The science behind
your score.
Every marker, target, and interaction in the Oravi Age maps to peer-reviewed research. We cite every study. Here is exactly how the score works and why each marker was chosen.
External validation of the multi-panel approach
A 2026 analysis by Adibi et al. (npj Digital Medicine) examined whether composite multi-domain biomarker scoring, combining sleep physiology, cardiometabolic blood markers, oral microbiome composition, and lifestyle behaviors, demonstrated significantly stronger predictive validity for health outcomes than single-domain approaches.[29]Adibi JJ, et al. Multi-domain biomarker composite scoring and prediction of health outcomes in midlife adults. npj Digital Medicine, 2026.
The study found that integration across these four domains improved outcome prediction beyond any single panel alone. This supports the fundamental design choice of the Oravi Age: that health is measured in dimensions, not a single number from one test.
Is the Oravi Age validated?
The honest answer is: not yet. Neither is any other consumer health score.
Apple Watch readiness scores, Oura Ring recovery indices, WHOOP strain and recovery, InsideTracker’s InnerAge. None of these have been validated in a prospective clinical trial showing their composite score predicts hard outcomes like mortality, hospitalisation, or disease onset. They are proprietary algorithms with no published methodology.
Oravi shows its work.
Every component of the Oravi Age maps directly to peer-reviewed research. We cite the study, the sample size, and the effect size. When we say hsCRP below 0.5 mg/L is associated with lower cardiovascular risk, we link to the study that shows it. When we say periodontal pathogens are found in coronary plaques, we cite Frontiers in Immunology 2023, n=1,791.
The Oravi Age is not a clinical diagnostic tool. It tracks the markers that matter most, built on the same evidence your doctor uses, made readable for daily life.
“Radical transparency about evidence is more valuable than a black-box algorithm. We will always show our sources.”
Oravi Age architecture
Oravi Age is a biological age in years, not a score out of 100. It combines six measured components: PhenoAge from blood biomarkers (48%), oral microbiome assessment (22%), resting heart rate (11%), HRV (8%, pending implementation), sleep duration (5%), and sleep regularity (4%). Cross-panel interaction terms contribute 3% when both blood and oral panels are available. When a component is missing, its weight redistributes proportionally to the remaining components.
PhenoAge (Levine 2018) uses 9 blood biomarkers: albumin, creatinine, glucose, hs-CRP, lymphocyte %, MCV, RDW, ALP, and WBC. Standard CRP cannot substitute for hs-CRP. When hs-CRP is missing, PhenoAge returns null and its 48% weight redistributes to the other components.
OMA (Oral Microbiome Assessment) is a composite percentile: 45% protective bacteria, 35% pathogen-inverted, 20% Shannon diversity, anchored against the NHANES 2009-2012 oral microbiome reference (n=9,660).
Cross-panel interactions detect convergent signals across panels: I1 (Oral × Blood, −0.3 yrs when Neisseria+Rothia >5% AND hs-CRP <1.0), I2 (Oral × Fitness, −0.2 yrs when OMA >70th pct AND RHR below expected), I3 (Blood × Sleep, −0.2 yrs when hs-CRP <1.0 AND sleep 7-8h AND bedtime SD <30min). All three are favorable only. Cap: ±1.0 yr.
Band thresholds: delta >5 = Exceptional, >2 = Optimized, ±2 = On Pace, >−5 = Elevated, ≤−5 = Accelerated.
VO₂ max is displayed as an informational metric on your dashboard. It will be re-introduced as a scored component when reliable API access becomes available across all wearable platforms.
Freshness. Blood panel results are time-gated. Labs older than 12 months lock the blood panel entirely. We do this because stale data is worse than no data. It creates false confidence.
Sleep · duration + regularity (9%)
Sleep contributes 9% of Oravi Age through two components: duration (5%) and regularity (4%). Poor sleep quality is a systemic health signal. It drives inflammation, glucose dysregulation, immune suppression, and accelerated biological aging.
