hallmarks of aging Archives

OXIDATIVE STRESS: Deterioration of Our Cells

Oxidative stress is a term that refers to the deterioration of our cells and tissues due to an imbalance between the production of free radicals and antioxidants. Free radicals are highly reactive molecules with unpaired electrons, which can cause harm when they interact with other important molecules in our cells. Antioxidants, on the other hand, work by donating their extra electron to neutralize free radicals before they can do any damage. This balance between free radical production and antioxidant protection is essential for health because it has been shown that oxidative stress plays a role in many chronic diseases such as cancer, diabetes mellitus type 2, cardiovascular disease (CVD), Alzheimer’s Disease (AD) and Parkinson’s Disease (PD), and more. There are many risk factors for oxidative stress including genetics, diet, exercise habits and environmental pollution. In this blog post we will be discussing what oxidative stress is, how it affects our body, and more!

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WHAT IS OXIDATIVE STRESS?

Oxidative stress is a natural phenomenon that occurs through metabolic processes in the body. It’s made by the release of free radicals during the process of lipid peroxidation, which involves an enzyme called lipoxygenase producing ROS while breaking down fats under oxidative conditions.[i] In other words, oxidative stress occurs when the production of reactive oxygen species (ROS) exceeds the body’s ability to protect itself with antioxidants. Reactive oxygen species refers to oxygen molecules that have unpaired electrons, making them “reactive”. ROS is made when oxygen interacts with other compounds; this can be caused by many external factors such as air pollution or cigarette smoke. When the produced ROS exceeds the body’s protection (antioxidants), it causes the oxidation of important molecules like DNA, proteins, and lipids (fats). These ROS include free radicals such as superoxide anions, hydrogen peroxide, and hydroxyl radicals, which form during normal metabolic processes. Superoxide anions refer to the combination of two oxygen molecules to form a free radical. This compound lacks an electron and can damage different types of biomolecules such as DNA, proteins, and lipids through oxidation. Hydrogen peroxide is made when superoxide anions break apart and are known as the primary toxic molecule of ROS. Hydrogen peroxide can also damage DNA, proteins, and lipids by oxidizing them. The hydroxyl radical is formed when hydrogen peroxide reacts with the superoxide ion, producing highly reactive OH-radicals that break down cell membranes and tissues in the body.

The release of these free radicals increases when there is damage to mitochondria in our cells, which is crucial for producing energy. Mitochondria (the part of our cells that turns food into energy) has to work harder during oxidative stress and requires large amounts of antioxidants.[ii]

HOW DOES OXIDATIVE STRESS AFFECT OUR BODY?

Because oxidative stress involves the production of free radicals, it can damage many types of molecules in our cells such as lipids (fats) and DNA. This is important because cell membranes and DNA are largely made up of lipids and contain genetic information that tells our body how to function. A study found that when there is an imbalance between ROS and antioxidants, it can cause oxidative damage to lipids in our cells. This is important because lipids are the fatty molecules that form cell membranes and protect our cells from foreign objects. When lipid peroxidation occurs, free radicals attack the lipids in cell membranes damaging them. When the cell membrane becomes damaged, it increases permeability which allows molecules to leak into the cell causing further damage to proteins and other important molecules. Free radicals can also directly cause oxidative stress through DNA damage. [iii]This occurs when free radicals combine with oxygen in essential parts of our DNA such as the mitochondrial genome, which is crucial for producing energy within cells. The combination of these oxidative damages creates a domino effect throughout our body cells. Damage to DNA results in the inability of cells to divide properly, which leads to uncontrolled cell growth. This can cause tumors and cancerous tumor cells to form all over our bodies. Damages caused by oxidative stress on lipids (fats) is important because fats are part of the lipid bilayer that forms the outer membrane of every living cell. When the lipid bilayer is damaged by ROS it leads to improper functioning in cells throughout our body.

When our body is under oxidative stress, there’s an accumulation of free radicals in our cells which results in damages to molecules like lipids (fats) and DNA. This can cause many problems in different parts of the body including:

– Increased atherosclerosis, is where plaque build-ups form in arteries causing them to harden.

– Increased risk for developing cancer and tumors because of DNA damage caused by ROS.

– Damages to cell membranes that lead to improper functioning in cells throughout our body.

COMMON SOURCES OF OXIDATIVE STRESS

Oxidative stress can be caused by many factors including environmental pollutants such as cigarette smoke, ultraviolet (UV) radiation from the Sun, and chronic infections like hepatitis. There are several other common sources of oxidative stress including:

– Smoking tobacco

– Eating high-calorie meals that contain a lot of fat, which can lead to obesity and increase the risk for cardiovascular disease.

