In recent years, we have started to look at health from a different perspective. For a long time, the goal was clear: prevent disease and extend lifespan. However, this approach falls short when we try to understand what actually happens in the body over time.

The reality is more nuanced. A person may have no diagnosis and yet have already begun to lose part of their physical, metabolic, or cognitive capacity. This is not a sudden or obvious change, but a gradual process that often goes unnoticed for years.

Dr. Carlos Martí – Neolife Medical Team

It’s Not Just About Being Healthy, but Understanding How Your Body Functions

When we think about health, we usually reduce it to the absence of disease. However, this perspective does not reflect how the body truly evolves over time.

Each system in the body has a point of peak performance, typically reached in relatively early adulthood. From that point onward, a gradual decline begins—one that is not always immediately noticeable. This is not an abrupt change, but a progressive reduction in function that affects multiple levels: physical capacity, metabolic function, cognitive performance, and immune response.

In this context, the concept of Peakspan has been introduced. It refers to the period during which the body remains close to its maximum functional potential, typically within a range near that peak. It is not about how long we remain disease-free, but how long we can maintain a high level of functioning.

What is particularly relevant is that this period is much shorter than we intuitively assume. Although life expectancy has increased significantly, most physiological functions begin to move away from their optimal point decades before any disease or clear clinical limitations appear.

The Silent Decline: When the Change Really Begins

One of the most important insights is that loss of capacity does not coincide with the onset of disease. Between these two points, there is a long period during which the body is still clinically “healthy” but already functioning below its optimal level.

This decline begins earlier than we tend to think. Many functions reach their peak in the third decade of life and then gradually decline. Initially, this is not clearly perceived, but it manifests through subtle changes: reduced endurance, slower recovery after exertion, decreased adaptability to stress, or more frequent infections.

This leads to what can be described as a state of being “healthy but with reduced performance,” where no diagnosable pathology is present, yet there is a growing gap from maximum functional potential.

As a result, two individuals with similar lab results may be at very different stages of this process. One may still be functioning close to their peak, while the other has already moved significantly away from it—even though both are considered clinically healthy.

Understanding this decline as part of the process allows for earlier intervention. The goal is not to wait for abnormalities to appear, but to identify when capacity begins to decrease and how it evolves in each individual.

When the Body Really Starts to Change

When different physiological functions are analyzed separately, as described in recent research on Peakspan, a clear pattern emerges: there is no single starting point for aging, but multiple trajectories that begin earlier than we typically perceive.

In the cognitive domain, abilities related to processing speed and working memory peak between the ages of 20 and 30, and then begin to decline, while other skills linked to experience are maintained for longer.

At the cardiorespiratory level, aerobic capacity and lung function reach their peak in the second or third decade, followed by a gradual decline. Similarly, muscle strength and mass peak between the ages of 20 and 35, with a period of stability before a more noticeable decline begins.

Other systems also show early changes. Kidney function begins to decline as early as the third decade, the endocrine system experiences gradual hormonal decreases from mid-adulthood, and the immune system shows reduced responsiveness from early adulthood.

Sensory and digestive systems follow a similar pattern, with changes appearing earlier than expected, such as high-frequency hearing loss or alterations in gastrointestinal motility and liver function from midlife onwards.

Overall, functional aging is an early and non-uniform process, in which different systems move away from their optimal state long before diseases or evident limitations appear.

Maintaining Capacity for as Long as Possible

This shift in perspective requires redefining what we mean by prevention. It is not only about avoiding disease, but about intervening in the functional trajectory before the decline becomes established.

The value of the Peakspan concept lies not only in describing the problem, but in identifying the point where there is the greatest opportunity for intervention: when function begins to move away from its near-optimal range. Acting at this stage allows us to modify the rate of decline and extend the period during which different systems maintain high performance.

This approach requires a more precise assessment, focused not only on isolated parameters but on the integration of functional, metabolic, and structural data to understand where each patient stands. The combination of biomarkers, functional testing, and lifestyle assessment provides a more complete view of this trajectory.

At Neolife, this model is part of daily clinical practice. Evaluation is aimed at early identification of which systems have begun to lose efficiency, followed by targeted interventions on the underlying mechanisms. This includes addressing cardiorespiratory capacity, muscle mass, metabolic balance, hormonal function, and sleep quality—all key determinants of functional capacity over time.

The goal is not only to delay the onset of disease, but to sustain the highest possible level of functioning for longer. This is the true paradigm shift in longevity medicine.

BIBLIOGRAPHY

(1) Zhavoronkov A, Ying K, Wilczok D. Peakspan: Defining, Quantifying and Extending the Boundaries of Peak Productive Lifespan. Aging Dis. 2026 Feb 25. doi: 10.14336/AD.2026.0080. Epub ahead of print. PMID: 41747171.

(2) López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: An expanding universe. Cell. 2023 Jan 19;186(2):243-278. doi: 10.1016/j.cell.2022.11.001. Epub 2023 Jan 3. PMID: 36599349.

La entrada It’s Not Just About Living Longer, but Living Longer in Your Best Version se publicó primero en Neolife.

Pulse wave velocity (PWV) is now the most accurate tool for the early detection of arterial aging and for understanding when hypertension truly begins—even when office blood pressure values are still within the normal range.

Added to this is the value of the renin/aldosterone ratio, which allows us to identify the underlying mechanism driving blood pressure elevation in each individual and to personalize management with unprecedented precision. This is what hypertension looks like in 2026: true anticipation and treatment tailored to each patient’s physiology.

Dr. Carlos Martí – Neolife Medical Team

For years, hypertension was understood as a number: above 140/90 mmHg meant “disease”; below that threshold, “everything was fine.”

Today we know this approach is insufficient. The most recent evidence points to something more profound: elevated blood pressure is the late consequence of accelerated arterial aging—now recognized as vascular aging—which can be detected long before the blood pressure cuff shows abnormal values.

What truly matters is no longer just measuring blood pressure, but understanding what is happening inside the arteries during that silent phase that determines future risk, even when everything appears normal. This represents one of the most important evolutions of recent years: hypertension is no longer seen solely as a diagnosis, but as an opportunity for early detection. A paradigm shift that reshapes how we assess cardiovascular risk and opens the door to earlier, more precise intervention with a real capacity for long-term prevention.

Over the past decade, we have learned that:

• Vascular damage begins 5–10 years before blood pressure readings become elevated.
• Arterial stiffness predicts real cardiovascular risk more accurately than brachial blood pressure.
• Many individuals with “normal–high” blood pressure already show signs of arterial aging.

For this reason, the latest updates prioritize the assessment of vascular physiology rather than interpreting numbers alone.

Arterial stiffness: the first “surname” of hypertension

One of the parameters that has gained the most relevance in recent years is pulse wave velocity (PWV), an essential marker of arterial stiffness. Understanding it is simple if we imagine our arteries as household pipes: when they are new, flexible, and well maintained, they absorb pressure and allow smooth flow. Over time, as they become stiffer, each pressure wave travels faster and with greater force.

PWV measures exactly how fast the pressure wave travels along the aorta.

When this wave travels too quickly, the artery has lost elasticity. And this can occur years before blood pressure rises. In other words, a person may have “normal blood pressure” and yet already display the first surname of future hypertension: increased arterial stiffness, indicating premature vascular aging.

SphygmoCor: measuring what very few can

Assessing arterial stiffness cannot be done with a conventional blood pressure monitor. At Neolife, we use SphygmoCor, the international reference technology used in advanced cardiovascular research.