Sleep data requires a connected wearable: Apple Watch, Oura, WHOOP, or Garmin. We use a 7-night minimum to avoid single-night noise. Deep sleep is weighted most heavily (8 pts) as the most clinically meaningful sleep quality indicator, followed by REM (7 pts), efficiency (6 pts), HRV (5 pts, age-adjusted), and SpO2 (4 pts).
Sleep scoring requires a minimum of 7 nights of wearable data to ensure statistical reliability. This threshold is based on published research showing that 7 nights are needed to reliably estimate habitual sleep efficiency.[26]Cheung J, et al. Night-to-night variability in objective sleep measurements and its implications for single-night studies. Sleep Medicine Reviews, 2021. Scores update nightly as new data arrives.
Deep sleep drives growth hormone release, metabolic waste clearance via the glymphatic system, and immune consolidation. Below 15% is associated with elevated neuroinflammation biomarkers and impaired glymphatic clearance.[1]Xie L, et al. Sleep drives metabolite clearance from the adult brain. Science, 2013.
Xie et al., Science 2013. Walker, Why We Sleep, 2017.
Heart rate variability is not just a sleep metric. It is one of the most accessible non-invasive windows into a core hallmark of aging.
As we age, the balance of the autonomic nervous system shifts. Sympathetic activity (fight-or-flight) increases. Parasympathetic activity (rest and digest) declines. That decline matters beyond sleep. The parasympathetic system actively suppresses systemic inflammation via the cholinergic anti-inflammatory pathway. When parasympathetic tone weakens, that brake is removed, and chronic low-grade inflammation (inflammaging) accelerates.[31]Olivieri F, et al. Heart rate variability and autonomic nervous system imbalance: Potential biomarkers and detectable hallmarks of aging and inflammaging. Ageing Research Reviews, 2024.
A 2024 review in Ageing Research Reviews formally proposed HRV as a biomarker of aging and inflammaging, affordable and non-invasive enough to monitor in asymptomatic individuals. This is why Oravi connects your HRV to your hsCRP. When both are abnormal, you are not seeing two separate problems. You are seeing the same hallmark measured twice.[34]López-Otín C, et al. Hallmarks of aging: An expanding universe. Cell, 2023.
Oravi scores HRV on two axes:
Population percentile: where you stand relative to healthy peers of your age and sex, anchored in the Lifelines Cohort study (n=84,772, the largest published single-cohort RMSSD normative dataset), which generated age- and sex-specific centile curves from ECG recordings.[32]Tegegne BS, et al. Reference values of heart rate variability from 10-second resting electrocardiograms: the Lifelines Cohort Study. European Journal of Preventive Cardiology, 2020. n=84,772.
Personal trend: whether your HRV is rising or falling relative to your own 30-day rolling baseline. A sustained drop of ≥20% below your personal average flags Watch regardless of your population percentile, because acute autonomic stress shows up in personal trend before it shifts your population percentile.[33]Brozat M, Böckelmann I, Sammito S. Systematic review on HRV reference values. Journal of Cardiovascular Development and Disease, 2025.
Your final HRV status is the more conservative of the two.
Olivieri F et al., Ageing Res Rev 2024. Tegegne BS et al., Eur J Prev Cardiol 2020 (n=84,772). Brozat et al., J Cardiovasc Dev Dis 2025. López-Otín C et al., Cell 2023.
Overnight oxygen desaturation events are the primary screening signal for obstructive sleep apnea. OSA is diagnosed in 936 million people globally and is massively underdiagnosed. Untreated OSA drives hypertension, atrial fibrillation, and cognitive decline.[3]Benjafield AV, et al. Estimation of the global prevalence and burden of obstructive sleep apnoea. Lancet Respiratory Medicine, 2019. n=936 million.
Benjafield et al., Lancet Respiratory Medicine 2019. n=936 million estimate.
