In 1970, an expedition to Greenland gave rise to the legend of omega-3 as a cardioprotective nutrient. Half a century later, science has taken decades to fully test it.

In the 1970s, Bang and Dyerberg linked the Inuit’s high-fat diet to their supposedly low cardiovascular risk. In 2014, it was revealed that they had never actually measured this incidence: they had relied on unreliable Greenlandic records. The founding myth of omega-3 was based, at least in part, on an assumption that had never been properly verified.

Dr. Carlos Martí – Neolife Medical Team

From an expedition to Greenland to a $1.1 billion industry

In the summer of 1970, two Danish researchers, Hans Olaf Bang and Jørn Dyerberg, travelled to the northwest coast of Greenland to investigate a medical mystery: the Inuit, whose diet was rich in seal and whale fat, appeared to experience very few heart attacks. That expedition gave rise to one of the most widely repeated nutritional recommendations of the past half-century — eating oily fish, or supplementing with fish oil, protects the heart — and laid the foundations for what is now an industry generating more than $1.1 billion in the United States alone.

What the legend leaves out is that, in 2014, a review published in the Canadian Journal of Cardiology compiled 48 subsequent studies on the cardiovascular health of the Inuit and concluded that their prevalence of coronary heart disease is actually similar to — or even higher than — that of the reference Caucasian population. Bang and Dyerberg never directly measured the incidence of heart attacks: they relied on annual reports from Greenland’s chief medical officer, a source that the reviewers themselves considered unreliable for a dispersed population with limited access to healthcare.

Although the original fieldwork had methodological gaps that took decades to identify, Bang and Dyerberg’s observations were not without value: their blood analyses did show a favourable lipid profile among the Inuit, and that finding — well supported by evidence, unlike the heart-attack figures — fuelled decades of biochemical research into EPA and DHA, including their role in platelet aggregation, endothelial function and systemic inflammation.

The distinction matters: the part of the story that withstood scientific scrutiny was not “the Inuit hardly ever suffer heart attacks,” but rather “EPA and DHA have real, measurable biological effects on the cardiovascular system.” This solid biochemical foundation eventually gave rise to an entire supplementation market, which in Spain has now become one of the best-selling product categories in pharmacies, parapharmacies and health-food stores.

What modern clinical trials have taken 50 years to answer

The question that Bang and Dyerberg left unresolved with sufficient scientific rigour — does omega-3 actually reduce the risk of heart attack and stroke? — has, half a century later, received a much more sophisticated and considerably less comfortable answer than the original legend suggested. Two major clinical trials using pharmacological doses (4 grams per day) have produced opposing results in recent years: REDUCE-IT (2019), using pure, purified EPA, found a significant reduction in major cardiovascular events among high-risk patients. STRENGTH (2020), using the same combination of EPA and DHA found in most over-the-counter supplements, found no benefit and was stopped early for lack of efficacy.

The scientific community continues to debate the reasons for this discrepancy — ranging from the type of placebo used in each trial to the possibility that DHA may attenuate EPA’s cardioprotective effects — but there is broader agreement on one point: the promise of “heart-attack prevention” repeated by many over-the-counter supplements does not have the same level of support today that it had a decade ago, when the Inuit legend was still widely accepted without sufficient qualification.

Between myth and uncertainty: what the evidence does support

Beyond the more controversial cardiovascular debate, there is an area in which the evidence surrounding EPA and DHA is solid and does not depend on any Greenlandic legend: the EFSA has authorised health claims based on consistent physiological evidence for the maintenance of normal cardiac function, from 250 mg/day of combined EPA+DHA, and for the maintenance of normal brain function and vision, from 250 mg/day of DHA. The reduction of triglyceride levels with high doses (2,000–4,000 mg/day, already within the pharmacological range) is, alongside these two authorised claims, one of the best-supported uses across the omega-3 supplement category.

The common mistake is not taking omega-3 for these reasons — they have a genuine scientific basis — but extrapolating this evidence to the broader and less well-supported promise of universal cardiovascular prevention precisely the part of the story that originated from data that had never been properly verified.

The question that really matters today: are we eating enough fish?

Regardless of the debate surrounding heart-attack prevention, there is one fact that does not depend on any controversial clinical trial: how much omega-3 we actually consume. The ANIBES study, a reference survey on dietary intake in Spain, found in 2023 that the average daily intake of EPA among the Spanish population was just 30 mg, while DHA intake was 60 mg — 90 mg combined, compared with the 250–500 mg consistently recommended by EFSA and most international scientific societies. The same study found that 65% of the adult population does not meet recommended fish consumption levels, particularly among younger people.

By far, this is the least controversial scientific argument in the entire article: regardless of the ultimate outcome of the cardiovascular debate, most of the Spanish population starts from a dietary omega-3 intake that is well below recommended levels — something that no review has called into question.

A half-truth myth, a real argument

Fifty years after that expedition to Greenland, omega-3 still has a real argument in its favour — a documented dietary gap and well-supported health claims — while having lost, at least in part, the myth that originally made it famous. It is a good example of how a story can be partially wrong at its origin and still point towards something true: the Inuit narrative turned out to have less scientific basis than initially believed, but the biochemical interest it generated has, decades later, produced much more rigorous evidence — with its own strengths and limitations — about what EPA and DHA can and cannot actually achieve.

At Neolife, we assess omega-3 supplementation within the context of each patient’s diet and biomarkers, rather than as an automatic recommendation or as a promise of universal prevention.

When appropriate, we offer NeOmega 3, which combines EPA and DHA at clearly defined doses with olive leaf extract for additional antioxidant support — designed as a maintenance foundation, not as a substitute for a diet containing sufficient oily fish.

BIBLIOGRAPHY

(1) Bang HO, Dyerberg J, Nielsen AB. Plasma lipid and lipoprotein pattern in Greenlandic West-coast Eskimos. Lancet. 1971;1(7710):1143-1146. doi: 10.1016/s0140-6736(71)91658-8.