This highly validated system allows us to:

• Accurately measure PWV.
• Calculate central blood pressure, which is the pressure that truly loads the heart and brain.
• Determine whether a patient’s arterial stiffness is appropriate for their age or reflects accelerated vascular aging.

This technology, although widely validated, is still largely limited to centers with an advanced approach to vascular assessment. Its true value lies in its ability to detect alterations during the silent phase, when intervention is still both effective and highly personalized.

This is the foundation of true prevention—not merely reactive care.

RAAS and the renin/aldosterone ratio: the second surname of hypertension

In recent years—and particularly in the most recent updates—the renin/aldosterone ratio has gained greater importance, as it allows us to go beyond blood pressure values and understand the internal mechanism driving blood pressure elevation in each individual.

The RAAS (renin–angiotensin–aldosterone system) is the body’s mechanism for regulating blood pressure, salt balance, and fluid volume. It functions as an internal blood pressure thermostat: when the body perceives insufficient pressure or volume, it activates the system to raise it; when there is excess, it suppresses it.

• Renin is the initial signal, released when the body detects low pressure or volume.
• Renin triggers the formation of angiotensin, which constricts arteries and rapidly increases blood pressure.
• Angiotensin then stimulates the release of aldosterone, a hormone that promotes sodium and water retention, increasing circulating volume and sustaining elevated blood pressure.

By analyzing the renin/aldosterone ratio, we can identify which part of the system is altered—essentially determining the physiological mechanism pushing blood pressure upward in that specific individual. This is key to personalizing treatment and identifying the “second surname” of hypertension: whether there is excessive system activation, aldosterone predominance, or abnormally low renin levels.

This approach allows us to move away from the uniform “one-size-fits-all” strategy. While some profiles clearly benefit from ACE inhibitors or angiotensin II receptor blockers (ARBs), others respond better to calcium channel blockers, beta-blockers, aldosterone antagonists, or even targeted supplementation and lifestyle optimization strategies.

Lifestyle in 2026: interventions that truly rejuvenate the vasculature

New guidelines emphasize something we know well at Neolife: not all lifestyle recommendations impact arterial health in the same way. Certain interventions directly improve arterial stiffness and central blood pressure.

Resistance training combined with high-intensity intervals improves aortic elasticity more effectively than moderate exercise alone. Reducing visceral fat decreases hemodynamic load and improves central pressure.
Achieving deep, stable sleep—particularly restoring the normal “dipper” pattern—acts as a powerful nocturnal cardiovascular protector.
The dipper pattern refers to the natural nighttime reduction in blood pressure, typically around 10–20%. When this decline does not occur, cardiovascular risk increases significantly. It is assessed through 24-hour ambulatory blood pressure monitoring (ABPM), which tracks blood pressure behavior during sleep.

Importantly, these changes are not applied intuitively, but through a personalized approach: identifying the dominant mechanism in each individual and directing lifestyle interventions toward that specific target.

Because hypertension is not prevented with generic advice, but by optimizing arterial physiology through precise and measurable interventions.

The true antiaging approach: acting before disease appears

Traditional medicine diagnoses hypertension once blood pressure crosses a defined threshold. Longevity medicine prefers to intervene when physiology begins to deviate—before pathological numbers appear—helping the body return to its natural, physiological balance.

If a patient already shows a first surname (increased arterial stiffness), a second surname (altered RAAS), or even rising central blood pressure, we are facing an early but still manageable process. This is the window of opportunity to get ahead of arterial aging and prevent long-term complications.

That is the Neolife approach: anticipate, identify early changes, and act with precision to keep arterial health on its youngest possible trajectory.

BIBLIOGRAPHY

(1) Mancia G, Kreutz R, Brunström M, Burnier M, Grassi G, Januszewicz A, Muiesan ML, Tsioufis K, Agabiti-Rosei E, Algharably EAE, Azizi M, Benetos A, Borghi C, Hitij JB, Cifkova R, Coca A, Cornelissen V, Cruickshank JK, Cunha PG, Danser AHJ, Pinho RM, Delles C, Dominiczak AF, Dorobantu M, Doumas M, Fernández-Alfonso MS, Halimi JM, Járai Z, Jelaković B, Jordan J, Kuznetsova T, Laurent S, Lovic D, Lurbe E, Mahfoud F, Manolis A, Miglinas M, Narkiewicz K, Niiranen T, Palatini P, Parati G, Pathak A, Persu A, Polonia J, Redon J, Sarafidis P, Schmieder R, Spronck B, Stabouli S, Stergiou G, Taddei S, Thomopoulos C, Tomaszewski M, Van de Borne P, Wanner C, Weber T, Williams B, Zhang ZY, Kjeldsen SE. 2023 ESH Guidelines for the management of arterial hypertension The Task Force for the management of arterial hypertension of the European Society of Hypertension: Endorsed by the International Society of Hypertension (ISH) and the European Renal Association (ERA). J Hypertens. 2023 Dec 1;41(12):1874-2071.

(2) McEvoy JW, McCarthy CP, Bruno RM, Brouwers S, Canavan MD, Ceconi C, Christodorescu RM, Daskalopoulou SS, Ferro CJ, Gerdts E, Hanssen H, Harris J, Lauder L, McManus RJ, Molloy GJ, Rahimi K, Regitz-Zagrosek V, Rossi GP, Sandset EC, Scheenaerts B, Staessen JA, Uchmanowicz I, Volterrani M, Touyz RM; ESC Scientific Document Group. 2024 ESC Guidelines for the management of elevated blood pressure and hypertension. Eur Heart J. 2024 Oct 7;45(38):3912-4018.

(3) Herzog MJ. Arterial stiffness and vascular aging: mechanisms, clinical implications, measurement and future perspectives. Signal Transduct Target Ther. 2025;10:23.

(4) Adler, G. K., Brown, J. M., Vaidya, A., Calhoun, D. A., Carey, R. M., Funder, J. W., Stowasser, M., & the Endocrine Society. (2025). Primary Aldosteronism: An Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology & Metabolism. , ePub ahead of print.

(5) Manual MSD.

La entrada Hypertension in 2026: Preventing and Personalizing Cardiovascular Risk Management se publicó primero en Neolife.

In a clinical trial in women aged 45 to 60, 120 mg/day of hyaluronic acid significantly improved dermal hydration and elasticity after 12 weeks compared to the placebo group.

The deterioration of Skin and joints share the progressive loss of collagen, elastin, and hyaluronic acid in our tissues. These substances not only provide support and elasticity to the skin, but are also essential for maintaining the function of our joints.

Dr. Alfonso Galán – Neolife Medical Team

One of the most promising strategies, with the strongest scientific backing, is oral hyaluronic acid supplementation, both for skin care and for joint health.

As we age, two of the most frequent complaints among men and women are the appearance of wrinkles, loss of firmness and radiance in the skin, and the onset of joint discomfort, stiffness, or even the first signs of osteoarthritis.

Although these processes are natural, they share a structural cause: the gradual decline of collagen, elastin, and hyaluronic acid in our tissues. These substances not only provide support and elasticity to the skin, but are also essential for maintaining the cushioning function of our joints.

The good news is that today we know we can act from within, with safe and effective interventions that help reverse or slow down these changes.

One of the most promising and best-supported interventions is oral hyaluronic acid supplementation, both for skin care and joint health.

Skin hydration and firmness from within

As we age, the hyaluronic acid (HA) content in our skin decreases dramatically. This contributes to loss of volume, elasticity, and firmness, and to the formation of wrinkles.

