Osteoporosis and osteopenia are silent diseases that affect millions of people, especially as they age.

Diet, lifestyle, and certain daily habits play a key role in both their prevention and progression. In this article, we review what happens in the bones, which nutrients help protect them, and which foods should be limited to preserve their strength.

Meritxell Massons – Neolife Nutrition Unit

What Are Osteoporosis and Osteopenia?

Osteoporosis is a disease characterized by the progressive loss of bone mass and bone quality. The bone becomes more porous and fragile, significantly increasing the risk of fractures, even during everyday activities such as walking or bending down.

Osteopenia is a previous stage in which bone mineral density is lower than normal but does not yet meet the diagnostic criteria for osteoporosis. It is usually detected through a bone densitometry test and represents an important opportunity for prevention.

Why Do Bones Weaken With Age?

Bones are not static structures; they are constantly being renewed. Some cells build bone (osteoblasts), while others break it down (osteoclasts).

• Childhood and adolescence: bone formation predominates.
• Adulthood: a balance is maintained between formation and degradation.
• After the age of 50–60: degradation exceeds formation, especially after menopause due to the decline in estrogen levels.

This process explains why osteoporosis is more common in postmenopausal women and older men.

Preventing Osteoporosis Through Nutrition

Prevention begins long before symptoms appear. Achieving a good peak bone mass during adolescence and early adulthood is essential for long-term bone health.

Calcium: The Structural Basis of Bone

Adequate calcium intake prevents the body from extracting calcium from bones to maintain vital functions such as muscle contraction or blood clotting.

Main sources:

• Dairy products (milk, yogurt, aged and semi-aged cheeses)
• Legumes, nuts, and seeds
• Small fish eaten with bones (such as sardines)
• Vegetables such as broccoli
• Fortified foods (plant-based drinks, cereals)

Two daily servings of dairy products, within a varied diet, usually cover the needs of healthy adults.

Vitamin D: Essential for Calcium Absorption

Vitamin D allows calcium to be properly absorbed in the intestine and deposited in the bone.

Main sources:

• Moderate sun exposure
• Oily fish
• Eggs and dairy products
• Fortified foods

During winter or in individuals with limited sun exposure, deficiencies are common, and supplementation may be necessary under the supervision of a healthcare professional.

Physical Activity: An Essential Stimulus

Exercise, especially weight-bearing activities (walking, climbing stairs, dancing, or strength training), stimulates bone formation. Each muscle contraction sends a positive signal to the bone, helping maintain its density.

Nutrients That Support Bone Health

In addition to calcium and vitamin D, other nutrients play key roles:

• Protein: necessary for the bone matrix, although excessive intake from animal sources should be avoided.
• Magnesium: supports bone mineralization and hormonal activity.
• Zinc: involved in the formation and repair of bone tissue.
• Vitamin C: essential for collagen synthesis.
• Vitamin K: regulates calcium binding in bone.

A varied and balanced diet usually covers these requirements.

Foods and Substances to Limit in Osteoporosis

This does not mean strict prohibitions, but rather moderate and mindful consumption.

• Caffeine

High intake may increase urinary calcium excretion. Limiting coffee, tea, and energy drinks can help protect bone health.

• Excess Phosphorus

Found mainly in soft drinks such as cola and in ultra-processed foods. Excess phosphorus disrupts the calcium–phosphorus balance and negatively affects bone density.

• Alcohol and Tobacco

Both interfere with new bone formation and increase the risk of fractures. Reducing or eliminating them is a key preventive measure.

• Phytates and Oxalates

Present in whole grains, cocoa, coffee, and some leafy green vegetables. It is not necessary to eliminate them, but it is advisable to combine them appropriately and ensure they do not displace calcium-rich foods.

Nutrition and Hormones: A Key Relationship

The loss of estrogen during menopause and testosterone in older men accelerates bone loss. For this reason, osteoporosis is more common in postmenopausal women and in men over the age of 65.

Proper nutrition, together with exercise and medical monitoring, can significantly slow this process.

Conclusion

Taking care of bone health does not depend on a single food, but on an overall lifestyle. A nutrient-rich diet, regular physical activity, and reducing harmful habits are the best tools to prevent osteoporosis and improve quality of life in the long term.

BIBLIOGRAPHY

(1) World Health Organization. Prevention and management of osteoporosis: report of a WHO scientific group. Geneva: World Health Organization; 2003. (WHO Technical Report Series; no. 921).

(2) International Osteoporosis Foundation. Nutrition and bone health [Internet]. Nyon: International Osteoporosis Foundation; 2023 [cited 2026 Feb 9]. Available from: International Osteoporosis Foundation.

(3) National Institutes of Health, Office of Dietary Supplements. Calcium: fact sheet for health professionals [Internet]. Bethesda (MD): National Institutes of Health; 2022 [cited 2026 Feb 9]. Available from: National Institutes of Health.

(4) National Institutes of Health, Office of Dietary Supplements. Vitamin D: fact sheet for health professionals [Internet]. Bethesda (MD): National Institutes of Health; 2022 [cited 2026 Feb 9]. Available from: National Institutes of Health.

(5) European Food Safety Authority. Scientific opinion on dietary reference values for calcium. EFSA Journal. 2015;13(5):4101.

(6) European Food Safety Authority. Dietary reference values for vitamin D. EFSA Journal. 2016;14(10):4547.

(7) Weaver CM, Gordon CM, Janz KF, Kalkwarf HJ, Lappe JM, Lewis R, et al. The National Osteoporosis Foundation’s position statement on peak bone mass development and lifestyle factors. Osteoporosis International. 2016;27(4):1281–1386.

(8) Bonjour JP. Protein intake and bone health. Int J Vitam Nutr Res. 2011;81(2–3):134–142.

(9) Rizzoli R, Biver E, Brennan-Speranza TC, Bilezikian JP. Nutritional intake and bone health. Lancet Diabetes Endocrinol. 2021;9(9):606–621.

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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.

