One of the most widely discussed studies in recent preventive cardiology, involving first-time runners in the London Marathon, examined how six months of training affected aortic health.

The study, published in the Journal of the American College of Cardiology and funded by the British Heart Foundation, included 138 runners and showed that marathon preparation reduced aortic stiffness and central blood pressure. Participants achieved arterial rejuvenation equivalent to approximately four years, with the greatest benefits observed in those who began with poorer physical fitness.

Dr. Carlos Martí – Neolife Medical Team

The aorta: the forgotten shock absorber of the circulatory system

When cardiovascular health is discussed, attention usually focuses on the heart or on specific arteries such as the coronary arteries. The aorta tends to remain in the background despite being the body’s largest artery and being responsible for a little-known but essential function: cushioning the force of each heartbeat. In a young person, its wall is elastic thanks to the elastin fibers that compose it, and it expands and recoils with every contraction of the heart, transforming a pulsatile flow into a much more uniform one before it reaches the rest of the body.

With age, that elastin is gradually degraded and replaced by collagen, a much stiffer protein. The aorta loses its cushioning capacity, the pressure generated by each heartbeat reaches the brain, heart, and kidneys with greater force, and this ongoing mechanical wear underlies much of the increased risk of hypertension, stroke, and heart failure associated with aging, even in the absence of other identifiable risk factors.

The most surprising finding: the poorer the starting fitness, the greater the benefit

When the results were analyzed by subgroup, a pattern emerged that overturns the usual intuition about exercise and age: vascular rejuvenation was not greatest in the youngest or fastest runners, but rather in the older participants and those with slower finishing times. The stiffer the aorta was at the beginning of the study, the greater the improvement observed after six months of training.

The authors’ interpretation was clear and, for any sedentary person considering starting exercise after the age of 50 or 60, quite encouraging: the cardiovascular system retains a substantial capacity for adaptation throughout much of adult life, and one does not need to have been an athlete to benefit. In fact, the margin for improvement is often greatest precisely in those who start from a less favorable baseline.

How vascular age is measured today: from the research laboratory to the clinic

In the original study, aortic stiffness was measured using cardiovascular magnetic resonance imaging, a highly precise technique that, because of its cost and availability, is largely confined to research settings. To bring the same concept into clinical practice, the reference tool is pulse wave velocity (PWV): the speed at which the pressure wave generated by each heartbeat travels through the arteries. A stiffer arterial wall transmits that wave more quickly, making an elevated PWV an independent predictor of cardiovascular risk beyond traditional risk factors.

Devices such as SphygmoCor can obtain this measurement non-invasively using a blood-pressure cuff on the arm or tonometry sensors placed over the radial and femoral arteries, reconstructing the central aortic pressure waveform without any invasive procedure. This turns something that previously could only be estimated indirectly into an objective, reproducible measurement: a true snapshot of the biological age of the arterial system, useful both for detecting accelerated vascular aging and for assessing whether an intervention such as a training program is working.

What endurance exercise does that a drug cannot fully replicate

The mechanism behind this improvement is not a single factor but the sum of several. Sustained endurance exercise increases shear stress on the endothelium, the inner lining of blood vessels, which stimulates the production of nitric oxide, a molecule central to the arteries’ ability to relax and remain elastic. Added to this are the well-documented effects of aerobic exercise: lower blood pressure, improved lipid profile, reduced low-grade inflammation, and greater insulin sensitivity.

What this study contributed was not the discovery that exercise improves vascular health—that has been known for years from supervised laboratory training programs—but the demonstration that the same benefit can be achieved through real-world training, without clinical supervision and at moderate intensity, the kind of program followed by anyone who decides to run a first marathon.

From evidence to practice: what this means for someone starting from zero

Translated into a realistic plan, the training pattern followed by the study participants did not require becoming a competitive distance runner: gradual progression of training volume over several months, three to five sessions per week combining easy continuous running with some more demanding work, and consistency maintained over time. The reported benefit was achieved after six months of preparation, not through isolated efforts or occasional high-intensity sessions.

In sedentary individuals, in those with pre-existing cardiovascular risk factors, or in adults over 45–50 years of age, it is advisable to begin with a medical evaluation that includes basic cardiovascular screening before starting a program of this type. Knowing a patient’s true vascular age at baseline, rather than relying solely on a single blood-pressure reading taken in the office, provides much more comprehensive information and also allows objective monitoring of progress as training advances.

