In a world where technological advancements are reshaping our lives, the pursuit of longevity has become an increasingly prominent focus. Longevity medicine, with its promise of extending not just lifespan but healthspan, offers a revolutionary approach to wellness. This blog post delves into the core concepts of longevity medicine, addressing the current flaws in our healthcare model, exploring the distinction between healthspan and lifespan, and unveiling the hallmarks of aging. We’ll also discuss the concept of biological upgrades and our mission at the Institute for Human Optimization.

The Problem with Our Healthcare Model

Our current healthcare system is predominantly reactive, designed to treat illnesses rather than prevent them. This model often leads to the treatment of symptoms rather than addressing the root causes of diseases. The focus is on managing chronic conditions rather than promoting optimal health and preventing the onset of these conditions in the first place.

Longevity medicine challenges this paradigm by shifting the focus from disease treatment to health optimization. By leveraging cutting-edge technologies and scientific insights, longevity medicine aims to detect and address potential health issues before they become significant problems. This proactive approach can lead to improved overall health and well-being, thereby extending both lifespan and healthspan.

Healthspan vs. Lifespan

While the term “lifespan” refers to the total number of years an individual lives, “healthspan” is the period during which a person remains healthy and free from serious chronic diseases. Longevity medicine emphasizes the importance of healthspan, advocating for a life characterized by vitality and good health for as long as possible.

Extending lifespan without considering healthspan could result in more years of poor health and diminished quality of life. Therefore, the goal of longevity medicine is not merely to add years to life but to add life to years. This involves optimizing physical, mental, and emotional well-being to ensure a high quality of life throughout the aging process.

Hallmarks of Aging

To understand how to extend healthspan, it is crucial to comprehend the biological underpinnings of aging. Researchers have identified several “hallmarks of aging,” which are the fundamental processes that drive the aging process. These 12 hallmarks of aging include:

  1. Genomic Instability: Accumulation of DNA damage over time, leading to mutations.
  2. Telomere Attrition: Shortening of telomeres, which protect chromosome ends, resulting in cellular aging.
  3. Epigenetic Alterations: Changes in gene expression without altering the DNA sequence itself.
  4. Loss of Proteostasis: Decline in the ability to maintain protein integrity and function.
  5. Deregulated Nutrient Sensing: Disruption in the body’s ability to manage energy and nutrient levels.
  6. Mitochondrial Dysfunction: Impaired function of mitochondria, the energy-producing components of cells.
  7. Cellular Senescence: Accumulation of aged cells that no longer divide or function properly.
  8. Stem Cell Exhaustion: Decline in the regenerative capacity of stem cells.
  9. Altered Intercellular Communication: Disruption in the signals between cells, leading to chronic inflammation and other issues.
  10. Microbiome Dysbiosis: Imbalance in the gut microbiome, affecting overall health.
  11. Compromised Autophagy: Reduced efficiency in the body’s ability to remove damaged cells and regenerate new ones.
  12. Chronic Inflammation: Persistent inflammation contributing to various diseases and degenerative conditions.

Understanding these hallmarks allows scientists and clinicians to develop targeted interventions that address the root causes of aging.

Data Driven, Proactive, Personalized Healthcare

At the heart of longevity medicine lies the power of data. By harnessing vast amounts of information from genetic profiles, biomarkers, and lifestyle factors, healthcare professionals can gain a comprehensive understanding of an individual’s unique needs. Advanced analytics and artificial intelligence are employed to interpret this data, identifying trends and potential risks long before they manifest as clinical symptoms. This proactive stance enables early intervention strategies that can prevent or mitigate health issues, ultimately promoting a longer and healthier life.

Personalization is another cornerstone of longevity medicine. Unlike the traditional one-size-fits-all approach, personalized healthcare tailors interventions to an individual’s specific genetic and phenotypic characteristics. This bespoke method ensures that treatments and preventive measures are not only effective but also aligned with the patient’s lifestyle and preferences. Personalized nutrition plans, exercise regimens, and medication protocols can significantly enhance outcomes by addressing the unique drivers of aging in each person.

