A new study published in Psychoneuroendocrinology indicates that women who experience high levels of anxiety regarding their declining health tend to age faster at a molecular level compared to those who do not.

The concept of aging is often viewed simply as the passage of time marked by birthdays. However, scientists increasingly view aging as a biological process of wear and tear that varies from person to person.

Two individuals of the same chronological age may possess vastly different biological ages based on their cellular health. To measure this, researchers look at the epigenome. The epigenome consists of chemical compounds and proteins that can attach to DNA and direct such actions as turning genes on or off, controlling the production of proteins in particular cells.

One specific type of epigenetic modification is called DNA methylation. As people age, the patterns of methylation on their DNA change in predictable ways. Scientists have developed algorithms known as “epigenetic clocks” to analyze these patterns.

These clocks can estimate a person’s biological age and the pace at which they are aging. When a person’s biological clock runs faster than their chronological time, it is often a harbinger of poor health outcomes and earlier mortality.

Researchers have previously established that general psychological distress can accelerate these biological clocks. However, less is known about the specific impact of aging anxiety. This form of anxiety is a multifaceted stressor. It encompasses fears about losing one’s attractiveness, the inability to reproduce, and the deterioration of physical health. Women often face unique societal pressures regarding these aspects of life.

Mariana Rodrigues, a researcher at the NYU School of Global Public Health, led a team to investigate this issue. Rodrigues and her colleagues sought to understand if these specific anxieties became biologically embedded in women. They hypothesized that the stress of worrying about aging acts as a persistent signal to the body. They believed this signal might trigger physiological responses that degrade cells over time.

To explore this connection, the team utilized data from the Midlife in the United States (MIDUS) study. This is a large, national longitudinal study that focuses on the health and well-being of U.S. adults. The researchers analyzed data from 726 women who participated in the biomarker project of the study. These participants provided blood samples and completed detailed questionnaires about their psychological state.

The researchers assessed aging anxiety across three distinct domains. First, they asked women about their worry regarding declining attractiveness. Second, they assessed anxiety related to declining health and illness. Third, they asked about worries concerning reproductive aging, such as being too old to have children.

The study employed two advanced epigenetic clocks to measure biological aging from the blood samples. The first clock, known as GrimAge2, estimates cumulative biological damage. It is often used to predict mortality risk by looking at a history of exposure to stressors.

The second clock, DunedinPACE, functions differently. Instead of measuring total accumulated damage, DunedinPACE acts like a speedometer. It measures the current pace of biological aging at the time the blood sample was taken.

The researchers used statistical models to test the relationship between the different types of anxiety and the two epigenetic clocks. They accounted for various factors that could skew the results. These included sociodemographic factors like age, race, and income. They also controlled for marital status and whether the women had entered menopause.

The analysis revealed distinct patterns in how different worries affect the body. The researchers found that anxiety about declining health was linked to a faster pace of aging as measured by DunedinPACE.

Women who reported higher levels of worry about illness and physical decline showed signs that their bodies were aging more rapidly than women with lower anxiety. This association persisted even when the researchers adjusted for the number of chronic health conditions the women already had.

This suggests that the worry itself, rather than just the presence of disease, plays a role in accelerating the aging process. However, the connection weakened when the researchers factored in health behaviors.

When they accounted for smoking, alcohol consumption, and body mass index, the statistical link between health anxiety and faster aging diminished. This reduction indicates that lifestyle behaviors likely mediate the relationship. Women who are anxious about their health might engage in coping behaviors that are detrimental to their physical well-being.

The study did not find the same results for the other domains of anxiety. Worries about declining attractiveness showed no statistical association with accelerated aging. Similarly, anxiety about reproductive aging was not linked to the epigenetic clocks. This lack of connection may be due to the fact that appearance and fertility concerns often fade as women grow older. Health concerns, by contrast, tend to persist or increase with age.