Double-blind, placebo-controlled clinical studies have shown that oral hyaluronic acid supplementation:

• Significantly increases dermal hydration (up to +28% in 6–12 weeks)
• Reduces wrinkle depth by 10% to 20%
• Improves skin elasticity and overall texture
• Enhances fibroblast activity, stimulating the production of collagen and elastin

In a clinical trial in women aged 45 to 60, 120 mg/day of hyaluronic acid significantly improved dermal hydration and elasticity after 12 weeks compared to placebo.

Protected joints, restored movement

Hyaluronic acid is also a natural component of synovial fluid and joint cartilage, where it acts as a “natural lubricant.”

In patients with mild to moderate osteoarthritis, multiple clinical trials have shown that oral hyaluronic acid:

• Reduces joint pain (significant improvements on the WOMAC scale of osteoarthritis-related disability)
• Improves mobility and joint function
• Increases collagen and proteoglycan content in cartilage
• Reduces the need for anti-inflammatory medications in chronic joint degeneration

Effective doses used in studies range between 80 and 200 mg daily, with visible improvements in 8–12 weeks.

How does oral hyaluronic acid work?

Although for many years it was thought that hyaluronic acid had to be injected to be effective, we now know that:

• Oral hyaluronic acid is broken down in the intestine into bioactive units.
• These units are absorbed and stimulate CD44 receptors, inducing the synthesis of more endogenous hyaluronic acid and collagen.
• Increases in hyaluronic acid content in the dermis and cartilage have been documented after oral supplementation.

Powerful synergies

At Neolife, we recommend combining hyaluronic acid with other active ingredients that reinforce its action.

This combination has shown greater clinical and functional efficacy in studies than hyaluronic acid alone.

Moreover, as we discussed in another article on our blog, it has a wonderful synergy with Hormone Optimization Therapy.

What do the studies say?

Recent systematic reviews and meta-analyses conclude that:

• Oral hyaluronic acid increases skin hydration and elasticity compared to placebo.
• Reduces joint pain in knee and hand osteoarthritis.
• Improves quality of life and function in active older adults.
• Shows excellent tolerance and safety in the medium and long term.

Conclusion

Science supports the use of oral hyaluronic acid as an effective and safe intervention for:

• Care for your skin from within
• Prevent and improve joint wear
• Maintain functional youth for longer

Just one capsule a day can make a meaningful difference in your skin and joint health.

BIBLIOGRAPHY

(1) Fukui T, et al. The effect of hyaluronic acid ingestion on dry skin: a double-blind, placebo-controlled study. Clin Cosmet Investig Dermatol. 2017;10:267–273.

(2) Kalman DS, et al. Effect of a natural extract of chicken combs with a high content of hyaluronic acid on pain relief and quality of life in subjects with knee osteoarthritis. Nutr J. 2008;7:3.

(3) Oe M, et al. Oral hyaluronan relieves knee pain: A review. 2021;13(1):223.

(4) Sato H, et al. Clinical effects of hyaluronic acid on dry skin. J New Rem Clin. 2002;51:548–556.

(5) DuRaine GD, et al. Evaluation of oral hyaluronan for osteoarthritis symptom relief: A meta-analysis. Int J Rheum Dis. 2020;23(5):560–568.

La entrada The power of oral hyaluronic acid: hydration, youthfulness, and mobility from within se publicó primero en Neolife.

The genome, metabolome, and microbiome of a supercentenarian: clues for healthy aging.

At Neolife, we are always attentive to cutting-edge advances in aging science, and today we want to share a study that is generating significant interest. It is “The multiomics blueprint of the individual with the most extreme lifespan,” recently published in Cell Reports Medicine by Santos-Pujol and colleagues. This work deeply analyzes the multiple biological layers (genome, epigenome, transcriptome, metabolome, proteome, and microbiome) of a supercentenarian in an effort to understand how it is possible to age so extensively while maintaining exceptional health.

Dr. Sánchez – Neolife Medical Team

Study context

The individual analyzed (referred to as “M116” in the paper) was, at the time, the oldest person with verified longevity (117 years and 168 days), making her an exceptional case for studying the mechanisms underlying extreme lifespan.

The research team analyzed blood, saliva, urine, and stool samples, applying multiple omics techniques to compare her biological profile with that of older adults who were not supercentenarians.

One key conclusion is that extreme longevity does not occur simply by “avoiding” aging, but rather through an intriguing duality: clear markers of advanced age (e.g., very short telomeres) coexisting with protective mechanisms that appear to preserve health.

In other words: she had not “defeated” aging, but had managed it in an exceptional way.

Key findings relevant to anti-aging practice at Neolife

Below we summarize the most important discoveries that, from Neolife’s perspective, are relevant to our clinical vision and guidance.

1. Genomics and rare variants

Researchers identified approximately 3.8 million single nucleotide variants (SNVs) in the woman’s genome, of which about 91,666 were considered “variants of interest” (VOI) with potential effects on more than 25,000 genes. Among these, seven were homozygous and absent from the European control population. Notable genes affected included: DSCAML1 (immunity and cognition)
MAP4K3 (longevity regulation in model organisms)
TSPYL4 and NT5DC1 (lung function)
The PCDHA1-9 cluster (brain and heart health)

Functional enrichment analysis showed overrepresented pathways such as:
T-cell differentiation in the thymus
Response to bacteria
Antigen-receptor–mediated signaling
Other immune-related mechanisms
This highlights the potential importance of a robust immune system in healthy longevity.

An interesting observation: although her telomeres were extremely short (~8 kb on average and ~40% below the 20th percentile), she remained in good health. This suggests that telomere length functions more as a “chronological clock” than a direct predictor of disease. At Neolife, this reinforces the idea that aging biomarkers must always be interpreted in a broad clinical context.

2. Metabolomics and lipid/anti-inflammatory profile

She displayed a remarkably favorable lipid profile: extremely low VLDL cholesterol and triglycerides, and very high HDL cholesterol (“good cholesterol”). Likewise, she had many medium/large HDL particles and many large LDL particles, with low levels of small HDL particles — all pointing to very efficient lipoprotein maturation.

She also showed low levels of saturated fatty acids, esterified cholesterol, linoleic acid, and acetone (typically associated with poorer health), and high levels of free cholesterol, which have been linked to better prognosis.

Her inflammatory profile showed low concentrations of glycoproteins A and B, suggesting a reduced degree of systemic “inflamm-aging.”

Altogether, these findings support the clinical value of interventions aimed at:
Optimizing lipid metabolism
Controlling triglycerides
Improving lipoprotein particle composition
Reducing low-grade chronic inflammation
All areas that Neolife actively addresses in personalized programs.

3. Extracellular vesicle (EV) proteomics

The proteomic analysis of M116’s extracellular vesicles (compared to postmenopausal women aged 49–65) revealed 231 proteins with significant differences. Enriched functional groups included:
Coagulation
Immune system
Lipid metabolism
Apoptosis
Cellular detoxification
Cell adhesion
mRNA regulation

Notable patterns included increased lipid and cholesterol transport, enhanced lipoprotein remodeling and clearance, and greater oxidative stress response activity.

A surprising detail: the most overexpressed protein in M116 was SAA1 (serum amyloid A-1), typically associated with Alzheimer risk, although she showed no signs of neurodegeneration. This underscores the need to interpret proteomic elevations with nuance and within the individual’s full biological context.

4. Gut microbiome

M116’s gut microbiome displayed much greater diversity compared to control women aged 61–91, indicating an extraordinarily rich microbial ecosystem.