The integration of continuous monitoring technologies, such as wearable devices and at-home testing kits, further enhances the personalized approach. These tools provide real-time data on a range of health metrics, from blood glucose levels to sleep patterns, allowing for dynamic adjustments to health plans and fostering a proactive rather than reactive stance to healthcare.

Biological Upgrades: Pioneering the Future of Longevity

One of the most exciting frontiers in longevity medicine is the concept of biological upgrades. This transformative approach involves using advanced biotechnologies to enhance the body’s natural capabilities, thus improving resilience against aging and disease. Biological upgrades can take many forms, from gene editing techniques like CRISPR to regenerative medicine strategies that rejuvenate tissues and organs.

For instance, therapies that target telomere extension could potentially reverse cellular aging, leading to a decrease in age-related diseases and an increase in lifespan. Similarly, stem cell therapies offer the promise of regenerating damaged tissues, restoring function and vitality in aging bodies. Moreover, advancements in synthetic biology could enable the creation of novel proteins or even entirely new biological systems, designed to enhance human health in ways previously unimaginable.

These innovations not only hold the promise of extending healthspan and lifespan but also challenge us to rethink the very nature of human biology and aging. As we move forward, ethical considerations, accessibility, and equitable distribution will be crucial to ensure that these powerful technologies benefit all of humanity.

OUR MISSION at the Institute for Human Optimization

At the Institute for Human Optimization, a premier longevity and health optimization center located in Maryland, our mission revolves around harnessing the power of longevity medicine to create transformative health outcomes. We are committed to advancing the science of human longevity through innovative research, cutting-edge technologies, and individualized treatments. Founded by Anil Bajnath, MD focusing on prevention, early detection, and personalized interventions, we aim to redefine what it means to age.

Our interdisciplinary team of experts collaborates across various fields, including genetics, biochemistry, nutrition, and regenerative medicine. Together, we strive to uncover the most effective strategies for extending healthspan and enhancing quality of life. We believe in empowering individuals with the knowledge and tools to take control of their health, promoting a proactive and preventive approach to wellness.

Whether it’s through our advanced diagnostic services, bespoke wellness programs, or state-of-the-art therapeutic interventions, we are dedicated to pushing the boundaries of what’s possible in human health. At the Institute for Human Optimization, we envision a future where aging is not a passive decline but an active, enriching journey marked by vitality and well-being.

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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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]


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.


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.





Disclaimer: The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Additionally, the information provided in this blog, including but not limited to, text, graphics, images, and other material contained on this website, or in any linked materials, including but not limited to, text, graphics, images are not intended and should not be construed as medical advice and are for informational purposes only and should not be construed as medical advice. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Before taking any medications, over-the-counter drugs, supplements or herbs, consult a physician for a thorough evaluation. Always seek the advice of your physician or other qualified health care provider with any questions you may have regarding a medical condition or treatment and before undertaking a new health care regimen, and never disregard professional medical advice or delay in seeking it because of something you have read on this or any website.

Maryland Functional Medicine 

Maryland Functional Physician

Maryland Functional Doctor

Mitophagy is a process that occurs in cells, and it’s essentially the destruction of old or dysfunctional mitochondria. It’s important to know about mitophagy because as we age, our bodies lose their ability to carry out this process properly. When mitophagy does not occur properly it can lead to mitochondrial disease which has been linked to neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease. This blog post will provide an overview of what mitophagy is and why it matters.

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The word ‘mitophagy’ was coined in 2007 by the researchers who discovered this process. The prefix mit- means thread and phage means eat, so we define mitophagy as the destruction of mitochondria via a cellular mechanism called autophagy. Autophagy is a process that involves the degradation and recycling of cellular components. Mitophagy is the selective kind of autophagy mechanism that removes mitochondria.  A cell can digest its own organelles through this process, but it will only remove damaged structures and not healthy structures. This selective quality is what makes mitophagy so unique because most other forms of autophagy just degrade cellular components indiscriminately.