– Consuming caffeine or alcohol in excess, because these substances inhibit enzymes that produce antioxidants in our body.

– Consuming a poor diet which may lack the necessary vitamins and minerals needed to make antioxidants in our body.

– Living a sedentary lifestyle, because can lead to weight gain that results in cardiovascular disease.

– Exposure to pollutants, which can come from the workplace or even the local environment.

One of the biggest sources of oxidative stress is exposure to sunlight. [iv]UV radiation that comes from sunlight has many harmful effects on our body including skin cancer because it promotes free radical formation in our bodies. When we are exposed to UV radiation it causes oxidation reactions in the skin, which damage proteins like collagen. Collagen is what gives our skin its strength and elasticity. When it becomes damaged, these effects lead to wrinkles and sagging in our skin.

Oxidative stress is a term that refers to the deterioration of our cells and tissues due to an imbalance between the production of free radicals and antioxidants. But what does this have to do with longevity? Studies show that people who experience high levels of oxidative stress during their lifetimes may be at greater risk for developing dementia or other age-related diseases later on in life. There are many ways in which we can help reduce oxidative stress, such as with antioxidant rich foods. What are some easy ways you have increased your antioxidant intake lately? Share with us in the comments below or follow us on next week’s blog for more information related to oxidative stress and longevity.

[i] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551541/#:~:text=Oxidative%20stress%20is%20a%20phenomenon,to%20detoxify%20these%20reactive%20products.

[ii] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4145906/#:~:text=Oxidative%20stress%20is%20characterized%20by,homeostasis%20and%20mitochondrial%20defense%20systems.

[iii] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC484183/

[iv] https://pubmed.ncbi.nlm.nih.gov/29124687/#:~:text=The%20generation%20of%20reactive%20oxygen,mechanisms%2C%20oxidative%20stress%20can%20develop.

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Maryland Functional Medicine

Maryland Functional Physician

Maryland Functional Doctor

2021-12-01/0 Comments/by Anil Bajnath

Human Optimization

METABOLIC ENDOTOXEMIA

Metabolic endotoxemia is a condition that affects many people in America. In fact, recent studies estimate that over one-third of adults in the United States have this health issue. It’s been estimated that it may soon be indirectly a leading cause of death. Follow us on this week’s blog to learn what it is and how to prevent metabolic endotoxemia.

Metabolic Endotoxemia

Metabolic endotoxemia is the presence of too much LPS (lipopolysaccharides) in the blood. LPS are toxins that reside on the outer membrane of bacteria that would otherwise not be allowed into our bloodstream. The American Diabetes Association identified bacterial lipopolysaccharide (LPS) as the inflammatory factor causative of the onset of insulin resistance, obesity, and diabetes. LPS triggers a cascade of immune responses. For example, after binding to its receptor TLR4 (TLR4 is a receptor found on the surface of cells that can detect LPS) or CD 14, there is an elevated level of tumor necrosis factor-alpha (TNFα). TNFα is a protein signaling molecule that is an inflammatory mediator that triggers the innate immune response. The innate immune system, as its name implies, is a primitive type of immunity that all living organisms have. In contrast to the adaptive immune system (which is found in humans and other higher-order species), there are no actual distinguishing features between cells belonging to the innate system or adaptive immune system – they simply look different. TNFα activates more TLR4 which results in more TNFα. As you can see, it becomes a vicious cycle leading to chronic inflammation.

LPS also induces cytokine production by activating inflammatory transcription factors known as nuclear factor kappa B (NF-κB). NF-κB is a protein complex that controls the expression of genes involved in immunity and inflammation. Inducing cytokine production helps our bodies fight off infections. However, it also activates the immune response to clear away cells that are injured or damaged by short-term inflammation. If this clearing of dead cells occurs chronically, it can lead to tissue damage and autoimmune diseases where the body starts attacking its own healthy tissues.

DIET & METABOLIC ENDOTOXEMIA

Paracelsus, a Renaissance physician said: “All things are poison; everything is poisonous; there is nothing without poisonous qualities. Only the dose permits something not to be poisonous.”

The severity of this disorder depends on how much LPS enters circulation and how sensitive an individual’s body is to these inflammatory agents. As expected, diet and lifestyle are critical when it comes to metabolic endotoxemia and other diseases.

Inflammatory transcription factors are also activated in response to a high-fat diet rich in saturated fats and low in fruits and vegetables. Inflammatory transcription factors are transcription factors that contribute to the initiation, regulation, and mediation of inflammation.

