Category: 8. Health

Corticosteroids, which are commonly prescribed to alleviate cancer-related symptoms in patients with non–small cell lung cancer (NSCLC) treated with immunotherapy, may be the reason certain immunotherapies fail in treating the disease, according to new research published by Polyakov et al in Cancer Research Communications.

The study results showed that high doses of steroids, when given before and/or during immune checkpoint inhibitor therapy, caused patients’ tumors to shrink less than those of patients not on steroids. Those patients also did not live as long. 

“Steroids were the biggest predictor of why certain immunotherapies may not be effective, even when considering multiple other factors such as stage and progression of the disease,” said Keck Medicine of USC oncologist and immunologist Fumito Ito, MD, PhD, lead author of the research. 

Additionally, researchers believe they have found the mechanism behind why steroids and some immunotherapies may not mix.  

“Our findings reveal that steroids stop the body’s natural cancer-fighting cells, T cells, from maturing. This makes them unable to attack the cancer as vigorously as they usually would, leading to worse outcomes for patients,” explained Dr. Ito, who is also a member and co-leader of the translational and clinical sciences research program at USC Norris Comprehensive Cancer Center. “While other research has indicated steroids may negatively impact immunotherapy’s efficacy, we are one of the first [groups] to pinpoint a probable cause and effect.”  

Dr. Ito and his colleagues also discovered that steroids blocked circulating biomarkers in the body. “Without the presence of circulating biomarkers to inform our decisions, oncologists cannot treat the cancer as effectively and patients may miss out on the best treatment for their cancer,” he noted.  

The study examined the effect of steroids on immune checkpoint inhibitors, which are often used to treat NSCLC. Steroids are often prescribed to alleviate symptoms of the cancer or treatments given for a variety of reasons, such as fatigue and vomiting, or more serious side effects like brain swelling and lung inflammation. Steroids suppress the immune system, which reduces the inflammation that can cause these conditions. 

Study Methodology

The researchers retrospectively studied the medical records of 277 patients with stage II to IV NSCLC who were treated with immune checkpoint inhibitors alone or in combination with other therapies. They compared outcomes (tumor shrinkage and survival rate) between patients who were prescribed steroids and those who were not at three centers. They analyzed up to 8 years of data to determine that steroids were the sole factor impeding the effectiveness of the immunotherapy.  

They also determined that the T cells of significant numbers of patients on steroids were not fully matured and launched a preclinical study using mice to observe the effects of steroids on immune checkpoint inhibitor therapy in real time. This mouse model study led to the discovery that steroids given before or during immunotherapy inhibit T cells from fully maturing.  

The Future of Steroid Use in NSCLC

While this new research indicates steroids can interfere with immune checkpoint inhibitor efficacy, the authors acknowledged that for some patients with NSCLC, steroids may be necessary to manage their cancer-related symptoms.  

“We know that steroids will continue to play an important role in lung cancer care, but it is important to understand their potential limitations,” said Dr. Ito. “Each patient should talk to their oncologist to make sure they have the best possible care plan tailored to their specific needs.”  

The investigators hope this research will lead to more studies examining the effect of steroids on immunotherapy, so oncologists can make fully informed decisions that will best benefit their patients.  

Disclosures: The study was supported with grants from the National Cancer Institute as well as the Department of Defense Lung Cancer Research Program and the Uehara Memorial Foundation. For full disclosures of the study authors, visit aacrjournals.org/cancerrescommun.

Automated surgery could be trialled on humans within a decade, say researchers, after an AI-trained robot armed with tools to cut, clip and grab soft tissue successfully removed pig gall bladders without human help.

The robot surgeons were schooled on video footage of human medics conducting operations using organs taken from dead pigs. In an apparent research breakthrough, eight operations were conducted on pig organs with a 100% success rate by a team led by experts at Johns Hopkins University in Baltimore in the US.

The Royal College of Surgeons in the UK called it “an exciting development that shows great promise”, while John McGrath, a leading expert on robotic surgery in the UK, called the results “impressive” and “novel” and said it “takes us further into the world of autonomy”.

It opens up the possibility of replicating, en masse, the skills of the best surgeons in the world.

The technology allowing robots to handle complex soft tissues such as gallbladders, which release bile to aid digestion, is rooted in the same type of computerised neural networks that underpin widely used artificial intelligence tools such as Chat GPT or Google Gemini.