There are two other forms of autophagy: chaperone-mediated autophagy and micropexophagy. [i]

  1. Chaperone-mediated autophagy is a process that degrades damaged proteins and this type of degradation occurs in the lysosome or sac like structure.
  2. Micropexophagy on the other hand targets  mitochondria for degradation.


The mitochondria is an organelle that is responsible for converting energy into a form of molecules that our cells can use.[ii] Inside the mitochondria are enzymes called electron transport chains (ETCs) which take electrons and try to pair them with hydrogen atoms to produce chemical energy. This process also creates free radicals as by products, so our cells must have an enzyme called superoxide. Superoxide dismutase (SOD) eliminates superoxides and turns them into hydrogen peroxide. Hydrogen peroxide (H2O2) is broken down by catalase and glutathione peroxidase into water and oxygen gas.

This cellular structure is responsible for helping generate ATP (Adenosine triphosphate) which stores energy in the form of phosphate bonds. Cells need ATP to get rid of excess calcium ions that build up due to metabolism, and also to open up calcium ion channels for muscle contraction. Severing of the mitochondria from the rest of a cell triggers apoptosis, which is a programmed form of cellular death. The lack of a link to other organelles and its proximity to calcium ions makes it susceptible to damage. Because of this susceptibility, cells have developed a mechanism which allows them to dispose of defective mitochondria.


Mitophagy is a type of autophagy and there are three steps that must occur for this mechanism to carry out successfully:[iii]

1. The first step is the creation of an isolation membrane which surrounds the mitochondria, so the rest of the cellular components aren’t degraded.

2. The isolation membrane which elicits the form of selective degradation known as mitophagy is created by a multi-protein complex called PINK1 and Parkin.

3. The last step involves the elimination of the mitochondrion through fusion with lysosomes (the cellular structure responsible for degrading other organelles) via a double membrane structure called an autophagosome.


There are two types of mitophagy that exist: Macro-autophagy and Micro-autophagy.

Macroautophagy begins with the formation of an isolation membrane around the mitochondria from a multi-protein complex composed of several proteins such as Nix, Parkin, AIFm2 and FUNDC1.

This isolation membrane then fuses with a lysosome which creates an autophagosome. The autophagosomes carry the mitochondria to the cytoplasm for degradation into amino acids, fatty acids, and nucleotides.

Microautophagy is a process that creates a small isolation membrane around the mitochondria from a single protein called Ulk1. This process is often used in response to stress, but there hasn’t been direct evidence of this process occurring in mammalian cells.


A protein complex called PINK1-Parkin is believed to be the primary regulator of mitophagy.  This complex is required for creating the isolation membrane that leads to mitophagy.

PINK1 has been found to regulate this process by promoting mitochondrial fission, imparting an isolation membrane around the mitochondria, and recruiting Parkin which becomes phosphorylated in response. When PINK1 is degraded or loses function through mutations, it can lead to PINK1-associated Parkinson’s disease.

Parkin is also required for mitophagy, and it acts in a parallel pathway to that of the PINK1-Parkin complex by creating an isolation membrane around mitochondria through phosphorylation of proteins involved in fission which leads to the formation of an autophagosome.

This suggests that PINK1-Parkin play a major role in the regulation of mitophagy.


Mitophagy is often found to be defective in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease[iv]. This is because faulty mitochondria are not properly eliminated, leading to cellular damage.

Since mitophagy is important in neuronal function, it follows that this process would be affected in cancer disorders. Cancer cells often have uncontrolled mitochondrial biogenesis, and this leads to extreme energy demands in cancerous cells which can be exploited. Mitochondrial biogenesis refers to the creation of new mitochondria from the division of existing ones.[v] This process is regulated by a protein complex that includes PGC1α and NRF1, which are often over-activated in tumor cells.

Cancer cells also need the ability to oxygenate themselves, so putting selective pressure on these cells through drugs that inhibit mitochondrial function can lead to their death. Inhibiting mitophagy could potentially decrease the effectiveness of such chemotherapy treatments, however research has shown that some chemotherapy drugs stimulate mitophagy so it may still have some use.

