Dementia prevention · early testing

Dementia Prevention Starts With Numbers You Can Measure Now

Before symptoms, measure fasting insulin as its own number, a formal memory and thinking score, fat versus muscle, and B12 and omega-3 status, and screen for sleep apnea. A routine checkup rarely includes any of them.

A dementia diagnosis is a late milestone, not the start of the disease. The quiet years before it are when measurement helps most, and when almost nobody thinks to ask for it.

Dementia prevention has a timing problem. The changes that lead to memory loss build for years while you feel fine, and by the time something is clearly wrong, the window for correction has narrowed. In the final video of The Starved Brain, You Can Protect a Struggling Neuron, Dr. Gurpreet Singh Padda, MD, MBA, MHP, reduces it to one idea: a struggling nerve cell can be protected, a lost one cannot be brought back. Measura [Cardiometabolic and Autonomic Health Analysis] exists for the part of that problem you can act on today, which is knowing your numbers before a diagnosis delivers them for you.

Why check dementia risk before symptoms?

When the process is most reversible, very little seems wrong. You misplace your keys, lose a word now and then, and someone says it is normal for your age. Nobody orders anything, because there is nothing to chase. Compare that with blood pressure, cholesterol and colon cancer screening, where everyone accepts that catching a problem early is the whole point. The brain has not been given the same logic, partly because the system organizes itself around diagnoses, and this diagnosis arrives late.

Dr. Padda counts himself among the reassurers. He spent years telling patients with prediabetes that an A1c like theirs was “not too bad.” He changed his practice when the physiology showed him that the number he was using to reassure people was the last one to move.

What raises dementia risk years before symptoms?

The first driver is insulin resistance. In the Whitehall II study of 6,538 British civil servants, insulin sensitivity was already falling about five years before a diabetes diagnosis, while fasting glucose held steady until roughly three years out. Glucose is a late witness. Fasting insulin, reported as its own number, catches the slide sooner. Dr. Padda’s clinic treats a fasting insulin above 10 µIU/mL as a high-risk finding; that is his practice cutoff, not a laboratory standard.

The second driver is the supply of repair materials and the inflammation that wears them down. In the VITACOG trial of older adults with mild cognitive impairment, B vitamins slowed brain shrinkage by 40 percent, but only in people whose omega-3 levels were already in the top third. In the bottom third, the same vitamins did nothing measurable. One nutrient’s benefit depended on another nutrient nobody had checked.

The third driver sits on the grocery shelf. In a cohort of 72,083 British adults, every 10% of the diet that came from ultra-processed food was tied to roughly a quarter more dementia risk. That is an observational link, not proof of cause, but it points at a food supply engineered for shelf life and repeat purchase rather than for the brain eating it.

What does a routine checkup leave out?

A standard physical checks fasting glucose, A1c, a basic cholesterol panel and blood pressure. Those matter. What it rarely includes:

• Fasting insulin reported on its own, not folded into a calculation.
• A formal memory and thinking score, recorded while nothing is wrong.
• A breakdown of fat and muscle, rather than weight alone.
• Functional markers of how the B12 and omega-3 systems are working.
• A screen for sleep apnea, which in one Wisconsin study went undiagnosed in 82% of men and 93% of women with moderate-to-severe disease.

None of these is exotic. Each one is simply not the default.

The measurements Measura can add

Measura measures; it does not diagnose dementia or treat it, and your results go to your physician. Within that role, several tests speak directly to the terrain described above:

• Laboratory panels capture the blood markers behind the metabolic picture, and they are the place to ask that fasting insulin be reported as a number.
• Cognitive assessment sets a baseline. The US Preventive Services Task Force found insufficient evidence to screen adults over 65 who have no symptoms, but a baseline for someone with a concern serves a different purpose: it is the number the next number gets compared with.
• Bioimpedance body composition separates fat from lean mass. Waist size is a rough stand-in for the fat around your organs, and muscle is the tissue that soaks up glucose, so knowing both compartments adds detail a tape measure cannot.
• Autonomic nervous system testing describes how your body regulates heart rate and blood pressure. That baseline matters for anyone on blood pressure medication, because cutting carbohydrate sheds sodium and water, and dizziness on standing is often the first sign a dose needs review by the prescriber.

Sleep studies and dental exams are done elsewhere, and both belong on the list.

How often should you repeat these tests?

One set of results is a snapshot. The value comes from the repeat. Insulin, glucose and triglycerides move within weeks of a real change in eating; homocysteine takes months; the omega-3 index takes closer to six months to settle; hs-CRP is the slowest and least reliable of the group. A sensible rhythm is about three months for the fuel markers and six months for the rest. Plan the timing with your physician, and read how often to repeat cardiometabolic testing.

Safety comes before any diet change. People taking insulin or a sulfonylurea can drop to dangerously low blood sugar quickly when they restrict carbohydrate, and an SGLT2 inhibitor combined with carbohydrate restriction can cause ketoacidosis while glucose looks normal. Those decisions belong to the prescribing physician before the first meal changes. Do not adjust a medication on your own.