(2) Fodor JG, Helis E, Yazdekhasti N, Vohnout B. “Fishing” for the origins of the “Eskimos and heart disease” story: facts or wishful thinking? Can J Cardiol. 2014;30(8):864-868. doi: 10.1016/j.cjca.2014.04.007.

(3) Nicholls SJ, Lincoff AM, Garcia M, et al. Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk: The STRENGTH Randomized Clinical Trial. JAMA. 2020;324(22):2268-2280. doi: 10.1001/jama.2020.22258.

(4) Redruello-Requejo M, Samaniego-Vaesken ML, Puga AM, Montero-Bravo A, Ruperto M, Rodríguez-Alonso P, Partearroyo T, Varela-Moreiras G. Omega-3 and Omega-6 Polyunsaturated Fatty Acid Intakes, Determinants and Dietary Sources in the Spanish Population: Findings from the ANIBES Study. Nutrients. 2023;15(3):562. doi: 10.3390/nu15030562.

La entrada The Greenland Legend That Invented Omega-3 (and What Science Has Taken Half a Century to Answer) se publicó primero en Neolife.

Minerals are involved in thousands of essential biological processes, including energy production, immune function, muscle health and healthy aging. Are we really meeting our needs?

The most reasonable approach is to start with a varied, high-quality diet and use supplementation on an individualized basis when there is insufficient intake, increased demand, or a clinical context that justifies it. NeoMineral Plus is a combination of minerals and trace elements in highly bioavailable forms, designed as a multimineral foundation within a comprehensive preventive medicine and longevity strategy.

Dr. Mercè Triviño – Neolife Medical Team

Minerals: Essential for Health and Aging

When we think about nutrition and health, the focus is usually on proteins, carbohydrates, healthy fats or vitamins. However, there is another group of micronutrients that is equally crucial to the body’s functioning and yet, paradoxically, often receives far less attention: minerals.

Although they are required in relatively small amounts, minerals are essential for virtually every cell in the body to perform its functions. They act as cofactors in enzymatic reactions involved in energy production, protein synthesis, muscle and nerve function, regulation of the immune response and protection against oxidative damage.

In recent years, growing interest in preventive medicine and Healthy Aging has shifted the focus towards a concept that goes beyond preventing deficiency diseases. The goal is to preserve biological function, maintain functional capacity and promote a good quality of life for as long as possible.

In this context, minerals play an important role. They are involved in processes closely related to aging, including mitochondrial function, energy metabolism, oxidative balance, immune response and the maintenance of muscle and bone mass. However, it is important to distinguish between the physiological importance of a nutrient and the existence of clinical evidence supporting its supplementation as a longevity intervention.

Why Are Minerals So Important?

Minerals act as key facilitators of metabolism. Many function as cofactors or structural components of enzymes and proteins that are essential for life.

One of the most representative examples is the mitochondrion, the organelle responsible for producing much of the ATP used by our cells. Magnesium participates in ATP metabolism and numerous energy-producing reactions; iron forms part of proteins involved in electron transport; and copper is involved in essential enzymes within the respiratory chain. Other minerals, such as manganese, zinc and selenium, contribute to antioxidant defense systems.

The importance of minerals goes beyond energy production. Zinc contributes to immune function, protein synthesis and tissue repair. Selenium forms part of selenoproteins involved in antioxidant defense and thyroid metabolism. Iodine is essential for the synthesis of thyroid hormones, while iron enables oxygen transport and contributes to energy metabolism.

Therefore, talking about minerals means talking about a metabolic network. Not all minerals have the same level of evidence, nor do they all require supplementation, but adequate availability is necessary for multiple physiological processes to function properly.

Minerals and Healthy Aging: Much More Than Preventing Deficiencies

For years, clinical nutrition has focused largely on preventing deficiency diseases. Longevity medicine has introduced a complementary approach: preserving biological function and reducing factors that may accelerate the loss of functional capacity.

Within this framework, minerals can contribute to maintaining fundamental physiological processes. Mitochondrial function depends on multiple cofactors; antioxidant systems require minerals such as zinc, selenium, copper and manganese; and thyroid function depends on adequate availability of iodine and selenium.

Muscle mass and bone health are equally relevant. Aging is accompanied by a progressive loss of muscle mass and function, as well as changes in bone metabolism. Magnesium contributes to muscle and bone function, while other minerals are involved in processes related to connective tissue and mineral metabolism. However, a multimineral supplement does not replace interventions with stronger evidence for preserving function: strength training, adequate protein intake, vitamin D when indicated, and a healthy diet.

Something similar applies to immunity and inflammaging, the chronic low-grade inflammation associated with aging. Zinc and selenium are important for immune function and antioxidant defense. However, maintaining adequate intake does not mean that high-dose supplementation will prevent aging or extend lifespan.

This distinction is fundamental. Nutritional optimization may be reasonable when there is insufficient intake, increased requirements or factors that impair absorption. However, physiological plausibility should not be turned into claims of anti-aging effects that have not yet been clinically demonstrated.

Does a Multimineral Supplement Make Sense?

Mineral supplementation is often focused on a single nutrient: magnesium for certain muscle-related symptoms, iron in the presence of a documented deficiency, or zinc in specific situations. This approach may be the most appropriate when there is a specific need. However, in preventive medicine, the goal may be different: improving overall mineral coverage in selected individuals.

Minerals do not act in isolation. Energy production, antioxidant defense, thyroid function and other processes depend on several cofactors. Therefore, a balanced multimineral formulation may make sense as a nutritional foundation when diet or clinical circumstances make inadequate mineral intake more likely.

The quality of the formulation is essential. It is not enough to include a large number of minerals: they should be selected in forms with good bioavailability, provided in functional amounts, and unnecessary or duplicative intake should be avoided. In addition, the presence of iron, iodine, selenium and chromium means that the indication should be individualized.

