Your Recovery Blueprint, Decoded.

This analysis reveals how your genetic signals influence sleep structure, restoration efficiency, and overall sleep satisfaction.

• Deep sleep quality – Methylation patterns in genes that regulate slow-wave sleep generation—the most physically restorative sleep phase linked to memory consolidation, immune function, and cellular repair. These patterns help explain individual variations in recovery capacity and how effectively your body restores itself during sleep.
• Reported sleep quality – Epigenetic markers affecting the subjective experience of sleep satisfaction—revealing why some individuals might feel unrested despite adequate sleep duration or why sleep tracking data might not match your personal sleep experience.
• Excessive sleepiness risk – Methylation sites associated with daytime alertness and fatigue patterns—potentially explaining persistent tiredness despite sufficient sleep and suggesting targeted approaches for enhancing wakefulness and energy balance.

This component examines the biological markers that govern your circadian rhythm, sleep duration needs, and sleep maintenance capacity.

• Ideal sleep window – Methylation patterns affecting your chronotype—determining whether you're genetically predisposed to function better as a morning lark, night owl, or somewhere in between. These patterns influence not just preferred sleep times but optimal windows for cognitive performance, physical activity, and food intake.
• Ideal total time in bed – Epigenetic sites influencing your body's natural sleep duration requirements—revealing why standard eight-hour recommendations might not be optimal for your unique biology and explaining individual variations in sleep needs.
• Sleep deprivation sensitivity – Methylation patterns associated with resilience or vulnerability to reduced sleep—potentially explaining why some people experience significant cognitive and mood impairment after sleep loss while others remain relatively functional.
• Micro-awakening propensity – Epigenetic markers affecting brief awakenings during sleep that may not reach conscious awareness but can significantly impact sleep quality and next-day performance—helping explain fragmented sleep experiences despite good sleep hygiene.

This section maps the epigenetic indicators associated with physical restlessness during sleep and movement-related sleep disruptions.

• Jittery legs risk – Methylation patterns influencing nervous system activity that may contribute to restless legs and limb movements during sleep—potentially explaining disrupted sleep despite good sleep hygiene practices.
• Sleep movement risk – Epigenetic markers affecting general body movement during sleep—revealing tendencies toward restlessness that may fragment sleep cycles and reduce overall sleep quality.
• Sleep continuity factors – Methylation sites associated with the ability to maintain uninterrupted sleep throughout the night—offering insights into why some people naturally experience more fragmented sleep and guiding targeted interventions.

This evaluation identifies the biological markers governing your response to compounds that can influence sleep quality.

• Caffeine effects on sleep – Methylation patterns affecting how caffeine impacts your sleep onset, quality, and duration—potentially explaining individual differences in sensitivity to caffeine consumption, even hours before bedtime.
• Caffeine metabolism (CYP1A2) – Epigenetic markers influencing the CYP1A2 enzyme that breaks down caffeine—determining how quickly your body processes caffeine and how long its stimulating effects persist in your system, with direct implications for sleep timing and quality.
• Melatonin metabolism – Methylation sites affecting your natural sleep hormone production, timing, and clearance—key factors in sleep onset and maintenance that help explain individual variations in natural sleepiness timing and response to darkness or light exposure.

This assessment examines the biological markers related to how your body activates, manages, and recovers from stress responses.

• Stress adaptation – Methylation patterns in genes regulating your HPA axis—the biological system connecting your brain and adrenal glands during stress. These markers influence how quickly you enter a stress response, how intensely you experience it, and how efficiently you recover afterward.
• Cortisol level propensity – Epigenetic sites affecting how your body produces and processes this primary stress hormone—impacting everything from sleep quality to immune function and cognitive performance, with implications for both stress resilience and recovery capacity.
• Recovery efficiency – Methylation patterns affecting parasympathetic nervous system activation—your body's natural relaxation response that restores balance after stress. These markers may explain individual differences in recovery time following stressful events.

This module evaluates DNA methylation patterns in genes controlling mood, emotional processing, and psychological resilience.

• Anxiety propensity – Methylation sites affecting the amygdala and fear processing centres—potentially explaining individual differences in worry patterns, anticipatory anxiety, and the neurological basis of disruptive thinking that can interfere with both sleep and daily function.
• Depression tendency – Epigenetic patterns influencing serotonin, dopamine, and other mood-regulating neurotransmitters—offering insights into biological factors affecting emotional stability, motivation, and mood-induced sleep disruption.
• Mood-induced sleeplessness risk – Methylation markers specifically associated with how emotional states affect sleep onset and maintenance—providing targeted approaches to managing the sleep-emotion connection.