The surgical robots were slightly slower than human doctors but they were less jerky and plotted shorter trajectories between tasks. The robots were also able to repeatedly correct mistakes as they went along, asked for different tools and adapted to anatomical variation, according to a peer-reviewed paper published in the journal Science Robotics.

The authors from Johns Hopkins, Stanford and Columbia universities called it “a milestone toward clinical deployment of autonomous surgical systems”.

Almost all the 70,000 robotic procedures carried out annually in the NHS in England were fully controlled under human instruction, with only bone-cutting for hip and knee operations semi-autonomous, McGrath said. Last month the health secretary, Wes Streeting, said increasing robotic surgery was at the heart of a 10-year plan to reform the NHS and cut waiting lists. Within a decade, the NHS has said, nine in 10 of all keyhole surgeries will be carried out with robot assistance, up from one in five today.

In the Johns Hopkins trial, the robots took just over five minutes to carry out the operation, which required 17 steps including cutting the gallbladder away from its connection to the liver, applying six clips in a specific order and removing the organ. The robots on average corrected course without any human help six times in each operation.

“We were able to perform a surgical procedure with a really high level of autonomy,” said Axel Krieger, assistant professor of mechanical engineering at Johns Hopkins. “In prior work, we were able to do some surgical tasks like suturing. What we’ve done here is really a full procedure. We have done this on eight gallbladders, where the robot was able to perform precisely the clipping and cutting step of gallbladder removal without any human intervention.

“So I think it’s a really big landmark study that such a difficult soft tissue surgery is possible to do autonomously.”

McGrath, who chairs NHS England’s robotics steering committee, said autonomous surgery, while still years away, could one day lead to a human surgeon overseeing several autonomous robotic operations at the same time, carrying out simple procedures such as hernia operations or gall bladder removals more rapidly, with greater precision than humans and with less damage to surrounding bodily structures.

But he cautioned that autonomous surgery remained a long way from being clinically deployable, because tests on dead pig organs do not test the robots’ capacity to react to a patient moving and breathing, blood running in the field of operation, an inadvertent injury, smoke from cauterisation or fluid on the camera lens.

Nuha Yassin, who leads on robotic surgery at the Royal College of Surgeons of England, said: “The next step must involve a careful exploration of the nuances within this rapidly evolving field to assess how these findings can be safely and effectively translated into a human pilot. Only then can this approach move toward, becoming a sustainable model for the future.”

She said training, education and patient safety must remain at the forefront.

High and rising levels of tetracycline resistance globally will likely limit the ability of doxycycline post-exposure prophylaxis (doxyPEP) to prevent gonorrhea infections, according to a study published today in JAC-Antimicrobial Resistance.

In a systematic review and meta-analysis, researchers from the University of Melbourne examined data from 67 studies of tetracycline resistance in Neisseria gonorrhoeae, the bacterium that causes gonorrhea, covering 51 countries and 80,645 isolates. Overall, the median tetracycline resistance was 54.2% (range, 4% to 100%), with the highest resistance observed in East Asia and the Pacific (82.1%; range, 18% to 100%) and sub-Saharan Africa (81.6%; range, 44% to 100%). The lowest tetracycline resistance levels were reported in North America (26.5%; range, 4% to 78%). For other regions, median resistance ranged from 38.9% to 61.6%.

Among the 80,645 isolates studied, 91.4% were collected from 2010 through 2013, and the rest from 1996 through 2009. The largest increases in tetracycline resistance between the two reporting periods were seen in South Asia (a 3.8-fold increase) and North America (a 4.1-fold increase). 

Only 11 studies (16%) provided tetracycline resistance data specifically from men who have sex with men (MSM), who are considered a high-risk group for gonorrhea, and only 6 (9%) included women. 

Limited role in gonorrhea control

Although randomized clinical trials have found that doxyPEP, which involves taking a dose of doxycycline within 72 hours of unprotected sex, is highly effective at reducing the incidence of chlamydia and syphilis in high-risk groups (MSM and transgender women), effectiveness against gonorrhea has been more modest. The study authors say these data suggest it may be unreliable for preventing incident gonorrhea infections.

“While tetracyclines are not used to treat N. gonorrhoeae globally, our finding suggests doxyPEP would have a very limited role in N. gonorrhoeae control when used to reduce incidence of other STIs such as chlamydia and syphilis, and as such, doxyPEP policies should make clear statements to prescribers and users regarding this,” they wrote. 