In addition, mitophagy is important for cardiovascular function and the development of stem cells. Mitochondrial biogenesis is a crucial process for stem cell formation and differentiation into progenitor cells. Mitophagy also ensures that damaged mitochondria are eliminated in cardiovascular cells.

Mitophagy is important to our longevity and healthspan because it allows the removal of faulty mitochondria that could potentially lead to cell death. Cell death leads to the death of the organism, so this process is critical for cellular health. Maintaining optimal cellular health is a key component in healthy aging, and efficient mitophagy is necessary for elimination of damaged mitochondria. We would love to see you next week on another blog post – Tune in then!

Disclaimer: The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Additionally, the information provided in this blog, including but not limited to, text, graphics, images, and other material contained on this website, or in any linked materials, including but not limited to, text, graphics, images are not intended and should not be construed as medical advice and are for informational purposes only and should not be construed as medical advice. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Before taking any medications, over-the-counter drugs, supplements or herbs, consult a physician for a thorough evaluation. Always seek the advice of your physician or other qualified health care provider with any questions you may have regarding a medical condition or treatment and before undertaking a new health care regimen, and never disregard professional medical advice or delay in seeking it because of something you have read on this or any website.






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.


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.


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.  


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.



With many major diseases linked to chronic inflammation, persistent inflammation is our enemy. What is the answer? It is not found in our medicine cabinet or the pharmacy. The best way to reduce inflammation can be found in our refrigerator through proper nutrition. But what is inflammation? Could you benefit from promoting an anti-inflammatory diet? 

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What is Inflammation

There are five cardinal signs of inflammation. One of the greatest medical writers, Aulus Cornelius Celsus described the first four of the main signs of inflammation as redness, heat, swelling, and pain. The fifth sign was later identified by Galen as a disturbance of function. Inflammation refers to the body’s immune system response to e.g., a foreign pathogen, injury, or infection. Our body’s inflammatory response is a remarkable protective part of our immune system. If you fall and scrape your skin, your immune system will release an army of white blood cells to immerse and protect the area which results in the visible redness and swelling commonly seen after an injury. When you have a cold the symptoms you experience such as a scratchy throat, sneezing, runny nose, are all by-products of inflammation as our body’s immune cell signaling to destroy virus particles. If you have ever experience green mucus, that is caused by myeloperoxidase, a green-colored protein that is found in infection-fighting white blood cells. It becomes green due to the white blood cell numbers increasing while you are sick (white blood cells are low in the early stages of inflammation) and therefore the amount of green myeloperoxidase increases ultimately changing the color of mucus.  So how can inflammation be bad?

Acute vs Chronic

Acute inflammation is obvious as it is a brief inflammatory response. Chronic inflammation on the other hand is another story that can lead to adverse health consequences. Simply put, your body is not designed to live in a state of chronic inflammation. When your body is in a chronic state of inflammation, your body is constantly under attack with your immune system on overdrive. This means that white blood cells that would go to an injured or infected area, may end up attacking healthy tissues and organs.

How so? Let’s say you carry visceral fat, which is the type of fat that is stored within the abdominal cavity near vital organs like the liver, stomach, intestines. This type of fat is considered “active” fat because it can actively increase your individual risk of disease. Visceral fat is a known link to metabolic disorders and inflammation. If you suffer from chronic inflammation, your white blood cells may perceive those visceral fat cells as a threat and begin to attack them. 

Prolonged State of Inflammation 

While inflammation is your body’s first line of defense, being in a prolonged state of inflammation can cause lasting damage. Let’s look at how inflammation plays a role in disease:

Alzheimer’s Disease: Anyone who has had a loved one with Alzheimer’s knows how terrible this disease is. Alzheimer’s disease is a progressive neurodegenerative disorder that destroys memory and affects many essential mental functions. While the exact answer is still unknown, Alzheimer’s is thought to be a result of an abnormal buildup of the proteins in and around brain cells specifically, the proteins called amyloid and tau. With many neurodegenerative disorders, chronic inflammation is a known core characteristic. Over the last decade, there have been studies show inflammation as a central mechanism in Alzheimer’s disease. Recent literature shows how inflammation accelerates Alzheimer’s disease pathologies as it exacerbates both amyloid and tau pathologies. 

