Can Stress Cause a Fever? The Surprising Body Response

Feeling overwhelmed can trigger unexpected physical symptoms, including an increase in body temperature. While fevers are typically associated with infections, stress can also cause a measurable rise in temperature, sometimes referred to as “stress fever.” This phenomenon, though not widely recognized, has been observed in both medical research and real-world cases.

Understanding how stress affects body temperature involves examining hormonal responses, nervous system activity, and immune reactions. Although stress-induced fevers differ from infectious ones, they can still be uncomfortable and concerning.

Stress-Linked Body Temperature Changes

Psychological stress can cause noticeable fluctuations in body temperature. Research has shown that individuals experiencing acute stress often exhibit a measurable rise in core body temperature, even in the absence of infection. A study published in Psychosomatic Medicine found that participants subjected to intense cognitive stress experienced an increase of up to 0.5°C (0.9°F), suggesting a direct physiological response to mental strain.

The hypothalamus, which regulates thermoregulation, plays a central role in this process. When stress levels rise, it signals for increased heat production through metabolic changes and altered blood flow. Vasoconstriction, or narrowing of blood vessels, can reduce heat dissipation, leading to a buildup of warmth. In some cases, stress triggers vasodilation, causing flushing and a sensation of heat, particularly in the face and upper body. These responses vary based on genetic predisposition, baseline stress tolerance, and environmental factors.

Chronic stress can further disrupt thermoregulation by affecting circadian rhythms. Normally, body temperature follows a daily cycle, peaking in the late afternoon and dipping during sleep. However, prolonged psychological distress has been linked to irregular temperature patterns, with some individuals experiencing sustained elevations or unexpected fluctuations. A study in Neuroscience & Biobehavioral Reviews found that individuals with generalized anxiety disorder or post-traumatic stress disorder often exhibit higher baseline body temperatures, suggesting long-term stress exposure may recalibrate the body’s thermal set point.

Hormonal Mechanisms Of Stress Fever

The rise in body temperature associated with stress is driven by hormonal changes originating from the hypothalamic-pituitary-adrenal (HPA) axis. When the brain perceives a threat, the hypothalamus releases corticotropin-releasing hormone (CRH), prompting the pituitary gland to secrete adrenocorticotropic hormone (ACTH). This stimulates the adrenal glands to produce cortisol, a glucocorticoid involved in metabolism and immune regulation. Elevated cortisol levels can increase metabolic activity, generating heat and contributing to temperature elevations.

Norepinephrine, released by the sympathetic nervous system during stress, further enhances metabolic rate by stimulating brown adipose tissue (BAT), which produces heat through non-shivering thermogenesis. Research in The Journal of Clinical Investigation has shown that acute stress activates BAT, leading to a measurable rise in core temperature. This effect is more pronounced in individuals with higher baseline sympathetic nervous system activity. Additionally, norepinephrine promotes vasoconstriction, reducing heat loss through the skin.

Thyroid hormones also play a role in stress-related temperature changes. Under prolonged stress, thyroid-stimulating hormone (TSH) levels can fluctuate, influencing the production of thyroxine (T4) and triiodothyronine (T3). These hormones regulate basal metabolic rate, and even slight increases in their activity can lead to greater heat production. A study in Endocrinology found that individuals with chronic stress exhibited altered thyroid hormone levels, correlating with mild but persistent temperature elevations.

Influence Of The Autonomic Nervous System

The autonomic nervous system (ANS) regulates body temperature, and its response to stress can cause significant fluctuations. Comprising the sympathetic and parasympathetic branches, the ANS controls involuntary physiological functions, including thermoregulation. When stress activates the sympathetic nervous system (SNS), it triggers physiological adaptations designed for survival, including increased heat production.

SNS activation leads to the release of catecholamines such as norepinephrine and epinephrine, which stimulate metabolic processes that generate heat. This effect is particularly evident in brown adipose tissue, a thermogenic organ that produces heat through mitochondrial uncoupling. Thermographic imaging studies have shown that individuals exposed to acute stress exhibit increased BAT activity, leading to measurable rises in core temperature.

Vasomotor control, another function of the ANS, also influences stress-related temperature shifts. Under stress, blood vessels in the skin constrict, reducing heat dissipation and creating a sensation of warmth. Some individuals experience stress-induced flushing, where transient vasodilation follows initial constriction, causing redness and heat in the face and upper body. These temperature fluctuations can mimic fever-like symptoms, even in the absence of infection.

Fever-Like Immune Responses To Stress

Psychological stress affects the immune system, sometimes triggering inflammatory responses similar to those seen in infections. When the body perceives a threat—whether physical or emotional—it mobilizes immune cells, leading to the release of pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). These molecules act on the hypothalamus, inducing a fever-like state even without pathogens.

Research has shown that individuals experiencing chronic stress often have elevated baseline levels of these cytokines, suggesting a sustained low-grade inflammatory response. A study published in Brain, Behavior, and Immunity found that participants under prolonged psychological distress had significantly higher circulating IL-6 levels. Similar immune activity has been observed in conditions such as major depressive disorder and post-traumatic stress disorder, where systemic inflammation is frequently detected. The persistent presence of inflammatory mediators can contribute to temperature fluctuations, fatigue, and other symptoms commonly associated with fever.

Distinguishing Infectious Fever From Stress Fever

Since both infectious and stress-induced fevers result in elevated body temperature, distinguishing between them is essential for proper management. Infectious fevers typically involve pathogen-specific immune responses, while stress-related temperature increases stem from neuroendocrine and autonomic changes.

One reliable way to differentiate the two is by assessing accompanying symptoms. Infectious fevers often present with chills, body aches, fatigue, and localized inflammation, while stress fever is more likely associated with anxiety, rapid heart rate, and excessive sweating. Temperature patterns also differ—infectious fevers tend to follow a sustained or biphasic pattern, sometimes exceeding 38°C (100.4°F), whereas stress-induced temperature increases are usually transient, rising during acute stress and subsiding once the stressor is removed.

How the fever responds to external factors can also provide insight. Infectious fevers rarely resolve quickly without medical intervention, whereas stress-related temperature elevations can be reduced through relaxation techniques, hydration, and breathing exercises. Additionally, antipyretics like ibuprofen or acetaminophen effectively lower fever caused by infection but may have little effect on stress-induced temperature changes. Monitoring these patterns can help individuals and healthcare providers distinguish between the two, avoiding unnecessary antibiotic use while addressing underlying stress-related health concerns.