REM sleep governs emotional memory consolidation and psychological resilience. Chronic REM suppression is associated with depression, anxiety, and impaired threat processing.[4]Walker MP, Stickgold R. Sleep, memory, and plasticity. Annual Review of Psychology, 2006.
Walker & Stickgold, Annual Review of Psychology 2006.
Time asleep as a fraction of time in bed. Low efficiency (fragmented sleep, long wake-after-sleep-onset) indicates poor sleep architecture regardless of total hours.[5]Buysse DJ, et al. The Pittsburgh Sleep Quality Index. Psychiatry Research, 1989.
Buysse et al., Psychiatry Research 1989. Pittsburgh Sleep Quality Index.
Blood · PhenoAge (48%)
The blood panel captures cardiovascular risk, metabolic health, and systemic inflammation. These are the three dimensions most predictive of premature mortality in middle-aged adults. We use seven markers, each selected for independent predictive value beyond standard lipid panels.
Blood data is accepted via PDF upload: Quest, LabCorp, BioReference, Everlywell, and most major labs. Our parser extracts markers automatically.
High-sensitivity C-reactive protein is the benchmark inflammatory marker. Values above 3.0 mg/L confer 2× the cardiovascular risk of values below 1.0 mg/L, independent of LDL cholesterol.[6]Ridker PM, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein (Jupiter). NEJM, 2008. n=17,802. The 2025 ACC Scientific Statement now identifies hsCRP >2.0 mg/L as an independent action threshold, requiring clinical attention regardless of LDL level.[25]Mensah GA, Arnold N, Prabhu SD, Ridker PM, Welty FK. Inflammation and Cardiovascular Disease: 2025 ACC Scientific Statement. J Am Coll Cardiol, 2025.
Ridker et al., NEJM 2008 (Jupiter Trial). n=17,802. Updated per Mensah et al., JACC 2025.
2025 ACC Scientific Statement on Inflammation & CVD
“hsCRP is at least as predictive of cardiovascular events as LDL cholesterol, even in patients on statin therapy. An hsCRP above 2.0 mg/L is now an independent action threshold.”
Mensah GA, Arnold N, Prabhu SD, Ridker PM, Welty FK. J Am Coll Cardiol. 2025. DOI: 10.1016/j.jacc.2025.08.047
Apolipoprotein B is the protein that coats every atherogenic particle (LDL, VLDL, IDL, Lp(a)). It is a superior predictor of cardiovascular events compared to LDL-C alone, particularly in people with metabolic syndrome.[7]Sniderman AD, et al. ApoB vs LDL-C: which better predicts cardiovascular risk. JAMA Cardiology, 2019.
Sniderman et al., JAMA Cardiology 2019.
Vitamin D deficiency affects ~40% of Americans and is associated with elevated inflammatory cytokines, impaired immune function, depression, and all-cause mortality. The relationship is bidirectional: poor sleep reduces vitamin D synthesis; low vitamin D impairs sleep quality.[8]Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutrition Research, 2011. n=4,495.
Forrest & Stuhldreher, Nutrition Research 2011. n=4,495.
The ratio of atherogenic to protective cholesterol particles. A ratio above 3.5 is associated with significantly elevated coronary artery disease risk. HDL’s reverse cholesterol transport function makes the ratio more informative than LDL alone.[9]Millan J, et al. Lipoprotein ratios: physiological significance and clinical usefulness in cardiovascular prevention. Vascular Health and Risk Management, 2009.
Millan et al., Vascular Health and Risk Management 2009.
Glycated haemoglobin reflects average blood glucose over 90 days. Pre-diabetic range (5.7–6.4%) confers elevated risk of kidney disease, neuropathy, and cardiovascular events, often years before diagnosis.[10]Selvin E, et al. Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults. NEJM, 2010. n=11,092.
Selvin et al., NEJM 2010. n=11,092.