You may not know that in Spain between one third and nearly half of adults have hypertension. This means that between 1 and 2 out of every 4 people suffer from high blood pressure, even though they may not be aware of it.

You may also be unaware—or not fully conscious—that, much like diabetes mellitus, arterial hypertension (HTN) is one of the main “silent killers” affecting our society. It often causes no symptoms, yet gradually damages our blood vessels and internal organs, increasing the risk of serious and potentially life-threatening complications. Every millimeter of mercury (the unit used to measure blood pressure) that is controlled represents time gained and health preserved. Would you like to understand why this is so?

Dr. Minguito – Neolife Medical Team

Risk factors

In part 1 of this article, we discussed what hypertension is and its consequences. In this second part, we will review risk factors and pharmacological treatment.

There are several risk factors that contribute to the development of arterial hypertension. Some cannot be changed, but others are within our control.

1. NON-MODIFIABLE RISK FACTORS

• Age

Blood pressure tends to increase with age because blood vessels gradually lose elasticity, hormonal changes affect fluid and salt balance, and the cumulative effects of unhealthy habits build up over time. While approximately 5–10% of women aged 20–44 have hypertension, prevalence rises dramatically to 85% in women aged 75 or older (comparable figures for men are 10–15% and 80%, respectively).

• Race

High blood pressure affects people of all races, but African Americans have a significantly higher risk of developing hypertension. African American women, in particular, have higher rates than men from other racial groups. For this reason, African Americans should begin monitoring their blood pressure and adopting healthy habits from a young age. Other racial groups have similar risk levels, although Asian women tend to have a lower risk. Despite this, many Hispanic and Asian individuals with hypertension are unaware of their condition and remain untreated, highlighting the importance of blood pressure monitoring for everyone.

• Family history and genetics

Having parents or close relatives with hypertension increases your risk, as approximately 50% of blood pressure variability is hereditary. More than 800 genetic variants influence blood pressure; although each has a small effect individually, their cumulative impact can accelerate the development of hypertension with age. Therefore, genetic predisposition requires regular monitoring and awareness of family history. Nevertheless, healthy lifestyle habits can offset a large part of this risk.

2. MODIFIABLE RISK FACTORS

Lifestyle modifications often provide effective, non-pharmacological ways to control or reduce blood pressure, sometimes with results comparable to medication. A large proportion of hypertension cases are due to an unhealthy diet (and associated obesity), lack of exercise, excessive alcohol consumption, or a combination of these factors.

• Obesity

One of the most effective lifestyle interventions for blood pressure control is weight loss. Excess body weight overloads the heart and promotes insulin resistance, both of which contribute to elevated blood pressure. Research shows a direct and consistent relationship between body mass index (BMI) and hypertension. Large studies suggest that obesity may account for 40–78% of hypertension cases.

Even modest weight loss can produce significant blood pressure reductions. A 2003 meta-analysis of 25 randomized clinical trials in overweight and obese adults found that for every kilogram of weight lost, systolic blood pressure decreased by approximately 1 mmHg and diastolic pressure by 0.92 mmHg.

Weight loss can be achieved through caloric restriction, intermittent fasting, or dietary changes, and the best approach depends on what is most sustainable for each individual.

• Dietary salt (sodium)

The relationship between dietary sodium, hypertension risk, and overall health is complex. Some individuals and groups are more sensitive to the blood-pressure-raising effects of salt. These include African Americans, older adults, people with diabetes, chronic kidney disease, or pre-existing hypertension. For these groups, sodium intake should be reduced, ideally to 2,000 mg per day or less.
Although organizations such as the American Heart Association recommend even lower limits (1,500 mg/day), it is important to note that excessively low sodium intake can also cause problems. Studies have shown that very low sodium consumption may be associated with headaches, mental status changes, lethargy, cramps, nausea, dehydration, and excessively low blood pressure, increasing the risk of falls and injuries in older adults. Therefore, moderate sodium reduction is advised for low-risk individuals, with more aggressive reduction reserved for those who are salt-sensitive.

In addition to reducing sodium, increasing potassium intake—a mineral essential for muscle function, kidney health, and blood vessel relaxation—can help lower blood pressure. In hypertensive adults, potassium intake can reduce systolic pressure by 3–6 mmHg and diastolic pressure by 1–4 mmHg. The sodium-to-potassium ratio appears to be more important than absolute intake levels. Foods rich in potassium, such as bananas, potatoes, and legumes, are especially beneficial for individuals with high salt intake.

• Exercise and blood pressure

Aerobic exercise is highly effective. A meta-analysis of clinical trials lasting at least four weeks found that aerobic training can reduce systolic blood pressure by up to 8 mmHg and diastolic pressure by at least 5 mmHg. The optimal dose is 90–150 minutes per week at 65–75% of maximum heart rate (the so-called “Zone 2”). At Neolife, we recommend at least three hours per week.

• Dynamic resistance training

Strength training may temporarily raise blood pressure during exercise, but in the long term it reduces systolic pressure by about 2 mmHg and diastolic pressure by 3 mmHg, when performed for 90–150 minutes per week using weights ranging from 50–100% of one-repetition maximum.

• Isometric resistance training (no weights)

This type of exercise has shown even greater reductions in systolic blood pressure—around 6 mmHg—and 3 mmHg in diastolic pressure, despite its seemingly low intensity.

• Alcohol

Current evidence shows that alcohol raises blood pressure in a dose-dependent manner. Genetic studies using Mendelian randomization confirm that even small amounts increase risk: each additional daily drink raises hypertension risk by 30%, and in heavy drinkers this risk can increase by up to 160%. There is no “safe” level of alcohol consumption for blood pressure. The good news is that reducing or stopping alcohol intake significantly lowers risk and improves cardiovascular health, even in former heavy drinkers.

3. OTHER FACTORS

• Sleep

Poor sleep—whether due to insufficient or excessive duration, or disorders such as insomnia, snoring, or sleep apnea—is associated with a higher risk of hypertension. Evidence shows a U-shaped relationship, with increased risk below 7 hours and above 9 hours of sleep. Optimizing sleep quality is essential; up to half of hypertension cases could potentially be managed without medication through lifestyle changes alone.

