The COVID-19 pandemic may be over, but our immune systems are still feeling the impact. After years of battling constant viral threats, from COVID-19 to seasonal flu and other infections, our body’s defense system is exhausted. Many people continue to experience lingering inflammation, frequent illnesses, and slower recovery times. This extended state of immune stress has compromised us further to chronic illness, including autoimmune diseases and even neurodegenerative diseases such as Parkinson's. So why is our immune system still in trouble? And how do we give it its power back? Understanding immune exhaustion is the beginning of rebuilding our body's natural immunity.

A weakened immune system makes people more susceptible to disease, mental illnesses, and even sleep disorders. Now, new research indicates that immune system depletion may play an important role in the onset of Parkinson's disease, a degenerative neurologic disorder that compromises movement and cognition.

Role of Inflammation in Parkinson's Disease

Dysfunctional immune response is a leading cause of long-standing inflammation within the body, that has been found to contribute towards a multitude of conditions, including cardiovascular conditions, diabetes, depression, and neurodegenerative diseases such as Alzheimer's.

As people age, their immune system naturally becomes less effective. This deterioration, referred to as immune exhaustion, may be a key contributor to the onset and progression of Parkinson’s disease. Rebecca Wallings, a Parkinson’s Foundation Launch Award grant recipient and senior postdoctoral fellow at the University of Florida, believes that an accumulation of exhausted immune cells could be driving neurodegeneration in Parkinson’s patients.

How a Tired Immune System Might Affect Parkinson's?

Parkinson's disease is most commonly linked with the degeneration and loss of dopaminergic neurons—motor nerve cells that produce dopamine, an essential neurotransmitter for movement. While researchers have long suspected inflammation is involved in this neurodegeneration, the mechanisms are not yet well understood.

Wallings' study is on immune cell exhaustion, a process by which aging immune cells fail to control immune responses effectively. Her research indicates that instead of dampening inflammation in Parkinson's patients, attempts should be made to rejuvenate the immune system to regain its functionality.

Energy Deficiency in Immune Cells

One of the major findings of Wallings' work is the function of mitochondrial impairment in immune cell exhaustion. Mitochondria are commonly called the powerhouses of cells, as they are vital for generating energy. As mitochondria age and become inefficient, immune cells fail to function well, potentially accelerating neurodegeneration in Parkinson's disease.

Wallings has found that mutations in the LRRK2 gene, a recognized genetic risk factor for Parkinson's disease, are linked with defective mitochondrial function and immune cell exhaustion. Her current work includes testing various therapeutic approaches to restore mitochondrial function in immune cells with the potential to enhance the immune system and potentially prevent or treat Parkinson's disease.

Will Rejuvenating the Immune System Help in Treatment?

For decades, the standard practice in treating Parkinson's has been to suppress brain inflammation. Yet Wallings' work indicates that instead of slowing down immune responses, restoring the immune system could be a more successful strategy. By addressing mitochondrial impairment and immune resilience, researchers can potentially reverse or slow down Parkinson's disease.

Wallings is now looking into how to rejuvenate immune cells by fixing mitochondria. She studies immune cells from patients with Parkinson's as well as from healthy subjects and performs experiments on animal models to determine if rejuvenation of the immune system could result in improved disease outcomes.

Lifestyle Factors That May Affect Parkinson's Risk

While there is no cure for Parkinson's disease, some lifestyle adjustments may decrease the chances of developing the illness. Since neurodegenerative diseases are associated with chronic inflammation and immune dysfunction, developing habits that enhance immune function might prove helpful.

Diet: There is evidence to suggest that eating in accordance with the Mediterranean or MIND diets, both high in antioxidants, healthy fats, and anti-inflammatory foods, can encourage brain wellness and reduce Parkinson's risk.

Avoiding Dangerous Substances: Restricting alcohol and nicotine use can maintain a robust immune system and suppress inflammation.

Reducing Stress: Chronic stress weakens immune function, so methods such as meditation, exercise, and sufficient sleep can lead to improved overall well-being.

Athletes who spend years training their bodies undergo remarkable physiological changes. Athlete's heart is one of them. It becomes stronger, more efficient, and sometimes even larger. This natural adaptation is known as athlete's heart, a condition that is completely normal in most cases but can occasionally resemble serious heart disease.

