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Scientists Discover Way to Send Information into Black Holes Without Using Energy

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The Secret Reason Your Body Stops You From Losing Weight

For decades, weight loss has been explained through a simple formula: eat less, move more, burn more calories than you consume. Yet anyone who has struggled with stubborn body fat knows that the human body often resists weight loss, even when we think we are doing everything right. We blame metabolism, hormones, genetics, or lifestyle—but now, scientists have discovered an entirely new player in the weight-loss battle: the immune system.

Researchers at the University of California San Diego School of Medicine have uncovered a surprising biological mechanism showing that certain immune cells—specifically neutrophils, a type of white blood cell—actually work to prevent excessive fat loss. Their findings, published in Nature, reveal that the immune system steps in during stressful situations, such as exposure to cold temperatures, and sends signals to slow down fat breakdown.

This discovery opens a new chapter in our understanding of metabolism, energy balance, obesity, and even unintentional weight loss. What we’ve long viewed solely as fat-burning biology is now known to involve a delicate partnership between fat cells and immune cells—one that helped our ancestors survive harsh environments, but may also make weight management more difficult today.

Why Our Bodies Hold Onto Fat: A Survival Strategy Built Into Our Biology

Before diving into the new study, it’s important to understand the essential role of fat in the body.

Fat Is Not Just Stored Calories—It’s a Life-Preserving Organ

Most people think of white adipose tissue (WAT)—commonly known as body fat—as something purely undesirable. But fat is actually a highly active and important organ. It:

  • Stores energy for times when food is scarce

  • Helps maintain body temperature

  • Produces hormones that regulate hunger, mood, reproduction, and metabolism

  • Supports immune function

  • Protects vital organs

In ancient times, having enough stored fat meant the difference between surviving a long winter or famine and starving to death. Our biology evolved to defend fat stores fiercely, even when we intentionally try to lose weight.

The new research shows that the immune system plays a key role in this defense.

The Discovery: Immune Cells That Slow Down Fat Burning

The UC San Diego team focused on two major stressors that cause fat to break down rapidly:

  1. Cold temperatures, which force the body to burn fat to stay warm

  2. Sympathetic nervous system activation, the same “fight or flight” response triggered by stress

When fat breaks down, fat cells release stored energy in the form of molecules called fatty acids. This is supposed to help keep us warm or supply energy during emergencies.

But too much fat breakdown can be harmful. Excessive fat loss can threaten survival, disrupt hormone balance, and even damage organs.

So the body has built-in ways to prevent runaway fat burning.

This is where neutrophils come in.

What Are Neutrophils, and Why Are They Going Into Fat?

Neutrophils are immune cells best known for fighting infections. They are the first responders when bacteria enter the body, quickly rushing to the site of injury or infection.

But the new study shows they do something completely unexpected:

Neutrophils travel into fat tissue and signal fat cells to slow down fat breakdown.

This happens when:

  • The body senses metabolic stress

  • Fat breakdown becomes too rapid

  • The sympathetic nervous system is activated

In the experiments, the scientists observed that within a short time after cold exposure or similar stress, neutrophils flooded into visceral fat—the fat surrounding internal organs.

This was surprising, because fat tissue is not normally considered a major site of immune activity. But the researchers discovered it has a crucial metabolic purpose.

How Neutrophils Slow Down Fat Burning

Once neutrophils enter fat tissue, they release specific signaling molecules. These molecules essentially tell nearby fat cells:

“Stop burning fat so quickly. You need to preserve energy.”

When these signals are present:

  • Fat breakdown slows

  • Fat stores are protected

  • The body resists further weight loss

To test how important these neutrophils are, researchers removed them or blocked the molecules they release. The result?

Without neutrophils or their signals, mice burned significantly more fat under stress.

This means neutrophils act as a natural “safety switch” that prevents excessive fat loss.

Why Would the Body Want to Prevent Fat Loss?

From a modern perspective, where obesity rates are climbing and weight loss is often a health goal, it can seem counterproductive that the body tries to prevent fat burning.

But from an evolutionary standpoint, it makes perfect sense.

In ancient times, survival depended on having strong fat reserves.

Early humans regularly faced:

  • Long winters

  • Food shortages

  • High physical demands

  • Unpredictable environments

Cold exposure was especially dangerous. If the body burned fat too fast during a cold spell or famine, it could run out of energy entirely.

So the body evolved mechanisms to preserve fat in stressful situations, ensuring survival.

Today, we rarely face those threats. But our bodies still hold onto fat as if we might.

The Role of Fat Cells in Signaling for Help

One of the most fascinating elements of this study is the discovery that fat cells themselves call for help.

When fat cells begin rapidly breaking down stored fat, they activate inflammatory pathways inside the cells. These pathways send distress signals that recruit neutrophils.

This means:

  • Fat cells sense when they are burning too much energy

  • They signal for immune reinforcement

  • Immune cells respond by helping conserve energy

It’s an intricate communication network designed to maintain balance.