The researchers also combined the scores to look at cumulative aging anxiety. They found that the total burden of aging worries was associated with a faster pace of aging. Like the findings for health anxiety, this association was largely explained by health behaviors and existing chronic conditions.

It is worth noting that the findings were specific to the DunedinPACE clock. The researchers did not observe statistically significant associations between any form of aging anxiety and the GrimAge2 clock.

This discrepancy highlights the difference between the two measures. DunedinPACE captures the current speed of decline, which may be more sensitive to ongoing psychological stressors like anxiety. GrimAge2 reflects accumulated damage over a lifetime, which might not be as responsive to current subjective worries.

The authors propose that health-related anxiety operates as a chronic cycle. Fear of health decline leads to heightened body monitoring. This vigilance creates psychological distress. That distress triggers physiological stress responses, such as inflammation. Over time, these responses contribute to the wear and tear observed in the epigenetic data.

There are limitations to this study that affect how the results should be interpreted. The data was cross-sectional, meaning it captured a snapshot in time. Because of this design, the researchers cannot definitively prove that anxiety causes accelerated aging.

It is possible that the relationship works in the opposite direction. Perhaps women who are biologically aging faster feel physically worse, leading to increased anxiety.

Additionally, the measures for aging anxiety were based on single items in a questionnaire. This might not capture the full depth or nuance of a woman’s experience. The sample also consisted of English-speaking adults in the United States. Cultural differences in how aging is perceived and experienced could lead to different results in other populations.

Future research is needed to clarify the direction of these associations. Longitudinal studies that follow women over many years would help determine if anxiety precedes the acceleration of biological aging. Tracking changes in anxiety levels and epigenetic markers over time would provide stronger evidence of a causal link.

The study supports a biopsychosocial model of health. This model suggests that our subjective experiences and fears are not isolated in the mind. Instead, they interact with our biology to shape our long-term health. The findings suggest that addressing psychological distress about aging could be a potential avenue for improving physical health.

The study, “Aging anxiety and epigenetic aging in a national sample of adult women in the United States,” was authored by Mariana Rodrigues, Jemar R. Bather, and Adolfo G. Cuevas.

A new study published in the journal Brain, Behavior, and Immunity provides evidence that sexual minority adults may experience a distinct physiological reaction to mental health challenges compared to heterosexual adults. The findings indicate that while depression and anxiety are more common in sexual minority populations, these conditions are also accompanied by stronger inflammatory responses for this group.

Health disparities affecting lesbian, gay, bisexual, and other non-heterosexual individuals are well-documented in medical literature. Statistics indicate that these groups face a higher risk for chronic physical conditions like heart disease, asthma, and diabetes compared to heterosexual adults. They also report rates of anxiety and depression that are often significantly higher than those seen in the general population.

Scientists often utilize the minority stress theory to explain these gaps. This framework suggests that the unique social stressors faced by marginalized groups create a burden that wears down physical health over time.

A key biological mechanism that might explain how stress becomes physical illness is inflammation. While acute inflammation is a necessary immune response to heal injuries or fight infection, chronic low-grade inflammation is damaging to the body.

Elevated levels of inflammatory markers are linked to a range of age-related conditions, including cardiovascular disease and cognitive decline. This process is sometimes referred to as “inflammaging,” where chronic inflammation contributes to accelerated biological aging.

“Sexual minority adults face well-documented disparities in both mental and physical health, including higher rates of depression, anxiety, and chronic conditions like cardiovascular disease,” said study author Lisa M. Christian, a professor and member of the Institute of Brain, Behavior and Immunology at The Ohio State University.

“While minority stress theory provides a framework for understanding these disparities, there has been very little research on the biological mechanisms that link psychological distress to physical health in this population. Specifically, data on inflammation, a key pathway to chronic disease, are scarce. Our study aimed to address this gap by examining whether depressive symptoms and anxiety are associated with greater inflammatory responses among sexual minority adults compared to heterosexual adults.”

The research team analyzed data from the National Couples’ Health and Time Study (NCHAT). This project involves a population-representative sample of married and cohabiting adults across the United States.