Therefore, a multimineral supplement should not be understood as a universal treatment for deficiencies. Its role is to provide nutritional coverage and optimization, particularly in people with low nutrient-density diets, increased nutritional demands, middle-to-older age, sustained stress or certain pharmacological treatments.

NeoMineral Plus: A Formulation Designed Around Physiology

NeoMineral Plus is an advanced nutritional food supplement providing minerals and trace elements in a single daily tablet. Within Neolife, it complements the vitamin foundation with cofactors involved in energy metabolism, immunity, oxidative stress, thyroid function, glucose metabolism, oxygen transport and structural support.

The formulation contains magnesium bisglycinate, zinc citrate, selenium as L-selenomethionine, chromium picolinate and other minerals and trace elements. The aim is to provide an organized and traceable mineral foundation, rather than treating a specific disease in isolation.

Magnesium deserves specific consideration. NeoMineral Plus provides 250 mg of magnesium bisglycinate, a relevant amount within a multimineral formulation. This intake should be understood as part of the product’s overall strategy and not as a specific magnesium treatment. When the primary clinical goal is to optimize magnesium intake, combining it with NeoMagnesium may be considered.

The indication should be individualized based on its iron, iodine and selenium content. For example, in patients with hemochromatosis, elevated ferritin or iron overload, a multimineral supplement containing iron should not be used automatically. Similarly, thyroid conditions should be assessed according to the clinical context and the individual’s overall iodine and selenium intake.

In practice, a basic assessment may include a complete blood count, ferritin, transferrin saturation, kidney function, TSH and free T4, glucose and HbA1c, with additional parameters depending on the individual case. It is also important to review potential duplication and possible interactions with levothyroxine, bisphosphonates, tetracyclines or quinolones.

Conclusion

Minerals are essential micronutrients for maintaining cellular function and are involved in processes as important as energy production, immune response, thyroid function, oxidative balance, and muscle and bone health. Their importance in Healthy Aging is physiologically clear, although the evidence that mineral supplementation on its own can extend longevity is much more limited.

The most reasonable approach is to start with a varied, high-quality diet and use supplementation on an individualized basis when there is insufficient intake, increased demand or a clinical context that justifies it. In this setting, a well-formulated multimineral supplement can be a useful tool for optimizing overall nutritional status.

NeoMineral Plus follows this approach through a combination of minerals and trace elements in highly bioavailable forms, designed as a multimineral foundation within a comprehensive preventive medicine and longevity strategy. The goal is not to identify a single nutrient capable of modifying the aging process, but rather to support an appropriate nutritional environment in which the physiological systems that sustain health can function as efficiently as possible.

LITERATURE

(1) López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The Hallmarks of Aging. Cell. 2013;153(6):1194-1217.

(2) López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of Aging: An Expanding Universe. Cell. 2023;186(2):243-278.

(3) Franceschi C, Garagnani P, Parini P, Giuliani C, Santoro A. Inflammaging: a new immune-metabolic viewpoint for age-related diseases. Nat Rev Endocrinol. 2018;14:576-590.

(4) Gröber U, Schmidt J, Kisters K. Magnesium in Prevention and Therapy. Nutrients. 2015;7:8199-8226.

(5) de Baaij JHF, Hoenderop JGJ, Bindels RJM. Magnesium in Man: Implications for Health and Disease. Physiol Rev. 2015;95:1-46.

(6) Prasad AS. Zinc in Human Health: Effect of Zinc on Immune Cells. Mol Med. 2008;14:353-357.

(7) Rayman MP. Selenium and Human Health. Lancet. 2012;379:1256-1268.

(8) Camaschella C. Iron Deficiency. N Engl J Med. 2015;372:1832-1843.

(9) Gombart AF, Pierre A, Maggini S. A Review of Micronutrients and the Immune System. Nutrients. 2020;12:236.

(10) Ames BN. Optimal micronutrients delay mitochondrial decay and age-associated diseases. Mech Ageing Dev. 2010;131:473-479.

(11) Manson JE, Bassuk SS. Vitamin and Mineral Supplements: What Clinicians Need to Know. JAMA. 2018;320(9):979-980.

La entrada Beyond Vitamins: The Role of Minerals in Healthy AgingMás allá de las vitaminas: el papel de los minerales en el Healthy Aging se publicó primero en Neolife.

The COSMOS study provides new evidence on the role of multivitamin supplements in healthy adults, after years of debate about their benefits.

The finding that has attracted the most attention was not related to the heart or cancer, but to the brain: taking a daily multivitamin significantly reduced age-related cognitive decline across three independent study groups. This is not definitive evidence, but it is the strongest evidence to date on the impact of this type of supplementation on brain health.

Dr. Carlos Martí – Neolife Medical Team

A Study Designed to Provide Answers, Not More Questions

COSMOS was designed at Harvard and led by Drs. JoAnn Manson and Shari Bassuk. More than 21,000 people over the age of 60 participated for almost four years: half took a daily multivitamin, while the other half took a placebo containing no active ingredients. Neither the participants nor the physicians responsible for follow-up knew which group they belonged to, eliminating the influence of expectations on the results.

What makes COSMOS particularly valuable in the field of brain health is that the same question was investigated in three different groups using different methods: one completed memory tests by telephone each year (COSMOS-Mind, more than 2,200 participants), another completed them online (COSMOS-Web, more than 3,500 participants), and a third group underwent detailed in-person assessments (COSMOS-Clinic, nearly 600 participants). The fact that all three reached the same conclusion is what makes this study more than just an isolated finding.

What They Found: Memory Improved and Cognitive Decline Slowed

Across all three groups, people who took the multivitamin daily performed better on tests of memory and mental agility than those who took the placebo. The most frequently cited finding is that, in COSMOS-Mind, the multivitamin appeared to delay cognitive aging by approximately 1.8 years over a three-year follow-up period, equivalent to slowing cognitive decline by around 60%.

