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.

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

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

Dr. Carlos Martí – Neolife Medical Team

Cardiovascular Prevention

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

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

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

Beyond Cholesterol: Understanding What We Really Measure

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

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

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

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

From Estimating Risk to Detecting Disease

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

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

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

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

A More Precise, Not More Complex Approach

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

In practice, this translates into:

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

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

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

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

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

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

Understanding Risk Before It Becomes Visible

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

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

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

BIBLIOGRAPHY

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

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

La entrada How Our Understanding of Cholesterol and Cardiovascular Risk Is Changing se publicó primero en Neolife.

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

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

Meritxell Massons – Neolife Nutrition Unit

What Are Osteoporosis and Osteopenia?

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

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

Why Do Bones Weaken With Age?

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

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

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

Preventing Osteoporosis Through Nutrition

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

Calcium: The Structural Basis of Bone

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

Main sources:

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

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

Vitamin D: Essential for Calcium Absorption

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

Main sources:

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

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

Physical Activity: An Essential Stimulus

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

Nutrients That Support Bone Health

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

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

A varied and balanced diet usually covers these requirements.

Foods and Substances to Limit in Osteoporosis

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

• Caffeine

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

• Excess Phosphorus

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

• Alcohol and Tobacco

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

• Phytates and Oxalates

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

Nutrition and Hormones: A Key Relationship

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

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

Conclusion

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

BIBLIOGRAPHY

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

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

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

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

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

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

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

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

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

La entrada Osteoporosis and Nutrition: What to Avoid and How to Protect Your Bones se publicó primero en Neolife.

Not everything is about the glycemic index, and you don’t need to “eat unlimited protein.”

If you want to lose body fat, you have probably heard that you should avoid foods with a high glycemic index and significantly increase your protein intake. But what truly matters? Does the glycemic index influence weight loss as much as we think? And how much protein do you actually need? Below, we clarify both concepts based on scientific evidence and practical application.

Adriana Martín Peral – Neolife Nutrition Unit

What Is the Glycemic Index?

The glycemic index (GI) measures how quickly a carbohydrate-containing food raises blood glucose levels compared with pure glucose.

• High GI → rapid rise in blood glucose
• Low GI → slower rise

However, there is a limitation: the glycemic index is measured under isolated conditions, with the food consumed alone and in standardized quantities. In real life, we eat combinations of foods. For this reason, a more practical concept is glycemic load, which takes into account both the quality and the quantity of carbohydrates.

Does the Glycemic Index Matter for Weight Loss?

Evidence shows that:

• Low-GI diets may improve glycemic control.
• They can be particularly beneficial in individuals with insulin resistance.
• However, when calories and protein intake are controlled, GI alone does not determine fat loss.

The factors that most strongly influence weight loss are:

• Sustained caloric deficit
• Adequate protein intake
• Long-term adherence

A high-GI food does not “cause weight gain” by itself. The overall dietary context is what truly makes the difference.

Protein: The Key Player in Fat Loss

If there is one macronutrient that becomes especially important when aiming to lose fat without losing muscle mass, it is protein. Why?

• It increases satiety.
• It reduces the loss of muscle mass during a caloric deficit.
• It has a higher thermic effect (the body expends more energy digesting it).

This leads to an important question:

How Much Protein Is Actually Needed for Weight Loss?

The standard recommendation for the general population is 0.8 g/kg/day.

However, for fat loss and preservation of muscle mass, current evidence suggests an intake of 1.6–2.2 g/kg of body weight per day. That said, before increasing protein intake, it is important to ensure that there is no medical condition requiring a different nutritional approach. Protein intake should always be individualized and supervised by a healthcare professional.

Practical example:

A person weighing 70 kg who wants to lose fat should consume between 112 and 154 g of protein per day. This does not mean “eating unlimited protein.” Beyond this range, the benefits do not increase significantly.

What You Should Really Focus On

Instead of becoming overly concerned with the glycemic index:

• Ensure sufficient protein intake at each meal.
• Combine carbohydrates with fiber, fats, and protein.
• Prioritize minimally processed foods.
• Evaluate your long-term adherence rather than focusing exclusively on GI.

Improving your daily protein distribution will have a much greater impact on body composition than focusing solely on the glycemic index.

Conclusion

The glycemic index can be a useful tool in certain contexts, particularly in individuals with metabolic disturbances, but it is not the decisive factor when it comes to fat loss. What truly makes a difference is maintaining a sustainable caloric deficit, ensuring adequate protein intake, and building a dietary pattern that can be maintained over time.