The authors add that countries implementing doxyPEP should ensure surveillance systems are in place to monitor resistance in N gonorrhoeae.

A new Scientific Statement released today by the Endocrine Society highlights potential research directions related to the pathogenesis of type 1 diabetes (T1D) that should help with the development of new and improved treatment options.

Type 1 diabetes is a chronic disease where the body’s immune system attacks and destroys insulin-producing cells in the pancreatic islet. Type 1 diabetes requires lifelong insulin administration and may result in complications such as eye, kidney, nerve, and heart disease. Type 1 diabetes is usually thought to be a disease of children and adolescents, but it is now recognized that T1D often has its onset in adults and can occur at any age.

The Endocrine Society develops Scientific Statements to explore the scientific basis of hormone-related conditions and diseases, discuss how this knowledge can be applied in practice, and identify areas that require additional research. Topics are selected on the basis of their emerging scientific impact. Scientific Statements are developed by a Task Force of experts appointed by the Endocrine Society, with internal review by the relevant Society committees and expert external reviewers prior to a comment period open to all members of the Society.

The Endocrine Society chose type 1 diabetes for a Scientific Statement because research related to T1D is rapidly expanding, and the field is poised for new advances. The hope is that the Scientific Statement will provide scientists, physicians, and funding agencies with a guide for areas of research that seem particularly promising.”

Alvin C. Powers, M.D., of Vanderbilt University Medical Center in Nashville, Tenn., member of the writing group

According to the International Diabetes Federation, 9 million people had type 1 diabetes in 2024 with considerable variation in the rates across countries.

The causes and factors that lead to type 1 diabetes are unknown. The Scientific Statement summarized research and suggested directions for new research in these areas related to T1D: genetics, heterogeneity, pathology of the pancreas, assessment of β cell function and mass, immunologic biomarkers in peripheral blood, changes in the exocrine pancreas, and screening to identify individuals at-risk for T1D.

“The data highlights the need for population-based screening for type 1 diabetes and more research into the causes of the disease,” Powers said. “We hope addressing these research gaps and incorporating more widespread screening efforts will help identify those at risk sooner and improve treatment and long-term health outcomes for people living with type 1 diabetes.”

The statement is based on the authors’ updated version of the widely cited and often modified Eisenbarth model, which outlines the different stages of progression to type 1 diabetes. The Scientific Statement proposes that Stage 0 be added to this model which already included Stages 1, 2, and 3, to highlight that there are likely events occurring earlier in the disease that currently are not understood or being studied.

“We hope that research in these areas infused with information from the application of emerging technological and analytical tools will lead to a new understanding of the pathogenesis of type 1 diabetes,” Powers concluded.

Other statement authors are Aaron Michels of University of the Colorado School of Medicine in Denver, Colo.; Todd Brusko of the University of Florida in Gainesville, Fla.; Carmella Evans-Molina of Indiana University School of Medicine and the Roudebush VA Medical Center in Indianapolis, Ind.; Dirk Homann of the University of Miami, Miami, Fla.; and Sarah Richardson of the University of Exeter Medical School in Exeter, U.K.

The statement, “Challenges and Opportunities for Understanding the Pathogenesis of Type 1 Diabetes: An Endocrine Society Scientific Statement,” was published online in the Society’s journal, The Journal of Clinical Endocrinology & Metabolism.

It’s been recognized for some time that Alzheimer’s disease affects brain regions differently and that tau – a protein known to misbehave – plays an important role in the disease. Normally, tau helps stabilize neurons, but in Alzheimer’s disease, it begins to misfold and tangle inside neurons. It spreads across the brain forming toxic clumps that impair neuronal function and ultimately lead to cell death.

Brain areas like the entorhinal cortex and hippocampus succumb early to tau tangles, while other areas, like the primary sensory cortices, remain resilient to the disease. In the quest to better understand this selective vulnerability (SV) or resilience (SR) to Alzheimer’s disease, researchers have looked to gene association and transgenic studies to identify Alzheimer’s risk genes. But past research has not shown a clear link between the location of genetic risk factors and associated tau pathology.

Now, a new study by UC San Francisco researchers has made a leap toward answering that question – by combining brain imaging, genetics, and advanced mathematical modeling into a powerful new lens. The study, published July 9 in Brain, shows multiple distinct pathways by which risk genes confer vulnerability or resilience in Alzheimer’s disease.