As always, the Neolife approach

This study illustrates a central idea in preventive and longevity medicine: biological age does not always match the age printed on an ID card, and much of that difference depends on modifiable factors. At Neolife, our preventive checkups include the assessment of cardiovascular biomarkers, including indicators of arterial stiffness, precisely to understand each patient’s true baseline beyond a blood-pressure number measured at a single moment.

Based on that assessment, we design personalized follow-up programs that combine exercise prescription, nutrition, and medical intervention when necessary, with the aim of addressing the aspects of vascular aging that can be modified. The study by Bhuva and Manisty leaves a simple message that is easy to apply: sometimes, the path toward a younger aorta begins with setting a first goal, no matter how distant it may seem at the start.

BIBLIOGRAPHY

(1) Bhuva AN, D’Silva A, Torlasco C, Jones S, Nadarajan N, Van Zalen J, et al. Training for a First-Time Marathon Reverses Age-Related Aortic Stiffening. J Am Coll Cardiol. 2020;75(1):60-71. doi: 10.1016/j.jacc.2019.10.045.

(2) University College London Hospitals Biomedical Research Centre. Training for first-time marathon “reverses” ageing of blood vessels. Comunicado de prensa, mayo de 2019.

(3) Townsend RR, Wilkinson IB, Schiffrin EL, et al. Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness: A Scientific Statement From the American Heart Association. Hypertension. 2015;66(3):698-722.

(4) Butlin M, Qasem A. Large Artery Stiffness Assessment Using SphygmoCor Technology. Pulse (Basel). 2017;4(4):180-192.

La entrada A First Marathon, A Younger Aorta: What a Group of Recreational Runners in London Demonstrated se publicó primero en Neolife.

Last May, The Lancet published the outcome of an unprecedented international consensus process: polycystic ovary syndrome (PCOS) will no longer be known by that name and will instead be renamed polyendocrine metabolic ovarian syndrome (PMOS). Led by Monash University and endorsed by the World Health Organization, this change is far more than a cosmetic adjustment in terminology; it is the result of fourteen years of scientific work.

Behind the new name lies an extensive process involving iterative global surveys, modified Delphi methods, and the participation of more than 14,000 individuals—both patients and healthcare professionals—from every region of the world. The goal was to identify a name that accurately reflects what is truly happening in the bodies of those living with this condition.

Dr. Carlos Martí – Neolife Medical Team

A new name to better reflect clinical reality

For decades, the term “polycystic” focused attention—and diagnosis—on a specific ultrasound finding: the presence of multiple follicles within the ovary. Yet these follicles are not pathological cysts, but rather immature structures that failed to complete their development, and many women with the condition do not even exhibit this ovarian morphology.

This discrepancy between the name and the clinical reality had important consequences: delayed diagnoses, fragmented care, and a stigma that remains associated with the word “polycystic.” The new name aims to put an end to this confusion and to acknowledge, from the terminology itself, that this is a multisystem disorder involving hormonal, metabolic, and reproductive dysfunction simultaneously.

The magnitude of the problem justifies the change. According to the WHO, PMOS affects one in eight women of reproductive age worldwide, and up to 70% of cases are estimated to remain undiagnosed. The transition to the new terminology will be implemented gradually over the next three years, with updates to clinical guidelines, diagnostic classifications, and educational materials for patients.

From PCOS to PMOS: the anatomy of a global consensus

The process, published on May 12, 2026, and led by Professor Helena Teede together with the Global Name Change Consortium, involved 56 academic, clinical, and patient organizations. The aim was not merely to select a new name based on the opinion of a few experts, but rather to build it upon scientific evidence and the real-world experiences of individuals living with the condition.

The new terminology was officially presented during the European Congress of Endocrinology in Prague and simultaneously published in The Lancet. According to the authors, the priority was to find a precise term, even if this meant leaving behind the familiar PCOS acronym that had defined the condition for decades.

The three pillars of the new name

The term polyendocrine metabolic ovarian syndrome encapsulates three key concepts.
“Polyendocrine” acknowledges that the disorder extends beyond the ovaries and involves multiple hormonal systems, including androgens, insulin, and, in some cases, thyroid function.
“Metabolic” places insulin resistance and cardiovascular risk at the center of the condition, rather than treating them as secondary complications.
“Ovarian” preserves the reproductive origin of the syndrome while removing the misleading reference to cysts.

