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.

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

For years, weight loss has mainly been approached from a simple perspective: eat less and move more. However, current evidence shows that this approach is insufficient to explain what happens in clinical practice.

Most diets do not fail because of a lack of knowledge, but because they fail to take into account how the body responds and how eating behavior is regulated over time.

Meritxell Massons – Neolife Nutrition Unit

What Happens in the Body When We Diet?

When calorie intake is reduced, the body activates adaptive mechanisms whose purpose is not aesthetic, but survival.

One of the main factors explaining why long-term diets fail is metabolic adaptation.

Metabolic adaptation

One of the main reasons why long-term diets do not work is metabolic adaptation, which occurs when a calorie deficit is maintained:

• Resting energy expenditure decreases.
• Activity-related energy expenditure is reduced.
• The body becomes more energy efficient.

Appetite Regulation: Hormonal Changes

Weight loss induces changes in key hormones:

• Decreased leptin levels (satiety signal).
• Increased ghrelin levels (hunger stimulation).

The result is a greater tendency to eat, even in individuals with high initial adherence.

Loss of Muscle Mass

Poorly structured or overly restrictive diets can lead to muscle mass loss, which results in:

• Reduced basal metabolic rate.
• Decreased ability to oxidize energy.
• Regain of body fat.

Behavior: The Key Factor

Beyond physiology, the success of a nutritional plan depends on whether it is sustainable. Evidence shows that weight loss does not depend solely on calorie deficit, but on the ability to maintain it over time.

This is where behavior becomes essential, as strict diets:

• Are difficult to maintain.
• Increase cravings for restricted foods.
• Promote episodes of loss of control.

In addition, external factors such as stress, lack of time, or food availability contribute additional strain on the body.

The Restriction–Loss of Control Cycle

A common pattern seen in clinical practice is:

Restriction → increased cravings → loss of control → guilt

This cycle makes adherence more difficult and promotes treatment abandonment.

The Solution in Clinical Practice

In clinical practice, this translates into:

• Avoiding aggressive calorie deficits.
• Prioritizing the preservation of muscle mass.
• Ensuring adequate protein intake.
• Evaluating long-term sustainability.
• Promoting healthy lifestyle habits.

The goal is not only to induce weight loss, but to create a metabolic and behavioral context that allows it to be maintained.

Conclusion

Most diets fail not because of a lack of discipline, but because they fail to consider the body’s physiological response and eating behavior.

The body adapts by reducing energy expenditure and increasing appetite, while restrictive strategies make adherence more difficult.

Therefore, long-term success does not depend on extreme measures, but on designing interventions that respect physiology, adapt to the individual, and can be maintained over time.

Ultimately, losing weight is not just a matter of calories, but of strategy, context, and sustainability.

BIBLIOGRAPHY

(1) Thom, G., et al. (2021). Weight loss-induced increase in fasting ghrelin concentration is a predictor of weight regain. Diabetes, Obesity and Metabolism.

(2) Nunes, C. L., et al. (2021). Adaptive thermogenesis after weight loss: a systematic review.

(3) López-Torres, S. Y., et al. (2024). Adaptive thermogenesis at the level of resting energy expenditure after diet-induced weight loss. Obesity (Silver Spring).

(4) Hall, K. D., & Kahan, S. (2023). Maintenance of lost weight and long-term management of obesity. Medical Clinics of North America.

La entrada Why Many Diets Fail in the Long Term: Beyond Calories se publicó primero en Neolife.

Discover why taking care of your gut means taking care of your entire body — from your immune system to your mood.

For a long time, the gut was thought to be responsible only for digesting food. Today, we know its role goes far beyond that. Inside it lives a complex ecosystem of microorganisms — the gut microbiota — that directly influences key aspects of our health. Taking care of it not only improves digestion, but can also help you feel more energetic, less inflamed, and emotionally more balanced.

Adriana Martín Peral – Neolife Nutrition Unit

What Is the Microbiota and Why Does It Matter?

The gut microbiota is the collection of trillions of microorganisms — bacteria, viruses, fungi, and others — that live in your intestines. Although it may sound strange, these tiny inhabitants play a crucial role in your health.

Among the microbiota’s main functions are:

• Digesting food and producing nutrients such as B vitamins and vitamin K
• Training the immune system
• Producing neurotransmitters such as serotonin (90% of which is produced in the gut!)
• Protecting against harmful pathogens

This is why the gut is often called “the second brain.” There is a direct connection between the gut and the brain, known as the gut-brain axis, which allows what happens in one to affect the other.

The Microbiota and Its Impact on Mental and Immune Health

The connection between the gut and the brain has been one of the most fascinating scientific discoveries in recent years. What was once considered solely a digestive organ is now recognized as a complex system that communicates directly with the brain through what is known as the gut-brain axis. This communication pathway allows changes in the gut microbiota to influence not only digestion, but also emotional state, behavior, and even the way our body responds to disease.