Saturated fatty acids trigger macrophages to create a cascade of inflammatory signals. Saturated fats refer to a type of dietary fat with no double bonds between the carbon atoms. They are typically solid at room temperature and found in foods such as beef, pork, poultry, butterfat (in dairy products), palm kernel oil, lard (in meat products), and cocoa butter. Inflammatory foods have been linked to causing an inflammatory immune response that results in endotoxemia, which is the presence of bacterial endotoxin (LPS) in the bloodstream.

METABOLIC ENDOTOXEMIA AND DISEASE

The relationship between metabolic endotoxemia and the onset of diabetes, obesity, and heart disease is well established. Metabolic endotoxemia causes the body to have increased cortisol levels. This causes increased insulin resistance, which can contribute to type 2 diabetes. Metabolic endotoxemia causes the body to have increased cortisol levels. This causes increased insulin resistance, which can contribute to type 2 diabetes. In a healthy body, insulin resistance may be caused by high cortisol levels in response to stress. This insulin resistance is typically temporary as a protective mechanism for the body, but in most people who are insulin resistant, a high carbohydrate diet makes them even more insulin resistant. So, these individuals will typically crave carbohydrates when their blood sugar is low from the stress cortisol is causing on their bodies with elevated insulin resistance.

Metabolic endotoxemia causes an increase in persistent free radicals, which contributes to chronic inflammation and aging of the cells. An increase in persistent free radicals is not optimal as this can result in the accelerated development of chronic disease. Chronic inflammation is cause for concern because it is associated with elevated risks of cardiovascular disease, Alzheimer’s disease, cancer, and many other chronic diseases. Metabolic endotoxemia also causes oxidative stress. Oxidative stress refers to the process whereby free radicals in cells cause damage to molecules leading to tissue and organ dysfunction. The human body has both antioxidant and anti-inflammatory mechanisms in place that operate in a feedback loop, such as red blood cells, white blood cells, vitamins C and E, uric acid, nitric oxide synthase (NOS), and more. This feedback loop works by protecting the cells from oxidative damage and removing damaged cells. However, there are many variables that can break the loop using mechanisms called hormesis. Hormesis refers to acute stress that leads to a beneficial effect. For example, exercise causes the body to emit oxidizing free radicals because it requires large amounts of ATP (energy) for muscle contraction. Metabolic endotoxemia however is not a beneficial mechanism. It is the result of an overload of free fatty acids (FFAs), cytokines, and NOS-derived NO which cause circulating endotoxins to disrupt the host’s metabolism.

Additionally, oxidative stress decreases cellular DNA repair. Cellular DNA repair is critical to our overall health and well-being. As we have discussed in recent blogs, DNA repair is critical for maintaining metabolic homeostasis. Failure to maintain metabolic homeostasis due to DNA damage from oxidative stress can lead to obesity, insulin resistance, and even type 2 diabetes.

In addition to causing insulin resistance and oxidative stress, metabolic endotoxemia has been linked to dysfunction of the hypothalamic-pituitary-adrenal axis. Our HPA Axis is critical for maintaining metabolic homeostasis. Our HPA Axis is responsible for the release of cortisol, our main stress hormone. We often think of the HPA Axis as being involved in stress but it involves every organ system in the body and is critical for maintaining normal body functions, including inflammation. Recent studies have established that in vivo administration of bacterial lipopolysaccharide (LPS) enhances hypothalamic-pituitary-adrenal (HPA) axis function by a mechanism involving endotoxin-stimulated cytokine release.

IMPORTANCE OF DECREASING INFLAMMATORY ALLOSTATIC LOAD

Deceasing our allostatic load is a component of reaching our optimal health. Allostatic load refers to the wear and tear on the body through stress. Metabolic endotoxemia contributes to the reduction in our allostatic load. Meeting one’s optimal health includes having a healthy weight, healthy blood sugar levels, and low inflammation among many things. The decreasing allostatic load can be done by increasing physical activity and mindfulness, improving nutrition, reducing stress, maintaining social connections, and getting enough sleep. Decreasing the number of factors involved in the allostatic load will help decrease the overall inflammatory response.

Don’t know where to start? At the Institute for Human Optimization, we will work with you directly to optimize your well-being. No two patients are the same, so we work with you and create a personalized and individual approach to your health concerns. Contact us today to get started.