At the phylum level, Actinobacteriota were markedly elevated, especially the family Bifidobacteriaceae and genus Bifidobacterium, which normally decline with age—but here remained abundant.

In contrast, Proteobacteria and Verrucomicrobiota were decreased relative to controls, patterns typically linked to better health in advanced age.

Dietary records showed that M116 consumed about three yogurts per day containing Streptococcus thermophilus and Lactobacillus delbrueckii subsp. bulgaricus, which support Bifidobacterium growth. Although causality is not proven, these findings open practical avenues worth exploring.

5. Epigenetics and “biological age”

Globally, M116’s estimated biological age (based on epigenetic methylation clocks) was significantly lower than her chronological age. For example, her “age pace” was −17.34 years, suggesting a slowing of epigenetic aging.

This confirms the value of incorporating epigenetic clocks into aging assessments, while acknowledging their limitations: epigenetics is modifiable, and the goal is to realign biological age toward younger values.

Implications for healthy aging practice at Neolife

This study matters deeply to us at Neolife, and here is what it teaches when translated into clinical practice:

Extreme longevity is not the result of a single miraculous intervention, but of a synergistic set of genetic, metabolic, immune, microbiological, and epigenetic mechanisms. At Neolife, we emphasize exactly this comprehensive approach.

Efficient lipid profiles, low inflammation, a favorable microbiome, and slowed epigenetic aging emerge as “health markers” rather than indicators of chronological age. For this reason, we promote a personalized strategy: thorough diagnostics, tailored interventions (nutrition, microbiota modulation, lifestyle optimization, lipid and epigenetic management), and continuous monitoring.

This case demonstrates something powerful: extreme longevity does not have to be accompanied by extreme disease. Some individuals can live over a century while maintaining functional, remarkably balanced biology.

Although the study examines a single subject —and therefore cannot be fully generalized— it offers valuable hypotheses applicable to individualized clinical programs:

• Assessing lipid metabolism beyond traditional cholesterol measures (lipoprotein profiling, HDL/LDL particle analysis)
• Monitoring low-grade inflammation (glycoproteins, EV markers)
• Analyzing the gut microbiome with special attention to Bifidobacterium and reduction of pro-inflammatory taxa
• Integrating genomics into longevity assessments, recognizing that there are no “magic genes,” but rather many variants whose effects accumulate and are modulated by lifestyle

This research reinforces the idea that age is an important factor but not an unavoidable destiny: aging and disease can be decoupled, as shown by this case. In the authors’ own words, “extreme age” does not necessarily equate to “poor health.”

For us, it emphasizes the importance of analyzing multiple layers of biology —inflammation, genetics, epigenetics, microbiome— all of which add up. And above all, it reminds us that there is no single formula for successful aging, but there are measurable patterns we can understand and, to some extent, modulate.

We believe this study by Santos-Pujol et al. opens the door to future interventions in epigenetics, microbiome modulation, and personalized prevention. And although much remains to be explored, it reinforces our daily mission at Neolife: to translate cutting-edge science into actionable strategies that help patients preserve —and even elevate— their quality of life as they age.

Our commitment at Neolife is precisely to translate these cutting-edge advances into practical strategies for our patients, helping them optimize their aging instead of resigning themselves to the passage of time.

If you would like to explore any of these biomarkers in more depth or understand how to incorporate them into your follow-up protocol, we would be delighted to assist you.

Thank you for joining us on this journey toward smarter, healthier aging.

BIBLIOGRAPHY

(1) Santos-Pujol, A., Matalonga, J., Calleja, N., Moratal, T., López-Montes, A., et al. (2025).
The multiomics blueprint of the individual with the most extreme lifespan.
Cell Reports Medicine, 6, 102368.
https://doi.org/10.1016/j.xcrm.2025.102368

La entrada Decoding the Secrets of Superlongevity: The Multi-Omics Map of the Longest Life in History se publicó primero en Neolife.

You’ve probably heard of medications like Ozempic, Wegovy, or Mounjaro, which are primarily used for weight loss or blood sugar control in people with diabetes.

But did you know that these therapies might be opening new doors in the field of longevity? We’d like to share how these small weekly injections can have powerful effects far beyond what was originally imagined…

Dr. Yéssica Sánchez – Neolife Medical Team

Less Inflammation, More Vitality, and… a Healthier Heart

Chronic inflammation—a silent process we often don’t notice but that progressively damages the body—is one of the main accelerators of aging. It’s involved in diseases like Alzheimer’s, certain cancers, and cardiovascular conditions.

Semaglutide, commercially known as Ozempic® or Wegovy®, not only supports weight loss but also significantly reduces inflammation. Studies have shown that it can lower inflammatory markers (like C-reactive protein, or CRP) by up to 43%, even beyond the weight-loss effect.

This anti-inflammatory action is especially enhanced by the reduction of visceral fat—the most dangerous type due to its strong link to cardiometabolic risk. For this reason, semaglutide is increasingly used in people who are overweight or obese, even if they are not diabetic, as part of a comprehensive strategy to improve metabolic health and reduce systemic inflammation.

Semaglutide has been shown to reduce vascular and cardiac inflammation, improving endothelial function, decreasing leukocyte (immune cell) adhesion, and lowering the expression of pro-inflammatory molecules like ICAM-1 and VCAM-1. It has also been associated with reduced myocardial inflammation, which may help reverse microvascular rarefaction (the loss of capillaries and arterioles that impairs microcirculation and is typical of metabolic syndrome).

All of this translates into less arterial stiffness, improved tissue perfusion (blood flow), and a reduced risk of cardiovascular events, such as heart attacks. Moreover, several studies have demonstrated that semaglutide lowers the incidence of major cardiovascular events (cardiovascular death, heart attack, or stroke) in people with obesity or type 2 diabetes.

Brain Protection

At the brain level, multiple studies suggest that these treatments may reduce the risk of cognitive decline and Alzheimer’s—even in people without diabetes. They are currently being investigated as potential allies in preserving memory and preventing age-related brain damage. This is largely due to their ability to reduce vascular inflammation and restore the integrity of the neurovascular unit.

In animal models, GLP-1 receptor agonists reduce amyloid plaques, neuroinflammation, and induce changes in microglia that promote a neuroprotective state. Additionally, observational clinical studies in people with diabetes show that semaglutide is associated with a 40–70% lower risk of being diagnosed with Alzheimer’s. In older individuals, GLP‑1 use is linked to lower incidence of 42 chronic diseases, including dementia.

One of the most interesting human studies in my opinion is a pooled analysis of seven clinical trials involving 1,094,761 patients (both men and women around 60 years old), selected from a U.S. patient database and followed for three years. The study cohort included 17,104 new semaglutide users and 1,077,657 new users of other antidiabetic medications. The efficacy of semaglutide was compared to each of the other antidiabetics studied.

Despite significant heterogeneity in insulin and semaglutide receptor profiles based on ethnicity, age, sex, obesity diagnosis, cardiovascular disease, and Alzheimer’s risk factors, these groups were balanced using propensity score matching. Patients with type 2 diabetes prescribed semaglutide had a significantly lower likelihood of being diagnosed with Alzheimer’s during a three-year follow-up visit compared to those prescribed other antidiabetic medications—regardless of sex, gender, or obesity status. In fact, the overall risk of a first Alzheimer’s diagnosis within three years was nearly double in the general elderly population.