• Stress

Chronic stress is a major contributor to hypertension. Stress hormones such as cortisol increase heart rate and constrict blood vessels. Unhealthy coping mechanisms—overeating, smoking, or alcohol use—can further worsen blood pressure. Mindfulness, meditation, deep breathing, and physical activity are recommended strategies. Relaxation techniques and biofeedback have shown modest blood pressure reductions in some patients.

• Caffeine

Caffeine can temporarily raise blood pressure, particularly in people who do not consume it regularly. However, habitual consumption does not appear to cause sustained hypertension or increase long-term risk.

• Insulin resistance

Insulin resistance and type 2 diabetes significantly impact blood pressure by reducing nitric oxide bioavailability, impairing vasodilation and increasing vascular resistance.

Pharmacological treatment

As discussed, blood pressure control is a cornerstone in reducing cardiovascular disease, stroke, and kidney damage. Lifestyle modifications are the first-line approach, but when insufficient, pharmacological treatment becomes necessary.

Antihypertensive therapy must always be prescribed by a physician, who will select the most appropriate option based on individual characteristics and comorbidities.

There are four main first-line drug classes:

1. Thiazide diuretics
2. Calcium channel blockers
3. Angiotensin-converting enzyme inhibitors (ACE inhibitors)
4. Angiotensin II receptor blockers (ARBs)

All typically reduce systolic blood pressure by 12–15 mmHg and diastolic pressure by 9–11 mmHg.

ACE inhibitors, for example, can reduce blood pressure by up to 12.5/9.5 mmHg. It is recommended to initiate treatment at half of the maximum dose to minimize the risk of adverse effects. ARBs (angiotensin II receptor blockers) offer similar efficacy but with fewer side effects. In many cases, they are even considered superior, although ACE inhibitors tend to be less expensive because they have been on the market longer.

When ACE inhibitors cause cough—a common side effect—patients can be easily switched to an ARB. Thiazide diuretics and calcium channel blockers are also effective, achieving reductions of up to 15/10 mmHg, but they are more frequently associated with adverse effects. For this reason, they are often used as adjunctive therapy, once treatment with ACE inhibitors or ARBs has been optimized. As always, treatment decisions must be individualized.

This raises an important question: are there factors that determine which medication is best for a particular individual? The answer is yes. The optimal choice of antihypertensive therapy is patient-specific and depends on the presence of comorbid conditions and tolerance to potential side effects. For example, most calcium channel blockers are contraindicated in heart failure with reduced ejection fraction, and thiazide diuretics are generally considered less appropriate for patients with diabetes or prediabetes, as they may worsen metabolic parameters. ACE inhibitors and ARBs are contraindicated during pregnancy, although they are generally associated with fewer adverse effects than calcium channel blockers and thiazide diuretics.

Summary

It is important to emphasize that while medications are often more effective than any single lifestyle intervention, the combined effect of multiple lifestyle improvements can match the benefits of pharmacological therapy.

At Neolife, we believe that blood pressure management is one of the most important pillars of longevity. It may not seem as glamorous as the latest anti-aging treatments, but it remains one of the most effective and well-established approaches in preventive medicine for reducing morbidity and mortality.

BIBLIOGRAPHY

(1) Banegas JR, Graciani A, López-García E, et al.
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La entrada “Silent Killer”: Understanding What Arterial Hypertension Is and Its Consequences (Part 2) se publicó primero en Neolife.

May not know that in Spain, between one third and nearly half of adults have hypertension. This means that between 1 and 2 out of every 4 people have high blood pressure—although they may not always be aware of it.

And may also not know, or may not be fully aware, that—much like diabetes mellitus—arterial hypertension (HTN) is one of the main “silent killers” affecting our society. It often causes no symptoms, yet it gradually damages our blood vessels and internal organs, increasing the risk of serious and potentially fatal complications. Every millimeter of mercury (the unit used to measure blood pressure) that is brought under control represents time gained and health preserved. Would you like to learn why this is so?

Dr. Minguito – Neolife Medical Team

What Is Arterial Hypertension?

Arterial hypertension is one of the leading cardiovascular risk factors in our society. At Neolife, we aim to provide you with a clear perspective so you can understand what it is, why it is so important to keep it well controlled, and what poor control can lead to. Here’s a spoiler: if you care about your brain, your heart, and your kidneys, you need low blood pressure.

When we talk about blood pressure, we are referring to the force exerted by the blood against the walls of the arteries as the heart beats. We have all heard, during a doctor’s visit, two measurements: the “upper” and the “lower” numbers—but what do they actually mean?

The cardiac cycle has two main phases: systole and diastole. During systole, the heart’s ventricles (the lower chambers) contract to eject blood. The left ventricle is especially important in this process because it is more muscular than the right and is responsible for pumping blood throughout the body, overcoming the resistance of the peripheral circulatory system.
It is worth noting that here we are referring to systemic or peripheral circulation—the circulation that supplies the body in general—and not to pulmonary pressure, which is a different measurement. Blood pressure, commonly reported as “120 over 80,” refers to pressure in the peripheral circulation. Pulmonary pressure, which is mainly regulated by the right ventricle, is considerably lower.

During systole, the left ventricle contracts and pushes blood out of the heart through the aortic valve into the aorta (the large artery leaving the heart), from where it is rapidly distributed throughout the body. In this phase, the blood exerts pressure against the arterial walls—this is the systolic pressure (the “upper” number).

The second phase of the cycle is diastole, which is equally important. During diastole, the heart relaxes after ejecting blood, allowing the ventricles to fill again from the atria. This is also the phase during which the heart itself receives its blood supply through the coronary arteries. Although blood pressure is lower during diastole, there is still a constant or tonic pressure within the arteries—this is the diastolic pressure (the “lower” number).

What Does It Mean to Have High Blood Pressure, and Why Is It So Important to Keep It at Optimal Levels?

Since 2017, guidelines have changed following the publication of the SPRINT clinical trial (Systolic Blood Pressure Intervention Trial) in 2015. Current recommendations, in effect for approximately six years, establish new blood pressure categories.