Heart Attacks & Strokes: When we look at heart attacks and strokes, atherosclerosis is usually the culprit. Atherosclerosis refers to a build-up of cholesterol-rich plaque inside arteries. Recent research from Harvard recognized that chronic inflammation sparks atherosclerosis. When cholesterol-rich plaque inside arteries causes inflammatory cells to cover and obstruct flowing blood, this results in blood clots that obstruct blood flow to the heart or brain. An artery to the heart that is blocked results in a heart attack. A blocked artery in or leading to the brain results in an ischemic stroke. 

Rheumatoid Arthritis (RA): RA is a chronic inflammatory disorder that usually begins by causing pain in the joints of your hands and feet. This occurs because your body is in a state of chronic inflammation and mistakes your e.g., joints for a threat.

Type 2 Diabetes: Diabetes is a complex multifaceted metabolic disorder that results in your blood glucose or blood sugar levels being too high. In type 2 diabetes, your body does not produce enough or insulin or cannot use the insulin it is producing effectively. It is common knowledge that obesity and inactivity are positively associated with the development of type 2 diabetes. Obesity and inactivity are also positively linked to chronic inflammation. Researchers have shown how an inflammatory state alters insulin’s action and drives the development of type 2 diabetes. The role of inflammation has generated interest to improve clinical outcomes with the control of the disease. Recent studies show how inflammation is linked to diabetes and targeting inflammatory pathways may prevent type 2 diabetes.

Is your lifestyle contributing to your inflammation?

Certain habitual lifestyle choices promote inflammation. For example, if you are not getting regular quality sleep, you may be contributing to inflammation. Sleep and our immune system are regulated by circadian rhythms. When we are not getting adequate sleep, we disrupt our circadian rhythm and subsequently, our immune system. Inactivity is also associated with a weakened immune system and inflammation. In a recent Harvard study, they show a molecular connection between exercise and inflammation. In this study, they put one group of laboratory mice with treadmills which resulted in mice running as much as six miles a night.  The second group of mice had no treadmills. At the end of the 6-week study, the mice in the group with the treadmills had substantially lower HSPC activity and level of inflammatory leukocytes than the group of sedentary mice. 

In a recent blog article, we discussed the role of vegetable oils and how they can contribute to inflammation.  A recent research study shows meal-induced inflammation plays role in chronic inflammation. Meal-induced inflammation is more common than we think due to the American diet being filled with ultra-processed foods. Processing is what changes food from its organic state. Ultra-processed foods are foods made with several industrial processes and ingredients that result in food being nothing like the original food (think strawberry cupcakes vs strawberries).  In general, ultra-processed foods are high in calories, fat, sugar, salt, and additives with little to no nutrients. What are some examples of inflammatory foods? Hint: They are the foods that we know to avoid regularly.

Examples of Inflammatory Foods:

  • Fried Foods
  • Soda 
  • Some Red Meat –Not all red meat is the same. It is important to look at how you eat red meat, the quality, and the quantity. 
  • Processed Meats – such as Hot Dogs, Sausage
  • Trans fats (partially hydrogenated oils) 
  • Added sugars
  • Refined carbohydrates
  • Vegetable Oils
  • Margarine
  • Alcohol

While foods can be inflammatory, there are so many food options that are anti-inflammatory, nutrient-dense, high quality, and delicious. Some great anti-inflammatory food options include:

  • Berries
  • Dark Leafy Greens
  • Nuts
  • Extra Virgin Olive Oil
  • Chia Seeds
  • Ground Flax Seeds
  • Omega 3-Fatty Fish such as Wild Caught Salmon
  • Cruciferous Vegetables
  • Avocados
  • Peppers
  • Mushrooms

Chronic Inflammation is something you can see and feel but can be hard to detect clinically.  Our best offense towards chronic inflammation is an anti-inflammatory lifestyle. Your comprehensive dietary patterns and lifestyle can promote longevity or an inflammatory response among many other undesirable health outcomes. In fact, the lifestyle factors Physicians warn against such as stress, sleep deprivation, inactivity, poor diet, smoking, are ALL contributory to inflammation. At the Institute for Human Optimization, we use food sensitivity testing and/or assess inflammatory markers to create a personalized approach to reduce inflammation as needed.