In the field of mental health, various studies have shown that an imbalance in the gut microbiota — known as dysbiosis — may be linked to disorders such as anxiety, depression, and chronic fatigue. This is because many intestinal bacteria participate in the production of key neurotransmitters such as serotonin, which is responsible for generating feelings of well-being and happiness. In fact, it is estimated that more than 90% of the body’s serotonin is produced in the gut, which explains why digestive discomfort is often accompanied by emotional disturbances.

On the other hand, the microbiota plays a crucial role in the functioning of the immune system. Approximately 70% to 80% of the body’s immune cells are located in the gut, making it a true defense center. When the microbiota is balanced, it helps train the immune system to respond appropriately to viruses, bacteria, and toxins. However, when this balance is disrupted, it can lead to a state of chronic low-grade inflammation that, over time, weakens our defenses and increases the risk of developing autoimmune diseases, allergies, recurrent infections, and even metabolic conditions such as obesity and type 2 diabetes.

In addition, the modern lifestyle — characterized by low-fiber diets, excessive consumption of ultra-processed foods, frequent antibiotic use, lack of sleep, and high levels of stress — has a direct negative impact on the microbiota. These factors reduce bacterial diversity, promote the growth of harmful microorganisms, and alter the protective functions of the gut. For this reason, caring for the microbiota should not be seen merely as a strategy to improve digestion, but as a fundamental tool for strengthening the immune system, balancing the mind, and preventing disease.

How to Care for Your Microbiota: Practical Guide

Taking care of your microbiota does not have to be complicated. Despite its biological complexity, this intestinal ecosystem responds very positively to simple lifestyle and dietary changes. What you choose to eat, how you manage stress, and how much sleep you get can shape your microbiota day by day, strengthening its diversity and promoting beneficial bacteria. In other words, every daily decision is an opportunity to nourish your health from within.

One of the fundamental pillars of maintaining a balanced microbiota is the regular consumption of fiber-rich foods. Fiber acts as food for the good bacteria in the gut, allowing them to grow, multiply, and perform their functions properly. This type of fiber, known as prebiotic fiber, is naturally found in:

• Garlic
• Onion
• Asparagus
• Leeks
• Artichokes
• Whole grains such as oats
• Less ripe fruits, such as green bananas

Unlike regular fiber, prebiotic fiber not only regulates intestinal transit, but also directly nourishes the microbiota, helping improve its diversity and stability.

Alongside prebiotics, fermented foods have special value for gut health. These foods contain live bacteria, known as probiotics, which can temporarily colonize the intestine and support digestive, immune, and metabolic functions.

• Kefir
• Plain unsweetened yogurt
• Sauerkraut
• Kimchi
• Artisan kombucha are some accessible and effective examples

Including them regularly in your diet can help restore microbial balance, especially after antibiotic treatments or prolonged periods of stress and poor eating habits.

In addition to diet, other lifestyle factors significantly influence the microbiota. Chronic stress, sedentary behavior, lack of sleep, and excessive consumption of ultra-processed foods are silent enemies of intestinal health. Stress, for example, alters intestinal motility and can change bacterial composition within just a few days, causing digestive symptoms such as bloating, gas, constipation, or diarrhea. Sleeping well, staying physically active, and finding time to disconnect are essential habits that work together to protect the balance of the intestinal ecosystem.

Conclusion

Taking care of your microbiota is not a fad or a passing trend. It is a real investment in your long-term health. Starting with small, sustainable changes — such as adding more vegetables to your meals, avoiding added sugars, or choosing fermented options instead of industrialized products — can make a big difference in how you feel and how your body functions. Remember that a healthy gut not only improves digestion, but also strengthens your defenses, helps you manage stress more effectively, and enhances emotional well-being.

Your gut has memory. Every choice you make either builds it up or weakens it. That is why caring for your microbiota is a smart and conscious way to care for your entire body, from the defenses that protect you to the thoughts that accompany you. Today is a good day to start.

BIBLIOGRAPHY

(1) Cryan, J. F., & Dinan, T. G. (2012). Mind-altering microorganisms: the impact of the gut microbiota on brain and behaviour. Nature Reviews Neuroscience, 13(10), 701–712.

(2) Dinan, T. G., & Cryan, J. F. (2017). The microbiome-gut-brain axis in health and disease. Gastroenterology Clinics of North America, 46(1), 77–89.

(3) Belkaid, Y., & Hand, T. W. (2014). Role of the microbiota in immunity and inflammation. Cell, 157(1), 121–141.

(4) Round, J. L., & Mazmanian, S. K. (2009). The gut microbiota shapes intestinal immune responses during health and disease. Nature Reviews Immunology, 9(5), 313–323.

(5) Kau, A. L., Ahern, P. P., Griffin, N. W., Goodman, A. L., & Gordon, J. I. (2011). Human nutrition, the gut microbiome and the immune system. Nature, 474(7351), 327–336.

(6) Valdes, A. M., Walter, J., Segal, E., & Spector, T. D. (2018). Role of the gut microbiota in nutrition and health. BMJ, 361, k2179.