Blood pressure classification (according to current guidelines)

For example, a person with a blood pressure of 120/83 mmHg would already fall into the category of stage 1 hypertension, even though their systolic pressure remains within the traditionally “normal” range.

Where Do These Values Come From? The SPRINT Trial (2015)

The aim of the SPRINT study was to evaluate the benefits of intensive blood pressure control. Nearly 10,000 individuals with a systolic blood pressure of 130 mmHg or higher and a high cardiovascular risk—but without type 2 diabetes—were included. This population was selected because a higher probability of cardiovascular events over a short period was expected, making it easier to assess clinical outcomes.

Participants were randomly assigned to two groups:

• Intensive treatment: target systolic blood pressure below 120 mmHg.
• Standard treatment: target systolic blood pressure below 140 mmHg.

At baseline, the average blood pressure of participants was approximately 140/78 mmHg. After one year of treatment, average systolic blood pressure was 121.4 mmHg in the intensive-treatment group and 136.2 mmHg in the standard-treatment group.

The most striking aspect of the study was that it was stopped early due to the clear clinical benefits observed in the intensive-treatment group. The most notable finding was a reduction in all-cause mortality—not only from cardiovascular causes, but also from kidney disease, accidents, suicides, and even homicides. This benefit was unexpected and surprised many experts.

This study was one of the most compelling demonstrations that intensively controlling systolic blood pressure below 120 mmHg can save lives and reduce cardiovascular events, even over a relatively short period.

The study also reminds us that conditions such as hypertension, smoking, and elevated apoB levels (a marker of atherogenic cholesterol) cause cumulative damage over time. Hypertension mechanically damages the vascular endothelium, smoking causes chemical damage to the same tissue, and LDL cholesterol (which contains apoB) infiltrates the damaged endothelium, initiating the atherosclerotic cascade. For this reason, early reduction of all these risk factors has an enormous cumulative effect over time.

Years later, in 2021, the STEP study in China once again demonstrated that strict blood pressure control reduces cardiovascular events and cardiovascular mortality.

We may still hear—or hold on to—the outdated belief that a blood pressure of 140/90 mmHg is acceptable. However, in light of all this evidence, it is clear that this is not the case. We need to change our mindset and pursue intensive control, aiming for a target of approximately 120/80 mmHg.

As early as the 1960s, the first data from the Framingham Heart Study had already shown the harmful effects of elevated blood pressure (at that time, hypertension was defined as any value above 140/90 mmHg). Lowering blood pressure from levels above that threshold already demonstrated clear benefits.

More recently, other meta-analyses have confirmed these findings. In individuals aged 40 to 70, for every 20 mmHg increase in systolic pressure or 10 mmHg increase in diastolic pressure, the risk of death from heart attack, stroke, or vascular disease doubles. This refers not only to a higher incidence of disease, but to a higher probability of death. For example, having a blood pressure of 140/90 instead of 120/80 doubles the risk of vascular death.

Other Organs Affected

The heart is not the only organ sensitive to hypertension. The brain is particularly vulnerable to high blood pressure, as both depend on proper perfusion through small vessels. Hypertension exerts a mechanical force that damages these vessels, increasing the risk of stroke and dementia.

The SPRINT-MIND trial, a substudy of SPRINT focused on cognitive decline, evaluated whether intensive treatment could prevent dementia. With more than 9,000 participants, the results showed an absolute reduction in dementia risk of 0.6% and a relative reduction of 16%. Thus, controlling blood pressure protects the brain.

The kidneys are another organ extremely sensitive to elevated blood pressure. Despite accounting for only 1–2% of body weight, they receive 20–25% of cardiac output (the amount of blood the heart pumps each minute to deliver oxygen and nutrients throughout the body). This implies a highly specialized and vulnerable vascular network. Hypertension accelerates the decline in glomerular filtration rate (GFR), reducing kidney function.
The situation worsens when elevated glucose levels are also present—a common combination, for example, in metabolic syndrome (which includes hypertension and insulin resistance). This leads to a progressive and dangerous decline in kidney function, often undetected if only creatinine is measured. For this reason, at Neolife, when kidney function impairment is suspected, we use cystatin C, a more sensitive marker.

The key message from these studies is that lowering blood pressure—even in individuals already diagnosed with hypertension—can significantly reduce the risk of heart disease, stroke, and other serious health conditions. While preventing blood pressure elevation in the first place is ideal, these trials show that reducing blood pressure after it has already exceeded optimal ranges still offers enormous cardiovascular benefits.

Caution: Low Blood Pressure, but Not Too Low

While high blood pressure is dangerous, excessively low blood pressure can also cause problems—although in this case, symptoms matter more than numbers. Technically, low blood pressure is defined as below 90/60 mmHg, but what truly matters is how the person feels.

Common symptoms of low blood pressure include dizziness, lightheadedness, nausea, fainting or syncope, dehydration or excessive thirst, difficulty concentrating, blurred vision, cold and pale skin, rapid and shallow breathing, and fatigue.

Not everyone with low blood pressure experiences symptoms. Some people may feel perfectly well with readings such as 100/70 mmHg, while others may not tolerate these levels, especially if they have lost weight or are taking antihypertensive medications.

For this reason, blood pressure management requires a personalized approach. As weight is lost, exercise increases, or other factors change, blood pressure may decrease naturally, and medications must be carefully adjusted to avoid adverse effects such as fainting or loss of balance.

Blood Pressure Variations Throughout the Day and With Exercise

Blood pressure naturally fluctuates throughout the day. A key observation is that during the night, it should decrease by 10–20% compared to daytime values. This is partly due to the horizontal position during sleep, which reduces the effort the heart needs to send blood to the brain. Additionally, sympathetic tone (the body’s “alert” system) should decrease at night, while parasympathetic tone—especially vagal activity—increases, promoting relaxation. Continuous blood pressure monitoring seeks precisely this nocturnal dip as a marker of cardiovascular health.

