Diabetes is a metabolic disease in which blood glucose levels remain elevated due to abnormal insulin function. In type 1 diabetes, the body does not produce this hormone; in type 2 diabetes (T2D), the body does not use it effectively. In Spain alone, 13% of the adult population lives with diabetes, a figure that continues to grow, driven by sedentary lifestyles, poor diet, and obesity.

Now, a scientific breakthrough provides a key piece of the puzzle. An international team of researchers has identified a gene called SMOC1, which plays a fundamental role in the development of type 2 diabetes. The study, published in the journal Nature Communications, explains why the beta cells of the pancreas—responsible for producing insulin—lose their function as the disease progresses.

When the pancreas “gets confused”: the origin of the problem

Inside the pancreas are the pancreatic islets, groups of cells that regulate blood sugar. There, two main players exist:

• Beta cells: produce insulin and decrease blood glucose
• Alpha cells: produce glucagon and increase blood glucose

Maintaining the balance between the two is essential for stable glucose levels.

The study reveals that in type 2 diabetes something surprising happens: some beta cells “forget” their original function, stop producing insulin, and begin to behave like alpha cells, generating glucagon. The result is devastating: less insulin, more blood glucose, and greater metabolic imbalance.

The role of the SMOC1 gene

To understand this “cellular identity crisis,” scientists analyzed pancreatic islets from 26 people (with and without diabetes) using advanced RNA sequencing techniques. This allowed them to classify five different types of cells and observe the progressive transformation from one into another.

The results pointed to a clear protagonist: the SMOC1 gene.

• In healthy individuals, SMOC1 is only active in alpha cells
• In people with type 2 diabetes, it begins to appear in beta cells, where it should not be

When SMOC1 is activated in the wrong place:

– insulin production is reduced

– the genetic identity of the beta cell is blocked

– the cell begins to produce glucagon

– blood glucose levels rise

Researchers even identified a third hybrid cell type, which they called “AB cells”, capable of producing both insulin and glucagon, confirming the ability for “role switching” within the pancreatic islet.

A new therapeutic target for type 2 diabetes

Until now, most treatments for T2D have focused on:

• Increasing insulin production
• Improving tissue sensitivity
• Reducing circulating glucose

But this research opens up a completely different approach: preventing beta cells from losing their identity and protecting their original function, by blocking or regulating the expression of the SMOC1 gene.

The next steps for the scientific team will be:

– Deciphering what activates SMOC1 in diabetic beta cells

– Understanding how its expression is regulated

– Developing drugs that block or modulate its activity

If successful, we could be looking at treatments capable of preserving beta cells and slowing disease progression, something no current drug fully achieves.

Conclusion

The discovery of the role of the SMOC1 gene offers a new explanation for the progressive deterioration of the pancreas in type 2 diabetes and points to a novel therapeutic target. This finding not only improves our understanding of the disease but also opens the possibility of future treatments that act at the cellular origin of the problem—not just its consequences.

 

In Spain, osteoarthritis is the leading cause of work disability, affecting nearly 75% of people over the age of 55. This cartilage degeneration causes chronic pain, with no definitive cure, and conventional options—medication and surgery—are not always viable, especially for patients with risk factors such as obesity, uncontrolled diabetes, or heart

A New Hope from NYU Langone Health

A team from the NYU Grossman School of Medicine has shown that a minimally invasive procedure, performed in less than two hours under mild sedation, can significantly reduce chronic knee pain in patients with osteoarthritis.

The treatment, known as Genicular Artery Embolization (GAE), selectively blocks abnormal blood vessels supplying the inflamed joint, reducing neovascularization, the influx of inflammatory cells, and therefore both pain and disease progression.

How GAE Works

A catheter guided by imaging is inserted into the genicular arteries, where embolic microspheres are injected to block them. In the NYU study, more than 60% of the 25 patients treated experienced significant improvements one year after the procedure, with no major complications. Additionally, researchers observed an average reduction of 12% in VEGF and 15% in IL-1Ra, key biomarkers linked to inflammation and joint damage.