This new terminology is not only more accurate; it also provides a better framework for treatment. A condition that simultaneously affects metabolism, multiple endocrine pathways, and the reproductive system cannot realistically be managed from a single specialty.

What is PMOS and how is it diagnosed?

Beyond the name change, PMOS continues to be diagnosed using the well-established Rotterdam criteria. At least two out of three conditions must be present:
Ovulatory dysfunction (irregular menstrual cycles or anovulation).
Excess androgen levels, either clinically (acne, hirsutism, hair loss) or demonstrated biochemically.
Characteristic ovarian morphology on ultrasound or elevated anti-Müllerian hormone levels.
In adolescents, diagnostic criteria are applied more cautiously, and only the first two criteria are considered.

These combinations give rise to different phenotypes; not all women with PMOS share the same profile. Some present with hyperandrogenism and irregular cycles together with polycystic ovarian morphology, whereas others exhibit the same hormonal abnormalities without the ultrasound findings. Still others maintain normal ovulation while showing androgen excess and multiple follicles. This variability is precisely what the new terminology aims to capture more effectively.

Although insulin resistance is extremely common in PMOS, it is not part of the formal diagnostic criteria. Nevertheless, it strongly influences prognosis and treatment, which explains why the metabolic component now occupies a central place in the disease’s name.

Why naming matters for health

Women with PMOS experience a wide range of manifestations: irregular cycles, difficulty conceiving, persistent acne, excessive hair growth, and hair loss, but also an increased risk of type 2 diabetes and cardiovascular disease. The previous terminology, focused mainly on the ovaries, tended to overlook these metabolic implications, which are often the most significant determinants of long-term health.

Accurately naming a disease is not merely symbolic. When terminology reflects the true complexity of a condition, it improves clinical recognition, accelerates diagnosis, and facilitates coordinated care among different specialties.

The cardiovascular component: why it is not a minor detail

Cardiovascular risk is not a secondary consequence of PMOS but one of the fundamental reasons behind the name change. Insulin resistance is present in approximately 85% of affected individuals and represents one of the central mechanisms driving the syndrome. Compensatory hyperinsulinemia stimulates ovarian and adrenal androgen production, reduces sex hormone-binding globulin (SHBG), and increases circulating free testosterone levels.

Ese mismo desequilibrio favorece la acumulación de grasa visceral y hepática, un estado proinflamatorio de bajo grado y disfunción del endotelio vascular, ingredientes que, sostenidos en el tiempo, derivan en hipertensión arterial, dislipemia y aterosclerosis prematura. El riesgo de diabetes tipo 2 y de diabetes gestacional también aumenta de forma proporcional al peso corporal.

For this reason, current guidelines recommend that all women newly diagnosed with PMOS undergo a metabolic evaluation including a lipid profile and an oral glucose tolerance test, regardless of age or body mass index. Early identification of these abnormalities allows intervention before overt cardiovascular disease develops, in line with the preventive approach that we apply at Neolife to cardiometabolic risk factors.

How PMOS is treated

Treatment of PMOS has never relied on a single solution, and this does not change with the new terminology. Management remains individualized and depends on the patient’s predominant symptoms, reproductive goals, and degree of metabolic impairment.

For most women, the first step consists of lifestyle interventions: adopting a diet that improves insulin sensitivity, engaging in regular physical activity, and achieving moderate weight loss when appropriate. These measures alone can improve menstrual regularity, reduce hyperandrogenism, and lower long-term cardiometabolic risk.

When metabolic dysfunction is significant, insulin-sensitizing agents such as metformin are often used. Combined hormonal contraceptives and antiandrogens are commonly prescribed to regulate menstrual cycles and manage acne or hirsutism, with spironolactone remaining one of the most widely used medications because of its effectiveness against excessive hair growth and acne. However, it should be avoided in women seeking pregnancy because of its teratogenic potential.
For women wishing to conceive, ovulation induction therapies such as letrozole or clomiphene citrate are available, and if necessary, assisted reproductive technologies such as in vitro fertilization may be considered.