The study introduced a model of disease spread called the extended Network Diffusion Model (eNDM). The researchers applied this model on brain scans from 196 individuals at various stages of Alzheimer’s. They subtracted what the model predicted from what they saw in the scans. The leftovers, called “residual tau,” pointed to areas where something else besides brain connections influence the buildup of tau – in this case, genes.

Using brain gene expression maps from the Allen Human Brain Atlas, the researchers tested the degree to which Alzheimer’s risk genes explain the patterns of both actual and residual tau. This allowed them to tease apart genetic effects that act with or independently of the brain’s wiring.

We think of our model as Google Maps for tau. It predicts where the protein will likely go next, using real-world brain connection data from healthy people.”

Ashish Raj, PhD, senior study author, UCSF professor of Radiology and Biomedical Imaging

This upends traditional view of how tau moves in the brain

The study team uncovered four distinct gene types based on how much and in what manner they were predictive of tau: Network-Aligned Vulnerability (SV-NA), which are genes that boost tau spread along the brain’s wiring; Network-Independent Vulnerability (SV-NI), which are genes that promote tau buildup in ways unrelated to connectivity; Network-Aligned Resilience (SR-NA), which are genes that help protect regions that are otherwise tau hotspots; and Network-Independent Resilience (SR-NI), which are genes that offer protection outside of the network’s usual path – like hidden shields in unlikely spots.

“Vulnerability-aligned genes dealt with stress, metabolism, and cell death; resilience-related ones were involved in immune response and the cleanup of amyloid-beta – another Alzheimer’s culprit,” said study first author Chaitali Anand, PhD, a UCSF post-doctoral researcher. “In essence, the genes that make parts of the brain more or less likely to be affected by Alzheimer’s are working through different jobs – some controlling how tau moves, others dealing with internal defenses or cleanup systems.”

This research built on another recent UCSF study in mice, published May 21 in Alzheimer’s & Dementia, which demonstrated that tau does not travel randomly or diffuse passively; instead, it follows the brain’s wiring pathways with a distinct directional preference. Using a system of differential equations called the Network Diffusion Model (NDM), the research team was able to show the dynamics of tau spread between connected brain regions, challenging the traditional view that tau spreads simply by diffusing through extracellular space or leaking from dying neurons.

“Our research showed that tau propagates trans-synaptically, traveling along axonal projections driven by active transport processes rather than passive diffusion, and exploiting active neural pathways in the preferred retrograde direction,” said Justin Torok, PhD, a post-doctoral researcher working in the Raj lab.

In the current study, network-based analyses complemented the existing approaches for validating and identifying gene-based determinants of selective vulnerability and resilience. Genes that respond independently of the network having different biological functions than those genes that respond in concert with the network.

“This study offers a hopeful map forward: one that blends biology and brain maps into a smarter strategy for understanding and eventually stopping Alzheimer’s disease,” said Raj. “Our findings offer new insights into vulnerability signatures in Alzheimer’s disease and may prove helpful in identifying potential intervention targets.”

 

When a stroke goes unnoticed, it can have serious consequences later in life. According to the Centers for Disease Control and Prevention, around one-quarter of strokes in the United States occur in people who have had a prior stroke. Asymptomatic, or silent, strokes often require a brain scan to be detected.

Toby Gropen, M.D., a professor in the Department of Neurology at the University of Alabama at Birmingham, explains how to recognize the signs of stroke and how response time affects recovery.

“In a stroke emergency, every minute counts,” Gropen said. “Recognizing the signs of a stroke, and getting proper treatment quickly, can prevent long-term damage and improve overall outcomes.”

Immediate medical attention is the first step in treatment. Earlier intervention improves the likelihood of preserving brain function and reducing long-term disability. Some treatment options include clot-removal procedures, medications and rehabilitation.

What is a stroke?

A stroke happens when there is a sudden lack of blood flow to the brain. This causes brain cells to die and may lead to severe, rapid brain damage.

The effects of a stroke vary depending on size and which part of the brain is affected. The brain controls everything from movement to emotions, behavior and sensory functions. Damage in one area can lead to impairments in vision, speech, mood or personality.

Stroke risk factors

Gropen says understanding the causes of strokes is essential in practicing prevention.

Most strokes are associated with common risk factors, which fall into two categories: non-modifiable and modifiable. Non-modifiable risk factors include age, sex, family history, race and ethnicity. Modifiable factors, like physical inactivity, some medications or smoking, are addressed through lifestyle changes.