(7) Giulia Enders (2014). La digestión es la cuestión. Editorial Uranito

(8) Michael Mosley (2017). El Código de la Comida: cómo tu flora intestinal puede cambiar tu vida. Editorial Urano.

La entrada Your Second Brain: How the Gut Microbiota Impacts Your Mind, Immunity, and Overall Health se publicó primero en Neolife.

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

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

Dr. Carlos Martí – Neolife Medical Team

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

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

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

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

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

The Silent Decline: When the Change Really Begins

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

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

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

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

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

When the Body Really Starts to Change

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

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

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

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

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

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

Maintaining Capacity for as Long as Possible

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

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

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

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

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

BIBLIOGRAPHY

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

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

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

What intermittent fasting is, how it works in the body, its potential benefits, and the risks of applying it incorrectly.

Intermittent fasting has become one of the most popular nutritional strategies in recent years, especially among individuals looking to lose weight. While it can offer metabolic and health benefits, it is not without risks if practiced without proper knowledge or supervision.

Adriana Martín Peral – Neolife Nutrition Unit

What Is Intermittent Fasting?

Intermittent fasting is not a diet per se, but rather an eating pattern that alternates periods of food intake with periods of fasting. It focuses less on what you eat and more on when you eat. Unlike traditional diets, it is not based on restricting specific foods, but on structuring the timing of meals.

Main Types of Intermittent Fasting

16:8 Fasting

This involves fasting for 16 hours and concentrating food intake within an 8-hour window. It is the most popular protocol due to its ease of integration into daily life.

14:10 Fasting

A more flexible version, recommended for beginners or individuals with higher energy demands.

5:2 Method

Five days of normal eating and two non-consecutive days with significantly reduced caloric intake.

Alternate-Day Fasting

Alternates days of normal eating with days of complete or partial fasting. It is more demanding and less sustainable for many people.

How Does Intermittent Fasting Work in the Body?

During the first hours of fasting, the body uses stored glucose in the form of glycogen. Once these reserves are depleted, it begins to rely on body fat as a source of energy.

This process is accompanied by:

• A decrease in insulin levels
• An increase in glucagon
• Activation of cellular repair mechanisms

These changes explain many of the effects associated with intermittent fasting.

Positive Effects of Intermittent Fasting

When properly implemented and adapted to the individual, intermittent fasting may offer several benefits:

1. Improved Insulin Sensitivity

Lower insulin levels promote better blood glucose control, which may be beneficial for individuals with insulin resistance or risk of type 2 diabetes.

2. Fat Loss

By promoting fat utilization as fuel, it may contribute to weight loss, especially when combined with a balanced diet.

3. Metabolic Health

Some studies associate intermittent fasting with improvements in markers such as cholesterol, triglycerides, and blood pressure.

4. Possible Activation of Autophagy

Fasting activates cellular recycling processes known as autophagy, which are linked to cellular health and longevity, although their impact in humans is still under investigation.

Negative Effects if Done Incorrectly

Intermittent fasting is not suitable for everyone, and improper implementation may lead to adverse effects:

1. Nutritional Deficiencies

Reducing eating windows without proper planning may result in insufficient intake of protein, vitamins, and minerals.

2. Digestive Issues and Fatigue

Skipping meals without prior adaptation can cause dizziness, weakness, constipation, headaches, or gastrointestinal discomfort.

3. Unhealthy Relationship with Food

In some individuals, it may promote disordered eating behaviors, binge eating, or a rigid relationship with food.

4. Not Recommended in Certain Cases

It is not advisable for:

• Pregnancy and breastfeeding
• Individuals with eating disorders
• Individuals with eating disorders
• People with certain medical conditions without professional supervision

Common Mistakes When Practicing Intermittent Fasting

• Overeating during the eating window
• Prioritizing ultra-processed foods
• Not meeting protein requirements
• Forcing excessively long fasting periods
• Ignoring the body’s signals

Recommendations for Safe Intermittent Fasting

• Start gradually (14:10 before 16:8)
• Prioritize fresh, nutrient-dense foods
• Maintain proper hydration
• Adapt fasting to lifestyle and activity level
• Consult a nutrition professional

Conclusion

Intermittent fasting can be a useful tool within a healthy eating approach, but it is not a universal solution. Its success depends on the individual, the context, and proper nutritional planning. When practiced with knowledge and supervision, it may provide benefits; when applied incorrectly, it can lead to more harm than good.

BIBLIOGRAPHY

(1) Mattson, M. P., Longo, V. D., & Harvie, M. (2017). Impact of intermittent fasting on health and disease processes. Ageing Research Reviews, 39, 46–58.

(2) Anton, S. D., et al. (2018). Flipping the metabolic switch: understanding and applying the health benefits of fasting. Obesity, 26(2), 254–268.

(3) Patterson, R. E., & Sears, D. D. (2017). Metabolic effects of intermittent fasting. Annual Review of Nutrition, 37, 371–393.

(4) Organización Mundial de la Salud (OMS). Healthy diet factsheet.

La entrada Ayuno intermitente: qué es, beneficios y riesgos de una práctica cada vez más popular se publicó primero en Neolife.