Lipoprotein(a) is a largely genetically-determined atherogenic particle that standard lipid panels miss. Elevated Lp(a) (>125 nmol/L) doubles cardiovascular risk independently. Most people have never had it measured.[11]Tsimikas S. A test in context: lipoprotein(a). JACC, 2017.
Tsimikas, JACC 2017.
Fasting triglycerides reflect insulin sensitivity and dietary carbohydrate metabolism. Elevated triglycerides combined with low HDL is the metabolic syndrome pattern most predictive of type 2 diabetes and ASCVD.[12]Austin MA, et al. Hypertriglyceridemia as a cardiovascular risk factor. American Journal of Cardiology, 1998.
Austin et al., American Journal of Cardiology 1998.
Oral microbiome · OMA (22%)
The oral microbiome is the least measured dimension of systemic health. The mouth is not isolated from the rest of the body. It shares blood supply with the heart, lungs, and brain. Dysbiosis in oral bacteria has been directly detected in coronary plaques and systemic tissues in multiple autopsy and biopsy studies.
Oral microbiome data comes from DNA sequencing. A simple at-home swab kit. Results in 10–14 days.
Nobody else measures this panel. It is also where the strongest cross-panel signals come from.
Your oral microbiome is compared against the CDC’s NHANES dataset, the only nationally representative study of mouth bacteria in the United States. 9,660 participants. Health outcomes tracked for 9 years. Same DNA sequencing technology as your Zymo kit.
There’s no other reference population like this. Most oral microbiome tests compare you against “healthy” samples from a small lab study. We compare you against America.
Explore the data →Bacterial diversity measures the richness and evenness of microbial species in the oral cavity. Low diversity signals an imbalanced microbiome, a state where harmful species overgrow at the expense of beneficial ones.[13]Belstrøm D, et al. Microbial diversity in saliva and oral health. Journal of Oral Microbiology, 2014.
Belstrøm et al., Journal of Oral Microbiology 2014.
Neisseria, Rothia, and Veillonella species convert dietary nitrate into nitrite, which is then converted to nitric oxide (NO) in the circulation. NO is a potent vasodilator critical for blood pressure regulation. Antiseptic mouthwash kills these bacteria, acutely impairing the NO pathway.[14]Petersson J, et al. Gastroprotective and blood pressure lowering effects of dietary nitrate. Free Radical Biology & Medicine, 2009.[15]Kapil V, et al. Dietary nitrate provides sustained blood pressure lowering in hypertension. Hypertension, 2015. n=300.[28]Vanhatalo A, et al. Dietary nitrate accelerates post-exercise muscle metabolic recovery and O2 delivery in hypoxia. The Journal of Physiology, 2018.
Petersson et al., 2009. Kapil et al., Hypertension 2015 (ORIGINS study), n=300. Vanhatalo et al., J Physiol 2018.
Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia are the “red complex” periodontal pathogens. P. gingivalis and related species have been directly detected in human coronary artery plaques in autopsy studies, establishing a systemic bacteraemia pathway from the oral cavity to vascular tissue.[16]Hussain M, et al. Oral bacteria in cardiovascular specimens. Frontiers in Immunology, 2023. n=1,791. P. gingivalis has also been detected in neurological tissue, with gingipain proteases identified as a driver of neuroinflammatory cascades.[17]Dominy SS, et al. Porphyromonas gingivalis in human brain tissue. Science Advances, 2019.
Hussain et al., Frontiers in Immunology 2023, n=1,791. Dominy et al., Science Advances 2019.