“This study utilizes data from Wave 1 of the National Couples’ Heath and Time (NCHAT) Stress Biology Study (NCHAT-BIO),” Christian noted. “NCHAT-BIO the first US-based study focused on stress biology within a large, diverse sample of married/cohabiting sexual minority and heterosexual adults.”

“NCHAT-BIO capitalized on the unique opportunity of NCHAT, a population-representative US sample which intentionally oversampled sexual minority respondents. Wave 1 NCHAT-BIO data have been deposited at ICPSR for public release to all researchers. We encourage interested researchers to take advantage of this unique and impactful dataset.”

The researchers focused on a subset of participants who provided biological samples. The final analysis included 572 participants. There were 321 individuals who identified as heterosexual and 251 who identified as sexual minorities, a group that included lesbian, gay, bisexual, and other non-heterosexual identities.

Participants completed detailed surveys assessing their mental health. To measure anxiety, they used the Generalized Anxiety Disorder scale (GAD-7). This tool asks respondents how often they have been bothered by problems such as feeling nervous or being unable to stop worrying.

To evaluate depressive symptoms, the researchers used the Center for Epidemiologic Studies Depression scale (CES-D 10). This measure asks participants how often they felt specific ways, such as fearful or lonely, during the past week.

The study also assessed adverse childhood experiences (ACEs) to understand early life stress. Participants reported if they had experienced events before age 18 such as abuse, neglect, household dysfunction, or parental incarceration.

Additionally, the survey asked about experiences of everyday discrimination and aggression. This included questions about being treated with less respect, being harassed, or facing physical attacks.

To measure biological markers, participants provided dried blood spots. They collected these samples at home by pricking a finger and placing blood drops on a special collection card. The researchers analyzed these samples for two specific markers of systemic inflammation: Interleukin-6 (IL-6) and C-reactive protein (CRP).

IL-6 is a cytokine that signals the immune system to respond to trauma or infection, while CRP is a protein produced by the liver in response to inflammation. Higher levels of these markers generally indicate a state of higher systemic inflammation.

The results showed that sexual minority participants reported higher levels of both anxiety and depressive symptoms compared to heterosexual participants. This aligns with prior statistics regarding mental health in these communities.

A statistical analysis revealed that this difference was partially explained by a higher number of adverse childhood experiences among the sexual minority group. Sexual minority respondents reported an average ACE score that was significantly higher than that of heterosexual respondents.

The most distinct finding emerged when the researchers analyzed the relationship between these mental health symptoms and inflammation levels. The data revealed a physiological pattern for sexual minority adults that was absent in heterosexual adults.

Among sexual minority participants, higher scores on the depression scale were associated with higher levels of both IL-6 and CRP. Similarly, higher anxiety scores were linked to higher CRP levels in the sexual minority group.

“We expected sexual minority adults to have higher depression and anxiety, which is consistent with prior research,” Christian told PsyPost. “What surprised us was the pattern of inflammatory response: sexual minority adults showed greater elevations in CRP with rising anxiety and depression. This effect was not seen in heterosexual adults. This suggests a unique physiological sensitivity among sexual minority individuals that warrants further investigation.”

The researchers adjusted their statistical models to account for potential confounding factors. They controlled for age, race, sex assigned at birth, education level, and existing health conditions.

They also ran sensitivity analyses that included body mass index and tobacco use. Even with these behavioral and physical factors included, the connection between distress and inflammation remained significant for sexual minority adults.

The study authors propose that this heightened inflammatory response is not an inherent trait of sexual minority individuals. Instead, it is likely a consequence of living in a marginalized social context.

Chronic exposure to stressors, such as discrimination or the threat of judgment, can sensitize the immune system. This sensitization means that when an individual experiences depression or anxiety, their body mounts a stronger inflammatory defense than it otherwise would.

This sensitization contributes to a “double burden” for sexual minority adults. First, they experience a higher prevalence of anxiety and depression, largely due to adverse childhood experiences and minority stress.