Stress also plays an important role. Transient stressful events can significantly raise blood pressure. Leaving excess cortisol (hypercortisolemia) uncontrolled can be just as harmful as persistent hypertension.

It is completely normal for systolic blood pressure to rise during exercise, as the heart needs to pump more blood to deliver oxygen to the muscles. In contrast, diastolic pressure usually remains stable or decreases slightly. This occurs because, during exercise, blood vessels in the muscles dilate (vasodilation), reducing resistance in the circulation. Thanks to this mechanism, exercise acts as a natural regulator of blood pressure: it improves arterial elasticity, reduces vascular resistance, and over time helps control resting blood pressure.

Primary vs. Secondary Hypertension

Another important concept is that hypertension may be due to an identifiable cause—this is known as secondary hypertension. It is caused by an underlying medical condition that may potentially be corrected. It is estimated that about 10% of hypertension cases have a secondary cause, so it is important not to assume that all hypertension is “essential” or primary.

There are warning signs that suggest secondary hypertension, such as lack of response to medications, loss of response to previously effective treatments, extremely high blood pressure (above 180 mmHg), or sudden onset. It is also suspicious when a young person with no family history or risk factors develops high blood pressure.

Other secondary causes that should not be overlooked include kidney disease, renal artery stenosis, thyroid disorders, sleep apnea, and hyperaldosteronism (which may result from prolonged corticosteroid use or adrenal gland disorders), among others.

At Neolife, we believe that blood pressure management is one of the most important pillars of longevity. It may not sound as glamorous as the latest anti-aging treatments, but it is one of the most effective and well-proven strategies in preventive medicine to reduce morbidity and mortality.

BIBLIOGRAPHY

(1) Banegas JR, Graciani A, López-García E, et al.
Prevalence, awareness, treatment and control of hypertension in Spain: results of a nationwide population-based study.
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Guía práctica sobre el diagnóstico y tratamiento de la hipertensión arterial en España.
Hipertens Riesgo Vasc. 2022;39(4):155–170.
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(4) Sociedad Española de Médicos de Atención Primaria (SEMERGEN).
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SEMERGEN; mayo 2024. Disponible en: SEMERGEN PDF.

(5) Banegas JR, et al.
Prevalence of hypertension in Spain 2019: population-based nationwide study.
J Hypertens. 2024;42(3):431–440.
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(6) SPRINT Research Group; Wright JT Jr, Williamson JD, Whelton PK, et al.
A randomized trial of intensive versus standard blood-pressure control.
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(7) Zhang W, Zhang S, Deng Y, et al; STEP Study Group.
Trial of intensive blood-pressure control in older patients with hypertension.
N Engl J Med. 2021;385(14):1268–1279.
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2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults.
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(9) Neter JE, Stam BE, Kok FJ, Grobbee DE, Geleijnse JM.
Influence of weight reduction on blood pressure: a meta-analysis of randomized controlled trials.
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Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials.
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Effect of dose and duration of reduction in dietary sodium on blood pressure levels: systematic review and meta-analysis of randomised trials.
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(12) Brouillard AM, Kraja AT, Rich MW.
Trends in dietary sodium intake in the United States and the impact of USDA guidelines: NHANES 1999–2016.
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Exercise training for blood pressure: a systematic review and meta-analysis.
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La entrada “Silent Killer”: Learn What High Blood Pressure Is and Its Consequences (Part 1) 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.

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.

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.

The habits we cultivate day by day have a direct impact on our physical health, emotional well-being, and how we age. Eating better, moving more, sleeping well, managing stress… it all adds up. And most importantly: everything can be trained.

We know it’s not easy. Changing a habit—especially an unhealthy one—requires consistency, patience, and often more willpower than we think we have. But we also know something else: it’s worth it.

Dr. Cristina Minguito – Neolife Medical Team

The Power of Habits: Your System Defines Your Destiny

In this newsletter, we want to help you start that change. We’re not talking about overnight transformations, but small daily decisions that, over time, can have a huge effect on your vitality, mood, and longevity.

Because yes, changing a habit can change your life. And you don’t have to do it alone. We’re here to help you find a strategy that works for you—one that inspires and motivates you, and that you can sustain over time.

This is your moment. Your health is in your hands, and we want to walk with you every step of the way.

You may have clear health goals, but what will truly determine whether you reach them is your system—that set of habits you repeat each day, often without realizing it. As James Clear explained in his book Atomic Habits, about 40–50% of what we do daily is automatic. That’s why building good habits isn’t just helpful—it’s essential.

Today, we’re sharing the four key steps from the book to build lasting habits, and how to apply them to your health, well-being, and longevity.

1. Make It Obvious

A habit needs a clear cue to be triggered. If we don’t see the “trigger,” we’ll likely forget. Visual reminders are your best allies—the more obvious, the better.

Examples:

• Want to read before bed? Leave the book on your pillow.
• Want to drink more water? Use a bright, fun bottle and place it on your desk.
• Want to improve your posture? Put a sticky note on your computer that says “Sit up straight!”

Pro Tip: For those starting strength training, leave a dumbbell in a visible spot: next to the coffee maker, by the couch, or even in the bathroom. Associating the new habit with a daily action (like making coffee) helps integrate it seamlessly into your routine.

2. Make It Attractive

We’re drawn to what feels pleasurable or fun. If the new habit feels like a punishment, it’ll be hard to stick to. But if we make it desirable, we’re already halfway there.

Examples:

• Cutting sugar? Try sweet fruit-based recipes or healthy, tasty snacks.
• Struggling with exercise? Play your favorite music or listen to a podcast you only allow during workouts.
• Turn habits into rituals: light a candle before meditating, or wear workout clothes you love.

Pro Tip: Team up. Train with a friend, do intermittent fasting with your partner, or go for a walk with your child or dog. Turning a habit into a shared moment boosts motivation and enjoyment.

3. Make It Easy

Never underestimate the power of starting small. If a habit is too demanding at first, you’ll probably quit. The key is to remove friction and make the action easier.

