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A new report shows that certain mental health conditions escalate the risk of developing heart disease by 50-100%—and adverse outcomes from existing heart conditions by 60-170%.

Every 34 seconds, someone in the United States dies from heart disease. As nearly half of the country suffers from some form of cardiovascular disease (CVD), another 1 in 4 adults experience a mental health disorder in their lifetime, signaling an inevitable overlap.

The new report in The Lancet Regional Health-Europe summarizes cardiovascular health disparities among those diagnosed with depression, anxiety, schizophrenia, bipolar and post-traumatic stress disorders (PTSD). The article is part of a series aiming to raise awareness around disparities in CVD health in four populations: women, the elderly, racial minorities, and those with mental health conditions.

Emory University professor Viola Vaccarino led this metareview linking mental health conditions to CVD, along with coauthors Amit Shah and Douglas Bremner, also Emory professors.

The report associated the following conditions and their corresponding risks of developing CVD:

• Major depression, 72%
• PTSD, 57%
• Bipolar disorder, 61%
• Panic disorder, 50%
• Phobic anxiety, 70%
• Schizophrenia, nearly 100%

The research also shows that these conditions are associated with a poorer prognosis, greater risk for readmission, and higher mortality from existing heart conditions. For example, major depression more than doubles the mortality rate in those with existing CVD.

Additionally, the report emphasizes a bidirectional relationship. “More than 40% of those with cardiovascular disease also have a mental health condition,” adds Vaccarino.

According to the report, a well-documented relationship exists among depression, schizophrenia, PTSD, and abnormal stress responses in the autonomic nervous system (ANS) and hypothalamic-pituitary adrenal axis (HPA).

The former allows the brain to manage involuntary responses, such as functions of the liver, heart, sweat glands, and eye muscles. The ANS also manages both acceleration and deceleration of these functions, regulating inflammatory responses. Since most major organs have ANS nerve endings, this system affects most bodily functions.

The HPA also influences immune response and metabolism, which can affect cardiovascular function.

According to the report, dysregulation of these systems creates “adverse downstream effects that can affect cardiovascular risk chronically, including increased inflammation, metabolic abnormalities, high blood pressure, enhanced systemic vascular resistance, and autonomic inflexibility.”

Inflammation has also been implicated in both the development of heart disease and mental health conditions.

The role of social determinants of health in CVD disparities is critical. Those with mental health conditions may face disruptions and barriers in the continuum of care, such as affordability and accessibility. Compromised health literacy or communication can also impede access to health screenings and treatment.

Clinicians could also be challenged to care for patients with certain mental conditions, which can be compounded by stigma and existing models that fragment mental and physical health care. Stigmas are also present in the field of clinical research, where having a mental health condition is often an exclusionary criterion in randomized trials.

Moreover, according to the report, current prediction models don’t account for mental health disorders when forecasting the risk of developing heart disease.

To address the disparities of CVD among people with mental health disorders, the authors recommend an integrated approach with interdisciplinary care encompassing behavioral, mental and cardiovascular health.

“The tight connection between cardiovascular and psychological health warrants changes in the health care system that are more amenable to patients with comorbidities,” says Vaccarino.

“A clinical team would be ideal for the care of these patients—a team of specialists, social workers, and nursing staff who work in collaboration to provide multidisciplinary care and resources.”

The report concludes that closing the health disparity gap upholds the rights of those living with a mental health condition to achieve the highest level of health and fully participate in society.

Source: Emory University

A single dose of penicillin works just as well to cure early syphilis as the three-injection regimen now used by many doctors, a new clinical trial says.

Second and third doses of benzathine penicillin G don’t provide any additional benefit in treating early-stage syphilis, researchers reported in the New England Journal of Medicine.

“Benzathine penicillin G is highly effective against syphilis, but the three-dose regimen can be burdensome and deter people from attending follow-up visits with their health care providers,” said Carolyn Deal, chief of the enteric and sexually transmitted infections branch of the National Institute of Allergy and Infectious Diseases.

“The new findings offer welcome evidence for potentially simplifying treatment with an equally effective one-dose regimen, particularly while syphilis rates remain alarmingly high,” Deal said in a news release. She was not involved in the research, which NIAID funded.

Syphilis continues to be a health threat for sexually active Americans, researchers said in background notes. In 2023, the nation saw more than 209,000 syphilis cases, up 61% from 2019 levels.

Without treatment, syphilis can cause brain damage, organ failure, pregnancy complications and birth defects, researchers said. The bacterial infection also increases a person’s likelihood of acquiring or transmitting HIV.

BPG is one of the few antibiotics known to be effective against syphilis. It’s imported into the U.S. now to resolve a nationwide shortage, researchers noted.

For the new study, 249 people with early syphilis were recruited at 10 U.S. medical centers, nearly all men and 61% living with HIV.

Participants were randomly chosen to receive either one shot of BPG or the three-dose series at weekly intervals.

About 76% of people in the single-dose group responded to the penicillin, based on blood tests, compared to 70% of those in the three-dose group. Overall, the difference between the groups was not statistically significant, researchers said.

“Syphilis has been studied and treated for more than a century, and BPG has been in use for more than 50 years, yet we are still acquiring knowledge to help us optimize treatment,” said lead researcher Dr. Edward Hook III, an emeritus professor of medicine and epidemiology at the University of Alabama at Birmingham.