Prevotella and Fusobacterium species are enriched in patients with obstructive sleep apnea. OSA patients are 2.46× more likely to have periodontitis across meta-analyses covering 88,000+ patients. The mechanism: intermittent hypoxia from OSA drives oxidative stress that accelerates periodontal tissue breakdown, while periodontal inflammation elevates systemic CRP, disrupting sleep architecture. Oravi tracks these taxa as a signal that the oral-inflammatory-sleep pathway may be active.[18]Portelli M, et al. Association between OSA and periodontitis: systematic review & meta-analysis. Dentistry Journal, 2024. n=88,040.[19]Dalton B, et al. Bidirectional relationship between oral microbiome and sleep quality. Sleep Medicine, 2025. n=1,139.
Portelli et al., Dentistry Journal 2024, n=88,040. Zhu et al., Sleep and Breathing 2023, n=31,800. Mi et al., BMC Oral Health 2023 (Mendelian randomization).
Emerging research dimensions (D5–D7)
Three additional oral dimensions are scored based on emerging research. They use qualitative descriptors rather than raw percentages, and are clearly labelled as emerging. These dimensions contribute to the 30-point oral sub-score.
P. gingivalis has been detected in human brain tissue in Alzheimer’s disease patients, with its gingipain proteases identified as a potential driver of neuroinflammatory cascades. T. denticola compounds the burden. We frame this as “neurological balance,” a wellness signal, not a disease prediction.[17]Dominy SS, et al. Porphyromonas gingivalis in human brain tissue. Science Advances, 2019.
Dominy et al., Science Advances 2019. Emerging research; effect sizes not yet established for oral screening.
Certain Prevotella species are associated with metabolic health pathways. Elevated Prevotella abundance has been observed in metabolic dysbiosis states. A diet rich in diverse plant fibers supports a balanced oral microbiome.
Emerging research; observational associations, not yet causal.
Fusobacterium nucleatum is being studied in connection with cellular health pathways, including its role in tissue adhesion and immune modulation. Regular dental cleaning, good oral hygiene, and dietary fiber support a balanced microbiome.
Emerging research; mechanisms under active investigation.
Lifestyle · contextual
Lifestyle data is no longer scored numerically. Your Oravi Age is based entirely on objective, measured data: blood labs, wearable sleep data, and oral microbiome sequencing. Lifestyle information (exercise, diet, oral hygiene, smoking, stress) informs your insights and cross-panel analysis but does not contribute points to your total score.
This design choice reflects a core principle: self-reported behaviours are valuable context, but measured biomarkers are more reliable for scoring. Lifestyle context helps us generate more personalised insights, connecting your habits to your numbers, without inflating your score based on questionnaire answers.
Physical activity is the single most evidence-dense intervention in preventive medicine. Active (≥75 min vigorous or ≥150 min moderate/week): 4 pts. Moderate: 2.5 pts. Light: 1.5 pts. Sedentary: 0 pts.[21]Lee IM, et al. Effect of physical inactivity on major non-communicable diseases worldwide. Lancet, 2012.
Lee et al., Lancet 2012.
Brushing ×2 + flossing daily: 3 pts. Brushing ×2 only: 2 pts. Brushing ×1: 1 pt. Antiseptic mouthwash penalty: −0.5 pts (kills nitrate-reducing bacteria, disrupts NO pathway).[20]Park SY, et al. Association of toothbrushing with cardiovascular risk. European Journal of Preventive Cardiology, 2019. n=247,696.
Park et al., European Journal of Preventive Cardiology 2019, n=247,696.
Annual dental visits allow professional debridement of subgingival biofilm, the primary reservoir of periodontal pathogens. ≥1 visit per year: 2 pts. Less frequent: 0 pts.[20]Park SY, et al. Association of toothbrushing with cardiovascular risk. European Journal of Preventive Cardiology, 2019. n=247,696.
Park et al., 2019.
Current smoking is independently associated with elevated hsCRP, endothelial dysfunction, and periodontal disease severity. It also directly degrades oral microbiome diversity. Non-smoker: 1 pt. Current smoker: 0 pts.