The authors themselves are clear: the study has not demonstrated that a multivitamin prevents Alzheimer’s disease or reverses existing cognitive decline. What the results suggest is that it may act as a protective factor during the years before cognitive decline becomes noticeable. And that is precisely the stage at which there is still the greatest opportunity to intervene.

Why the Brain May Respond Better Than the Heart

Previous studies involving tens of thousands of participants have investigated the effects of multivitamins on heart disease and cancer, without finding clear results. The brain appears to be a different case, and the reason is fairly intuitive: it is the body’s most energy-demanding organ and one of the organs that relies most heavily on vitamins to function properly on a daily basis.

As we age, the absorption of some vitamins gradually becomes more difficult, while our needs do not necessarily decrease. A daily multivitamin could help fill the nutritional gap that even a reasonably varied diet does not always cover. COSMOS is the first large-scale study to provide real-world data—not just theoretical arguments—in support of this idea.

What the Study Does Not Say (and What You Should Know)

The results are real, but they should be interpreted in context. The multivitamin used in COSMOS was a standard generic product, so the study cannot determine which specific vitamins were responsible for the effect, nor whether a formulation containing higher-quality ingredients would have produced better or worse results.

We also do not know whether the benefit persists beyond the three-year follow-up period, or whether it applies equally to people aged 45 and those aged 70. And although the observed difference was consistent, it was not enormous in everyday life: we are not talking about restoring the memory someone had twenty years ago, but rather about a protective effect that accumulates over time and makes much more sense as a sustained habit than as an effect that can be noticed from one day to the next.

A Multivitamin Foundation as Part of a Longevity Program: The Role of NeoVitamin Plus

The practical conclusion from COSMOS is not that everyone should take a multivitamin. Rather, it suggests that in middle-aged and older adults whose diets are not always optimal, a daily vitamin foundation may have a favorable benefit-risk profile and, for the first time, solid experimental evidence supporting its potential role in cognitive health. This is precisely the type of intervention that makes sense within a preventive longevity program, where the goal is not to treat a disease but to preserve function before it begins to decline.

At Neolife, we use NeoVitamin Plus as a vitamin foundation within this context. Its formulation includes B vitamins involved in homocysteine regulation (B6, active-form B12, folate, and betaine), antioxidant vitamins C and E, and nutrients such as choline, which are less common in standard multivitamin formulations. The study does not support any specific formulation, but the mechanisms highlighted by COSMOS are precisely those addressed by NeoVitamin Plus in the design of its formula. Because if there is one thing this trial makes clear, it is that the brain, like the rest of the body, is better cared for before it starts asking for help.

BIBLIOGRAPHY

(1) Yeung LK, Alschuler DM, Wall M, Luttmann-Gibson H, Copeland T, Hale C, et al. Multivitamin supplementation improves memory in older adults: a randomized clinical trial. Am J Clin Nutr. 2023;118(1):273-282. doi: 10.1016/j.ajcnut.2023.05.011. [COSMOS-Web]

(2) Vyas CM, Manson JE, Sesso HD, Cook NR, Moorthy MV, Buring JE, et al. Effect of multivitamin-mineral supplementation versus placebo on cognitive function: results from the clinic subcohort of the COSMOS randomized clinical trial and meta-analysis of 3 cognitive studies within COSMOS. Am J Clin Nutr. 2024;119(3):692-701. doi: 10.1016/j.ajcnut.2023.12.011. [COSMOS-Clinic + metáanálisis]

(3) Manson JE, Bassuk SS, Cook NR, et al. COSMOS (COcoa Supplement and Multivitamin Outcomes Study): design and baseline characteristics of a randomized controlled trial. Contemp Clin Trials. 2020;94:106033. doi: 10.1016/j.cct.2020.106033.

La entrada 21,000 People, Three Years, and a Daily Multivitamin: What the COSMOS Study Changed About Brain Health se publicó primero en Neolife.

Your ID card tells you how many years you have lived. Your biological age helps us understand how you are living those years and what you can do to age better.

We all know our chronological age, but two people born in the same year can have very different levels of health. Biological clocks analyze different signals from the body to provide a more personalized picture of how we are aging.

Dr. Marta López – Neolife Medical Team

Chronological Age and Biological Age Are Not the Same

Chronological age is straightforward: it is the number of years that have passed since we were born. It cannot be changed and progresses at the same rate for everyone.

Biological age tries to answer a different question: how is our body doing for our age? We see this constantly in clinical practice. There are 60-year-olds with excellent physical capacity, good muscle mass, and optimal metabolic parameters, while others of the same age may experience greater fatigue, inflammation, loss of strength, or several risk factors.

That is why, when we talk about longevity, we are not only interested in adding years to life. We want to understand how we are reaching those years and what we can do to maintain energy, independence, and quality of life for longer.

Living Longer and Living Better: Lifespan vs. Healthspan

In longevity medicine, we distinguish between two closely related concepts. Lifespan is the total length of life: how many years we live. Healthspan, on the other hand, is the amount of time we live in good health, with independence, energy, and the ability to carry out our daily lives normally. It is not simply about adding more years to the calendar, but about making as many of those years as possible years of quality. Knowing our biological age can help us identify which areas deserve greater attention in order to bring these two goals closer together: living longer, but above all, living better.

What Influences Our Biological Age?

Our genes play an important role, but they do not tell the whole story. Diet, exercise, sleep, stress, body composition, and exposure to toxins also leave their mark on the body.

This is good news: we cannot change our date of birth, but we can influence many of the factors that affect how we age.

Biological Clocks: A Snapshot of How We Are Aging

Biological clocks are tools that combine different biomarkers and transform them into an estimate of biological age or aging rate.

We could compare them to a car’s dashboard. The number of kilometers tells us something, but we also want to know the condition of the engine, fuel consumption, tire pressure, or whether there are any warning signals. Something similar happens in our bodies: chronological age is an important piece of information, but it is not the only one.