Importantly, PMOS does not necessarily imply infertility. Many women with the condition achieve spontaneous or assisted pregnancies. The key lies in comprehensive follow-up involving gynecology, endocrinology, and nutrition, together with psychological support whenever necessary, given the emotional burden associated with living with a chronic condition.

What changes—and what does not—for patients

The symptoms do not change. A woman with PMOS experiences exactly the same manifestations previously associated with PCOS. What changes is the framework used to understand and integrate these manifestations into a single clinical picture, as well as the way healthcare professionals communicate and coordinate care.

The transition will be gradual. Over the next three years, clinical guidelines, classification systems, medical records, and educational resources for both patients and professionals will be updated. The goal of the consensus initiative is not to transform clinical practice overnight, but rather to ensure an orderly evolution toward this new diagnostic framework.

The Neolife approach

At Neolife, we have long approached female hormonal disorders through a comprehensive perspective, integrating endocrinology, gynecology, and nutrition to understand what happens beyond the ovary itself. This change in terminology reinforces something that has always been part of our clinical practice: evaluating each patient’s hormonal, metabolic, and reproductive profile as a whole, rather than treating individual symptoms in isolation.

Because giving a disease the right name is often the first step toward treating it better.

BIBLIOGRAPHY

(1) Teede HJ, Bahri Khomami M, Morman R, et al; Global Name Change Consortium. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. Lancet. 2026 Jun 6;407(10545):2329-2339. doi: 10.1016/S0140-6736(26)00717-8. Epub 2026 May 12.

(2) Teede HJ, Moran LJ, Morman R, et al. Polycystic ovary syndrome perspectives from patients and health professionals on clinical features, current name, and renaming: a longitudinal international online survey. EClinicalMedicine. 2025;84:103287.

La entrada The polycystic ovary syndrome gets a new name: the polyendocrine metabolic ovarian syndrome (PMOS) is finally born se publicó primero en Neolife.

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.

The recently published American guidelines for the management of dyslipidemia reinforce an important shift in how we understand cardiovascular risk. This is not so much about new targets, but about a more precise way of interpreting what is actually happening in each patient.

For many years, dyslipidemia has been understood as an alteration in numbers: elevated LDL cholesterol implied increased risk, and reducing it was the primary treatment goal. While useful, this approach oversimplifies a much more complex process.

Dr. Carlos Martí – Neolife Medical Team

Cardiovascular Prevention

For a long time, the focus has been on identifying out-of-range values. However, we now know that the atherosclerotic process (the accumulation of fat in the arteries) begins long before these values change or symptoms appear.

This explains why some individuals experience cardiovascular events despite having apparently normal blood tests, while others with elevated levels remain stable for years. The difference lies in what is not always visible in conventional testing: particle number, cumulative burden, or the presence of subclinical disease. Today’s tools allow access to this information and enable a better understanding of where each patient stands in the disease process.

The goal, therefore, is not only to detect abnormalities once they become evident, but to interpret earlier signals that allow for more proactive intervention. In cardiovascular health, it is not just about treating risk when it appears, but about understanding how it develops from much earlier stages.

Beyond Cholesterol: Understanding What We Really Measure

LDL cholesterol has traditionally been the cornerstone of diagnosis and treatment. However, not all LDL particles have the same impact, and a normal value does not guarantee low risk. In this context, apolipoprotein B (ApoB) has gained importance. It is a protein present in all particles capable of forming plaques in the arteries, meaning that measuring it is essentially counting how many “potentially harmful particles” are circulating in the bloodstream.

Unlike LDL, which measures how much cholesterol these particles carry, ApoB indicates how many particles are actually present. This is particularly useful in individuals with overweight, diabetes, or elevated triglycerides, where LDL may appear normal despite high risk.

But not all risk depends on lifestyle or metabolism. There is also a genetic component that may go unnoticed in standard blood tests. This is where lipoprotein(a), or Lp(a), becomes relevant. It is a particle similar to LDL but with unique characteristics that make it especially atherogenic (more likely to promote plaque formation in the arteries). Its levels are largely genetically determined, meaning a person may have elevated Lp(a) from birth without knowing it. As a result, even with apparently normal cholesterol levels, cardiovascular risk may be higher than expected if Lp(a) is elevated. For this reason, current guidelines recommend measuring it at least once in a lifetime.

The integration of these biomarkers provides a more comprehensive assessment of risk, moving beyond a model based solely on total cholesterol or LDL.