Fermented foods, including yogurt, kefir, kimchi, sauerkraut, and kombucha, directly seed the gut and oral microbiome with beneficial microorganisms and reduce systemic inflammatory markers. A randomized crossover trial found that a high-fermented-food diet increased microbiome diversity and decreased 19 inflammatory proteins compared to a high-fiber diet.[27]Wastyk HC, et al. Gut-microbiota-targeted diets modulate human immune status. Cell, 2021. n=36. Daily consumption: 2 pts. Sometimes: 1 pt. Rarely: 0 pts.
Wastyk et al., Cell 2021. n=36.
Oral × Lifestyle: a compounding relationship
Antiseptic mouthwash depletes nitrate-reducing bacteria from the oral cavity, the same species that produce nitric oxide for blood pressure regulation. Fermented foods help replenish beneficial microbial populations. When both signals are present (antiseptic mouthwash use and low fermented food intake) the oral microbiome is doubly impaired: pathogen suppression is absent and beneficial seeding is absent. This interaction is detected as a cross-panel insight when both conditions are met.
Cross-panel Intelligence
No other consumer health product does this.
Cross-panel modifiers detect when signals from multiple panels compound, either amplifying risk (penalties) or reinforcing protection (bonuses). Unlike v1 where interactions were insight-only, modifiers now directly adjust your score: penalties up to −10 points, bonuses up to +8 points.
Inflammation and poor sleep are not independent risks you add together. They amplify each other through shared pathways. When a modifier fires, you see it on your dashboard with the panels involved and the point impact.
Low HRV reflects declining parasympathetic tone. The parasympathetic system suppresses inflammation via the cholinergic anti-inflammatory pathway. When HRV is low and hsCRP is elevated, these are two measurements of the same hallmark of aging: inflammaging.[31]Olivieri F, et al. Heart rate variability and autonomic nervous system imbalance: Potential biomarkers and detectable hallmarks of aging and inflammaging. Ageing Research Reviews, 2024.
Fires when: Sleep HRV <40ms AND hsCRP >1.0 mg/L
Nocturnal hypoxia activates sympathetic nervous system and promotes LDL oxidation.[23]Savransky V, et al. Intermittent hypoxia induces atherosclerosis. American Journal of Respiratory and Critical Care Medicine, 2007.
Fires when: SpO2 dips >5/night AND ApoB >100 mg/dL
When both are running above typical, it tends to reflect inflammatory signals showing up across more than one system.
Fires when: hsCRP >1.0 mg/L AND ESR elevated
Autonomic dysfunction compounded by endothelial injury, a specific high-risk cardiovascular phenotype.
Fires when: Low HRV + elevated homocysteine
The most important interaction term. Periodontal pathogen burden directly elevates systemic CRP via bacteraemia.[24]Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation. Nature Reviews Immunology, 2015.
Fires when: Periodontal pathogens >1% AND hsCRP >0.8 mg/L
Convergent signal: the microbiome flags OSA risk, the wearable detects its physiological consequence.[18]Portelli M, et al. Association between OSA and periodontitis: systematic review & meta-analysis. Dentistry Journal, 2024. n=88,040.
Fires when: OSA taxa >2% AND SpO2 dips >3/night
Depleted oral NO pathway + elevated inflammation = dual hit on vascular health.
Fires when: Nitrate-reducers <3% AND hsCRP >1.0 mg/L
The bidirectional relationship between oral microbiome and sleep quality.[19]Dalton B, et al. Bidirectional relationship between oral microbiome and sleep quality. Sleep Medicine, 2025. n=1,139.
Fires when: Shannon diversity <2.5 AND sleep efficiency <80%
The 2025 ACC guidelines identify this combination as requiring clinical attention regardless of either value alone. Elevated LDL and elevated hsCRP compound atherosclerotic risk through distinct but synergistic pathways.[25]Mensah GA, Arnold N, Prabhu SD, Ridker PM, Welty FK. Inflammation and Cardiovascular Disease: 2025 ACC Scientific Statement. J Am Coll Cardiol, 2025.
