February 2021

Biohacking, BLOG, Health Optimization, Human Optimization

TELOMERE ATTRITION – The Wear and Tear of Our Chromosomal Guardians

We have a sophisticated and specialized part of our DNA that protects all of the genetic information in our cells. Let’s take a look at how the break-down of these important complexes contributes to the acceleration of aging.

. . .

I’ve said it before, and I’ll say it again: Age is the number one independent risk factor for all chronic diseases. The biological definition of aging is the many processes of cellular damage accumulation in the body and these are known in the scientific literature as the Nine Hallmarks of Aging. I’ve also talked about how the first four hallmarks are considered primary since they are believed to be actual causes of aging and have a definitively negative effect on DNA.

We talked about the first hallmark of aging, genomic instability, in our last blog. This week, we will look at the second hallmark of aging: telomere attrition. In order to understand what this particular process of aging means, we must again revisit high school biology.

The rungs on the twisted ladder

Our DNA is made up of smaller units called nucleotide bases. There are 4 bases: adenine (A), guanine (G), thymine (T), and cytosine (C). Each of these bases forms a pair that shows the iconic visual of rungs on a twisted ladder. Adenine forms a base pair with thymine, and cytosine forms a pair with guanine. These base pairs spell out a letter code that allows the DNA to function in different ways in our bodies.

Remember that our DNA carries our genetic blueprint or instructions in the form of genes. Our DNA is tightly woven around protein to structure our chromosomes, which are found in the nucleus, or control center, of our cells.

Now picture the rungs of base pairs on that twisted ladder – there are millions of them. The middle section of rungs is made up of long stretches of our genes. The last few thousand rungs on ends of that twisted DNA ladder are called telomeres. They are repetitive, short sequences of non-coding nucleotide bases, bound by a special protein called shelterin. They protect the ends of our DNA, and thus our genetic information, in the same way, that the aglets, or plastic tips, on our shoelaces keep them from fraying.

This is extremely important as we age and our cells divide to produce new cells to replace those that are old and worn-out. Telomeres allow our cells to divide, and thus our DNA to replicate, without harming our genetic information. They do this by preventing the ends of chromosomes from fusing together, which would cause considerable genomic instability.

Telomeres do this with the help of the aforementioned protein called shelterin, which masks the ends of the chromosomes and suppresses the signaling process in the body that cleans up damaged DNA. The enzyme telomerase also helps to replenish the repetitive telomere sequences during each cell cycle.

Good things don’t last forever

This amazing protective mechanism in the body sadly does not last forever. In my book, The Longevity Equation, I point out that, “Our natural DNA replication mechanisms do not duplicate all of the telomeres when each cell divides, so each chromosome has fewer telomeres. Once the telomeres run out, you hit what’s called a cell growth arrest. This means you are limited to how much new tissue you can regenerate as you age.” Some say that telomeres are the molecular clock that stops cell division.

Each time a cell divides, 25-200 bases are lost from the ends of the telomeres on each chromosome. As telomeres start to fray and become shorter, they start to resemble broken DNA and become more likely to be targeted by a process called DNA damage response (DDR), which ultimately leads to cell death. Shorter telomeres are associated with most diseases of aging in humans.

Maintenance requirements

Telomerase is an enzyme that adds DNA to the ends of chromosomes, which helps maintain chromosomal length. However, it is only found in low concentrations in somatic cells (any cells other than the reproductive cells) but in high concentrations of stem cells and germ cells (egg and sperm). For this reason, as we age, our telomeres reduce in normal function. Unfortunately, telomerase is also found in high levels in cancer cells, which enables these cells to divide indefinitely.

What all of this means is that we need to have enough telomerase activity to keep our cells healthy and prevent them from degrading prematurely, but not so much that it contributes to the growth of cancer cells. So in a word: moderation.

If our cells are exposed to stress or injury – such as hormonal stress, inflammatory stress, and oxidative stress – they will be forced to divide more frequently, and consequently, our telomeres will shorten more quickly. The end result: accelerated aging.

Some easy ways we can maintain our telomere length, and possibly extend them:

· Regular, moderate exercise

· Stress reduction

· Healthy diet

· Weight loss

· Smoking cessation

Let us provide you with guidance

Since telomeres are essential in cellular functioning, they continue to be actively researched as a therapeutic intervention in nearly every known disease state. They are considered a biomarker of aging, and thus we have the ability to test and measure telomeres directly. However, because of their direct and significant role in genomic instability, we suggest another way of looking at the current state of your DNA.

My best-selling book, The Longevity Equation, provides a step-by-step blueprint to hack your genes, optimize your health and master the art of existence. In my book, I take an in-depth look at aging, explore what it means to extend your healthspan, and outline the pathways and factors that lead to a lifelong solution to the burdens of aging.

In collaboration with TruDiagnostic™, I have developed The Longevity Equation Epigenetic Consult. We are offering a revolutionary new way to access your health using an epigenetic test called TruAge™. This test will help tell you what your body is actually doing right now and what that means.

TruAge™ works by using mathematical models and a powerful algorithm to measure DNA methylation-based biomarkers. Methylation is what modifies the function of the genes in the body by adding what’s called a methyl group to DNA, which is what signals genes to turn on or off. DNA methylation is the best indicator of age-related changes and is the best-studied biomarker of age. This comprehensive testing method determines your epigenetic, or biological age, and can detect the acceleration of aging before the signs of aging even begin to appear.