When you are young, your brain has 100 billion brand-new cells called neurons, and they help your brain hum like a well-oiled machine. But as you get older, things start to change.

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Aging is the number one risk factor for chronic disease. Buck Institute asserts that maintaining cognitive function is the key to living better longer.

It is estimated that 45 million of currently living Americans will develop Alzheimer’s disease. One in three people will develop memory problems so severe they may die prematurely. Unfortunately, despite the billions spent every year on drug development, pharmaceutical companies have no drug that can cure severe memory loss at this time.

How the brain ages

A study published in Archives of General Psychiatry concluded that the minor memory lapses we have been told to accept as ‘normal’ age-related memory loss are actually signs of early-stage cognitive decline. Lifestyle factors such as lack of physical activity, excessive consumption of sugar, and stress can even accelerate this decline.

Typically after the age of 40, a certain protein called amyloid beta starts to accumulate in your brain. It forms into plaques that cause inflammation and damage your neurons from the inside. Some researchers have shown that this is a mechanism in the body to protect the brain from the effects of nutrient deficiency, chronic inflammation, and excessive toxin buildup, among other things. Yet there is general agreement that although this is this case, it still contributes to clinical cognitive impairment.

Another consequence of aging in the brain is oxidative stress. Your brain weighs only 2% of your body weight, but it uses 20% of your body’s oxygen, and oxygen is the primary catalyst of oxidation. Your brain also contains high levels of iron and copper, making it extremely vulnerable to oxidative damage. This slowly erodes your memory and makes you lose mental sharpness. Symptoms like forgetfulness, trouble concentrating, and brain fog have all been linked to oxidative stress.

Some say the main cause of oxidative stress is the consumption of refined carbohydrates from processed foods, like white bread, muffins, doughnuts, cakes, and so on. According to a study published in the journal, Behavioral Neuroscience, even otherwise healthy young people who ate lots of refined carbohydrates had impaired memory. Another study looked at folks over 65 and similarly found that the more refined carbohydrates were consumed, the worse their memory was.

An additional contributor to the aging brain is when your brain cells can’t communicate with each other, which threatens the brains of 95% of people over 50. Your memory neurons can’t just work by themselves – they have to be connected to other neurons, and it’s those connections that make your memory work.

One very important chemical your brain needs for these neuronal connections to work is acetylcholine (uh-seet-l-koh-leen). It acts as a communication line between your neurons and you need it to form new memories. If your brain is low on acetylcholine, your neurons can’t talk to each other, which means your memory recall will slow down, you’ll become forgetful, and lose the ability to focus. A study done at King’s College in London found that a lack of acetylcholine leads to severe age-related memory loss.

A cause for hope

Your brain has the ability to grow new neurons, which is a process called neurogenesis. Nerve growth factor (NGF) is one of a group of small protein-like molecules called neurotrophins that are responsible for neurogenesis. NGF acts like a protective bodyguard for all these new brain cells, as well as the ones you already have. Researchers at Johns Hopkins University found that NGF halts the breakdown and death of your brain cells as you age!

To help support this process in the body, I’ve developed a state-of-the-art cognitive supplement perfect for anyone looking to enjoy crystal clear thinking, rapid memory, and a clear memory that won’t let them down.

Puromind provides you with the nutrients you need to maintain healthy, sharp, lifelong cognitive health. You will find an improved ability to recall the things most important to you, enjoy a heightened sense of well-being and peace of mind, and benefit from your mind operating better than it ever has. If you want to learn a new language, have a sharper wit, or simply want to stop dealing with those annoying ‘senior’ moments that interrupt your life, Puromind can give your brain the fuel it needs to function at 100%.

