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The two things my DNA told me that eleven years of blood tests never could

Times of India Published Jul 9, 2026 Reviewed Jul 12, 2026 ✓ Reviewed by citations.press editors
In August 2015, at age 43, a coronary calcium scan showed a score of 266, placing him in the 98th percentile for his age.
266 score · coronary calcium scan98 percentile · percentile ranking Nickhil Jakatdar, author
He has taken 20 mg of rosuvastatin every day.
20 mg · rosuvastatin dose Nickhil Jakatdar, author
His LDL‑C remains above the under‑50 mg/dL target recommended for someone with his cardiovascular risk.
less than 50 mg/dL · LDL‑C target Nickhil Jakatdar, author

By Nickhil Jakatdar, Ph. D.I thought eleven years of blood tests had answered the important questions about my health. I was wrong.Readers of my blogs know the backstory: in August 2015, In 2015, at the age of 43, a coronary calcium scan showed a score of 266, placing me in the 98th percentile for my age.

Since then, I've taken 20 mg of rosuvastatin every day. It has worked well. My LDL-C and ApoB have fallen significantly, and I assumed I already knew everything important about how my body responded to treatment. Then I sequenced my genome as part of my Mira One report, which combines bloodwork, pharmacogenomics, and whole-exome sequencing into a single picture.

I wasn't expecting any surprises. But I found two.The first was about my statin. The report showed that my body processes rosuvastatin more slowly than average because of a variant in a gene called ABCG2. At my current dose, that's not a problem. But my LDL-C is still above the under-50 mg/dL target recommended for someone with my cardiovascular risk.If my LDL-C remains above target in the future, one option my cardiologist might naturally consider is increasing the dose.

But my genetics suggest that may not be the best approach. Because my body clears rosuvastatin more slowly, a higher dose could expose me to much more of the drug than expected. The better strategy may be a different approach chosen with my cardiologist. The test didn't change what I take today but did change how I'll think about future treatment decisions with my doctor.The second finding was about another habit that's been part of my routine for years.

I've practiced intermittent fasting for a long time. Like many people interested in longevity, I believed it was almost universally beneficial.But my genome told me a different story.It showed me that I carry a variant associated with Gilbert syndrome. This is a common and generally harmless condition in which the liver clears bilirubin more slowly than average.

And one of the most reliable things that raises bilirubin in people with Gilbert syndrome is prolonged intermittent fasting.That doesn't mean fasting is bad. It means my body responds to it differently.When I considered that alongside everything else I ask of my body (walking around 15 km a day during calls, playing intense soccer twice a week, and averaging about 6.5 hours of sleep), I realized I was stacking another source of physiological stress onto an already demanding routine.

What may be an excellent strategy for someone else wasn’t necessarily the best one for me.Neither of these findings was dramatic but they were rather nuanced and fine. I didn't discover a rare disease or need a new prescription overnight. But I avoided making what could have been the wrong medication decision, and I stopped assuming that one of my longevity habits was automatically the right fit for my biology.That was my biggest takeaway: Blood tests showed me where I was.

My DNA helped explain why I was there, and how I should think about the road ahead. Medicine is built around the average patient. The challenge is that none of us is average. Sometimes the most valuable thing a genetic test gives you isn't a diagnosis but the confidence to stop treating yourself like everyone else.Get the latest movie news, reviews, and celebrity updates.

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