The Longevity Equation Epigenetic Consult is intended to give you a snapshot of your biological age, as well as the lifestyle and environmental shifts you can make right away to start adding vitality and wellness into your life. Click here to schedule your consult!

More about The Institute for Human Optimization

The Institute for Human Optimization is committed to helping you create a personalized plan for living your longest, healthiest life possible. My team and I leverage the most cutting-edge advances in genetic testing, nutritional analysis, and functional medicine to get to the root biological imbalances that cause aging.

The Institute for Human Optimization was created with the intention of pursuing a highly personalized approach to longevity medicine to help enhance healthspan. Where lifespan is the actual number of years we’re alive, healthspan is how many of those years are spent in health and wellness.

We believe that a long healthspan – not just a long lifespan – is the most important thing you can cultivate. A long healthspan means you don’t miss out on life as you get older. It means remaining independent and having the vitality to travel and see the world. A long healthspan means that you can be there – in full body and mind – for the people who need you the most and that every day will feel like a gift.

We know that each person is truly unique. From DNA to iris, we all possess a blueprint that is genetically inherited and environmentally influenced. By gaining a deeper appreciation for the person on a molecular level and addressing the root causes driving disease, we can help promote optimized health through our unique scientific, N of 1, approach to individualized care.

The Institute for Human Optimization provides the most comprehensive, data-driven, personalized approach to wellness. It is:

· Predictive – We use genomics and advanced biomarker testing to risk stratification and empowerment.

· Personalized – We use data-driven health information to curate actionable change for disease mitigation and prevention.

· Preventive – We utilize highly individualized programs tailored to your unique genomic blueprint.

· Participatory – We empower engagement in personal choices, which allows for improved outcomes and enhanced results.

I am so excited about the possibility to support you on this cutting-edge journey to extend your lifespan AND your healthspan. Click here to schedule Your Longevity Equation Epigenetic Consult! Can’t wait to meet you!

2021-02-25/0 Comments/by Anil Bajnath

Biohacking, BLOG, Health Optimization, Human Optimization

GENOMIC INSTABILITY – A Root Cause of Aging

We accumulate genetic damage throughout our lives. Let’s begin to understand how this happens, how our bodies are programmed to respond and repair the damage, and what to do when that goes awry.

. . .

Age is the number one independent risk factor for all chronic diseases. As stated in a previous blog, aging is the many processes of cellular damage accumulation in the body and these are known in the scientific literature as the Nine Hallmarks of Aging.

The first four hallmarks – genomic instability, telomere attrition, epigenetic alterations, and loss of proteostasis – are considered primary, since they are believed to be actual causes of aging and have a definite negative effect on DNA. They could be what firstly initiates cellular damage, which then leads to accumulation and progressive loss of function.

The next three hallmarks – deregulated nutrient-sensing, mitochondrial dysfunction, and cellular senescence – are called antagonistic, as they ultimately respond to the damage caused by the primary hallmarks. However, they are initially designed to have protective factors. It is only when bodily conditions become chronic and/or aggravated that they contribute to cellular damage.

The last two hallmarks – stem cell exhaustion and altered intercellular communication – are thought to be integrative hallmarks because they “directly affect tissue homeostasis and function.” These come into play once the accumulated damage caused by the primary and antagonistic hallmarks can no longer be stabilized. Once this happens, functional decline is inevitable.

Defining the genome

In this blog, we will look at the first hallmark, genomic instability. It is a root cause of aging, thus the reason it is categorized as one of the primary hallmarks of aging. But first, let’s go back to high school biology and take a look at what comprises the genome.

We’re all familiar with the visual of the double-helix structure that is DNA – the complete set of instructions that we are all born with. This very long DNA molecule is made up of smaller units called nucleotide bases – of which we have 3 billion! They vary ever-so-slightly in each of us, which makes us all unique!

Combinations of these DNA bases form our 20,000 to 25,000 genes, which contain all of the information needed to produce one or more proteins. Some genes determine our physical characteristics, and some can influence our susceptibility to certain conditions and illnesses.

Our DNA is tightly woven around proteins to make structures known as chromosomes. We inherit 23 pairs from our mother and father, and they are stored in the nucleus of our cells. Some DNA is also stored in the mitochondria, which is like a power generator for the cells. Collectively, this is known as our genome. There is one copy of our genome in nearly every cell of our body, and every one of those cells knows what their jobs are.

Damage control

Our cells are obsessive about keeping our DNA safe. However, the integrity and stability of our DNA can be exposed to damage by many sources on a daily basis. This happens endogenously via DNA replication errors, chemical processes that impair DNA, and oxidative stress due to unstable molecules called reactive oxygen species (ROS). The damage also happens exogenously via overexposure to ultraviolet light from the sun and x-rays, smoking, and excessive alcohol use, among other sources. All of these assaults lead to an unstable environment for the genome.

Our body’s response to DNA damage has evolved. Our cells have intricate and sophisticated systems, such as DNA repair and cell cycle checkpoints, that can reduce the harmful effects of DNA damage. Unfortunately, this repair process is not perfect, and once the damage starts to accumulate, the nucleotide bases of the DNA start to mutate. And if not caught by this repair process, the mutations are passed on and replicated to daughter cells, which leads to conditions such as cancer.

The good news is that even studies as recently as 2020 are illustrating the connection between genomic instability and aging. While they confirm and elaborate on what researchers have been finding for years, what is promising is that they show us that there is hope. By searching for underlying causes, we’re learning more about DNA repair as we age and how that might translate into future treatment.

Until then, I have an opportunity