Alzheimer's and Ketones: The Coconut Oil That Doesn't Slow the Disease

Ketones vs. Alzheimer's: When the Brain Stops Eating Glucose

A 79-year-old woman wakes up not recognizing her husband or the house she lives in. Half an hour after taking four tablespoons of coconut oil, she remembers everything again. The episode is not a clinical trial; it is the testimony that fuels a hypothesis that has been circulating for years outside of impact journals: that Alzheimer's is, first and foremost, a problem of brain fuel.

The theory, in short: neurons can be fueled by glucose or ketones. When the brain develops insulin resistance, it loses access to that glucose and begins to starve. Some call it, without much rigor, "type 3 diabetes." And if the problem is fuel, the solution would not be a single drug, but changing the pump.

The Amyloid Plaque Fraud and 16 Years Going in the Wrong Direction

For nearly two decades, cutting-edge Alzheimer's research has focused on removing amyloid plaque from the brain. According to information released about amyloid protein research, that effort was partly based on manipulated results. Whether the target was correct or not is another discussion, but what is certain is that drugs approved along this line have yielded results that are between discrete and non-existent.

The counterargument circulating is compelling: if at least 36 factors influence cognitive decline, there is no single pill capable of keeping the brain on the right side of the scale. It is argued, along these lines, that the large pharmaceutical industry, working at the molecular level, has already lost that war. It is a seductive thesis. And like all seductive theses, it requires proof that is still scarce.

Glucose 112 → 84: The Analyses That Did Change

This is where the matter stops being philosophy and numbers appear. A documented case of a 79-year-old patient, subjected to coconut oil, vitamins, and a diet without bread or yogurt for a month, showed notable analytical changes between February and August 2022: glucose from 112 to 84 mg/dL, LDL from 163 to 111, triglycerides from 84 to 61, and vitamin D from 9.5 to 29.6 ng/mL. Ferritin dropped from 85.1 to 40.6.

The complete breakdown of these markers—including iron, B12, and HDL—paints a picture that is more surprising than the official narrative admits. However: improving analyses is not reversing dementia. They are two different things, and it is important not to confuse them, even if the temptation is enormous when the patient is your mother.

The Case That Doesn't Pan Out: When Coconut Oil Slows Nothing

Because there are also counterexamples, and they are what lend credibility to the whole. A family administered coconut oil for an entire year to a 93-year-old patient. The disease continued to pogre the same way. The woman, moreover, had never taken a pill and had always had impeccable test results. If the blood marker were the key, it should have worked there. It didn't.

And the uncomfortable detail continues: clinical consensus holds that when symptoms appear, it is already too late. That is the wall against which everything crashes, coconut oil, the ketogenic diet, and any laboratory promise.

From Coconut Oil to NAD+: P7C3-A20 and Anavex

The conversation doesn't stay in the kitchen. The focus has shifted towards compounds that restore NAD+ balance in the brain. In animal models, a compound called P7C3-A20 has managed to pharmacologically reverse advanced Alzheimer's, and some are closely watching the development of the biotech company Anavex and its pathway via the sigma-1 receptor. The problem, as almost always, is funding: it is difficult to find money to study what cannot be patented.

In parallel, other fronts are emerging. A team from Baylor College of Medicine described in October 2023 that when the brain is infected with a common fungus, it changes in a way similar to what is observed in Alzheimer's. Fungal infection thus joins the list of suspects, along with inflammation and the aforementioned energy metabolism.

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What if memories are not erased, but the key to accessing them is simply lost? An MIT study suggests that retrograde amnesia could be an access problem, not a storage problem. If that were true, reversibility would cease to be science fiction. The question today is whether anyone is willing to pay for the trial to prove it.