What Is Athlete’s Heart?

Understanding the difference between a healthy athletic heart and an underlying cardiac disorder is crucial, especially as awareness grows around sudden cardiac deaths in young athletes.

HealthandMe spoke to Dr. Ruchit Shah, Interventional Cardiologist at Saifee Hospital, Mumbai, who said, “If a person exercises too much, normally more than 60 minutes in most days of the week for a prolonged period of time, the body's need for oxygen and for blood to supply the oxygen rises significantly. This can often be seen in the very intense training regimens of competitive athletes. The heart muscle responds to this extra demand by getting "conditioned" and thickening with time.”

Just like skeletal muscles that get bigger and thicker and with training and exercise, the heart muscle can get bigger and thicker too.

Athlete's heart is usually characterised by a “conditioned heart rate”. People with athlete's hearts will now show symptoms or serious warning signs and thereby won't need a specific treatment for the condition.

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Common Signs Of Athlete’s Heart

Signs include:

• Slow resting heart rate (bradycardia)

• Mild enlargement of the heart on imaging

• Changes on an electrocardiogram (ECG)

• High exercise capacity with no symptoms

Athlete’s Heart Is Different From Cardiac Diseases

The expert also says that athlete's heart is different from serious cardiac diseases like cardiomyopathies, especially hypertrophic obstructive cardiomyopathy (HOCM).

He says, “HOCM is a serious disease, with heart muscle thickening also occurring and causing the left ventricular cavity to narrow. The left ventricle's outflow tract can also become obstructed from this excessive thickening. Athletes with HOCM have a risk of sudden cardiac arrest and death, unlike athletes with athlete's heart.”

An athlete‘s heart, by itself, is considered a benign physiological adaptation and does not require medical intervention.

However, it becomes important to investigate further if an athlete experiences:

• Chest pain during exercise

• Unexplained fainting

• Palpitations

• Shortness of breath out of proportion to exertion

• Reduced exercise performance

• A family history of sudden cardiac death or inherited heart disease

Ignoring these warning signs can delay the diagnosis of potentially serious cardiac conditions. Those who have an athlete’s heart must get periodic cardiac evaluation, do a temporary reduction in training if the diagnosis remains uncertain, and monitor when minor abnormalities are present.

Athlete's heart is proof of the body's extraordinary ability to adapt to sustained physical activity. For most athletes, it represents a healthy, efficient cardiovascular system rather than a medical problem. The challenge lies in distinguishing these normal adaptations from potentially dangerous heart conditions that can look remarkably similar.

Adults under 40 with obesity continue to face a higher risk of cardiovascular disease than their peers with a normal Body Mass Index (BMI), according to a new study published in The Lancet.

The international study, led by researchers at Imperial College London, found that differences in blood pressure and unhealthy cholesterol levels between older adults with obesity and those with a normal BMI have narrowed—or even disappeared—in several high-income countries over the past three decades. In contrast, little or no such improvement was seen among younger adults.

Younger Adults Show No Similar Improvement

The findings suggest that adults under 40 with obesity continue to have higher blood pressure and unhealthy cholesterol levels than those with a normal BMI.

Obesity is a key risk factor for heart disease.

Researchers also found that the use of cholesterol-lowering and blood pressure medications remains low in this age group, supporting the idea that medication has played a key role in reducing cardiovascular risk among older adults.

"While good news for older adults with obesity, our results suggest that cardiovascular health risks remain higher for adults under 40 than for their counterparts with a normal BMI,” said author Ysé d'Ailhaud de Brisis, from the School of Public Health at Imperial.

"Early lifestyle interventions, screening, and, when appropriate, medication in this younger group should be considered to prevent long-term cardiovascular complications linked to obesity," de Brisis added.

Older Adults See Reduced Risk

Since the 1990s, blood pressure and unhealthy cholesterol levels have fallen more rapidly among adults aged 40 to 79 with obesity than among those with a normal BMI in most of the seven high-income countries studied, including England and the US.