“While the overall risk increases with age, younger individuals are not immune,” Gropen said.

“Strokes in younger people can stem from less traditional causes, such as trauma, blood clotting disorders, heart abnormalities or even drug use. This can make diagnosis and prevention especially important in this age group.”

Signs and treatment

The common signs of stroke affect a person’s balance, eyes, face, arms and speech. These signs require timely action and are grouped into the acronym BE FAST:

• Balance: Loss of balance or coordination
• Eyes: Blurred or double vision
• Face: Facial drooping or numbness
• Arms: Tingling, numbness or weakness in one arm
• Speech: Slurred speech or difficulty understanding others
• Time: Act timely and calling 911

“Patients who receive treatment within the first few hours after symptom onset have significantly better outcomes, and those treated within the first hour often have the best outcomes,” Gropen said.

Learn more about treatment and prevention options through the UAB Comprehensive Stroke Center.

High doses of steroids, whether administered before or during treatment with an immune checkpoint inhibitor (ICI), caused the tumors of patients with non-small cell lung cancer (NSCLC) to shrink less than those not on steroids, according to recent study results published by investigators in Cancer Research Communications. The authors wrote that their findings could serve as a baseline for the steroids’ negative independent prognostic factor in patients with NSCLC undergoing ICI therapy.¹

ICI therapy has become revolutionary for patients with NSCLC, the authors wrote, with anti–PD-1/PD-L1 regimens becoming a foundation of treatment. Although improved clinical outcomes with the addition of chemotherapy to ICI have been recorded for some patients, there is ongoing research to understand how prognostic factors (eg, smoking history, tumor histology, performance status) can provide some predictive values for patient response to ICI therapy. Additionally, the authors wrote that, prior to this study, it was unclear whether the immunomodulatory mechanisms of steroids had negative impacts on ICI treatment outcomes. For this study, the authors specifically evaluated the impact of baseline steroid use on clinical outcomes and blood-based predictive correlates of response to ICI therapy in patients with NSCLC.¹

The investigators enrolled patients with stage II to IV NSCLC who were treatment-naïve or previously treated with an anti–PD-1 antibody alone (pembrolizumab [Keytruda; Merck] or durvalumab [Imfinzi; AstraZeneca]), anti–PD-1/CTLA-4 antibodies (nivolumab/ipilimumab [Opdivo/Yervoy; Bristol Myers Squibb]), or a combination of chemotherapy and anti–PD-1/PD-L1 antibody (pembrolizumab or atezolizumab [Tecentriq; Genentech]). Patients were treated at Roswell Park Comprehensive Cancer Center (RPCCC; n = 88) or at the University of Southern California (USC) Norris Comprehensive Cancer Center or Los Angeles General Medical Center (n = 189). A total of 277 patients (median age: 66 years; range: 30–89 years) with NSCLC who initiated treatment between October 2013 and August 2023 were enrolled.¹

The median time of follow-up was about 10.4 months for patients from RPCCC (range: 0.7–52.0 months) and 6.4 months for those from USC (range: 0.7–88.3 months). Among the 21 patients receiving steroids, indications included brain metastases (n = 17; 80%) or comorbid lung conditions (n = 4; 20%) such as chronic obstructive pulmonary disease. Of note, all 21 patients had remained on steroids for at least 12 weeks after initiating ICI therapy. The investigators had also observed mouse models with MC38 tumors to assess how steroid use influenced T cells.¹

In both RPCCC and USC, patients on baseline steroids were observed to have a lower overall response rate (RPCCC: P = .0141; USC: P = .0454) with noticeably shorter progression-free survival (PFS; RPCCC median: 10.7 months; USC median: 6.6 months) and overall survival (OS; RPCCC median: 21.0 months; USC median: 16.4 months) compared with those not receiving steroids (RPCCC respective median PFS and OS: 3.2 and 7.7 months; USC median PFS and OS: 3.0 and 3.7 months). Additionally, in multivariate analysis, steroid use was the only significant independent risk factor for disease progression and mortality in both the RPCCC and USC cohorts.¹