Examples:

• Hate running? Just put on your workout clothes. Once you do that, you’re already halfway there.
• Struggle with meditation? Start with just 2 minutes.
• Feel overwhelmed cooking healthy meals every day? Make double portions and freeze for the week.

Pro Tip: Travel often and worry about breaking your routine? Bring resistance bands or portable weights. Research nearby parks in advance. Planning ahead turns complicated into simple.

4. Make It Satisfying

We repeat what makes us feel good. Seeing tangible progress or receiving rewards makes our brain say, “This is worth it!”

Examples:

• Use an app to track your steps, sleep, or meals.
• Keep a journal to note how you feel after each workout.
• Make a “habit thermometer” and color in a square for every successful day.

Pro Tip: Celebrate your wins in meaningful ways. Did you complete a month of training? Treat yourself to new workout gear or a special class. Choose rewards that support your goal—not sabotage it.

And What About Breaking a Bad Habit?

Breaking a bad habit takes more than willpower—it requires strategy. Here are four key steps, along with real and powerful examples to inspire action today:

1. Make It Invisible

Temptation you don’t see is easier to resist.

Inspiring Examples:

• Quitting alcohol? Don’t keep it at home. Store it somewhere hard to reach—or better yet, don’t buy it.
• Don’t want to check your phone before bed? Leave it in another room. No excuses—if you use it as an alarm, get a real one.
• Want to cut back on TV? Delete streaming apps from your phone or block access with a parental control app.

“Your environment dictates your behavior. Change your environment, and your behavior will follow.”

2. Make It Unattractive

Turn momentary pleasure into a reminder of the harm it causes.

Powerful Examples:

• Quitting smoking? Keep a picture of damaged lungs in your wallet or cigarette case.
• Cutting sugar? Post a copy of your blood test results or a diabetes risk chart in your kitchen.
• Leaving a toxic relationship? Write down the most hurtful things that were said to you and read them when tempted to go back.

“Remember why you started. Your health, your peace of mind, your future—these are worth more than instant pleasure.”

3. Make It Difficult

The harder it is to access a bad habit, the less likely you are to do it.

Practical Examples:

• Want to stop eating junk food? Don’t buy it. Simple as that. No chips at home = no chips to eat.
• Spend too much time on social media? Delete the apps and only access them from a computer at designated times.
• Want to reduce phone time? Put it away as soon as you get home—and spend more time with family. Everyone will benefit.

“Put obstacles in your past self’s path. Make it easier for your future self to choose well.”

4. Make It Unsatisfying

Tie it to negative consequences so it’s no longer rewarding.

Impactful Examples:

• Each time you smoke, donate money to a cause you strongly disagree with. Painful, right? That’s the point.
• Struggling with procrastination? Make your goal public and give a friend permission to post it if you fail.
• Break your diet unnecessarily? Do 50 squats or clean the most annoying part of your house.

“When bad actions come with a cost, it’s harder to justify them.”

Breaking a bad habit isn’t about punishment—it’s about self-care. Make the healthy path the easy path. Remember: change isn’t magic—it’s a choice. Today could be your first step.

Conclusion

Habits don’t form overnight, but with the right tools, they can become sustainable. Think of them as long-term investments in your health, energy, and happiness.

Instead of setting unrealistic goals, start with simple, well-designed habits repeated daily. We’re here to help you choose the ones that fit you best, support you, and celebrate every step on your journey to a healthier, longer life.

BIBLIOGRAPHY

(1) James Clear, “Atomic Habits”.

La entrada How to Create Habits That Can Change Your Life se publicó primero en Neolife.

These enzymes have been investigated for many years and have been associated in particular with delayed aging and longevity. . According to research conducted by Libert, there are different compounds in foods that activate the production of these enzymes. 

Francisco Martínez Milla – Neolife Nutrition Unit

There are foods that activate the production of these enzymes, specifically stimulating SIRT1, the gene that encodes these proteins, which in turn have an anti-inflammatory and metabolic-enhancing effect in situations of obesity and glucose intolerance. 

Sirtuins (SIRTs) are a group of seven proteins found in the body that have been shown to regulate a variety of functions, including metabolism, inflammation, and lifespan, as documented in a study published in the Annual Review of Physiology by Sergiy Libert and Leonard Guarente of the Massachusetts Institute of Technology (USA). 

This group of researchers promotes the massive consumption of foods that stimulate the formation of SIRT proteins in the body. 

Low grade chronic inflammation 

Inflammation is a strategy used by our body, through which the immune system mobilizes and initiates the process necessary for repair to occur. Under normal conditions the threat is eliminated, repair is completed, and anti-inflammatory processes are activated to minimize damage. This is so-called acute inflammation, and it is necessary. 

The problem is when this process, for reasons that we will go into later, remains permanent and is maintained over time, silent, and very dangerous. It’s like having a wound that never heals. The constant activation of the immune system, designed to defend you, ends up hurting you. The correct action of sirtuins counteracts this mechanism. 

What exactly do sirtuins do? 

Sirtuins are protein enzymes that modify other proteins in such a way as to reduce oxidative stress in cells and help their survival under adverse conditions. They promote DNA repair and increase its energy efficiency.

What is the relationship between sirtuins and longevity? 

Much of the scientific literature links sirtuins to a longer and healthier life due to the cellular protection they provide. But almost all the research links it to calorie restriction. 

What foods contain sirtuins? 

Plant foods that are rich in antioxidants are the ones that most activate SIRT1. They do not contain sirtuins, but compounds, such as resveratrol, quercetin, curcumin, and catechins, which are capable of activating their production. These foods are: kale, broccoli, grapes, strawberries, onions, celery, red chicory, blueberries, soybeans, parsley, extra virgin olive oil, dark chocolate (85% cocoa), matcha green tea, buckwheat, turmeric, walnuts, arugula, chili, capers, and coffee. Let’s take a closer look at some of these.  

Resveratrol: This is the 3,5,4′- Trihydroxystilbene, polyphenol class: stilbenes. It is a polyphenolic phytoalexin (antimicrobial present in some plants) present in the grape (Vitis vinifera), studied for its in vitro and in vivo properties (antioxidant, anti-inflammatory, anticancer).