Within this framework, protein plays a key role because it helps preserve muscle mass, improves satiety, and facilitates adherence to the nutritional plan. However, more is not always better, and recommendations should be adjusted according to each individual’s characteristics and health status.

Ultimately, losing weight does not depend on demonizing foods based on their glycemic index or consuming unlimited protein, but rather on applying strategy, scientific evidence, and long-term consistency.

BIBLIOGRAPHY

(1) Thomas, D., Erdman, K., & Burke, L. (2016). Position of the Academy of Nutrition and Dietetics: Nutrition and Athletic Performance.

(2) Morton, R. W., et al. (2018). Protein intake and muscle mass: A meta-analysis.

(3) Wycherley, T. P., et al. (2012). Effects of energy-restricted high-protein diets on body composition.

(4) Livesey, G., et al. (2008). Glycemic index and body weight: systematic review and meta-analysis.

La entrada Glycemic Index and Protein: What Really Matters If You Want to Lose Weight se publicó primero en Neolife.

The menopausal transition promotes changes in body composition. We analyze the hormonal factors involved and the most effective nutritional strategies.

During menopause, many women experience weight gain, particularly in the abdominal area. Although this is often attributed exclusively to “hormones,” the phenomenon is more complex. The decline in estrogen levels, changes in muscle mass, and metabolic adaptations all play a significant role. We review what actually happens and how to intervene effectively.

Adriana Martín Peral – Neolife Nutrition Unit

Hormonal Changes in Menopause: What Really Happens?

Menopause is characterized by a progressive decline in estrogen levels, particularly estradiol. This hormonal shift impacts:

• Redistribution of body fat toward a more android (abdominal) pattern.
• Decreased basal energy expenditure.
• Increased insulin resistance.
• Higher cardiometabolic risk.

Estrogens play a protective role at the metabolic level. Their decline favors greater accumulation of visceral fat, which is metabolically active and associated with inflammation.

Is It Only a Hormonal Issue?

Not exclusively. In addition to hormonal changes, other factors are involved:

• Loss of Muscle Mass (Sarcopenia)

From the ages of 40–50 onward, there is a progressive decline in muscle mass if no strength stimulus is present. Since muscle is metabolically active tissue, its reduction decreases daily energy expenditure.

• Decreased Total Energy Expenditure

Lower levels of spontaneous physical activity, changes in sleep patterns, and increased stress contribute to a sustained positive energy balance.

• Changes in Appetite and Satiety

Some women report increased cravings for energy-dense foods, possibly related to hormonal fluctuations and sleep disturbances.

Evidence-Based Nutritional Strategies

• Prioritize Adequate Protein Intake: A sufficient protein intake (approximately 1.2–1.6 g/kg/day depending on individual profile) helps to:
  • Preserve muscle mass.
  • Improve satiety.
  • Support glycemic control.

Distributing protein evenly throughout the day optimizes muscle protein synthesis.

• Strength Training + Nutrition: Resistance training is key to counteracting age- and menopause-related muscle loss. When combined with adequate protein intake, it improves body composition beyond what is reflected on the scale.
• Control Energy Density: Reduce ultra-processed foods and prioritize:
  • Vegetables
  • Whole fruit
  • Legumes
  • Healthy fats (extra virgin olive oil, nuts)
  • Lean protein sources

This approach supports satiety while lowering overall caloric load.

• Fiber and Metabolic Health: A high fiber intake (25–35 g/day) improves:
  • Insulin sensitivity
  • Lipid profile
  • Gut health

The gut microbiota also appears to play a relevant role in weight regulation during this stage.

Sleep and Stress

Sleep deprivation is associated with greater insulin resistance and increased appetite. Therefore, intervention should be comprehensive and lifestyle-oriented.

What Does NOT Work

• Extremely restrictive diets maintained over time.
• Complete elimination of food groups without clinical indication.
• Focusing exclusively on weight without assessing body composition.

During menopause, the goal should be to improve body composition and metabolic health—not simply reduce body weight.

Conclusion

Weight gain during menopause is not inevitable, but it does require a different approach. The combination of appropriate nutrition, strength training, and a comprehensive lifestyle strategy can improve body composition and reduce cardiometabolic risk during this stage of life.

BIBLIOGRAPHY

(1) Lovejoy JC et al. Increased visceral fat and decreased energy expenditure during menopause.

(2) Lizcano F, Guzmán G. Estrogen deficiency and the origin of obesity during menopause.

(3) Stuenkel CA et al. Treatment of symptoms of menopause.

(4) Messier V et al. Menopause and sarcopenia: impact on metabolic health.

La entrada Menopause and Weight Gain: The Real Role of Hormones and How to Address It Through Nutrition se publicó primero en Neolife.