There are clocks based on clinical tests, proteins, metabolites, medical imaging, or data collected through digital devices. Among the best known are epigenetic clocks, which analyze certain chemical signals in DNA associated with the passage of time, health status, and lifestyle.

Epigenetics: When Lifestyle Communicates with Our Genes

Epigenetics studies how gene activity is regulated without changing the DNA sequence itself. One simple way to understand it is to imagine that DNA is a large instruction manual. Epigenetics helps determine which pages are read more, which are read less, and how the body responds to its environment.

Diet, physical activity, rest, stress, smoking, and metabolic health can all be associated with epigenetic changes. Based on these signals, epigenetic clocks estimate whether our body shows a pattern of aging that is faster, similar to, or slower than expected for our chronological age.

The value of this information is not simply knowing a number. Its importance lies in using it as a starting point to review our habits, identify areas for improvement, and develop a more personalized health strategy.

Telomeres: Protectors of Our Chromosomes

Telomeres are structures located at the ends of chromosomes. Their function is similar to the small plastic tips that protect the ends of shoelaces: they help prevent genetic material from deteriorating.

As time passes and cells undergo successive divisions, telomeres tend to shorten. Their length is influenced by age, but it has also been associated with oxidative stress, inflammation, smoking, sedentary behavior, and other health factors.

Measuring telomere length provides information about cellular aging and adds another piece to the set of data we use to assess how a person is aging.

Can We Improve Our Biological Age?

Biological age should not be understood as a sentence or a fixed label. Its greatest value lies precisely in reminding us that a significant part of how we age is related to modifiable factors.

There are simple measures, although not always easy to maintain, that can make a significant difference:

• Maintain good muscle mass and engage in strength training.
• Exercise regularly and take care of cardiovascular fitness.
• Follow a diet adapted to your individual needs.
• Sleep well and maintain healthy rest patterns.
• Monitor glucose, blood pressure, cholesterol, and body composition.
• Reduce smoking, excessive alcohol consumption, and exposure to other toxins.
• Take care of stress, emotional health, and social relationships.

Measuring allows us to better understand our starting point. And when we repeat an assessment after some time, we can also observe changes and determine whether the modifications we have introduced are moving us in the right direction.

The Neolife Approach: Measure to Take Action

At Neolife, we understand longevity medicine as preventive, personalized, and data-driven medicine. Our aim is not simply to know how old a person is, but to understand their current health status and identify the areas we can work on to improve their future health.

As part of our assessment, we offer two tests specifically related to biological age:

• Telomere length measurement: provides information about cellular aging and the condition of these protective structures at the ends of our chromosomes.
• Epigenetic biological age test: analyzes epigenetic signals associated with aging and helps assess how our lifestyle may be influencing this process.

We interpret these results alongside the patient’s medical history, blood tests, body composition, cardiovascular health, muscle mass, exercise, sleep, and lifestyle. In this way, the number stops being an isolated piece of data and becomes a tool for making informed decisions.

Knowing our biological age does not mean predicting the future. It means having more information to take better care of it. Because the goal is not simply to live more years, but to reach those years with greater health, independence, and quality of life.

BIBLIOGRAPHY

(1) de Magalhães JP. Biological aging clocks in health and disease. Nature Medicine. 2026. doi:10.1038/s41591-026-04495-3.

(2) Mavrommatis C, et al. An unbiased comparison of 14 epigenetic clocks in relation to 174 incident disease outcomes. Nature Communications. 2025;16:11164. doi:10.1038/s41467-025-66106-y.

(3) Belsky DW, et al. DunedinPACE, a DNA methylation biomarker of the pace of aging. eLife. 2022;11:e73420. doi:10.7554/eLife.73420.

(4) Horvath S. DNA methylation age of human tissues and cell types. Genome Biology. 2013;14:R115. doi:10.1186/gb-2013-14-10-r115.

(5) Levine ME, et al. An epigenetic biomarker of aging for lifespan and healthspan. Aging. 2018;10(4):573-591. doi:10.18632/aging.101414.

(6) Vaiserman A, Krasnienkov D. Telomere length as a marker of biological age: state-of-the-art, open issues, and future perspectives. Frontiers in Genetics. 2021;11:630186. doi:10.3389/fgene.2020.630186.

(7) Wang K, et al. A full life cycle biological clock based on routine clinical data and its impact in health and diseases. Nature Medicine. 2025. doi:10.1038/s41591-025-04006-w.

La entrada Biological Age: How Old Is Your Body Really? se publicó primero en Neolife.

Vitamin D3 supplementation, including doses of up to 4,000 IU/day in selected patients, has emerged as a safe and effective strategy to correct deficiency and preserve musculoskeletal health during aging.

Vitamin D deficiency remains highly prevalent, even in Mediterranean countries. The latest evidence supports an individualized approach to supplementation, highlighting that doses of up to 4,000 IU/day may be necessary to achieve optimal 25(OH)D concentrations in certain patients. Beyond its well-established role in bone metabolism, vitamin D is increasingly recognized as an important contributor to healthy aging.

Dr. Mireia Junyent – Neolife Medical Team

Why Is Vitamin D Deficiency Still So Common?

Despite the abundant sunlight typical of Mediterranean regions, vitamin D insufficiency continues to represent a significant public health issue. A substantial proportion of adults have inadequate 25-hydroxyvitamin D levels, particularly older adults, individuals with obesity, gastrointestinal disorders, limited sun exposure, or darker skin phototypes.

Aging reduces the skin’s ability to synthesize vitamin D, increasing the risk of chronic insufficiency that may negatively affect musculoskeletal health and physical function.

Recent meta-analyses consistently show that conventional supplementation doses (600–800 IU/day) may be insufficient to achieve adequate serum levels in patients with risk factors, reinforcing the importance of personalized supplementation strategies.