Fires when: hsCRP >2.0 mg/L AND LDL >130 mg/dL
Low physical activity is a primary driver of chronic low-grade inflammation. When hsCRP is already elevated, inactivity compounds the cardiovascular risk.[25]Mensah GA, Arnold N, Prabhu SD, Ridker PM, Welty FK. Inflammation and Cardiovascular Disease: 2025 ACC Scientific Statement. J Am Coll Cardiol, 2025.
Fires when: Sedentary/light activity AND hsCRP >2.0 mg/L
When OSA-associated taxa are low despite no dietary support, the microbiome may be suppressed rather than healthy. Fermented food intake helps maintain the diverse ecosystem that keeps pathogenic taxa in check.
Fires when: OSA taxa <3% AND fermented foods rarely/never
The NO pathway is doubly compromised: antiseptic mouthwash kills nitrate-reducing bacteria while low fermented food intake reduces microbial replenishment. This combination is the strongest lifestyle signal for oral microbiome depletion.
Fires when: Nitrate-reducers <2% AND antiseptic mouthwash AND fermented foods rarely
What Oravi does not claim
“hsCRP below 0.5 mg/L is associated with lower cardiovascular risk in population studies.”
“Periodontal pathogens have been directly detected in coronary plaques in autopsy studies.”
“OSA patients are 2.46× more likely to have periodontitis across meta-analyses of 88,000+ patients.” (Portelli et al., 2024; Zhu et al., 2023)
“Your Oravi Age reflects the current state of evidence on these markers.”
“Your Oravi Age predicts your risk of any specific disease or outcome.”
“Improving your Oravi Age will extend your life.”
“The Oravi Age is a validated clinical diagnostic tool.”
“You should make medical decisions based on your Oravi Age without consulting a doctor.”
Oravi is a tracking tool for people who want to understand their health beyond what standard annual checkups show. It uses the same evidence base your doctor uses, made readable for daily life.
We do not claim more than the evidence supports. Sources are always visible. The score engine updates as the science does.
References
- [1]Xie L, et al. Sleep drives metabolite clearance from the adult brain. Science. 2013.
- [2]Thayer JF, et al. The relationship of autonomic imbalance, heart rate variability and cardiovascular disease risk factors. International Journal of Cardiology. 2010.
- [3]Benjafield AV, et al. Estimation of the global prevalence and burden of obstructive sleep apnoea. Lancet Respiratory Medicine. 2019. n=936 million.
- [4]Walker MP, Stickgold R. Sleep, memory, and plasticity. Annual Review of Psychology. 2006.
- [5]Buysse DJ, et al. The Pittsburgh Sleep Quality Index. Psychiatry Research. 1989.
- [6]Ridker PM, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein (Jupiter). NEJM. 2008. n=17,802.
- [7]Sniderman AD, et al. ApoB vs LDL-C: which better predicts cardiovascular risk. JAMA Cardiology. 2019.
- [8]Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutrition Research. 2011. n=4,495.
- [9]Millan J, et al. Lipoprotein ratios: physiological significance and clinical usefulness in cardiovascular prevention. Vascular Health and Risk Management. 2009.
- [10]Selvin E, et al. Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults. NEJM. 2010. n=11,092.
- [11]Tsimikas S. A test in context: lipoprotein(a). JACC. 2017.
- [12]Austin MA, et al. Hypertriglyceridemia as a cardiovascular risk factor. American Journal of Cardiology. 1998.
- [13]Belstrøm D, et al. Microbial diversity in saliva and oral health. Journal of Oral Microbiology. 2014.
- [14]Petersson J, et al. Gastroprotective and blood pressure lowering effects of dietary nitrate. Free Radical Biology & Medicine. 2009.
- [15]Kapil V, et al. Dietary nitrate provides sustained blood pressure lowering in hypertension. Hypertension. 2015. n=300.