Additional Scientific Evidence

• A recent publication in Cardiovascular and Interventional Radiology analyzed 43 patients with moderate to severe osteoarthritis (Kellgren-Lawrence grade 2–4). It reported an average reduction of 2 points in walking pain scores after one year, with only minor side effects such as mild skin changes.
• A systematic review with meta-analysis concluded that GAE provides sustained pain reduction, with decreases of 30–41 points on the VAS scale after 1, 3, 6, and 12 months.
• Another retrospective study of 236 patients revealed a clinical success rate of 54% after one year, with better outcomes in younger patients and those with mild to moderate osteoarthritis.
• GAE is considered safe, with minor adverse effects such as temporary skin discoloration, bruising, or short-term paresthesia. Serious complications, like unintended embolization outside the target area, are very rare.

Why Is This a Significant Innovation?

• Outpatient and quick (1–2 hours), with almost immediate recovery.
• Provides sustained pain relief and functional improvement, even in cases unresponsive to conventional therapies.
• Serves as an effective intermediate treatment for patients who are not yet candidates—or cannot undergo—knee replacement surgery.
• Offers a new therapeutic pathway that clinically modifies the inflammatory process, not just the symptoms.

Conclusion

Genicular Artery Embolization (GAE) emerges as a safe, effective, and minimally invasive option to treat knee pain caused by osteoarthritis, particularly in patients with physical limitations or surgical risks. It represents a breakthrough in the management of this chronic disease, with growing support from clinical studies and systematic reviews.

 

An innovative sub-study of the VITAL trial—coordinated by Brigham and Women’s Hospital (Harvard), Harvard Medical School, and Augusta University (Mass General Brigham)—has revealed a promising link between daily vitamin D₃ supplementation and the preservation of telomere length, a key marker in cellular aging.

The Study:

• Rigorous design: Double-blind, placebo-controlled trial using 2,000 IU/day of vitamin D₃ and 1 g/day of omega‑3 in over 1,000 participants (men ≥ 50 years; women ≥ 55) over a five-year period.
• Analyzed sample: 2,571 white blood cell samples from 1,031 participants, evaluated at baseline, two years, and four years.
• Main finding: Participants taking vitamin D₃ experienced significantly less telomere shortening (140 fewer base pairs) compared to the placebo group—equivalent to delaying cellular aging by approximately two to three years.
• No impact from omega‑3: Omega‑3 supplementation showed no significant effect on telomere length.

Telomeres: Guardians of Aging

Telomeres are DNA sequences that protect the ends of chromosomes. As cells divide, telomeres gradually shorten, potentially leading to cellular senescence or programmed cell death—processes linked to aging and age-related diseases such as diabetes, cancer, or cognitive decline.

Why Does Vitamin D Help?

Beyond its well-known role in bone health and immune modulation, vitamin D₃ may also reduce inflammation—a key mechanism in DNA damage and telomere shortening—and potentially activate enzymes like telomerase, which could support DNA repair and preservation.

What Are the Real-Life Benefits of This Finding?

• Delayed cellular aging: Roughly equivalent to three additional years of cellular protection against normal aging.

• Potential prevention of chronic diseases: Preserving telomere length may reduce the risk of age-related illnesses.
• High scientific validity: This is the first large, long-term randomized clinical trial to support a specific protective effect of vitamin D on telomeres.

Warnings and Limitations

• Preliminary results: Researchers regard these findings as hypothesis-generating and stress the need for further studies to confirm biological mechanisms and effects across diverse populations.
• Technical concerns: The qPCR technique used to measure telomeres can be influenced by blood cell type distribution; experts like Nobel Laureate Carol Greider note limitations in its precision.
• Limited demographic: Participants were mostly white Americans aged over 50, so it’s unclear whether the benefits extend to other age groups or ethnicities.

Practical Recommendations

• The dose used—2,000 IU of vitamin D₃ daily—is considered safe for most adults, with no common adverse effects reported during the five-year study.
• Supplementation should not replace a balanced diet or sufficient sun exposure. It may be especially useful for people with low vitamin D levels or high inflammatory risk.
• Always consult a healthcare professional before starting vitamin D supplements, especially if you have underlying health conditions or take other medications.