4,000 IU/Day: An Evidence-Based Dose

Current recommendations emphasize that the optimal vitamin D dose should be tailored to each individual’s characteristics. Multiple clinical trials and systematic reviews have demonstrated that supplementation with 4,000 IU/day of cholecalciferol (vitamin D3) is more effective at correcting vitamin D deficiency than standard doses, particularly in patients with obesity, older age, or malabsorption.

This regimen has been shown to provide:

• A greater likelihood of achieving serum 25(OH)D concentrations > 30 ng/mL.
• Improved response in patients with increased volume of distribution or reduced bioavailability.
• An excellent safety profile when prescribed and monitored by healthcare professionals.
• No clinically significant increase in hypercalcemia in the available studies.

The most recent clinical practice guidelines consider 4,000 IU/day to be the upper tolerable intake level for healthy adults and a commonly used dosage in vitamin D deficiency correction protocols before transitioning to a maintenance regimen.

Vitamin D and Healthy Aging: Beyond Bone Health

Over the past decade, vitamin D has evolved from being viewed solely as a regulator of calcium and phosphorus metabolism to becoming an important component of longevity medicine.

Aging is associated with a progressive decline in muscle mass, immune system changes, and a chronic low-grade inflammatory state known as inflammaging. Within this context, maintaining adequate vitamin D levels may help preserve musculoskeletal function and support healthy aging.

The strongest evidence supports benefits in:

• Maintaining muscle strength and physical function.
• Reducing the risk of frailty.
• Preserving mobility in older adults.
• Optimizing bone health and reducing the risk of osteomalacia.

Although several studies have linked adequate vitamin D levels with improved immune function, lower systemic inflammation, and better cardiometabolic health, current evidence does not support recommending vitamin D supplementation specifically as an intervention to slow biological aging or extend lifespan.

From a clinical perspective, correcting vitamin D deficiency should therefore be considered a strategy to optimize overall health and functional capacity rather than an “anti-aging” treatment.

At Neolife, we offer NeoVit D3, a high-quality vitamin D3 supplement formulated to help maintain optimal vitamin D levels. Our medical team can assess your individual needs and recommend the most appropriate supplementation strategy based on your clinical profile.

BIBLIOGRAPHY

(1) Demay MB, et al. Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab.

(2) Bouillon R. Vitamin D and Healthy Aging. Nature Reviews Endocrinology.

(3) Ortiz-Prado E, et al. Cholecalciferol (vitamin D3): efficacy, safety and implications in public health. Front Nutr.

(4) Ogorek AN, Samara VA. New Clinical Practice Guidelines for Vitamin D Supplementation and Testing. Clin Chem.

(5) Goswami C, et al. Are there prophylactic effects of vitamin D among healthier adults? A systematic review of randomized controlled trials. BMC Nutrition.

(6) Figura 1. Metabolismo de la vitamina D y formación de 25(OH)D y calcitriol. Adaptado de Ortiz-Prado et al. Front Nutr. 2025 (CC BY).

La entrada Vitamin D: An Evidence-Based Pillar of Longevity se publicó primero en Neolife.

As Dr. Martí explained in the previous article, Poliendocrine Ovarian Metabolic Syndrome (POMS) encompasses a range of phenotypes and clinical presentations. Not all women experience the same symptoms, have the same hormonal or metabolic alterations, or pursue the same therapeutic goals.

This heterogeneity has a direct implication from a nutritional perspective: there is no single dietary approach for women with POMS. For many years, nutritional recommendations focused almost exclusively on weight loss and insulin resistance. However, the latest scientific evidence supports a broader, more individualized approach. Nutrition should be tailored to each patient, taking into account her clinical profile, symptoms, goals, and specific needs.

Meritxell Massons – Neolife Nutrition Unit

What many women with POMS have in common

Although important differences exist between patients, research has identified several mechanisms that frequently occur across different POMS phenotypes.

One of these is chronic low-grade inflammation. This is not the type of inflammation that produces obvious symptoms, but rather a persistent inflammatory state that can influence multiple hormonal and metabolic processes.

In this context, nutrition plays an important role. The most recent studies suggest that dietary patterns based on fresh, minimally processed foods are associated with a healthier inflammatory and metabolic profile, whereas a high intake of ultra-processed foods, products rich in added sugars, and foods with low nutritional density may contribute to a less favorable metabolic environment.

For this reason, rather than focusing on restrictive diets or specific eating strategies, the goal is generally to build a dietary pattern rich in vegetables, fruits, legumes, fish, eggs, nuts, seeds, extra virgin olive oil, and high-quality whole grains, always adapting it to each woman’s individual needs.

Gluten: one of the most common questions in the clinic

Interest in gluten-free diets as a possible strategy for improving symptoms associated with POMS has increased considerably in recent years.

However, there is currently no strong scientific evidence to support the routine elimination of gluten in all women with this condition.

Most available studies have not demonstrated clear benefits from removing gluten alone in women who do not have celiac disease or diagnosed gluten sensitivity.

This does not mean that every patient responds in the same way. Some women report feeling better after reducing foods made with wheat or other gluten-containing cereals. In many cases, however, this improvement may be related more to a reduction in ultra-processed foods and refined flours than to the elimination of gluten itself.

For this reason, current recommendations do not advocate routinely excluding gluten, but rather individualizing each case and focusing on the overall quality of the diet by prioritizing fresh, minimally processed foods over products made with refined flours.

The gut microbiota: a new piece of the puzzle

Another area attracting growing attention in recent research is the role of the gut microbiota.

We now know much more about the influence that intestinal microorganisms have on inflammation, metabolism, and hormonal regulation. Several recent studies have identified differences in the composition and diversity of the gut microbiota in women with POMS compared with women without the condition, suggesting that the microbiota may play a role in mechanisms related to inflammation, insulin resistance, and hormonal regulation.

Although many questions remain unanswered, these findings suggest that gut health may play a more important role than previously believed.