“We hope these promising results will be complemented by scientific advances in syphilis prevention and diagnosis,” he added in a news release.

Limiting syphilis treatment to a single dose could help prevent the bacteria from developing antibiotic resistance, researchers said, as well as helping limit the impact of drug shortages.

“During our trial, as on several occasions over the past several decades, benzathine penicillin G was in short supply in the United States,” researchers wrote in their paper.

“This shortage led public health authorities to prioritize which patients receive benzathine penicillin G and which should be treated with alternative therapies,” researchers wrote. “Global shortages of benzathine penicillin G are also common and undermine syphilis-control efforts in many countries.”

Although the trial provides evidence that a single dose of BPG is as effective as three doses, more research is needed to fully understand the potential of a shorter treatment strategy, researchers noted.

It’s also not clear whether a one-dose approach would work in people with late-stage syphilis or syphilis that has already invaded the nervous system, researchers added.

More information

Yale Medicine has more on syphilis.

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A research team at the Medical University of South Carolina reports in Cells that the complement system, part of the body’s natural immune defenses, is a key driver of inflammatory responses that contribute to fetal brain inflammation and preterm birth, the latter of which is the leading cause of complications and death in newborns. The study, led by Eliza McElwee, M.D., an assistant professor of Obstetrics and Gynecology, focuses on finding the root cause of preterm birth itself, rather than just treating the complications left in its wake.

A major health concern

Preterm birth, or delivery before 37 weeks, affects about 12% of pregnancies in the U.S. and is linked to serious complications, such as brain hemorrhage, cerebral palsy, sepsis and death. South Carolina ranks fifth in the nation for preterm deliveries, highlighting a significant public health concern for the Lowcountry.

A few options are available to mitigate preterm birth once it has already begun.

“We have some strategies and medications that have a goal of stopping preterm labor after it’s happening,” McElwee explained. However, there are limited therapies that prevent preterm birth by addressing its root cause. “As a result, rates of preterm delivery remain high in the U.S.”

Looking for root causes

Previous studies have shown a link between inflammation brought on by infection in the amniotic fluid and preterm birth, but the source of the inflammation remained unknown. Using a well-studied animal model, McElwee and her team set out to pinpoint what causes the inflammation associated with preterm birth. They focused on the complement system, an area of expertise for Stephen Tomlinson, Ph.D., professor of Pharmacology and Immunology, whose lab supported the study. Often referred to simply as complement, this group of proteins in the blood helps to defend the body against infection and plays an important role in immunity.

When activated, complement enlists leukocytes – white blood cells – to respond. These cells create and sustain inflammation, which can lead to weakening of the cervix. The cervix can be thought of as the gateway of the pregnancy, keeping the baby safely inside until birth, when it thins and dilates to allow the baby’s passage. When weakened by inflammation, the cervix can’t guard the gates effectively, leading to the baby being delivered prematurely.

To investigate complement’s role in preterm birth, researchers used a mouse model that simulates a uterine infection-induced inflammation in pregnant women. They found increased complement activation and leukocyte infiltration in the cervix as early as one hour after inducing inflammation, with a marked rise at nine hours, and that these immune changes were associated with preterm delivery. Team member Devin Hatchell, a trainee in the South Carolina Clinical and Translational Research Institute’s TL1 predoctoral training program, helped to perform these experiments and analyze the data.

The results strongly support the team’s theory that complement is a key factor in preterm birth. “We found that complement activation is increased in inflammatory-mediated preterm birth,” explained McElwee.

“I am never surprised to find that complement plays a significant role in a disease process,” Tomlinson said.

Setting the stage for potential new therapies

The team then went a step further – showing that these changes could be prevented in this animal model by administering a drug called a complement inhibitor, which blocks complement activation and limits its ability to recruit leukocytes. Compared to mice receiving a placebo, pregnant mice induced for preterm birth and treated with the complement inhibitor saw reduced inflammation in both the maternal uterus and the fetal brain. This treatment also reduced leukocyte infiltration and decreased levels of pro-inflammatory cytokines associated with fetal brain inflammation. Pregnant mice treated with the complement inhibitor carried their babies longer and gave birth to more viable offspring.

The hope is that these findings could provide the scientific groundwork for a new therapeutic approach.

By targeting complement with a complement inhibitor, we could decrease rates of preterm birth and reduce fetal neural inflammation.”

Eliza McElwee, M.D., Assistant Professor of Obstetrics and Gynecology, MUSC

Hatchell, whose research before joining the McElwee team focused on developing therapies to reduce brain hemorrhages in premature babies, says what stood out most for him about the results is the possibility of using complement inhibitors in mothers as a preventive therapy. “All the therapy was given to the mother,” he said. “This suggests that we can take care of the mother as well as take care of the offspring at the same time.”

In other words, treating mothers during pregnancy with complement inhibitors could stop preterm birth before it happens and prevent serious complications for both mother and child. “Healthy pregnancies mean healthy babies,” McElwee added.

Several drugs that block complement are in clinical trials, including one with a similar mechanism of action to the mouse complement inhibitor used in the study. However, very few have been approved for medical use – and none is approved for preventing preterm birth or fetal brain inflammation. Still, this study’s findings offer hope for future treatments of preterm birth and beyond.

“This study by Dr. McElwee certainly paves the way for expanding the investigation of complement inhibitors as potential therapies for infection-induced preterm birth, and it is noteworthy that many new complement inhibitors are in clinical development,” said Tomlinson.