Cellular Energy and Metabolism

These therapies optimize how our cells use energy, regulate insulin, and protect the mitochondria (the “powerhouses” of our cells)—all essential for slowing down aging from the inside by promoting a healthy metabolic environment.

So, Are They Just for Weight Loss?

Given all the points above, the answer is no. While they were initially introduced with that goal in mind, scientists are now studying them as potential anti-aging tools. In the future, they may become part of prevention programs targeting brain, cardiovascular, and metabolic health.

Should I Take Them?

Should I Take Them?
They’re not for everyone—but they may be worth considering for people with obesity, prediabetes, insulin resistance, or high cardiovascular risk. The decision should always be made together with a physician who can assess your case individually. At Neolife, we’d be happy to guide you and personalize this treatment to suit your needs.

BIBLIOGRAPHY

(1) Estato, V., Obadia, N., Chateaubriand, P.H. et al.Semaglutide restores astrocyte–vascular interactions and blood–brain barrier integrity in a model of diet-induced metabolic syndrome. Diabetol Metab Syndr 17, 2 (2025).

(2) William Wang, QuangQiu Wang, Xin Qi, et al. Associations of semaglutide with first-time diagnosis of Alzheimer’s disease in patients with type 2 diabetes: Target trial emulation using nationwide real-world data in the US. Alzheimer’s & Dementia. Vol.20, issue 12 (2024)

(3) Meca AD, Boboc IKS, Mititelu-Tartau L, Bogdan M. Unlocking the Potential: Semaglutide’s Impact on Alzheimer’s and Parkinson’s Disease in Animal Models. Curr Issues Mol Biol. 2024 Jun 13;46(6):5929-5949. doi: 10.3390/cimb46060354. PMID: 38921025; PMCID: PMC11202139.

(4) Guo X, Lei M, Zhao J, Wu M, Ren Z, Yang X, Ouyang C, Liu X, Liu C, Chen Q. Tirzepatide ameliorates spatial learning and memory impairment through modulation of aberrant insulin resistance and inflammation response in diabetic rats. Front Pharmacol. 2023 Aug 28;14:1146960. doi: 10.3389/fphar.2023.1146960. PMID: 37701028; PMCID: PMC10493299.

(5) Shayan Yaghmayee, Atefeh Sadat Moazzeni, Tannaz Jamialahmadi, Sercan Karav, Habib Yaribeygi, Prashant Kesharwani, Amirhossein Sahebkar, Neuroprotective and cognitive benefits of Semaglutide: Insights into the underlying molecular mechanisms, Neuroscience, Volume 579, 2025, Pages 187-197, ISSN 0306-4522

(6) Zheng, Z., Zong, Y., Ma, Y. et al.Glucagon-like peptide-1 receptor: mechanisms and advances in therapy. Sig Transduct Target Ther 9, 234 (2024).

(7) Wang, W., Wang, Q., Qi, X., et al.(2024) Associations of semaglutide with first-time diagnosis of Alzheimer’s disease in patients with type 2 diabetes: Target trial emulation using nationwide real-world data in the US. Alzheimer’s and Dementia 1-12.

(8) Papakonstantinou I, Tsioufis K, Katsi V. Spotlight on the Mechanism of Action of Semaglutide. Curr Issues Mol Biol. 2024 Dec 23;46(12):14514-14541. doi: 10.3390/cimb46120872. PMID: 39728000; PMCID: PMC11674233.

La entrada Small Doses, Big Effects: GLP-1 and Longevity se publicó primero en Neolife.

It is truly a privilege for us to address you on the occasion of a milestone that marks a before and after in the history of our institution: the opening of our new clinic in Barcelona, located at 8 Ferran Agulló Street.

This is not simply a new location; it is about bringing to the Catalan capital all the medical excellence, knowledge, and experience accumulated over more than thirteen years dedicated to Preventive and Healthy Aging Medicine. It is about continuing to accompany our clients on their journey toward active longevity, with more resources, more human talent, and more commitment than ever.

Neolife Team

Medicine for Healthy Aging and Proactive Prevention

Neolife was a pioneer in Spain in the clinical application of what was then called Anti-Aging Medicine, a term that, over time, has evolved and deepened into what we now know as comprehensive age management.

From the very beginning, when this approach was barely known, we were clear about our mission: to transform the way people understand and experience the passage of time.

We have witnessed the evolution of science, technology, and evidence, and we have always been on the front line, applying everything that truly makes a difference in health, well-being, and longevity.

Today, with over 13 years of experience, we not only maintain that pioneering spirit—we reinforce it with the opening of a center that represents the very best of who we are. In our Barcelona clinic, you will find a space designed not only with functionality and cutting-edge technology in mind but also with warmth and humanity. Because at Neolife, we believe that the medicine of the future cannot be separated from human excellence.

We are at the forefront of all advances in the field of healthy aging and proactive prevention. We incorporate into our protocols everything that solid scientific evidence has proven effective in improving our clients’ health, quality of life, and longevity. What is discussed at international conferences, published in PubMed articles, and implemented by leading institutions worldwide is already part of our daily practice.

If you have heard of advanced tests to measure biological age, gut microbiome analysis, genetic predisposition and pharmacogenetics studies, maximum effort tests with oxygen consumption measurement, body composition analysis using DXA, intravenous NAD+ protocols, cardiovascular risk testing with molecular biomarkers, vascular assessments, early cancer screening using liquid biopsies or next-generation imaging… all of this is already available to you at our Barcelona clinic.

And not just available—guided by the best-trained, most dedicated, and most discerning medical and technical team in the sector. Professionals who not only have scientific knowledge but who also understand people. Because as important as knowledge is the judgment with which it is applied, and the ability to listen, empathize, and support each client with humanity and commitment.

One of our founding principles has always been providing exquisite, personalized care. At Neolife, the client is not just a number or a clinical case. Every client is a person with a story, expectations, fears, and goals. That is why each assessment, each check-up, and each program we design is fully personalized. We create tailor-made solutions adapted to the specific circumstances of each client, and we do so with the utmost respect, confidentiality, and dedication.

We offer hormonal optimization programs tailored to every stage of life, for both men and women. Because hormonal balance is neither a luxury nor a trend—it is a key factor in cardiovascular, cognitive, sexual, emotional, and metabolic health. And we know how to address it through science and precision, with the safety provided by clinical experience and ongoing training.

We also help our clients regain control over their metabolism and body composition. Excess visceral fat or loss of muscle mass are not just aesthetic issues; they are risk factors for chronic diseases that can and should be reversed with the right approach.

We often receive clients with diffuse symptoms, unclear diagnoses, or conditions that have not found answers in traditional medicine. Chronic fatigue, insomnia, brain fog, sexual dysfunctions, muscle pain, or mood changes that do not respond to conventional treatments. Thanks to the knowledge we have developed in integrative medicine, hormonal optimization, and the physiology of aging, we can offer solutions where others cannot. Because we look beyond the obvious, and because we have diagnostic and therapeutic tools that conventional medicine has not yet embraced.

Our new clinic in Barcelona is not just a physical space: it is an extension of our philosophy, our commitment, and our passion for health. We want it to be a benchmark not only in Catalonia but throughout Europe for those seeking a type of medicine that does not settle for treating diseases but aspires to prevent them, to anticipate, and to optimize every stage of life.

We warmly invite you to visit us, to discover firsthand what a truly comprehensive and personalized approach to health means, and to become part of this community that refuses to age according to statistics but instead chooses to do so with quality, vitality, and purpose.

Thank you for your trust, for your time, and for walking alongside us on this journey toward active, conscious, and fulfilling longevity.