Second, when they do experience these symptoms, their bodies react with greater inflammation. Over time, even modest elevations in markers like CRP and IL-6 can increase the risk for chronic illnesses, potentially explaining some of the physical health disparities seen in this population.

“The main takeaway is that sexual minority adults not only experience higher rates of depression and anxiety but also show stronger inflammatory responses when they do,” Christian explained. “Even modest elevations in inflammation can increase long-term risk for chronic illnesses. This means that mental health challenges in sexual minority populations may have ripple effects on physical health, underscoring the importance of integrated care and targeted prevention efforts.”

There are some limitations to consider. The study used data collected at a single point in time for the survey, with blood samples collected several months later. This timeline makes it difficult to determine causality.

It is possible that inflammation exacerbates mood symptoms, rather than the other way around. The gap between the survey and the blood collection introduces some statistical noise, though the findings remained robust despite this.

“It is notable that the current effects in sexual minority adults were observed despite the presence of this statistical ‘noise,'” Christian said. “However, future studies in which time of collection is both simultaneous and longitudinal would be ideal.”

“Indeed, it is plausible that the presence of associations between inflammation and mental health indicators among sexual minority respondents, but not heterosexual respondents, is a function of greater chronicity of symptoms among sexual minority respondents. This could not be tested in the current analyses.”

The sample consisted entirely of married or cohabiting adults. People who are partnered often have better health outcomes and more social support than single individuals. This means the results might not fully reflect the experiences of unpartnered sexual minority adults.

The researchers also caution against interpreting these results to mean that sexual minority adults are inherently less healthy. “There is nothing problematic or unhealthy about being a sexual minority,” Christian told PsyPost.

“The differences we observed reflect the physiological costs of living in a society where sexual minority individuals are exposed to higher levels of stress, discrimination, and adversity, not something intrinsic to their identity. In other words, the burden comes from external exposures, not from who people are.”

The researchers have received funding from the National Institute on Aging to extend this work into a longitudinal study. They intend to examine how inflammatory markers change as the participants age. They also plan to look at epigenetic aging, which uses DNA methylation to measure biological age. This will help determine if the observed inflammation is translating into accelerated aging at the cellular level.

“This manuscript is part of a larger longitudinal study,” Christian said. “As with NCHAT-BIO Wave 1 data, assay results from Wave 3 will be made publicly available to other researchers through ICPSR alongside the survey, time diary, and contextual data from NCHAT Waves 1 through 3, and biological data from NCHAT-BIO Wave 1. Together, these resources will provide an exceptional dataset for future researchers.”

The study, “Sexual minority adults exhibit greater inflammation than heterosexual adults in the context of depressive symptoms and Anxiety: Pathways to health disparities,” was authored by Lisa M. Christian, Rebecca R. Andridge, Juan Peng, Nithya P. Kasibhatla, Thomas W. McDade, Tessa Blevins, Steve W. Cole, Wendy D. Manning, and Claire M. Kamp Dush.

Social anxiety is commonly associated with shyness, silence, and a tendency to withdraw from social interactions. However, new research suggests that for some adolescents, this condition manifests through aggression and impulsivity rather than avoidance. This “atypical” presentation appears linked to specific narcissistic traits. The study was published in the journal Personality and Individual Differences.

“There is a prevailing assumption in the popular and professional literature that social anxiety is characterized solely by avoidance of tendencies and behavioral inhibition (i.e., shyness). This is likely a consequence from its formal classification of social phobia, which inadvertently shaped the way we study and understand the clinical phenomena,” explained study author Mollie J. Eriksson, a PhD Candidate in Louis Schmidt’s Child Emotion Lab at McMaster University.

“Nonetheless, this prototypical inhibited presentation does not reflect the lived experience of many individuals with social anxiety symptoms (for a comprehensive review see Kashdan & McKnight). And so, in the current study we aimed to examine the externalizing correlates of social anxiety that are less studied and correspondingly less understood, particularly in a population (i.e., adolescents) in which these dynamics might be especially conspicuous.”