From a practical standpoint, this knowledge reinforces recommendations that already form part of a healthy dietary pattern: increasing the variety of fruits and vegetables, regularly including legumes, consuming nuts and seeds, choosing whole grains, using extra virgin olive oil as the primary dietary fat, and incorporating fermented foods such as plain yogurt or kefir when well tolerated.

All of these foods provide fiber, polyphenols, and other bioactive compounds that help support a more diverse and functional gut microbiota.

What about insulin resistance?

Although insulin resistance is not present in all women with POMS, it remains a common and clinically significant finding in a substantial proportion of patients.

For this reason, an appropriate nutritional assessment should also consider each woman’s individual metabolic profile. The nutritional approach for a woman of normal weight with irregular menstrual cycles is not the same as for a patient who is overweight and has impaired glucose metabolism.

When insulin resistance is present, nutrition can become an especially valuable therapeutic tool. Current evidence supports dietary patterns that promote more stable blood glucose responses and reduce inflammatory burden.

In practice, this generally means prioritizing foods rich in fiber, high-quality protein, and healthy fats while reducing the regular consumption of sugary drinks, pastries, ultra-processed snacks, and other foods with a high glycemic load.

Rather than classifying foods as “allowed” or “forbidden,” the objective is to create an eating pattern that improves metabolic health while fitting each patient’s individual circumstances.

Nutrition tailored to every woman

Perhaps one of the most important messages emerging from current research is that nutrition in POMS should move away from rigid, one-size-fits-all approaches.

Just as there is no single form of POMS, there is no single diet that is appropriate for every woman living with this condition. The most effective nutritional approach is one that combines the best available scientific evidence with each patient’s individual characteristics, preferences, and therapeutic goals.

BIBLIOGRAPHY

(1) Teede HJ, Tay CT, Laven JJE, Dokras A, Moran LJ, Piltonen TT, et al. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Eur J Endocrinol. 2023

(2) Joham AE, Teede HJ, Boyle JA, Stener-Victorin E, Moran LJ, Piltonen TT, et al. Summary of the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Med J Aust. 2024.

(3) Hanna A, Abbas H, Yassine F, AlBush A, Bilen M. Systematic review of gut microbiota composition, metabolic alterations, and the effects of treatments on PCOS and gut microbiota across human and animal studies. Front Microbiol. 2025;16:1549499.doi:10.3389/fmicb.2025.1549499.

La entrada Nutrition in POMS se publicó primero en Neolife.

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.

Two opposite strategies, one common question: what is the best way to structure our meals?

For years, eating five meals a day was widely recommended to keep the metabolism “active,” control hunger, and promote a healthy body weight. More recently, intermittent fasting has gained popularity as an effective strategy for losing body fat and improving certain metabolic markers. But what does the scientific evidence actually say? Do we need to eat every few hours, or can we safely go for long periods without food?

Adriana Martín – Neolife Nutrition Unit

The Origin of the Five-Meal Myth

The recommendation to eat five meals a day was largely based on the idea that eating frequently keeps the metabolism “active” and prevents excessive hunger before the main meals.

However, the energy expenditure associated with digestion—known as the thermic effect of food—depends primarily on the total amount of calories and nutrients consumed, not on how many meals those calories are divided into. In other words, consuming 2,000 kcal spread across three meals or five meals produces a very similar energy expenditure.

Furthermore, the most recent studies show that increasing meal frequency does not provide a significant advantage for body weight or body composition when total calorie intake remains the same.

What Exactly Is Intermittent Fasting?

Intermittent fasting is not about eating specific foods or following a special diet. Instead, it involves restricting food intake to a defined eating window.

One of the most commonly used approaches is the 16:8 protocol, which consists of fasting for 16 hours and consuming all meals within an 8-hour window—for example, eating the first meal at noon and finishing the last meal by 8:00 p.m.

Its popularity stems from the fact that many people find it easier to reduce their overall energy intake by limiting the amount of time available for eating rather than consciously counting calories.

What Does the Scientific Evidence Say?

Meta-analyses published in recent years reach an interesting conclusion: when calorie and protein intake are matched, intermittent fasting and conventional meal patterns produce very similar results for weight loss.

However, some studies suggest that certain forms of time-restricted eating may offer additional benefits for insulin sensitivity, blood glucose control, and several cardiometabolic health markers.

Even so, these benefits tend to be modest and depend largely on long-term adherence.

Overall, the evidence suggests that the quality of the diet, overall energy balance, and consistency of healthy habits matter far more than the number of meals consumed each day.

So, How Many Meals Should We Eat?

The short answer is that there is no single ideal number of meals that works for everyone.

Some people manage their hunger better by eating three main meals a day. Others prefer to include one or two additional meals or snacks. Likewise, some individuals feel comfortable practicing intermittent fasting, while others experience increased hunger, irritability, or find it difficult to maintain over time.

What truly matters is choosing an eating pattern that allows you to:

• Meet your nutritional requirements.
• Maintain an adequate protein intake.
• Promote long-term adherence.
• Fit your personal lifestyle and work schedule.

Which Strategy Works Best in Practice?

For most healthy individuals, eating three to four meals per day is generally sufficient to achieve adequate nutrition without making daily life unnecessarily complicated.

Intermittent fasting can be a useful tool for people who prefer to concentrate their food intake within a shorter period of the day, but it is neither a magic solution nor a requirement for improving health.

Likewise, eating five meals a day does not boost metabolism or guarantee greater weight loss.

Three Key Takeaways

• Your metabolism does not work faster simply because you eat five times a day.
• Intermittent fasting can be an effective strategy, but it is not superior to other approaches when calorie intake is the same.
• The best meal pattern is the one you can maintain consistently as part of a healthy lifestyle over the long term.

What You Can Do This Week

• Pay attention to the times of day when you feel hungriest and have the most energy.
• Try eating three or four meals a day for several days and assess how satisfied you feel.
• Focus on the quality of your food choices rather than the exact number of meals you eat.