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Aging is an inevitable biological process characterized by the progressive loss of cellular and physiological functions. This deterioration is the main risk factor for the development of chronic and degenerative diseases.

Although research on aging and age-related diseases is still in its early stages, recent years have seen significant advances in longevity studies. Notably, the increase in life expectancy and the prevalence of associated diseases make it urgent to develop effective preventive and therapeutic strategies. Today, researchers are faced with a major question: can we intervene externally to slow down the aging process?

Dr. Yessica Sánchez – Neolife Medical Team

Hallmarks of Aging

We’ve previously discussed the “Hallmarks of Aging.” In this article, we explore current advancements that directly address each of these hallmarks and attempt to answer the key question. Let’s examine the main mechanisms involved:

One of the most relevant processes is genomic instability, which arises when DNA repair systems stop functioning properly, allowing mutations to accumulate with significant functional consequences.

Another essential mechanism is telomere shortening—the structures that protect the ends of chromosomes. With each cell division, telomeres shorten until the cell loses its ability to replicate. It has been observed that activating the enzyme telomerase can slow this process in certain experimental models.

Epigenetic alterations also play a key role. Aging modifies gene expression without changing the DNA sequence itself, thereby affecting multiple cellular functions. These epigenetic changes are implicated in premature aging syndromes.

Proteostasis, or the maintenance of protein balance, is another pillar disrupted by aging. The body loses its ability to properly fold and recycle proteins, which leads to their accumulation. Diseases like Alzheimer’s are directly linked to this breakdown in protein quality control.

Alongside this is dysregulated nutrient sensing, in which cells lose sensitivity to key metabolic signals. It has been shown that a predominantly anabolic metabolism accelerates aging, while catabolic processes—promoted by practices such as fasting—favor longevity. In this area, compounds like rapamycin have demonstrated positive effects in animal models.

Mitochondrial dysfunction is another central factor. Mitochondria, responsible for cellular energy production, become less efficient with age, increasing the formation of reactive oxygen species and leading to progressive cellular damage.

Added to this is cellular senescence, a state in which cells stop dividing without dying. Although this initially serves as a defense against mutations, the accumulation of senescent cells contributes to inflammation and tissue deterioration.

Over time, there is also a decline in the number of functional stem cells, limiting the body’s capacity for regeneration. Lastly, altered intercellular communication, worsened by an inflammatory environment, undermines the coordinated function of tissues.

Strategies to Address Aging

Today, there are pharmacological, nutritional, and genetic strategies to target many of these aging processes. Even the gut microbiota plays a key role in regulating the immune system and thus is considered essential for longevity.

Of all available approaches, reducing chronic inflammation and eliminating senescent cells have drawn the most attention. Nutritional supplementation has also been recognized as important in preventing functional decline.

Research led by pioneering scientists like David Sinclair has shown that certain natural compounds can promote healthy aging. These compounds, known as caloric restriction mimetics, imitate the benefits of fasting by activating genetic pathways related to longevity.

These include spermidine, berberine, resveratrol, and quercetin. Trans-resveratrol and quercetin, for example, stimulate the activity of the SIRT1 gene, which is involved in DNA repair and other cellular processes that slow aging. Additionally, trans-resveratrol improves insulin sensitivity in a dose-dependent manner. Quercetin, a flavonoid with anti-inflammatory properties, primarily works by eliminating senescent cells, which are responsible for age-related degenerative processes.

A recent study by Murugesan et al. (2023) demonstrated that the combination of quercetin and trans-resveratrol significantly reduces fat deposits, further supporting their potential as a metabolic therapy.

Another important molecule is NAD⁺ (nicotinamide adenine dinucleotide), a coenzyme essential for energy metabolism and the activation of sirtuins. NAD⁺ production can be increased using precursors such as nicotinamide riboside or nicotinamide mononucleotides (NMN). However, at Neolife, we strongly recommend intravenous NAD⁺ therapy due to its superior effectiveness.

Spermidine also stands out for its ability to induce autophagy, a key process in cellular renewal that significantly impacts cell differentiation and maturation.

Lastly, berberine, a natural compound with mechanisms similar to metformin, activates the AMPK gene, regarded as a master regulator of metabolism. Its effects promote mitochondrial biogenesis, improve insulin sensitivity, and support blood glucose regulation.

Scientific Support for a Therapeutic Approach

A recent development in this field is the COSMOS study, presented in March 2025 during the American Heart Association’s scientific sessions. This randomized clinical trial assessed whether daily multivitamin supplementation could slow biological aging, as measured by DNA methylation-based epigenetic clocks.

The study included over 950 older adults (mean age: 70.2 years), who underwent blood testing at baseline, 12 months, and 24 months. In all five epigenetic clocks analyzed, the group receiving multivitamins showed a slower rate of biological aging compared to the placebo group. This effect corresponded to an approximate “deceleration” of four months in biological aging. The benefits were even greater in individuals with accelerated aging at the start of the study.

These findings add to the growing body of evidence, such as results from the Physicians’ Health Study II, which showed a reduction in the risk of invasive cancer with multivitamin use, as well as less age-related cognitive decline and memory loss.

Although further replication and clarification of mechanisms are still needed, studies like COSMOS, along with data from the Physicians’ Health Study II and USPSTF reviews, reinforce the idea that good nutrition and appropriate supplementation can be valuable allies in preventing age-related decline.

Healthy longevity is not the result of a single intervention but rather the integration of multiple factors: genetics, nutrition, lifestyle, metabolic health, hormonal balance, and inflammation control.

While supplements are not a substitute for a balanced diet or healthy lifestyle, they represent a valuable tool within a preventive approach and may help target key aging markers.

Thanks to science, we now have promising tools that allow us to intervene before disease appears. Among them, well-chosen supplements are gaining a more solid role. Studies like COSMOS open new doors to consider supplementation as a thoughtful, evidence-based component of longevity medicine.

BIBLIOGRAPHY

(1) Ni YQ, Liu YS, New Insights into the Roles and Mechanisms of Spermidine in Aging and Age – Related Diseases. Aging Dis. 2021 Dec 1;12(8):1948-1963.

(2) López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G, The hallmarks of aging, Cell. 2013 Jun 6;153(6):1194-217

(3) Sesso HD, Manson JE, Aragaki AK et al. COSMOS Research Group. Effect of cocoa flavanol supplmentation on preventing cardiovascular disease events: The COSMOS randomized clinical trial. Am J Clin Nutr. 2022; 115 (6): 1490-1500

(4) Gaziano JM, Sesso HD, Christen WG, Bubes V, Smith JP, MacFadyen J, Schvartz M, Manson JE, Glynn RJ, Buring JE. Multivitamins in the prevention of cancer in men: the Physicians’ Health Study II randomized controlled trial. JAMA. 2012 Nov 14;308(18):1871-80. doi: 10.1001/jama.2012.14641. Erratum in: JAMA. 2014 Aug 6;312(5):560. PMID: 23162860; PMCID: PMC3517179.

La entrada Supplementation and Longevity se publicó primero en Neolife.

From the age of 40, the symptoms of aging become more noticeable, often appearing earlier and negatively affecting many aspects of our lives. This is largely due to a decline in hormone levels.

Neolife offers optimal management of this hormonal imbalance, ensuring long-term effectiveness and safety. For over 10 years, we’ve been providing our patients in Madrid and Marbella with the best available options, which have consistently delivered successful results.