Conclusion

This VITAL sub-study provides compelling evidence that daily, moderate-dose vitamin D₃ supplementation may help preserve telomere length, effectively slowing cellular aging by up to three years. While not yet sufficient to alter medical guidelines, it offers a strong foundation for future research and highlights vitamin D’s potential as a preventive health tool.

 

Creatine is widely recognized as one of the most extensively studied supplements in the world of sports, traditionally associated with increased muscle mass and enhanced physical performance. However, recent research has broadened its scope, revealing its influence on cognitive function, mental health, and various life stages—sparking discussions about its classification and inclusion in everyday diets.

Essential Roles of Creatine in the Body

As reported by the BBC, creatine occurs naturally in the human body and plays a crucial role in the management and storage of cellular energy. This compound is primarily produced in the liver, kidneys, and pancreas, then transported to the muscles and brain, where it acts as an immediate energy source—especially during short bursts of intense physical effort.

Its primary mechanism involves the formation of phosphocreatine, an energy reserve system that allows cells to access quick energy when demand is high, such as during exercise or metabolic stress.

Why Supplementing with Creatine Is Recommended

Although the body can synthesize creatine, endogenous production is often insufficient to meet total needs. Therefore, many people also rely on dietary creatine. Foods like meat and fatty fish are key natural sources. For individuals with restrictive diets, such as vegans, or those seeking to enhance physical and mental performance, supplementation may be advisable.

Benefits include improved muscle function, physical endurance, and recovery. Emerging evidence also suggests broader health advantages.

Potential Benefits Beyond Muscle Growth

Recent studies explore creatine’s effects beyond sports performance. These include:

• Reduction of post-viral fatigue
• Improved cognitive function under stress
• Antioxidant potential
• Alleviation of menopausal symptoms
• Slower tumor progression (based on animal studies and epidemiological data)

One revealing finding showed that older adults consuming more creatine had a lower risk of cancer. Research also investigates its positive impact on memory and attention, especially in sleep-deprived or mentally overworked individuals.

Creatine and Cognitive Function

A study by Forschungszentrum Jülich in Germany, led by Ali Gordjinejad, showed that one-time supplementation enhanced cognitive processing speed in sleep-deprived individuals. The stress increased energy demands in the brain, explaining this result. However, the high dosage used warrants caution.

Terry McMorris from the University of Chichester notes that while cognitive improvement data is promising, it is not yet conclusive due to variability in doses and testing methods.

Creatine and Mental Health

A study combining creatine with cognitive-behavioral therapy in depression patients showed greater improvement than therapy alone. This is attributed to creatine’s role in brain energy and neural communication. Vegans, who have lower creatine levels, may particularly benefit.

According to the BBC, a study involving long COVID patients showed improvements in brain fog and concentration following creatine supplementation.

Creatine in Fertility and Development

Creatine plays a vital role even before birth, contributing to:

• Sperm motility
• Placenta formation
• Fetal growth

In complicated pregnancies like preeclampsia, the body increases creatine levels. During infancy, breast milk is the primary source of creatine.

Creatine in Aging

In older adults, creatine serves as a defense against sarcopenia (age-related loss of muscle mass and strength). Supplementation can improve strength and functionality, supporting active aging.

Consumption Recommendations

• Intake: Approximately 1 gram per day
• Sources: Usually met through diet unless in specific cases (e.g., vegans, pregnant women)
• Status: No official daily recommendations yet, but experts suggest considering it a semi-essential nutrient

Researchers recommend developing specific guidelines for groups such as women, older adults, and vegetarians.

Conclusion

Creatine is more than just a sports supplement. Its impact extends to brain, emotional, metabolic, and reproductive health. While research continues, it is already emerging as a key supplement for overall wellness across various stages of life.

A team of scientists from Columbia University has identified a type of neuron in mice that acts as a natural “switch” to control appetite. This discovery, published in Nature Neuroscience and reported by New Scientist, could revolutionize obesity treatment in humans.