This component examines the biological signals governing key hormone systems that affect sleep quality and stress resilience.

• Thyroid function markers – Methylation patterns affecting TSH levels and thyroid hormone conversion efficiency—crucial processes for regulating metabolism, energy, and sleep depth. These markers influence how efficiently your body can access energy and maintain stable core temperature during rest and recovery.
• DHEA-S propensity – Epigenetic sites related to this stress-protective hormone that serves as a precursor to other hormones—with implications for sleep quality, resilience, and recovery from challenging circumstances.
• Cortisol patterns – Methylation markers influencing your primary stress hormone's production, daily rhythm, and clearance—affecting both sleep architecture and stress recovery throughout the 24-hour cycle.

This analysis uncovers how your body processes essential nutrients that support nervous system function and recovery.

• Vitamin B12 level propensity – Methylation patterns affecting how your body absorbs, transports, and utilises this crucial nutrient for nerve function, energy production, and sleep regulation.
• Vitamin B9 need – Epigenetic markers influencing folate requirements and processing—essential for neurotransmitter production, mood regulation, and cellular repair during sleep.
• Vitamin B6 level propensity – Methylation sites related to this critical cofactor for neurotransmitter synthesis—directly impacting mood stability, dream recall, and overall sleep quality.
• MTHFR activity – Epigenetic patterns affecting this key enzyme in the methylation cycle—a biochemical pathway that supports neurotransmitter production, hormone processing, and cellular energy generation critical for sleep quality and stress management.
• Vitamin D metabolism – Methylation markers influencing vitamin D dietary absorption, deficiency risk, and conversion between inactive and active forms—essential for mood regulation, immune function, and sleep quality.

This module evaluates DNA methylation patterns in genes governing electrolyte balance and mineral utilisation.

• Sodium sensitivity – Methylation patterns affecting how your body responds to sodium intake—potentially impacting fluid balance, blood pressure regulation, and neurological function with implications for sleep quality.
• Potassium sensitivity – Epigenetic sites influencing cellular potassium transport and utilisation—crucial for nerve transmission, muscle function, and heart rhythm regulation that can affect sleep comfort and continuity.
• Magnesium deficiency risk – Methylation markers associated with this critical relaxation mineral's absorption, transport, and cellular use—essential for muscle relaxation, nervous system calm, and GABA production (the brain's primary inhibitory neurotransmitter).

This assessment identifies the biological markers responsible for cellular protection, antioxidant defence, and compound processing.

• Glutathione level propensity – Methylation patterns influencing your body's production of this master antioxidant—essential for cellular protection, detoxification support, and neutralising free radicals produced during stress and poor sleep.
• NRF2 activity – Epigenetic sites regulating this master switch for antioxidant enzyme production—a critical pathway that activates cellular defence mechanisms against oxidative stress from both environmental exposures and internal metabolic processes.
• Methylation efficiency – Methylation markers affecting this crucial biochemical process that regulates hormone activation, neurotransmitter production, and detoxification capacity—all vital for sleep quality and stress resilience.
• Choline need – Epigenetic patterns determining requirements for this essential nutrient—critical for neurotransmitter production, cell membrane integrity, and proper methylation support.

This module evaluates DNA methylation patterns in genes controlling inflammatory response, immune signalling, and cellular protection.

• CRP inflammation – Methylation patterns affecting baseline and reactive C-reactive protein levels—a key systemic inflammatory marker with implications for both sleep quality and recovery capacity.
• IL-10 inflammation risk – Epigenetic sites influencing this powerful anti-inflammatory cytokine—essential for resolving inflammation and maintaining tissue integrity, particularly during stress and sleep disruption.
• Mast cell/IgE activation – Methylation markers affecting these immune cells that release histamine and other inflammatory compounds—with implications for sensitivity to environmental triggers, food compounds, and stress-induced inflammatory responses.
• Benzene risk – Epigenetic patterns associated with processing of this environmental compound—potentially reflecting broader sensitivity to chemicals that might impact sleep quality or stress recovery.

This module evaluates DNA methylation patterns in genes affecting how psychological stress manifests physically.

• Teeth grinding tendency – Methylation sites influencing bruxism and jaw tension during sleep or stress—potentially explaining why some individuals express stress through teeth grinding even without conscious awareness, with implications for both dental health and sleep quality.
• TMJ sensitivity – Epigenetic markers affecting temporomandibular joint function and sensitivity—revealing connections between stress, facial tension, and physical discomfort that may disrupt sleep or amplify stress perception.
• Physical tension patterns – Methylation patterns influencing how muscle tone responds to psychological stress—determining whether stress tends to manifest as neck, shoulder, or other specific physical tension patterns.