Genetic information helped frame an individual plan; blood testing recorded what changed. Explore the metabolic results, both age scores and the priorities that remained.
K.A.R.’s follow-up ran from August 2025 to January 2026, five months. HOMA-IR fell from 1.4 to 0.7 and fasting insulin from 6.87 to 3.61 µIU/mL. ApoB fell from 98 to 87 mg/dL, hs-CRP from 1.22 to 0.64 mg/L and GGT from 17 to 9 U/L.
Genetic context and measured follow-up play different roles
The source records an APOE ε3/ε4 finding as context for K.A.R.’s plan. Her blood results then provide the follow-up evidence, including the HOMA-IR change and ongoing ApoB and ferritin priorities. That distinction helps explain personalisation without turning genetic information into a promised outcome.
Starting point and context
The source records an APOE ε3/ε4 genotype and describes a DNA-informed protocol, including a Mediterranean-style diet and individually selected supplements. Genetic information provided context for the care plan; this case does not demonstrate that a genetic risk was removed or that dementia was prevented. Her KDM-13 score fell by 1.5 years, and her PhenoAge score by 2.52 years.
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The recorded results
| Biomarker | Aug 2025 | Jan 2026 | Change |
|---|---|---|---|
| Metabolic | |||
| HOMA-IR | 1.4 | 0.7 | −50% |
| Fasting Insulin (µIU/mL) | 6.87 | 3.61 | −47% |
| Fasting Glucose (mg/dL) | 81 | 81 | Stable |
| Uric Acid (mg/dL) | 5.1 | 4.2 | −18% |
| Inflammation & Liver | |||
| hs-CRP (mg/L) | 1.22 | 0.64 | −48% |
| Homocysteine (µmol/L) | 10.7 | 7.84 | −27% |
| GGT (U/L) | 17 | 9 | −47% |
| Cardiovascular | |||
| ApoB (mg/dL) | 98 | 87 | −11% |
| Triglycerides (mg/dL) | 116 | 81 | −30% |
| HDL (mg/dL) | 63.4 | 58.4 | Slight dip |
| Nutrition & Methylation | |||
| Folate (ng/mL) | 9.85 | 17.79 | +80% |
| Homocysteine (µmol/L) | 11 | 7.84 | −29% |
| Ferritin (ng/mL) | 18 | 33 | +83% |
| Hormonal (significant) | |||
| Estradiol (pg/mL) | 38.67 | 65.08 | +68% |
| Progesterone (ng/mL) | 0.47 | 2.07 | +340% |
| DHEA-S (µg/dL) | 173.12 | 179.34 | +3.6% |
| Biological Age | |||
| KDM-13 Biological Age | 34.9 yrs | 33.4 yrs | −1.5 yrs |
| PhenoAge | 28.21 yrs | 25.69 yrs | −2.52 yrs |
Figures are reproduced from the case record, including qualitative entries and reported percentage changes. Source labels such as optimal describe the case’s interpretation, not a universal reference range. A dash indicates a value not supplied.
Context that matters
- K.A.R.’s age is not provided in the original case. No chronological age has been inferred.
- The source table contains two homocysteine baseline entries: 10.7 to 7.84 µmol/L with a 27% reduction, and 11 to 7.84 µmol/L with a 29% reduction. Both original entries are retained in the table; the record does not establish whether 11 is rounding or a separate value.
- Estradiol is reported at 38.67 then 65.08 pg/mL and progesterone at 0.47 then 2.07 ng/mL. Cycle timing and other sampling context are not supplied, so these are reported values rather than proof of a specific hormonal effect.
- The original’s PhenoAge headline rounds the 2.52-year change to 2.5 years. KDM-13 is the separate 1.5-year change.
- The source describes a future plan to consider pTau-217 testing at age 50. It is not a result already obtained.
The recorded protocol
The following items are recorded in this person’s plan. This is a historical description, not a protocol for readers to copy.
- Omega-3 EPA/DHA 2g daily (brain inflammation, ApoB)
- Berberine (ApoB, insulin sensitivity)
- L-Methylfolate sublingual (MTHFR, homocysteine)
- Methylcobalamin B12 sublingual
- Vitamin D3+K2 (inflammation, hormonal, brain)
- Creatine 5g daily (low creatine metabolism — DNA confirmed)
- Magnesium Bisglycinate (sleep, cortisol, insulin sensitivity)
- Iron Bisglycinate (ferritin restoration)
- Zinc Bisglycinate (immune, hormonal)
- Mediterranean-style diet (TCF7L2 & APOE4 directed)
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What remained in progress
ApoB at 87 mg/dL remained above the case’s stated target below 80 mg/dL. Ferritin rose from 18 to 33 ng/mL but remained below the source’s stated 70–120 ng/mL range. The record describes continued lipid and iron support. These targets belong to this individual plan and should not be used to self-prescribe treatment.
Reading the biological-age result
Biological-age scores are model outputs derived from the inputs available to that model. A lower score is not a measured gain in lifespan. Different models use different inputs and should be labelled and interpreted separately.
Does this case show that APOE-related risk was eliminated?
No. The record shows changes in measured blood markers during a DNA-informed plan. It does not measure a change in this person’s lifetime dementia risk or demonstrate prevention of a future diagnosis.
How this connects to EVA
EVA connects blood testing, clinician-reviewed personalised supplements and follow-up. Blood Intelligence uses your blood results; Elite DNA + Blood adds genetic information. DNA is optional. The aim is a personal plan grounded in your information, with review as new results become available.
Understand where DNA could add context
If you are considering DNA alongside blood testing, explore what each can contribute to a clinician-reviewed personal plan.
See how to start with EVAExplore blood testing, optional DNA and personalised supplements, with the current steps to get started in Dubai.
This is an individual observational case, not a controlled trial. Biomarker changes and biological-age scores do not establish the effect of a particular supplement, predict an individual’s lifespan or guarantee future results. The protocol described was personalised and is not a recommendation to self-prescribe. EVA supports informed health decisions and is not intended to diagnose, treat, cure or prevent disease. Consult a qualified healthcare provider for medical advice.
Source: EVA clinical case record supplied for publication. Observation dates and model names are shown in the case. Prepared for web publication in October 2026.