Resveratrol promotes longevity in simple organisms like the Saccaromyces cerevisiae yeast, the C.elegans worm, the Drosophila melanogaster fly, and the Nothobranchius guentheri fish. Some studies indicate that the molecule would be less effective in larger species.

It can apparently lead to a 60% increase in life expectancy in some animal models, but the results vary depending on dosage, sex, genetics, and diet composition.

Quercetin: The 3,5,7,3’,4’- Pentahydroxyflavone, polyphenol class: flavonoids, subclass: flavonols, can increase the longevity of yeasts and C.elegans by 60 and 15% respectively.

Foods like red onion, broccoli, apples, and grapes contain large amounts of quercetin.

Quercetin alone improves senescence markers in renal tubule cells and renal fibrosis in obese dyslipidemic mice with a diet rich in fats.

Curcumin: Polyphenol class: other polyphenols, subclass: curcuminoids. This is a dye that comes from turmeric (from its root).

A 10% decrease in the senescent cells of the intervertebral discs (from donors) was observed, as well as the proliferation of healthy cells with a dose of 5 mcM of curcumin. Additionally, the production of inflammatory cytokines was reduced.

Catechins: The catechins contained in green tea, similarly referred to as 3, 5, 7, 3′, 4′- Pentahydroxyflavone; polyphenol class: flavonoids; subclass: flavonols, administered to rats in water (0.02% dilution) are linked to an improvement in brain functions. The protective effect is evident in the reduction of beta-amyloid plaques.

Is it reasonable to base a diet on these foods? 

They are healthy foods, and their consumption is recommended. But there are also many other healthy foods that are not included in this selection, and there is no reason to exclude them. 

BIBLIOGRAPHY

(1) https://www.annualreviews.org/doi/10.1146/annurev-physiol-030212-183800

(2) Kawanishi, S., Hiraku, Y. and Oikawa, S. (2001). Mechanism of guanine-specific DNA damage by oxidative stress and its role in carcinogenesis and aging. Mutation Research/ revisions in mutation research, 488 (1), 65-76. 

(3) Datta, S., Iqbal, Z. and Prasad, KR (2011). Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease. Indian Journal of Clinical Biochemistry, 26 (2), 210-213. 

(4) The role of sirtuins in the aging of adult stem cells. García García, María. URL: https://digibuo.uniovi.es/dspace/handle/10651/17918 

(5) Emerging Roles of Sirtuin 6 in Alzheimer’s Disease. Mohamad Nasir NF1,2,3, Zainuddin A2,4, Shamsuddin S5,6. URL: https://www.ncbi.nlm.nih.gov/pubmed/29260452 

(6)  Hormesis defined. Author links open overlay panelMark P.Mattson. URL: https://www.sciencedirect.com/science/article/pii/S1568163707000712?via%3Dihub 

(7) Hormesis in Health and Chronic Diseases. Li X1, Yang T2, Sun Z3. https://www.ncbi.nlm.nih.gov/pubmed/31521464. 

(8) Mechanisms of aging and potential role of selected polyphenols in extending healthspan. Russo GL1, Spagnuolo C2, Russo M2, Tedesco I2, Moccia S2, CervelleraC2. URL: https://www.sciencedirect.com/science/article/abs/pii/S0006295219304186?via%3Dihub 

La entrada How Do We Activate Sirtuins to Combat Aging? se publicó primero en Neolife.

Peak oxygen consumption normally has an exclusive focus on performance, but according to the latest research, obtaining a high value means the absence of disease and the assurance of good health in the future. 

Dr. César Montiel – Neolife Medical Team

When we want to know our state of health, we usually use a medical check-up that includes blood pressure, heart rate, BMI, fat %, and blood tests to control the levels of sugar, triglycerides, transaminases, and cholesterol, and sometimes even spirometry and electrocardiogram at rest. 

However, the importance of a high VO2max is increasingly recognized as the first diagnosis of good health and longevity, well above the previous assessments; even the American Heart Association considers it necessary to perform a stress test every year and considers the assessment of VO2max the “gold standard” of health. 

Peak oxygen consumption normally has an exclusive focus on performance, but according to the latest research, obtaining a high value means the absence of disease and the assurance of good health in the future. Even longitudinal studies have shown that an increase of only 1 ml/kg/min reduces all-cause mortality by 11%, cardiovascular disease by 15%, and cancer by 16%.. The survival rate in a serious event (work accident, traffic accident, etc.) is much higher for those with higher metabolic efficiency. 

Recent research has provided a reference for predicting VO2max adjusted for age and weight. So if you are above this average, you have a very significant assurance of good health. 

What does it mean to have metabolic flexibility?

Currently, there is a growing interest in assessing the influence of metabolic flexibility, which can be defined as the ability of a system to adjust fuel oxidation to fuel availability. In other words, to have the capacity to quickly use the substrate that will allow us to have energy available, based on availability and need, or in other words, to have the capacity to use glucose in moments of intense activity with a limited duration and fatty acids for moments of less intensity and rest (stored in our adipocytes), which is what we have been designed for over the course of millions of years, and so, in this way, to always have energy available. 

All this will depend on the type and amount of nutrients available for oxidation at the cellular level, and so people with good metabolic flexibility will have better body fat oxidation and optimal sports performance. Having food easily and readily available at all times is not natural, nor is not having to move to get it, as the vast majority of today’s jobs are very inactive. But it’s also unnatural to eat 5 or more times a day, and if this food is processed (many kcal that do not generate satiety and are extremely easy to digest), this leads to the obesity epidemic we are currently living in.

However, the new way of life in developed societies has generated a phenomenon that is not accepted by our genes and triggers health problems. We have evolved over thousands of years, but in a very short time we have created a world for which our body is not prepared, full of comforts and without stimuli. We have lost our Metabolic Flexibility (MF), and in the long run, this makes us sick. 