Conclusion

The real question is not whether eating five meals a day is better than practicing intermittent fasting. Instead, the key is identifying the eating pattern that helps you nourish your body, manage your appetite, and maintain healthy habits in a sustainable way. Current scientific evidence indicates that both approaches can be effective, provided they are accompanied by a high-quality diet and tailored to each individual’s needs and preferences.

BIBLIOGRAPHY

(1) Moon S, Kang J, Kim SH, et al. Beneficial effects of intermittent fasting: a narrative review. Journal of Yeungnam Medical Science. 2020.

(2) Varady KA, Cienfuegos S, Ezpeleta M, et al. Clinical application of intermittent fasting for weight loss: progress and future directions. Nature Reviews Endocrinology. 2022.

(3) Schoenfeld BJ, Aragon AA. How much protein can the body use in a single meal? Implications for daily protein distribution. Journal of the International Society of Sports Nutrition. 2018.

(4) Bellisle F, McDevitt R, Prentice AM. Meal frequency and energy balance. British Journal of Nutrition. 1997.

La entrada Do You Need to Eat Five Meals a Day, or Is Intermittent Fasting Better? se publicó primero en Neolife.

GLP-1 medications are transforming weight loss. But there is one aspect that receives far less attention: how you eat during treatment can make all the difference.

Over the past few months, names such as Ozempic, Wegovy, and Mounjaro have moved from medical consultations into everyday conversations and social media feeds. Weight loss seems more accessible than ever, yet one important question often goes unaddressed: What happens to our nutrition when appetite decreases so dramatically?

Adriana Martín Peral – Neolife Nutrition Unit

The GLP-1 Revolution: What Is Happening?

A few years ago, the idea that medications could help people lose between 10% and 20% of their body weight might have sounded overly optimistic. Today, however, it is a reality.

Drugs such as semaglutide and tirzepatide have transformed the management of obesity and overweight. Their popularity has grown so rapidly that they have moved beyond endocrinology clinics into newspaper headlines, podcasts, and workplace conversations.

Amid all this discussion, however, one crucial point is often overlooked: Losing weight is not simply about losing pounds.

The real question is: What kind of weight are we losing?

How Do These Medications Actually Work?

Although many people describe them as “weight-loss injections,” their mechanism of action is far more interesting.

GLP-1 medications mimic gut hormones that help regulate appetite and blood glucose levels. In simple terms, they make people:

• Feel less hungry.
• Feel full sooner.
• Think less about food.
• Reduce caloric intake with little conscious effort.

And here lies an interesting paradox: Eating less does not necessarily mean eating better.

When appetite decreases significantly, it becomes easy to unknowingly adopt poorer eating habits—skipping meals, reducing protein intake, or avoiding essential foods simply because “nothing sounds appealing.”

The Underappreciated Risk: Losing Muscle Along with Fat

One of the most important—and least discussed—aspects of GLP-1 therapy is that not all weight loss comes from body fat.

Part of the weight lost may come from lean muscle mass, and this matters much more than many people realize.

Muscle is not only important for strength or body composition. It also plays a vital role in:

• Metabolism.
• Bone health.
• Future mobility.
• Healthy aging.
• Blood glucose regulation.

Losing fat can improve metabolic health, but excessive muscle loss may have the opposite effect in the medium and long term.

That is why the goal should not simply be to weigh less, but rather to improve body composition.

How Nutrition Changes When Taking GLP-1 Medications

This is where nutrition stops being secondary and becomes a central part of treatment.

1. Protein Is No Longer Optional

As appetite decreases, many people eat less of everything—including protein. Yet maintaining an adequate protein intake is essential to preserving muscle mass during weight loss.

In practice, this often means prioritizing:

• Fish.
• Eggs.
• Lean meats.
• High-protein dairy products.
• Legumes
• High-quality plant proteins.

Sometimes meals even need to be reorganized to ensure adequate protein intake, despite reduced hunger.

2. Strength Training Matters More Than Cardio

An increasingly common recommendation among specialists is this: If you are losing weight, you need to stimulate your muscles. Strength training—adapted to each individual’s abilities—helps send the body an important message: “This muscle tissue is still needed.”

There is no need to become an athlete or train six days a week. But it is important to understand that while walking is excellent for health, it may not be enough on its own.

3. Greater Satiety Does Not Mean Better Nutrition

Many people describe an experience like this: “I simply don’t feel like eating anymore.”
Although this may initially seem like an advantage, it can also lead to diets that are deficient in fiber, vitamins, and minerals. In other words: Less hunger does not automatically translate into better nutrition.

Food quality still matters.

So… Are They a Good Tool?

The short answer is: They can be, in the right context.

GLP-1 medications are producing very promising results and can significantly improve health when there is an appropriate medical indication. However, it is important to move beyond the simplistic notion that the medication “does everything.”

The reality is both more interesting and more useful: Treatment works best when combined with: A well-designed nutritional strategy. Strength training. Medical supervision. Sustainable lifestyle changes.
Because the goal is not simply to lose weight quickly. The goal is to improve health without sacrificing muscle mass, energy, or quality of life.

Conclusion

We are witnessing a major shift in the treatment of overweight and obesity. GLP-1 medications have opened possibilities that seemed unimaginable just a few years ago.

But perhaps the most important lesson is this: As appetite decreases, nutrition becomes even more important.

Eating less may be relatively easy. Eating better—while preserving muscle mass and metabolic health—still requires strategy. And that is where a well-designed nutritional approach truly makes the difference.

BIBLIOGRAPHY

(1) Wilding JPH, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. New England Journal of Medicine. 2021.

(2) Jastreboff AM, et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine. 2022.

(3) Wharton S, et al. Obesity in adults: a clinical practice guideline. CMAJ. 2020.

(4) Metaanálisis sobre cambios en composición corporal y pérdida de masa magra asociada a terapias GLP-1 en obesidad

La entrada The Weight-Loss Drug Boom (GLP-1): Why Nutrition Matters More Than Ever 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.

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