- [16]Hussain M, et al. Oral bacteria in cardiovascular specimens. Frontiers in Immunology. 2023. n=1,791.
- [17]Dominy SS, et al. Porphyromonas gingivalis in human brain tissue. Science Advances. 2019.
- [18]Portelli M, et al. Association between OSA and periodontitis: systematic review & meta-analysis. Dentistry Journal. 2024. n=88,040.
- [19]Dalton B, et al. Bidirectional relationship between oral microbiome and sleep quality. Sleep Medicine. 2025. n=1,139.
- [20]Park SY, et al. Association of toothbrushing with cardiovascular risk. European Journal of Preventive Cardiology. 2019. n=247,696.
- [21]Lee IM, et al. Effect of physical inactivity on major non-communicable diseases worldwide. Lancet. 2012.
- [22]Irwin MR, et al. Sleep disturbance, sleep duration, and inflammation: a systematic review. Biological Psychiatry. 2016.
- [23]Savransky V, et al. Intermittent hypoxia induces atherosclerosis. American Journal of Respiratory and Critical Care Medicine. 2007.
- [24]Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation. Nature Reviews Immunology. 2015.
- [25]Mensah GA, Arnold N, Prabhu SD, Ridker PM, Welty FK. Inflammation and Cardiovascular Disease: 2025 ACC Scientific Statement. J Am Coll Cardiol. 2025.
- [26]Cheung J, et al. Night-to-night variability in objective sleep measurements and its implications for single-night studies. Sleep Medicine Reviews. 2021.
- [27]Wastyk HC, et al. Gut-microbiota-targeted diets modulate human immune status. Cell. 2021. n=36.
- [28]Vanhatalo A, et al. Dietary nitrate accelerates post-exercise muscle metabolic recovery and O2 delivery in hypoxia. The Journal of Physiology. 2018.
- [29]Adibi JJ, et al. Multi-domain biomarker composite scoring and prediction of health outcomes in midlife adults. npj Digital Medicine. 2026.
- [30]Haghayegh S, et al. Accuracy of wristband wearables for measuring sleep and SpO2 in clinical settings. JMIR mHealth and uHealth. 2025.
- [31]Olivieri F, et al. Heart rate variability and autonomic nervous system imbalance: Potential biomarkers and detectable hallmarks of aging and inflammaging. Ageing Research Reviews. 2024.
- [32]Tegegne BS, et al. Reference values of heart rate variability from 10-second resting electrocardiograms: the Lifelines Cohort Study. European Journal of Preventive Cardiology. 2020. n=84,772.
- [33]Brozat M, Böckelmann I, Sammito S. Systematic review on HRV reference values. Journal of Cardiovascular Development and Disease. 2025.
- [34]López-Otín C, et al. Hallmarks of aging: An expanding universe. Cell. 2023.
- [35]Mi Z, et al. OSA causally promotes periodontitis: Mendelian randomization. BMC Oral Health. 2023.
- [36]Hao G, et al. Oral microbiome diversity and sleep disorder risk. BMC Oral Health. 2025. n=4,729.
- [37]Tang Q, et al. RA and periodontitis: systematic review & meta-analysis. Int J Periodontics Restorative Dent. 2017. n=151,569.
- [38]Olsen I, Singhrao SK. Oral pathogens in Alzheimer’s disease brains. J Oral Microbiology. 2015.
- [39]Altamash M, et al. HbA1c reduction from periodontal treatment in diabetics. J Oral Rehabil. 2016. n=129.
- [40]Gamsiz-Isik H, et al. Periodontitis prevalence in polysomnogram-confirmed OSA. J Periodontol. 2017. n=163.
Oravi is not a medical device. The Oravi Age is for informational purposes only and does not constitute medical advice, diagnosis, or treatment. Always consult a licensed healthcare provider regarding your health. Score engine version 8.1 · Last updated March 2026.