Further, a baseline peripheral blood neutrophil-to-lymphocyte ratio below 5 was observed to be a strong prognostic indicator; however, the prognostic value of the neutrophil-to-lymphocyte ratio was not present in patients receiving steroids. Additionally, the baseline frequency of circulating CX3CR1+CD8+ T cells was noticeably lower in patients on steroids. Using a bedside-to-bench approach, the investigators determined that concurrent steroid use had significantly decreased antitumor efficacy of anti–PD-1 therapy and weakened the increase of CX3CR1+CD8+ T cells in mouse models bearing MC38 tumors, whereas discontinuation of steroids at treatment initiation did not make a negative impact on survival. Generally, baseline steroid use was associated with worse outcomes and decreased frequency of circulating differentiated effector T cells in patients with NSCLC.¹

“Steroids were the biggest predictor of why certain immunotherapies may not be effective, even when considering multiple other factors such as stage and progression of the disease,” lead author Fumito Ito, MD, PhD, oncologist and immunologist at Keck Medicine, said in a news release. “Our findings reveal that steroids stop the body’s natural cancer-fighting cells, T-cells, from maturing. This makes them unable to attack the cancer as vigorously as they usually would, leading to worse outcomes for patients. While other research has indicated steroids may negatively impact immunotherapy’s efficacy, we are one of the first to pinpoint a probable cause and effect.”²

The authors emphasized that the findings show how high-dose baseline steroid use can decrease the efficacy of ICI in patients with NSCLC. Additionally, they noted that the findings regarding immune-related biomarkers in patients on steroids should be interpreted with caution.¹ However, they ultimately concluded that the findings could help oncologists and health care providers make informed decisions that can benefit patients.²

“Without the presence of circulating biomarkers to inform our decisions, oncologists cannot treat the cancer as effectively, and patients may miss out on the best treatment for their cancer,” Ito explained. “We know that steroids will continue to play an important role in lung cancer care, but it is important to understand their potential limitations. Each patient should talk to their oncologist to make sure they have the best possible care plan tailored to their specific needs.”²

REFERENCES

1. Polyakov L, Lim A, Meyer A, et al. Impact of Glucocorticoids on Immune Checkpoint Inhibitor Efficacy and Circulating Biomarkers in Non–Small Cell Lung Cancer Patients. Cancer Res Commun. 2025;5(7):1082–1094. doi:10.1158/2767-9764.CRC-25-0051

2. University of Southern California – Health Sciences. Common medication for lung cancer symptoms found to limit effectiveness of cancer treatment. News release. July 7, 2025. Accessed July 7, 2025. https://www.eurekalert.org/news-releases/1089842

Maintaining a healthy heart is essential for long-term well-being and quality of life. According to the CDC, heart disease remains the leading cause of death in the United States, affecting nearly half of all adults. The encouraging news is that many of the risk factors associated with heart disease, which includes high blood pressure, high cholesterol and chronic inflammation, can be managed—or even prevented—through intentional lifestyle and dietary changes.

The foods we eat each day can improve heart health, and by focusing on nutrient-dense foods, we can provide our bodies with what they need to thrive. While there are so many foods that can support heart health, we’re highlighting seven of our top heart-healthy picks to enjoy during the summer. Plus, we’re sharing a few simple strategies to help you care for your heart and take proactive steps toward long-term cardiovascular health.

1. Blueberries

Blueberries are one of nature’s most powerful heart-healthy fruits. Not only are they sweet and perfectly in season in July, but they are rich in anthocyanins, which are plant-based compounds that give them their vibrant blue hue and provide powerful antioxidant and anti-inflammatory effects. Studies show that consuming anthocyanin-rich berries, like blueberries, can significantly reduce total cholesterol levels and inflammatory markers like C-reactive protein.

Blueberries are incredibly versatile. They can be eaten fresh by the handful, blended into smoothies or baked into your favorite muffin recipe for a heart-healthy treat.

2. Avocados

Avocados are a great, heart-healthy addition to your diet. They provide nearly 20 vitamins, minerals and phytonutrients, along with 5 grams of monounsaturated fats (MUFA) in just one-third of a medium avocado. These “good fats” have been shown to help reduce LDL (bad) cholesterol levels, which may help lower the risk of heart disease and stroke. A 30-year study even found that higher avocado intake was associated with lower risk of cardiovascular disease and coronary heart disease.

Healthy eating patterns that promote longevity often include a variety of fruits, vegetables and unsaturated fats, which includes avocados. The American Heart Association encourages limiting saturated fat, added sugars and sodium and recommends choosing unsaturated fats whenever possible. Adding fresh avocados to salads, toast or smoothies or using them as a creamy topping for grain bowls is an easy way to meet these goals while supporting heart health.

