Key Benefits

• See how stress, inflammation, and immune balance may influence your mood.
• Spot cortisol imbalance tied to chronic stress, sleep loss, and low mood.
• Flag low-grade inflammation with hs-CRP that can worsen depressive symptoms and pain.
• Clarify immune activation using NLR when infection or fatigue may drive mood changes.
• Guide personalized care by targeting sleep, exercise, and anti-inflammatory nutrition when elevated.
• Protect heart health by revealing inflammation linked to depression and cardiometabolic risk.
• Track trends to monitor therapy response, relapse risk, and stress recovery over time.
• Interpret results with your symptoms, PHQ-9 scores, and absence of acute infection.

What are Depression

Depression biomarkers are measurable signals that reflect how the body’s mood-regulating systems are functioning. They do not diagnose depression on their own; rather, they reveal which biological pathways may be driving symptoms and where care can be personalized. Key domains include the stress response (cortisol and daily cortisol rhythm, the hypothalamic–pituitary–adrenal axis), inflammation (C‑reactive protein and cytokines such as interleukin‑6 and tumor necrosis factor‑alpha), and brain plasticity (brain‑derived neurotrophic factor, BDNF). Metabolic and endocrine signals can also shape mood (thyroid hormones, insulin sensitivity), as can nutrient cofactors for neurotransmitters (vitamin D, vitamin B12, folate). Some tests reflect neurotransmitter turnover (serotonin and dopamine metabolites), while circadian markers touch sleep–wake regulation (melatonin). Together, these measures translate a subjective experience into an objective biological profile—helping identify contributing factors to address, track response to therapy, and flag coexisting conditions that can mimic or worsen depression.

Why are Depression biomarkers important?

Depression biomarkers are measurable signals from the stress axis and immune system that show how the brain, hormones, and inflammation are interacting. They matter because mood emerges from this whole-body network: when the hypothalamic–pituitary–adrenal (HPA) axis and immune tone are off, sleep, energy, appetite, and cognition shift in predictable ways.

Cortisol follows a diurnal curve—high in the early morning, falling to low at night. A robust peak with an evening low is generally optimal; persistently high or a blunted, flat pattern signals dysregulation. For hs-CRP, values under 1 are typically low-risk, 1–3 average, and above 3 elevated; for mood, “better” tends to sit toward the low end. The neutrophil-to-lymphocyte ratio (NLR) is usually around 1–3, with the lower-middle part of that range reflecting quieter inflammation; higher numbers point to systemic inflammatory activation.

When values run low, they tell different stories. A globally low or flattened cortisol pattern suggests HPA-axis downregulation and often aligns with “atypical” depression—fatigue, hypersomnia, increased appetite, pain sensitivity, and cognitive fog. Very low NLR can reflect lymphocyte predominance or neutropenia, sometimes accompanying recurrent infections that amplify low mood via sickness behavior; low hs-CRP itself rarely causes symptoms but indicates minimal inflammatory drive. In women, inflammation–mood links are often stronger; during pregnancy hs-CRP and NLR rise physiologically, while postpartum shifts in cortisol can influence mood. Teens may show transient HPA changes as the axis matures.

Big picture, these biomarkers connect depression to cardiometabolic, immune, and sleep-circadian systems. Elevated inflammation and cortisol imbalance track with higher risks of treatment resistance, cardiovascular disease, diabetes, and cognitive decline, while more regulated profiles align with resilience and recovery potential.

What Insights Will I Get?

Depression reflects how stress, metabolism, vascular tone, and immune signaling interact across systems. Biomarkers clarify these pathways shaping energy, cognition, sleep, and cardiometabolic risk. At Superpower, we test Cortisol, hs-CRP, and NLR.

Cortisol is the primary stress hormone (HPA-axis output) that sets daily energy rhythm and vascular tone. In depression, rhythms often shift—average levels may be higher and the diurnal slope flatter, though some subtypes show lower output. A strong morning peak with low evening levels signals resilient stress regulation; persistent elevation or a blunted rhythm suggests allostatic load and mood vulnerability.

hs-CRP is a high-sensitivity measure of C-reactive protein, an acute-phase protein reflecting low-grade systemic inflammation (often IL-6–driven). Higher hs-CRP links to greater depression risk and severity and vascular dysfunction. Lower steady-state levels indicate quieter immune signaling; higher values suggest inflammatory tone that can alter neurotransmission and energy.

NLR (neutrophil-to-lymphocyte ratio) from a standard blood count indexes the balance between innate activation and adaptive regulation. Higher NLR associates with depressive symptoms, stress reactivity, and cardiometabolic comorbidity. A balanced NLR suggests coordinated immune surveillance without chronic activation, supporting normal synaptic plasticity and stress recovery.

Notes: Context matters: cortisol depends on time since awakening and shift work; acute infection, injury, vaccination, and strenuous exercise can raise hs-CRP and NLR; glucocorticoids, NSAIDs, antidepressants, and beta-blockers alter values; pregnancy, postpartum state, age, obesity, smoking, and assay differences affect baselines.