The research team recruited 298 adolescents for the study. The participants ranged in age from 12 to 17 years old. The sample was nearly evenly split between boys and girls. Data was collected through a series of online self-report questionnaires.

Participants answered detailed questions regarding their feelings of social anxiety and their levels of narcissism. The narcissism measure distinguished between vulnerable and grandiose traits. Additional surveys assessed impulsivity and general aggression.

The researchers used a statistical method known as Latent Profile Analysis to group the participants. This technique identifies distinct categories of people based on patterns in their responses. “This is a very robust statistical technique because it uncovers patterns in the data that reflect individual variation in people and not simply associations between data points,” Eriksson said.

The analysis revealed three distinct profiles among the adolescents. The largest group comprised about 46 percent of the sample. These individuals displayed low levels of social anxiety, narcissism, and aggression. This profile appears to represent a well-adjusted or normative group with few social difficulties.

The second group accounted for approximately 30 percent of the participants. Adolescents in this profile reported the highest levels of social anxiety. They also scored high on vulnerable narcissism but low on grandiose narcissism and aggression. This group fits the prototypical description of social anxiety. These teens appear to manage their fear of rejection through inhibition and withdrawal.

The third group made up roughly 25 percent of the sample. This profile was characterized by moderate levels of social anxiety but high levels of impulsivity and aggression. Notably, these adolescents scored the highest on both vulnerable and grandiose narcissism. This combination of traits represents the “atypical” presentation of social anxiety.

“Social anxiety is a broad and heterogeneous mental health problem that is characterized by several features, beyond shyness,” Eriksson told PsyPost. “Recognizing its heterogeneity is the first step in identifying individuals, particularly adolescents, who may be struggling with social anxiety. By providing the tools (i.e., additional features that characterize social anxiety) we can intervene sooner, ideally before symptoms become entrenched, which will ultimately set the adolescent up for greater intra-personal and inter-personal success later in life.”

The researchers also found sex differences in profile membership. Boys were more likely than girls to belong to the third, aggressive profile. This suggests that boys may be more prone to expressing social fears through externalizing behaviors. This aligns with broader socialization norms where boys may be discouraged from showing vulnerability.

“It was exciting that these results replicated previous adult findings, which really underscores the robustness of these findings,” Eriksson said. “Even though this was in line with our a priori hypothesis, it was also interesting that boys were more likely to be in the ‘moderate social anxiety/high externalizing profile.’ It makes me think about how sex/gender influence the expression of social anxiety.”

But the study, like all research, has some limitations. The data was collected at a single point in time. This prevents researchers from establishing a causal relationship between narcissism and the development of aggressive social anxiety. It is unclear if the personality traits precede the anxiety or if they develop concurrently.

“A common misinterpretation we would like to preempt is the assumption that these profiles represent fixed or diagnostic categories,” Eriksson explained. “Rather, they reflect patterns of co-occurring traits and symptoms within a specific developmental window. Additionally, because the data are cross-sectional, we cannot infer developmental pathways or causal mechanisms. Replication (particularly in longitudinal designs) is therefore essential for understanding how these profiles emerge and change over time.”

Tracking these traits from childhood into adolescence could reveal early warning signs. Identifying these patterns early could lead to more effective interventions. Standard treatments for social anxiety may not work for teens who react with aggression rather than fear.

“I hope to examine early childhood antecedents of atypical social anxiety symptomology both behaviorally and biologically,” Eriksson said. “This will really inform treatment and prevention efforts. I also hope to examine in more detail the novel hypothesis we articulated: social anxiety is driven by two divergent self-regulatory pathways. This hypothesis requires a longitudinal study design, which is something we plan to do in the very near future.”

The study, “Characterizing the dark side of social anxiety in adolescence: A replication and extension study,” was authored by Mollie J. Eriksson and Louis A. Schmidt.