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References

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4695328/

https://diabetes.diabetesjournals.org/content/56/7/1761

https://pubmed.ncbi.nlm.nih.gov/14965237/

https://pubmed.ncbi.nlm.nih.gov/8892362/

2021-10-19/0 Comments/by Anil Bajnath

Biohacking, BLOG, Health Optimization, Human Optimization

ALTERED INTERCELLULAR COMMUNICATION – Where Inflammation Meets Aging

As we age, cells show an increase in self-preserving signals that result in damage elsewhere in the body. Altered intercellular communication contributes to symptoms and diseases that are associated with declining health.

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Today, we conclude our nine-part series on the Hallmarks of Aging. If you have followed along, you will find that each hallmark either directly or indirectly affects the other. (Start here if you’d like to start with the first hallmark.)

The first four hallmarks are considered primary since they are believed to be actual causes of aging and have a definitive negative effect on DNA. They are what first initiate cellular damage, which then leads to accumulation and progressive loss of function. They are:

· Genomic instability

· Telomere attrition

· Epigenetic alterations

· Loss of proteostasis

The next three 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. They are:

· Deregulated nutrient-sensing

· Mitochondrial dysfunction

· Cellular senescence

The last two hallmarks are thought to be integrative 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, the functional decline is inevitable. They are:

· Stem cell exhaustion

· Altered intercellular communication

This week, we will cover the final hallmark: altered intercellular communication. The primary and antagonistic hallmarks each contribute to the variety of breakdowns in communication within and around our cells, thus the reason for altered intercellular communication is identified as one of the two integrative hallmarks.

Communication is everything

Our cells process millions of signals every day. Scientists have spent entire careers discovering how different signals and intercellular pathways work. It’s that important. When communication gets disrupted, it can allow disease to set in, such as cancer cells growing out of control. In fact, most diseases involve at least one breakdown in cell communication.

How a cell gives and receives messages with its environment and with itself is critical to its survival. It processes information from the outside, such as changes in temperature, variation in light levels, and availability of nutrients. It also communicates with other cells via chemical and mechanical signals, which cause alterations in their function.

Protein receptors embedded in the cell membrane connect membrane signals that affect the inner chemistry of the cell. This allows the direct passage of molecules between the internal and external compartments of the cell. All of this translates into how our cells adapt and change based on our environment and what our bodies need. This includes functions from gene expression and glucose regulation to our overall development.

Inflammation and aging don’t mix

As we age, the signals that send chemical messages across our bodies tend to become more inflammatory. This inhibits our immune system and can cause muscle wasting, bone loss, and other detrimental effects. This gradual increase of systemic inflammation in the body as we age is called inflammaging.

This consistent growth in inflammation leads to cells increasingly activating a chemical in their nuclei that regulate inflammation. This protein complex, called NF-kB, is involved in responses to heavy metals, free radicals, bacterial and viral antigens, and even stress. When it is over-produced, it leads to damaging consequences and becomes a significant risk factor as we age.

Cellular senescence, one of the antagonistic hallmarks of aging, is one of the main factors contributing to inflammaging. Senescent cells are known to negatively affect neighboring cells because they release pro-inflammatory cytokines, growth factors, and proteases that affect the function of nearby cells and incite local inflammation. This is a concept known as the bystander effect.

Inflammaging also hinders our immune system’s ability to effectively clear pathogens and dysfunctional cells, such as those that turn into cancer. This is known as immunosenescence.

And as inflammatory reactions accumulate, neurohormonal signaling also becomes deregulated as we age. When NF-kB is activated in the hypothalamus, it has been shown to inhibit the production of gonadotropin-releasing hormone (GnRH). The reduction of this hormone can lead to skin degradation, muscle weakness, and bone fragility. It can also affect food intake and metabolism.

How to improve intercellular communication

Dietary/caloric restriction, mentioned in many of our blogs in this series, is one of the most studied ways to potentially restore, or at least improve communication between our cells as we age. As recently as February 2020, scientists in the US and China collaborated to study the cellular effects of a calorie-restricted diet.

“The primary discovery in the current study is that the increase in the inflammatory response during aging could be systematically repressed by caloric restriction,” says co-corresponding author Jing Qu, also a professor at the Chinese Academy of Sciences.

Including more foods that are known to reduce inflammation, such as green leafy vegetables, fatty fish, berries, and olive oil can help to reduce the effects that inflammaging has on our bodies as we age. “A healthy diet is beneficial not only for reducing the risk of chronic diseases, but also for improving mood and overall quality of life,” Dr. Frank Hu, professor of nutrition and epidemiology in the Department of Nutrition at the Harvard School of Public Health, says.