The Brain Switch That Tells Us When to Stop Eating

The newly discovered neurons are located in the brainstem, specifically in the dorsal raphe nucleus, a region associated with feeding, mood, and sleep. These cells produce cholecystokinin (CCK), a hormone linked to the feeling of satiety.

How Do They Work?

• They detect signals such as the smell, taste, and texture of food.
• They respond to gut hormones released after eating.
• They send a signal to the brain to slow down food intake and eventually stop eating.

Controlling Appetite with Light (Optogenetics)

Researchers used optogenetics (light-based neuron activation) to control these cells in mice:

• When activated, the animals ate more slowly and stopped eating sooner.
• When inhibited, the mice continued eating uncontrollably.

Connection to Drugs Like Ozempic and Wegovy

The study revealed that these neurons also respond to GLP-1 agonists, the class of medications that includes semaglutide (Ozempic/Wegovy). This suggests that future treatments could combine:

• Existing drugs (to regulate hormones).
• Targeted therapies for these neurons (to enhance satiety).

Do Humans Have These Neurons?

Although the research was conducted in mice, study leader Alexander Nectow states:

“It is highly likely that humans have similar neurons, but this remains to be confirmed.”

Implications for Obesity Treatment

Obesity affects over 650 million adults worldwide (WHO). If confirmed in humans, this discovery could lead to:

• More precise therapies (with fewer side effects).
• Medical devices that modulate the activity of these neurons.
• Better combinations with current medications.

Next Steps

The team now aims to:

1. Confirm the presence of these neurons in humans.
2. Explore whether their malfunction explains eating disorders (such as binge eating).
3. Develop non-invasive methods to stimulate them.

The End of Extreme Dieting? While years of research are still needed, this breakthrough brings science closer to more effective and natural obesity treatments.

Chronic lower back pain is one of the most common and debilitating conditions worldwide, affecting millions of people and limiting their ability to perform daily activities. In search of relief, many patients turn to treatments such as epidural steroid injections. However, a recent guideline from the American Academy of Neurology (AAN) suggests that the evidence supporting their effectiveness is limited, particularly for certain types of chronic lower back pain.

What Are Epidural Steroid Injections?

Epidural steroid injections are a medical procedure in which a corticosteroid medication is administered into the epidural space of the spine. This treatment aims to reduce inflammation and relieve pain in patients with conditions such as radiculopathy (pain caused by a pinched nerve) or spinal stenosis (compression of the spinal cord or nerves).

Although this procedure has been used for decades, its long-term effectiveness has been debated. A recent systematic review published on February 12, 2025, in the journal Neurology sheds new light on this topic.

Key Findings of the Study

The study, led by Dr. Carmel Armon from Loma Linda University in California, analyzed 90 studies conducted over 16 years that evaluated the use of epidural steroid injections in patients with chronic lower back pain. The researchers focused on two main conditions:

a) Lumbar Radiculopathy:

• The injections provided a modest reduction in pain and disability.
• Compared to patients who did not receive injections, 24% more reported less pain, and 16% more experienced reduced disability for up to three months.
• 11% more patients reported reduced disability for six months or longer.

b) Lumbar Spinal Stenosis:

• The injections appeared to reduce disability but not pain.
• 26% more patients reported reduced disability for up to three months, and 12% more did so for six months or longer.
• No significant reduction in short-term pain was observed.

However, the researchers noted that there was insufficient evidence to assess the effectiveness of these injections for neck conditions such as cervical radiculopathy or cervical spinal stenosis.

Limitations and Concerns

While the results suggest that epidural steroid injections may offer some short-term benefits, the researchers highlighted several limitations:

• Long-term effectiveness: No studies were found evaluating whether repeated treatments are effective.
• Impact on daily life: It was not analyzed how these injections affect patients’ ability to return to work or perform daily activities.
• Lack of research in other areas: There is insufficient evidence regarding their use in treating cervical conditions.