Our muscle mass, liver, and adipose tissue are the great energy reservoirs, since they govern Metabolic Flexibility in a direct relationship with the endocrine system, so any alteration of this control may attract pathologies linked to the opposite, the dreaded Metabolic Inflexibility, which is present in people who have insulin resistance, diabetes, and obesity. 

What happens when we eat? 

The postprandial phase begins, where the body must decide what to do with each macronutrient ingested, in other words, use it as fuel or store it. It’s a complex process, but let’s explain it this way:  

We can’t store alcohol, it must be burned immediately, and this inhibits the use of other substrates, interfering with the burning of fat and with the proper functioning of the liver.  

Ingested protein has mainly a structural role (building muscle, hormones, neurotransmitters, etc.), although it may also be used in part as fuel. Surplus protein can’t be stored directly; it must first be converted into glucose through a process called gluconeogenesis.  

We also have carbohydrates that are converted into glucose, a fuel that can be used by any cell and easily stored in the form of glycogen (in muscles or the liver). If the available reserves are exceeded, glucose can also be stored as fat.  

Last but not least, dietary fats can be used as energy, for structural tasks (cell membranes, hormones…) or stored directly as subcutaneous or intramuscular fat. 

Imagine that the food you ate had X amount of calories and 60% was ultimately stored. A process called partitioning will occur, (some of those calories are stored as muscle, as protein or muscle glycogen) and some as fat. This depends partly on what you have eaten, but also on your metabolic flexibility. Once this selection phase is over, the post-absorptive phase begins, which is where you start to use the reserves, and it will not end until you eat again. 

Partitioning also occurs, but as output; if you expended 50% of your calories in this post-absorptive phase, how many came from glycogen and how many from fat?

The graph tells us that our weight is determined by the differences in energy, i.e. the energy expended and stored, but your body composition (muscle/fat ratio) will depend on the partitioning of input compared to output.  

This must be: 

1. In the postprandial state, we store almost all excess energy as muscle (protein + glycogen). 
2. In the post-absorptive state, we obtain almost all the energy required from stored fat, reserving glycogen for occasional high intensity efforts. 

How do we find out if we have the right metabolic flexibility? 

It is simpler than you think, and there is no need for blood tests or complex studies. Simply complete a period of fasting on an active day (more than 14-16h) and exercise at medium/low intensity. If you don’t feel any discomfort or dizziness (hypoglycemia) in these conditions, when glycogen stores are low, it is very likely that you were able to consume a large part of the energy used in the form of fatty acids. But if every time you don’t eat for 4-5h, you feel sick, there’s a problem, because it is an indication of metabolic inflexibility and future metabolic problems, even if you have blood tests that are within the normal range.  

There are other methods that could provide us with more specific values of metabolic flexibility such as the FAST MAX test, where after a fast of 5 to 6 hours, if you have high blood sugar levels, you will use this as the main source of energy because you have extra. We will then perform a gas analysis measurement at rest and during exercise, increasing the intensity progressively until reaching the anaerobic threshold. That is to say, it will not be demanding since we don’t need to reach maximum intensities as in a stress test; in this case, we will be able to see the CO2 you produce and the O2 you consume, and it would give us a Respiratory Exchange Ratio (RER) as a result, which tells us quite precisely the percentage of nutrients that serve as a source of energy.

Although there is a lot of research on performance, there is very little on the normal population and health. But more and more research is being done on the consumption of fats in different types of subjects and their health benefits.  

The differences between a person with high and low metabolic flexibility are maintained 24 hours a day. This means that consuming more or less fat is constant, at rest and during exercise, and even the response at meals is different. Having a better metabolic flexibility means benefits in health, but also in terms of appearance, since it is much easier to reduce the percentage of fat.  

In a few years’ time, future blood tests will not measure good and bad cholesterol, something that has already been shown not to have much influence on health. Occupational medical check-ups will be much more useful by radically changing the way of assessing patients to anticipate illnesses that for now can only be seen when they are already present. Here at NEOLIFE, we already use more useful means such as measuring the level of cellular oxidation and Redox potential to control metabolic damage and all mitochondrial diseases (type 2 diabetes, arteriosclerosis, obesity, cancer, neurodegenerative diseases, etc.), or a stress test to assess RER and VO2max, among others. 

Knowing how we use oxygen by knowing its volume and the oxidation capacity of our mitochondria is the best way to know more about our metabolic health, something that NEOLIFE wants you to know is highly recommended. If we complete a stress test once a year, trying not to decrease our VO2max (since it is the best reference), and knowing how to use nutrients, we could control our metabolic flexibility on a regular basis, and in this way we would be able to maintain healthy values (RER 0.8 or lower); this would indicate that we are able to use fats as a nutrient and we have an adequate insulin sensitivity. 

Don’t miss Part 2 of this article, where we will cover the tools to improve these areas. 

BIBLIOGRAPHY

(1) Bret H. Goodpaster, Ph.D. and Lauren M. Sparks, Ph.D. 2017 Metabolic flexibility in health and disease Bret H. Goodpaster, Ph.D. and Lauren M. Sparks, Ph.D. Cell Metab 25(5): 1027–1036 

(2) Corey A. Rynders, Stephane Blanc, Nathan DeJong, Daniel H. Bessesen and Audrey Bergouignan. 2018 Sedentary behaviour is a key determinant of metabolic inflexibility. J Physiol 596.8 pp 1319–1330 

(3) David E. Kelley. 2005 Skeletal muscle fat oxidation: timing and flexibility are everything. J. Clin. Invest. 115:1699–1702 

(4) Jönsson, T., Olsson, S., Ahrén, B. et al. Agrarian diet and diseases of affluence – Do evolutionary novel dietary lectins cause leptin resistance?. BMC Endocr Disord 5, 10 (2005). https://doi.org/10.1186/1472-6823-5-10

(5) De Luca C, Olefsky JM. Inflammation and insulin resistance. FEBS Lett. 2008;582(1):97-105. doi:10.1016/j.febslet.2007.11.057 

La entrada Are you Metabolically Flexible? Part 1 se publicó primero en Neolife.