How much can dementia prevention do at each stage?

Prevention, before symptoms, is where correcting the terrain has the most room. Early impairment still has real room: the vitamin and ketone trials that showed benefit were in mild cognitive impairment and mostly mild-to-moderate Alzheimer’s disease. Advanced disease calls for humility. In one small pilot, all 4 participants with moderate Alzheimer’s withdrew, each citing caregiver burden, and a study of 37,717 people in Korea found that those who were underweight after their dementia diagnosis had a hazard ratio of 1.57 for death. For someone with advanced dementia, a restrictive diet that causes weight loss can do real harm, which is why that decision rests with a physician who knows the patient.

The numbers are where your agency lives

Unmeasured is unmanaged. You cannot feel insulin resistance, a low omega-3 status or a memory score that has not dropped yet, but you can know them. Ask for the numbers while nothing is wrong, keep a copy, and repeat them. The trial-by-trial evidence and a list of questions for your physician are in the Chapter 10 companion evidence guide. The evidence on ketogenic therapy itself is in what the keto diet does and does not do for Alzheimer’s, and who should be tested explains where to begin.

Frequently asked questions

References

• Tabák, A. G., Jokela, M., Akbaraly, T. N., Brunner, E. J., Kivimäki, M., & Witte, D. R. (2009). Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. The Lancet, 373(9682), 2215–2221. https://doi.org/10.1016/S0140-6736(09)60619-X
• Jernerén, F., Elshorbagy, A. K., Oulhaj, A., Smith, S. M., Refsum, H., & Smith, A. D. (2015). Brain atrophy in cognitively impaired elderly: The importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial. American Journal of Clinical Nutrition, 102(1), 215–221. https://doi.org/10.3945/ajcn.114.103283
• Li, H., Li, S., Yang, H., Zhang, Y., Zhang, S., Ma, Y., Hou, Y., Zhang, X., Niu, K., Borné, Y., & Wang, Y. (2022). Association of ultraprocessed food consumption with risk of dementia: A prospective cohort study. Neurology, 99(10), e1056–e1066. https://doi.org/10.1212/WNL.0000000000200871
• Young, T., Evans, L., Finn, L., & Palta, M. (1997). Estimation of the clinically diagnosed proportion of sleep apnea syndrome in middle-aged men and women. Sleep, 20(9), 705–706. https://doi.org/10.1093/sleep/20.9.705
• US Preventive Services Task Force (Owens, D. K., Davidson, K. W., Krist, A. H., Barry, M. J., Cabana, M., Caughey, A. B., Doubeni, C. A., Epling, J. W., Kubik, M., Landefeld, C. S., Mangione, C. M., Pbert, L., Silverstein, M., Simon, M. A., Tseng, C.-W., & Wong, J. B.). (2020). Screening for cognitive impairment in older adults: US Preventive Services Task Force recommendation statement. JAMA, 323(8), 757–763. https://doi.org/10.1001/jama.2020.0435
• Huh, Y., Nam, G. E., Han, K., Jung, J.-H., Kim, B. S., Lee, D., Park, H. J., Yoo, M. Y., Yoon, S. Y., Kang, S. H., Kim, C. K., Kim, S. M., & Park, H. S. (2026). Body mass index levels and changes before and after dementia diagnosis and risk of all-cause mortality: A nationwide cohort study. Alzheimer’s Research & Therapy, 18(1), article 10.1186/s13195–026–02002–x (page not assigned in PubMed record). https://doi.org/10.1186/s13195-026-02002-x
• Taylor, M. K., Sullivan, D. K., Mahnken, J. D., Burns, J. M., & Swerdlow, R. H. (2018). Feasibility and efficacy data from a ketogenic diet intervention in Alzheimer’s disease. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 4, 28–36. https://doi.org/10.1016/j.trci.2017.11.002
• Johnson, J. L., Duick, D. S., Chui, M. A., & Aldasouqi, S. A. (2010). Identifying prediabetes using fasting insulin levels. Endocrine Practice, 16(1), 47–52. https://doi.org/10.4158/EP09031.OR
• Leslie, W. S., Ali, E., Harris, L., Messow, C. M., Brosnahan, N. T., Thom, G., McCombie, E. L., Barnes, A. C., Sattar, N., Taylor, R., & Lean, M. E. J. (2021). Antihypertensive medication needs and blood pressure control with weight loss in the Diabetes Remission Clinical Trial (DiRECT). Diabetologia, 64(9), 1927–1938. https://doi.org/10.1007/s00125-021-05471-x
• Peters, A. L., Buschur, E. O., Buse, J. B., Cohan, P., Diner, J. C., & Hirsch, I. B. (2015). Euglycemic diabetic ketoacidosis: A potential complication of treatment with sodium–glucose cotransporter 2 inhibition. Diabetes Care, 38(9), 1687–1693. https://doi.org/10.2337/dc15-0843

Related reading

• Keto Diet and Alzheimer’s: What to Measure Before You Believe It
• Laboratory Panels

Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP, medical director of Measura. Last reviewed September 12, 2026.