Dr. César Montiel – Medical Team Neolife

Hormonal deficiency

Adult male androgen deficiency is caused by low testosterone levels, which are associated with a series of symptoms: irritability, sadness, loss of muscle mass, decreased sexual desire, worsening of erection quality, fatigue, and lack of vitality. These hormone-related issues don’t stop there—they are clearly linked to certain health conditions such as cardiovascular disease, fall risk, osteoporosis, depression, aggressive prostate cancer, metabolic disorders (type 2 diabetes, obesity, dyslipidemia), and neurodegenerative diseases.

On the other hand, the symptoms caused by a lack of female hormones such as estradiolthe progesteron and the testosteronewhich we address in our treatments menopauseare numerous and varied: hot flashes, mood swings, depression, anxiety, irritability, weight gain (fat), muscle loss, vaginal dryness, pain during intercourse, loss of libido, urinary incontinence, memory issues, difficulty concentrating, insomnia… in addition to less noticeable effects such as increased cholesterol levels, insulin resistance, higher cardiovascular risk, loss of bone mass, and cognitive decline associated with Alzheimer’s disease, among others.

What are the steps to begin a Bioidentical Hormone Replacement Therapy (BHRT) program at Neolife?

1. Completion of a preliminary questionnaire, after which our medical team will assess whether you are a suitable candidate and determine which biomarkers need to be tested.
2. Initial consultation, where a personalized prescription for Bioidentical Hormone Replacement Therapy will be made.
3. Start of the hormone treatment prescribed by our medical team.
4. Ongoing monitoring and treatment maintenance. After the initial 4–5 weeks, a blood test will be requested to assess the early results. From there, blood tests will be scheduled every 3–5 months, with intervals adjusted to each individual’s needs. These results will be used to personalize the next phase of treatment.

If you’re interested, contact us!

• Madrid Clinic: 917 32 59 50
• Marbella Clinic: 951 30 44 88

La entrada WHY START A MENOPAUSE OR ANDROPAUSE PROGRAM AT NEOLIFE? se publicó primero en Neolife.

Aging is an inevitable biological process that involves changes in different body systems, increasing the risk of chronic diseases such as atherosclerosis, osteoporosis, insulin resistance, and neurodegenerative diseases. In this context, vitamin K has emerged as a key nutrient in preventing and slowing down these processes.

“Although it is often associated solely with blood clotting, recent research has shown that vitamin K plays a fundamental role in cardiovascular, bone, metabolic, and brain health, making it a pillar of anti-aging medicine. Once again, nutrition plays a crucial role in prevention and overall health!”

Estefanía Álvarez – Neolife Nutrition Unit

Types of Vitamin K and Their Differences

There are three main forms of vitamin K, each with specific functions in the body.

• Vitamin K1 (Phylloquinone or Phytomenadione): It is primarily found in leafy green vegetables such as spinach, kale, and broccoli. Its main function is the activation of clotting factors in the liver, preventing bleeding.
• Vitamin K2 (Menaquinone, MK): It is found in fermented foods, animal products, and is produced in small amounts by the gut microbiota. It plays a crucial role in regulating vascular calcification, bone health, and insulin metabolism.
• Vitamin K3 (Menadione): It is a synthetic form used in some supplements and medical treatments, but its use in humans is limited due to potential adverse effects.

Health and Anti-Aging Benefits of Vitamin K

1. Protection Against Cardiovascular Diseases

Aging is associated with increased arterial stiffness due to the accumulation of calcium in the arteries. Vitamin K2 plays a fundamental role in preventing this phenomenon by activating Matrix Gla Protein (MGP), a protein that inhibits vascular calcification.

Various studies have shown that higher vitamin K2 intake is associated with a lower risk of cardiovascular disease, including heart attacks and strokes.

2. Bone Strengthening and Osteoporosis Prevention

As we age, bone density decreases, increasing the risk of osteoporosis and fractures. Vitamin K activates osteocalcin, a protein that enables proper bone mineralization by binding calcium to the bones.

Studies have shown that people with optimal vitamin K levels have higher bone density and a lower risk of fractures, especially in postmenopausal women.

3. Improved Insulin Sensitivity and Diabetes Prevention

Insulin resistance is a key factor in metabolic aging and the development of type 2 diabetes. Vitamin K has been found to play an important role in glucose metabolism by stimulating active osteocalcin, a bone protein that improves insulin sensitivity.

A study published in Diabetes Care found that higher vitamin K2 intake was associated with a lower incidence of type 2 diabetes in older adults.

4. Protection Against Neurodegenerative Diseases

The brain is one of the most vulnerable organs to aging. Vitamin K is essential for the production of sphingolipids, key compounds in the structure and function of neuronal cell membranes.

Low vitamin K levels have been linked to an increased risk of cognitive decline and neurodegenerative diseases such as Alzheimer’s and Parkinson’s.

Additionally, its anti-inflammatory action may help reduce oxidative stress and protect the brain from aging-related damage.

5. Reduction of Inflammation and Oxidative Stress

Aging is associated with a state of chronic low-grade inflammation, known as inflammaging, which contributes to various chronic diseases.

The vitamin K Has anti-inflammatory properties that reduce the production of pro-inflammatory cytokines, helping slow down cellular aging and prevent chronic inflammatory diseases.ropiedades antiinflamatorias que reducen la producción de citocinas proinflamatorias, ayudando a ralentizar el proceso de cellular aging and prevent diseasesprevenir enfermedades chronic inflammatory

Sources of Vitamin K and Strategies to Optimize IntakeFuentes de vitamina K y estrategias para pptimizar su ingesta

To maintain adequate vitamin K levels, it is essential to include foods rich in its different forms in the diet:

• Vitamin K1: Spinach, kale, lettuce, broccoli, Brussels sprouts.
• Vitamin K2: natto (fermented soybeans), aged cheeses, egg yolk, liver, beef.

The gut microbiota also produces vitamin K2, but its bioavailability is limited, as many of its molecules remain associated with bacterial cell membranes.

To improve vitamin K absorption, it is advisable to consume it with healthy fat sources, as it is a fat-soluble vitamin.

Supplementation and Evaluation of Vitamin K Levels

Dietary recommendations establish an adequate intake of 70 µg of vitamin K1 per day, but there are no specific values for vitamin K2, despite its importance for cardiovascular and bone health.

To assess vitamin K levels in the body, the PIVKA-II marker (protein induced by vitamin K absence) is used, allowing for the detection of deficiencies and measurement of the vitamin’s biological activity in the body.

In certain cases, especially in individuals at risk of osteoporosis, cardiovascular diseases, or insulin resistance, supplementation with vitamin K2 (MK-7) may be beneficial, always under medical supervision.

It is important to note that those taking coumarin-based anticoagulants (such as warfarin) should consult their doctor before modifying their vitamin K intake, as it may interfere with the medication.

Thus, vitamin K is an essential nutrient that goes far beyond blood clotting. Its impact on cardiovascular, bone, metabolic, and neurological health makes it a key component in healthy longevity strategies.

Ensuring an adequate intake of vitamin K through diet and, in some cases, supplementation can be an effective strategy to slow aging and improve quality of life in adulthood.

La entrada Vitamin K and Anti-Aging: A Key Nutrient for Healthy Longevity se publicó primero en Neolife.

NAD or nicotinamide adenine dinucleotide is a derivative of vitamin B3, also known as niacin, niacinamide or nicotinamide (soluble form). NAD is used in over 500 reactions and has a crucial role in metabolism, cellular aging, DNA repair, and gene expression.