From Estimating Risk to Detecting Disease

Another key change reinforced by the new guidelines is the use of imaging techniques to refine risk assessment in selected patients. Coronary artery calcium (CAC) measures the amount of calcium deposited in the arteries of the heart. Its presence indicates that atherosclerosis already exists, even in the absence of symptoms.

Although not yet part of the main guideline recommendations, carotid ultrasound allows direct visualization of the neck arteries and the detection of plaques or arterial wall thickening (intima-media thickness, IMT, a marker of arterial health). While CAC identifies more advanced disease, carotid ultrasound can provide information about earlier stages of the process.

At Neolife, these tools are part of an advanced preventive medicine approach. This allows for more precise adjustment of treatment intensity and prioritization of interventions in patients who might otherwise appear low-risk based on conventional testing.

We combine biomarkers such as ApoB and lipoprotein(a) with imaging techniques, including carotid ultrasound, to obtain a more complete picture of vascular health. The goal is not only to estimate future risk, but to determine whether the disease process has already begun—even in its earliest stages.

A More Precise, Not More Complex Approach

The evolution in dyslipidemia management does not mean performing more tests on every patient, but rather selecting more effectively which information is needed in each case.

In practice, this translates into:

• Knowing when a basic blood test is sufficient
• Identifying when measuring ApoB or lipoprotein(a) is useful
• Considering markers such as high-sensitivity CRP (an indicator of low-grade inflammation), which can increase cardiovascular risk even with normal cholesterol levels
• Using imaging tests to clarify uncertainty about actual risk
• Adjusting treatment based on the patient’s overall profile, not just a single value

This approach allows for the identification of high-risk individuals who might otherwise go unnoticed with conventional testing, while also avoiding unnecessary treatment in those who do not need it.

At Neolife, this strategy has long included the assessment of low-grade inflammation, understood as a key factor in the development of atherosclerosis. It is not only about how much cholesterol circulates, but about the environment in which that cholesterol acts.

Applying a Comprehensive Strategy: Addressing the Cause, Not Just the Numbers

Lifestyle interventions remain the foundation of treatment, but their impact goes far beyond lowering cholesterol. Reducing visceral fat (fat stored around organs), improving insulin sensitivity, engaging in strength training and aerobic exercise, and ensuring adequate sleep all directly influence the formation of atherogenic particles, inflammation, and arterial health.

This explains why two individuals with the same cholesterol levels may have completely different risks. The goal is not just to improve lab results, but to modify the metabolic environment in which the disease develops.

Understanding Risk Before It Becomes Visible

Cardiovascular risk does not appear suddenly—it develops progressively over time. We now know that the atherosclerotic process begins long before laboratory values change or symptoms arise. This is why a conventional blood test does not always reflect true risk. Factors such as particle number, inflammation, and subclinical disease can make a critical difference. The real advancement lies in being able to access this information and understand where each patient stands in the process, allowing for earlier and more effective intervention.

At Neolife, this approach is part of daily clinical practice: integrating advanced laboratory testing, biomarkers, and vascular imaging to detect risk before it becomes clinically apparent and to address it in a personalized way.

Because in cardiovascular health, the goal is not simply to act in time—but to prevent the problem from developing in the first place.

BIBLIOGRAPHY

(1) Blumenthal RS, Morris PB, Gaudino M, Johnson HM, Anderson TS, Bittner VA, Blankstein R, Brewer LC, Cho L, de Ferranti SD, Gianos E, Gluckman TJ, Gradney KF, Isiadinso I, Lloyd-Jones DM, Marrs JC, Martin SS, McLain KH, Mehta LS, Mora S, Mulugeta WM, Natarajan P, Navar AM, Orringer CE, Polonsky TS, Reynolds HR, Saseen JJ, Shapiro MD, Soffer DE, Tynes SA, Villavaso CD, Virani SS, Wilkins JT. 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2026 Mar 13:S0735-1097(25)10254-4. doi: 10.1016/j.jacc.2025.11.016. Epub ahead of print. PMID: 41824590.

(2) Gráfico extraído del blog de https://peterattiamd.com/measuring-cardiovascular-disease-risk-and-the-importance-of-apob-part-1/

La entrada How Our Understanding of Cholesterol and Cardiovascular Risk Is Changing 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

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

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