The greatest improvements were seen among adults aged 60 to 79. In England and the US older adults with obesity—particularly those with severe obesity—had similar or even lower blood pressure and unhealthy cholesterol levels than those with a normal BMI by the end of the study period.

Heart Medications May Explain the Trend

The researchers said the narrowing gap is largely due to increased use of cholesterol-lowering medications, such as statins, and blood pressure medicines among adults over 40 with obesity.

For example, by the early 2020s, around 70% to 72% of older men with severe obesity in England and the US were taking cholesterol-lowering medication, compared with 40% to 48% of older men with a normal BMI.

“This latest analysis suggests that the observed convergence in cholesterol and blood pressure levels between people aged over 40 with obesity and those with a normal BMI is largely due to statins and other widely accessible medications to reduce cardiovascular risk. That is a significant public health success story, and one we should not lose sight of as new weight-loss medications enter the picture,” said author Lakshya Jain, from the School of Public Health at Imperial.

How Was the Study Conducted?

The researchers analyzed blood pressure and cholesterol data from nearly one million participants across 110 health datasets collected between 1990 and 2024.

The study included people with obesity, overweight and normal BMI from seven high-income countries: England, the US, Japan, South Korea, Taiwan, Thailand and Finland.

The authors also acknowledged limitations of the study such as, the findings may not apply to low- and middle-income countries, where access to cholesterol- and blood pressure-lowering medications is lower. Further, the study could also not assess the impact of different medication doses because prescription data were unavailable.

Popular GLP-1 medications such as Ozempic, Wegovy, and Zepbound are well established for improving metabolic health, lowering blood sugar and promoting weight loss. These blockbuster drugs are also known to reduce the risk of conditions such as heart disease and type 2 diabetes.

Now, researchers are exploring whether these medications could also help slow biological aging and potentially increase longevity.

Study Explores Anti-Aging Potential

A recent US National Institutes of Health (NIH)-backed study, published in the journal Nature, found that Ozempic slowed biological aging in people living with HIV and lipohypertrophy, a condition in which fatty deposits develop under the skin.

People with HIV often experience accelerated aging because of the infection, making them an important group for age-related research, said lead author Dr. Michael Corley, associate professor of medicine at the University of California, San Diego's Stein Institute for Research on Aging, according to The New York Times.

Although the trial was preliminary, Dr. Corley said it "provided us an opportunity to say, hey, is there any signal here that warrants all the hype?"

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Can GLP-1 Drugs Slow Aging?

Experts believe the findings are promising, but stressed that more research is needed.

Dr. Nicolas Musi, director of the Diabetes and Aging Center at Cedars-Sinai, told NYT that because these drugs reduce the risk of diseases associated with aging, they could potentially improve lifespan as well.

"GLP-1 agonists decrease the incidence of diseases that are related to aging and are associated with decreasing life span. One would assume that they're also potentially going to increase life span and be beneficial for longevity," Dr. Musi said.

Researchers also point to the drugs' anti-inflammatory effects. Chronic inflammation is one of the biological processes linked to aging, said Dr. Thomas Blackwell, professor of general internal medicine at the University of Texas Medical Branch in Galveston.

However, scientists caution that there is currently no evidence showing that GLP-1 drugs provide longevity benefits for people who are already metabolically healthy.

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What Are GLP-1 Drugs?

Drugs such as Ozempic and Wegovy contain semaglutide, a GLP-1 receptor agonist, while Zepbound and Mounjaro contain tirzepatide.

These medications are approved for the treatment of type 2 diabetes, and some are also approved for chronic weight management.

GLP-1 receptor agonists work by binding to GLP-1 receptors in the body. This increases insulin production in response to food, suppresses glucagon—a hormone that raises blood sugar—and helps regulate blood glucose levels.

What Does GLP-1 Do in the Body?

GLP-1 (glucagon-like peptide-1) is a hormone naturally produced by the small intestine after eating. It plays several important roles in regulating blood sugar and appetite by:

• Stimulating insulin release from the pancreas.
• Suppressing glucagon secretion, which helps prevent unnecessary increases in blood sugar.
• Slowing stomach emptying allows glucose to enter the bloodstream more gradually.
• Increasing feelings of fullness (satiety), which helps reduce food intake.