We manufacture each premium batch in an FDA-compliant, GMP-certified facility right here in the USA, and every bottle is tested for both purity and potency, so you can know that you are putting only the most nutritious, beneficial ingredients into your body. Puromind is crafted with the following five powerful, brain-boosting nutrients:

·         LION’S MANE MUSHROOM: Lion’s mane mushroom supports the production of NGF, the fuel your brain needs to build new neurons. Researchers have found that Lion’s Mane mushroom is the only proven stimulant of nerve growth factor that Mother Earth gives us. In one Japanese study, researchers discovered that lion’s mane mushroom could replenish natural NGF levels, and it’s been shown to significantly improve the cognitive function of patients in just four months! In 2019, doctors and researchers at Johns Hopkins University reviewed eight different studies and three clinical trials. At the end of the review, they wrote that Lion’s Mane ‘may have a beneficial effect on cognitive impairment.’ There was also a clinical trial at Tohoku University in Japan, where researchers found that the group of people who received lion’s mane mushroom ‘showed significantly increased scores on the cognitive function scale compared with the placebo group,’ and had no side effects!

·       BACOPA MONNIERI: Bacopa can help extinguish the oxidative damage that is damaging your neurons. An animal study published in the journal, Phytotherapy Research showed that bacopa both crosses the blood-brain barrier and has powerful antioxidant effects. When you clean the inflammation out of your neurons, it’s like you’re peeling away the curtain that’s been holding your brain back for all these years. Researchers in Thailand took 60 volunteers around 62 years of age and gave one group bacopa monnieri and the second group a placebo. At the end of the trial, the group who took 300mg of bacopa extract scored 20% better in working memory tests and their attention improved 33%! In yet another study published in the journal, Neuropsychopharmacology, researchers revealed that of the 76 adults aged between 40 and 65 involved in the study, the group that received 300 mg of bacopa daily had improved their memory recall and retention by 100%!

·         ALPHA-GPC:  Together with huperzine A (see below), alpha-glycerophosphocholine (alpha-GPC) works to boost levels of acetylcholine and help your brain cells communicate with each other. A study at Sapienza University in Italy showed it has a unique ability to cross the blood-brain barrier and directly raise acetylcholine levels, which protects your memory and gives you laser-sharp mental focus. A study published in the journal, Clinical Therapeutics, found that patients who supplemented with alpha-GPC experienced a dramatic improvement in their memory and ability to perform cognitive tasks.

·         HUPERZINE A: Acetylcholine is easily broken down by your body, so adding more of it is only the first step. The second step is making sure it remains in your brain to do its job. That’s where huperzine (hoop-ur-zeen) A comes in. Huperzine A is extracted from Chinese club moss. It protects acetylcholine from being broken down by your body and can help you maintain healthy acetylcholine levels. A clinical trial performed at the Traditional Chinese Medicine Epicenter in Shanghai separated older patients with severe memory loss into two groups. All patients were given memory tests after one group was given a placebo, and another huperzine A. At the end of the trial, 58% of patients who took Huperzine A showed 36% memory improvements compared to placebo! And when you combine Huperzine A with alpha-GPC, you get a powerful combination that can both help increase acetylcholine levels and prolong its memory-boosting benefits.

·         GINKGO BILOBA: Ginkgo biloba is sometimes referred to as a ‘living fossil’ because it is the last surviving member of an ancient type of plant. It boosts cerebral blood flow and makes it easier for your brain to absorb Puromind’s other ingredients, magnifying their powerful effects and delivering maximum cognitive support potential. Clinical studies also show that ginkgo is able to dramatically boost blood flow to your brain and the rest of your body almost immediately after taking it. For you, that means lightning-fast thinking and quicker memory recall.

These statements have not been evaluated by the FDA. Puromind is not intended to diagnose, treat, cure or prevent any disease.

How can The Institute for Human Optimization assist me?

At The Institute for Human Optimization, my team and I leverage the most cutting-edge advances in genetic testing, nutritional, and functional medicine to help our patients treat the root biological imbalances that cause aging. I 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.

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.

Let’s work together to make a long healthspan your reality!