Additionally, since the gut microbiome is an integral part of our immune system, it appears possible to extend healthy aging and lifespan by focusing on the health of our intestinal bacterial ecosystem.

What else can I do?

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.

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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.

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

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2021-04-20/0 Comments/by Anil Bajnath

Human Optimization

CELLULAR SENESCENCE – When Cells Undermine Their Purpose

Our bodies have a built-in process that is believed to be a protective mechanism called cellular senescence. As we age, this process slows down and can result in disease.

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The biological definition of aging is the many processes of cellular damage accumulation in the body. These are known in the scientific literature as the Nine Hallmarks of Aging. We’ve covered the first four, or primary, hallmarks: genomic instability, telomere attrition, epigenetic alterations, and loss of proteostasis, as well as the first two of the antagonistic: deregulated nutrient-sensing, and mitochondrial dysfunction.

The role of the antagonistic hallmarks is to respond to and block the damage caused by the primary hallmarks. Yet, when bodily conditions become chronic and/or aggravated, they end up contributing to cellular damage and can accelerate aging. The seventh hallmark, and third of the antagonistic, is cellular senescence. Senescence plays roles in normal development, maintains tissue homeostasis, and limits tumor progression. If you’ve read any of my blogs in the past, you know this is one of my favorite topics.

The miracle that is us

It varies depending on the cell, but the division cycle of a typical human cell averages 24 hours, which is mind-blowing considering the complexity of what takes place.

Figure 1: The cell cycle Courtesy: National Human Genome Research Institute

Our cell cycle has four stages:

· G1 (gap 1) stage: where the cell prepares to divide. This is the longest phase, where the cell is metabolically active and continues to grow, but does not replicate its DNA.

· S (synthesis) stage: where the cell copies its entire DNA.

· G2 (gap 2) stage: where cell growth continues and it organizes and condenses the genetic material and prepares to divide.

· M (mitosis) stage: where the cell separates the two copies of chromosomes into two daughter cells. This is the most dramatic stage, ending in the cell division in a process called cytokinesis.

A fine line between helping and hurting

In my best-selling book, The Longevity Equation, I point out that, “When your cells have had more than enough DNA damage, stress, and telomere shortening, they enter a state of growth arrest known as cellular senescence. This function is put in place to prevent damaged cells from turning into cancerous cells. However, in the process, it also stops allowing worn-out tissue to be replenished and rebuilt. Senescent cells often secrete inflammatory molecules that further damage the cellular environment, leading to chronic inflammatory conditions, including heart disease and osteoarthritis.”

Cellular senescence inevitably halts the cell cycle during the G2 stage, as a result of excessive intracellular or extracellular stress or damage, such as oxidative stress, DNA damage, and telomere erosion, or when they overexpress certain oncogenes (have the potential to transform into a tumor cell). Once this process starts, it is irreversible.

Similar to the other antagonistic hallmarks of aging, this process is meant to prevent the proliferation of damaged cells and helps to suppress malignant cell formation. However, as time goes by, our bodies begin to accumulate these senescent cells, which leads to the deterioration of the tissue repair mechanism that usually accompanies senescence.

Crossing the threshold

When a cell enters senescence and it stops producing copies of itself, it excretes hundreds of proteins, which in moderation in healthy tissue, signal the immune system to initiate cellular housekeeping, called autophagy, and start the repair process.

However, when disease and aging cause extensive damage in the tissues, senescent cells build up and stay in a state of suspended animation – not alive, but not quite dead. Some scientists call these twilight cells, and others go for a more Hollywood description of zombie cells because they can negatively affect surrounding cells if not cleared efficiently by the immune system.

Again, from my book, The Longevity Equation, “Unlike other damaged cells, zombie cells don’t self-destruct or clear out of the way to make room for healthy cells. Instead, they stick around and interfere with the body’s natural rebuilding and replenishing mechanisms. . .”

Senescent cells cross the threshold from being protective to deleterious when their accumulation causes them to excrete an overabundance of molecules like pro-inflammatory cytokines, growth factors, and proteases that affect the function of nearby cells and incite local inflammation.

Can we clean up the excess?

While there is no magic bullet and research is still learning how to extend our lifespan and our healthspan, studies on cellular senescence are very promising and it seems as though therapies are on the horizon.

“That getting rid of senescent cells is enough to effectively rejuvenate an animal—that tells you they’re a really important driver of aging,” says Lorna Harries, a molecular geneticist at the University of Exeter in the UK who studies cell senescence.

What else can I do?

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.