Dr. Pushpa Narayanaswami, co-author of the study and a member of Beth Israel Deaconess Medical Center in Boston, emphasized the need for further research:

“Our review confirms the limited short-term effectiveness of epidural steroid injections for certain forms of chronic back pain. Future studies should address these gaps.”

This is a simple headline

The AAN review confirms that epidural steroid injections can be a moderately effective treatment option for some patients with chronic lower back pain, particularly in cases of radiculopathy and spinal stenosis. However, their effectiveness is limited and not without risks.

Researchers urge the medical community to conduct more studies to assess the long-term effects of these injections and their impact on patients’ quality of life. In the meantime, patients should work with their doctors to develop a personalized treatment plan that addresses their specific needs.

 

Henriette van Praag, who grew up in the Netherlands and was always an active person, discovered something fascinating about the benefits of exercise while working as a scientist at the Salk Institute for Biological Studies in San Diego in the late 1990s. She revealed that exercise could stimulate the growth of new brain cells in older mice—a revolutionary idea at the time. This changed her perception of physical activity, and since then, she has adopted a more serious approach to her routine, including CrossFit and running eight to nine kilometers several days a week. From improving mood to strengthening cognitive functions, exercise offers a wide range of benefits for brain health.

Immediate Cognitive Boost

Exercise benefits the brain by enhancing short-term cognition. Studies have shown that people who engage in physical activity exhibit immediate improvements in working memory and other executive functions. This is partly because exercise increases the release of neurotransmitters such as epinephrine and norepinephrine, which are essential for maintaining attention and processing information, explains Marc Roig, a professor at McGill University.

Additionally, dopamine and serotonin—neurotransmitters associated with well-being and happiness—are also released during physical activity. These chemical changes contribute to the sense of well-being many people experience after running or playing sports.

Long-Term Benefits

While the immediate effects are remarkable, the greatest benefits of exercise for the brain are observed when maintaining a consistent routine. Those who exercise regularly perform better on cognitive tests compared to sedentary individuals. Moreover, research indicates that the benefits multiply over time, as participating in an aerobic exercise program for several months can improve overall cognition.

It’s important to note, however, that exercise’s effects on cognition are not miraculous. According to Roig, one cannot expect exercise to grant a “supermemory.” However, the long-term impact on the brain is significant and real.

Exercise and Mental Health

Those who regularly engage in physical activity report better mental health compared to sedentary individuals. Furthermore, exercise can be an effective treatment for depression. In fact, some psychiatrists and therapists prescribe exercise programs as part of a therapeutic plan.

The Centers for Disease Control and Prevention (CDC) recommend at least 150 minutes of moderate aerobic activity or 75 minutes of vigorous aerobic activity per week. This amount of exercise can serve as a good benchmark for those looking to improve their overall well-being.

Protection Against Neurodegenerative Diseases

One of the most notable benefits of exercise is its ability to protect against neurodegenerative diseases, such as Alzheimer’s and dementia. Michelle Voss, a professor at the University of Iowa, emphasizes that physical activity is one of the most effective health behaviors for improving cognitive function and reducing the risk of these conditions.

How Does Exercise Benefit the Brain?

The process by which exercise improves brain health begins in the muscles. When we exercise, muscles release molecules that travel through the bloodstream to the brain. Some of these molecules, such as irisin, have neuroprotective effects, meaning they can help protect and restore brain cells.

Additionally, exercise improves blood circulation, facilitating the flow of these molecules to brain regions and enhancing neuronal health. A key example is the brain-derived neurotrophic factor (BDNF), a hormone that plays a crucial role in creating new neuronal connections and repairing brain cells.

The Most Beneficial Type of Exercise

Experts agree that any type of exercise is good for the brain. However, most studies have focused on aerobic exercise, and high-intensity activities like cardiovascular training have been shown to provide greater benefits. Improving cardiorespiratory fitness is key to maximizing the cognitive benefits of exercise.

As Henriette van Praag demonstrates, incorporating intense exercise into daily life can make a difference. Although it may seem challenging on busy days, finding ways to include physical activity—like cycling uphill—can be an excellent way to stay active and continue enjoying the benefits of exercise.