What the Study Found in Humans

Although much of the research was conducted using mouse models, the team also analyzed human genetic data.

They discovered that obese individuals had higher activity in the genes related to this neutrophil-fat signaling pathway.

This suggests that:

  • In people with obesity, the body may be even more active in trying to preserve fat

  • The same biological defenses that once prevented starvation may now contribute to weight-loss resistance

  • Immune-metabolic communication is stronger in individuals with higher body fat

This does not mean obesity is caused by the immune system alone, but it highlights a new layer of complexity.

Why This Discovery Is Important

This research changes how scientists think about weight regulation in several key ways:

1. Weight loss is not just about calories—it’s also about immune activity.

The body actively engages the immune system to prevent fat loss when it perceives stress.

2. Fat tissue is not passive—it communicates with and recruits immune cells.

This relationship shows how tightly energy balance is controlled.

3. Obesity may involve overactive fat-preservation signals.

If the neutrophil pathway is more active in people with obesity, the body may be signaling to preserve fat even when it’s not needed.

4. Treating obesity may require new strategies beyond diet and exercise.

Targeting the signaling between fat cells and neutrophils could offer future therapeutic options.

How This Affects Weight-Loss Efforts Today

While this study doesn’t mean immune-based weight-loss therapies are around the corner, it offers several important insights that can change how we think about dieting and metabolism.

1. The body is designed to resist rapid weight loss

This is why:

  • Weight loss often slows down after an initial drop

  • The body “plateaus” even with consistent eating and exercise habits

  • Hunger and cravings increase during dieting

  • Metabolism changes under stress

Your body interprets fast weight loss as a threat, triggering biological defenses—including immune responses—to preserve energy.

2. Stress makes weight loss harder

Because stress activates the sympathetic nervous system, it can:

  • Increase fat-preservation signals

  • Slow down fat breakdown

  • Trigger hormonal changes that increase hunger

Managing stress may be as important as diet and exercise.

3. Cold exposure impacts fat metabolism differently than we thought

Cold is often promoted as a way to boost metabolism. But this study shows that cold also activates neutrophils that work to balance fat burning.

The relationship is more complicated than simply “cold burns fat.”

4. Inflammation and immunity are deeply connected to metabolism

Chronic inflammation is known to be higher in obesity. This study shows inflammation plays a role in preventing fat loss, not just causing metabolic issues.

What This Means for Future Obesity Treatments

Understanding that the immune system regulates fat breakdown opens up exciting possibilities for medical advances.

1. Targeted therapies could reduce the immune system’s fat-preservation signals

By blocking the specific molecules neutrophils release, doctors may one day be able to:

  • Increase fat burning

  • Help break through weight-loss plateaus

  • Treat metabolic disorders more effectively

2. Personalized medicine based on genetic profiles

People with highly active genes in this pathway may respond differently to dieting or medication. Genetic screenings could help tailor treatments.

3. New approaches for unintended weight loss

Just as some individuals struggle to lose weight, others—such as elderly patients or people with chronic illness—struggle with dangerous unintended weight loss.

Understanding the neutrophil-fat partnership could help preserve healthy fat levels in those individuals.

4. Better strategies for metabolic syndrome

Metabolic syndrome, which includes conditions like insulin resistance and fatty liver disease, may be influenced by these immune signals. Targeting them could improve treatments.

The Big Picture: A New Understanding of Weight Control

This research reinforces an important reality:

Weight loss isn’t just about willpower—it’s about biology.

The body is wired to maintain balance and protect energy stores, even when our goals conflict with these ancient survival mechanisms.

Fat cells, immune cells, the nervous system, and metabolic pathways work together in a highly coordinated way. This makes weight management complex and deeply personal—not a one-size-fits-all journey.

Key Takeaways

  • Neutrophils, a type of immune cell, help slow fat breakdown during metabolic stress.

  • This mechanism evolved to preserve energy and prevent dangerous fat loss.

  • Stress, cold exposure, and inflammation all activate this fat-preserving pathway.

  • Obese individuals show higher activity in the genes involved in this system.

  • Targeting the fat-immune communication network could lead to new obesity treatments.

  • Weight loss is influenced by far more than diet and exercise—the immune system plays a central role.

Conclusion: A New Chapter in Metabolism Research

The discovery that the immune system can stall weight loss is a major milestone in metabolic science. It sheds light on why losing weight is often so difficult and why the body seems to fight back against dieting efforts.

Understanding this powerful partnership between fat cells and immune cells not only transforms our view of fat, but opens the door to a new era of weight-loss research—one that looks beyond calories and into the complex biological systems that protect us.

As scientists continue exploring this pathway, we may soon see more effective treatments for obesity, metabolic syndrome, and other conditions linked to energy imbalance. For now, this study reminds us that our bodies are designed to survive, and sometimes that means holding onto fat for reasons far deeper than we ever realized.

Reference: Son, S., Xu, C., Fu, H. et al. Neutrophils preserve energy storage in sympathetically activated adipocytes. Nature (2025). https://doi.org/10.1038/s41586-025-09839-6

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