NAD intervenes vitally in two very important pathways in humans, namely the sirtuin and PARP pathways. It is essential in functions that influence the aging process, such as mitochondria synthesis, apoptosis, autophagy, inflammation, intracellular and systemic signaling, DNA repair, genomic stability, and programmed cell death.

Dr. Alfonso Galón González – Neolife Medical Team

Without the presence of NAD, much of the reactions that protect us from pathologies related to aging do not occur, we accumulate damage… and eventually we die.

Today I want to share information with you about a very important molecule that we have in our bodies, of which you’ve probably never heard of. It is NAD or nicotinamide adenine dinucleotide, which is a derivative of something that we’re already familiar with, vitamin B3, also known as niacin, niacinamide or nicotinamide (soluble form). NAD is used in over 500 reactions and has a crucial role in metabolism, cellular aging, DNA repair, and gene expression.

Additionally, they intervene vitally in two very important human pathways, which we’ve already mentioned in previous blog posts, namely the sirtuin and PARP pathways.

Sirtuins are a group of 7 enzymes, specifically deacetylase, which are highly preserved from an evolutionary standpoint, from bacteria to humans. They regulate functions that influence the aging process such as mitochondria synthesis, apoptosis, autophagy, inflammation, intracellular and systemic signaling, DNA repair, etc… They’ve been called the genes of longevity.

PARP (Poly-ADP-Ribose polymerase) are a family of polymerase involved in DNA repair, genomic stability, and programmed cell death.

These very important processes I have just mentioned do not occur if there is no NAD, which leads us to accumulate damage, age, and die.

That’s how important NAD is. Additionally, NAD levels drop as we age. In fact, it plays a role in the so called “Hallmarks of aging“.

NAD comes in two forms: NAD+ and NADH. NAD+ accepts electrons from other molecules, becoming NADH, and NADH donates an electron to another molecule, becoming NAD.

Why do its levels decline over the years?

Like most things in our bodies, it’s a balance between production and degradation; in this case, it is simple: not only does the body produce less, but it also degrades more.

As shown in this chart, there are two fundamental synthesis pathways:

The de novo pathway and the salvage pathway.

• The de novo pathway synthesizes NAD from the tryptophan we consume in our diet, but this pathway is not very efficient.
• The salvage pathway effectively uses as precursors recycled parts of the use of NAD as cofactors in various reactions or after it has been used by sirtuins, for example. This is the main pathway of NAD production, but it is limited as we age because of the activity of the enzyme NMPT.

In addition to the decline in its production, as already mentioned, its degradation increases, as well. The previously mentioned PARP increase their activity over the years. This totally makes sense: as we age, DNA damage accumulates, and they must increase their activity to repair it, thus consuming more NAD. And there is another enzyme called CD-38, whose activity doubles or triples as we age, and this directly degrades NAD. In fact, it is believed that the benefit of treatments that seek to combat the inflammation that occurs over the years (inflammaging) comes with the fact that they decrease their activity.

What can we do to keep our NAD levels from declining over the years?

The scientific community is investigating exactly this. It is considering the possibility of increasing de novo synthesis, promoting the salvage pathway, and lowering the activity of enzymes that degrade NAD. Sounds simple, right?

Let’s see what we know so far:

• Increasing de novo synthesis: As already mentioned, this pathway is not very efficient and increasing tryptophan intake does not seem like the best option.
• Promoting the salvage pathway: This can be done in two ways. One, by providing more precursors of the salvage pathway like Nicotinamide (NAM), Nicotinamide Riboside (NR), and Nicotinamide Mononucleotide (NMN), to which we will add what we know about Niacin or Nicotinic Acid (NA), which we may see in the chart for the Preiss-Handler pathway; and two, by increasing the activity of NAMPT.
  • Niacin is a great choice. Studies show that it may increase up to 2 times the levels of NAD in 10 months, and it’s affordable. One disadvantage is that extended-release niacin is toxic to our liver, and immediate release niacin may quite often cause what is called the “Niacin Flush”, skin redness accompanied by a greater or lesser degree of itching. However, this is usually the case with the first doses, and then after the body gets used to it, it no longer happens. Moreover, niacin raises our good cholesterol (HDL) level, one of the few treatments to achieve this result. We’ll cover this topic in future blog posts.
  • NMN: it’s the most promising. As shown in the chart, it only needs a small reaction to become NAD. The problem is that to this day it is a very expensive supplement, there are no studies that tell us exactly how much NAD levels go up, and there is controversy regarding how it enters the cell.
  • NR: It seems that it may double the levels of NAD with a dose of 1 g, but we don’t know if it must be converted into Nicotinamide before becoming NAD or if it does so directly.
  • Nicotinamide: This is the soluble form of Vitamin B3. But it’s not without controversy either. It has been shown that when we take it, we inhibit SIRT1 (one of the sirtuins) for 1h, but after 8h it increases its activity. Inhibiting the activity of our sirtuins is the last thing we want, so the way to prevent this from happening is being researched. Additionally, its use and that of any of its derivatives such as NMN, NA, or NR interferes with a very important process called methylation, which is essential for neurotransmitter synthesis, creatine synthesis, choline, and DNA methylation, so whenever we supplement with these precursors, we must add another compound to prevent this interference from happening, usually TMG (trimethylglycine).
  • Increasing NAMPT activity. As we have seen, its activity drops over the years, making it difficult to convert Nicotinamide into NMN. What strategies have been shown to increase its activity? Interestingly, but it should come as no surprise, two of the most consolidated, effective, and acclaimed antiaging measures appear here: exercise and nutrition. Aerobic activity has been shown to increase its activity by 12% in young people and 28% in older adults, while strength training increases its activity by 25% and 30% respectively. Calorie restriction (CR) or calorie restriction mimetics, mentioned in these blog posts, have also been shown to increase its activity.

• The last proposed strategy is to lower the activity of enzymes that consume NAD or degrade it. I think it is clear that we have no interest in lowering the activity of our sirtuins or PARPs. But we may do so in the case of CD-38.

So far we know that a flavonoid present in dry parsley, celery, and chamomile tea, called apigenin, may lower its activity.

I hope that I have been able to convey the vital importance of NAD and maintaining its proper levels. I hope this reinforces your use of good nutrition habits, exercise, and supplementation, as I’ve provided a few more reasons as to why we should exercise, eat well, and use vitamin supplements, as is the case with B3.

BIBLIOGRAPHY

(1) Imai S, Guarente L. NAD+ and sirtuins in aging and disease. Trends Cell Biol. 2014;24(8):464-471. doi:10.1016/j.tcb.2014.04.002

(2) De Flora A, et al. Autocrine and paracrine calcium signaling by the CD38/NAD+/cyclic ADP-ribose system. Ann N Y Acad Sci. 2004;1028:176–191.

(3) Lin S-J, et al. Calorie restriction extends yeast life span by lowering the level of NADH. Genes Dev. 2004;18:12–16.

(4) Imai S, Yoshino J. The importance of NAMPT/NAD/SIRT1 in the systemic regulation of metabolism and ageing. Diabetes Obes Metab. 2013;15(Suppl 3):26–33.

(5) Satoh A, et al. The role of mammalian sirtuins in the regulation of metabolism, aging, and longevity. Handb Exp Pharmacol. 2011;206:125–162.

(6) Lin SJ, et al. Life span extension by calorie restriction in S. cerevisiae requires NAD and SIR2. Science. 2000;289:2126–2128.

La entrada What NAD is and Why You Should Care About It se publicó primero en Neolife.