3. Collard Greens

Leafy greens, such as collard greens, are some of the most nutrient-dense foods you can eat for your heart. These leafy greens are packed with vitamins A, C and K and are a source of folate, calcium and potassium. Diets such as the DASH (Dietary Approaches to Stop Hypertension) Diet and the Mediterranean Diet, which are known for improving cardiovascular health, encourage the consumption of leafy greens, like collard greens, due to their role in lowering LDL cholesterol and improving vascular function.

For a quick side dish, try sautéing them with garlic and olive oil. You can also chop them finely and add them to soups or stews for a nutrient boost or use large collard leaves as a sturdy, low-carb wrap alternative and fill them with lean protein, grains and veggies.

4. Sardines

Sardines may be small, but they are rich in omega-3 fatty acids, specifically EPA and DHA, which have been shown to reduce inflammation, lower triglyceride levels and support the function of blood vessels, reducing the risk for heart disease and cognitive decline. Research shows that consuming fatty fish like sardines at least twice a week provides significant cardiovascular benefits, including a reduced risk of heart attacks and stroke.

Sardines can be eaten in a variety of ways. Add them to your avocado toast, or pair them with fresh herbs and a drizzle of olive oil for a flavorful, heart-healthy meal.

5. Tomatoes

Tomatoes are more than just a summer staple; they are rich in lycopene, which is a naturally occurring antioxidant that gives tomatoes their signature red color. Lycopene also helps reduce oxidative stress and inflammation, which are both underlying contributors to heart disease.

Tomatoes also contain a good source of potassium, which contributes to heart health. According to the American Heart Association, foods rich in potassium are important in managing high blood pressure. Potassium can reduce the effects of too much sodium in the body, which has been shown to increase blood pressure. Tomatoes can easily be incorporated into your meals. Slice them up and add them to salads, or roast them for a flavorful addition to your favorite pasta recipe.

6. Flaxseeds

Flaxseeds are a small but mighty addition to any heart-healthy diet. They are packed with omega-3 fatty acids, fiber and powerful antioxidants that have been shown to help lower LDL cholesterol, reduce inflammation and support healthy blood pressure levels. In fact, studies show that regular consumption of flaxseeds has been associated with improvements in arterial function and a lower risk of cardiovascular disease.

To reap the most benefits, choose ground flaxseeds, which are easier for the body to digest. Sprinkle them into oatmeal, stir them into smoothies or mix them into baked goods like muffins or pancakes for an easy, affordable way to support a healthy heart.

7. Garlic

Garlic is especially abundant during the summer months and packs a powerful punch when it comes to heart health. It contains natural sulfur-containing compounds, particularly allicin, which has been shown to help lower blood pressure and support overall cardiovascular function. In fact, a recent meta-analysis found that garlic supplementation significantly reduced both systolic and diastolic blood pressure, with results comparable to those when taking a low dose of blood pressure medications.

Garlic can be used in various recipes, making it easy to incorporate it into your everyday meals. Try adding it to a stir-fry or roasting it with your favorite summer veggies.

Strategies to Improve Heart Health

• Adopt a plant‑forward plate: When preparing meals, prioritize plant-based foods like fruits, vegetables, whole grains, nuts and legumes. These foods have been shown to help reduce blood pressure and cardiovascular risk.
• Limit added sugars: Excessive sugar intake has been shown to increase inflammation, raise triglyceride levels and contribute to insulin resistance, which can increase the risk of heart disease. Choosing naturally sweet foods like fruit and carefully reading nutrition labels are simple ways to limit added sugar intake.
• Stay active: Regular exercise has been shown to help lower blood pressure, improve cholesterol levels, boost circulation and support healthy blood vessel function. Just 150 minutes of moderate-intensity movement per week, such as walking, biking or dancing, can make a meaningful difference.

Our Expert Take

A healthy heart lays the foundation for a healthy life, and the foods we eat can have a big impact. Foods like berries, avocados, leafy greens, fatty fish, seeds, tomatoes and garlic offer several benefits that can support and protect your cardiovascular system while nourishing your body with nutritional goodness. In addition to consuming a variety of nutrient-dense foods, it’s also important to incorporate intentional lifestyle habits, like prioritizing more plants at meals, limiting added sugars and staying active. These small changes can lead to big, lasting heart-healthy benefits.

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