The ketogenic protocol at the centre of NKFB was not designed only for weight loss. The brain health dimension came from a different direction entirely — from watching what happens to the brain when glucose metabolism fails, and from understanding that ketones offer an alternative the brain can use when glucose no longer works.
For some people, this is the primary reason they are here.
The brain accounts for roughly 20% of the body's total energy consumption despite being 2% of its weight. On a standard diet, almost all of that energy comes from glucose. For most of a healthy life, this works. But in several neurological conditions, it stops working — not because glucose disappears, but because the brain loses the ability to use it efficiently.
In Alzheimer's disease, reduced glucose metabolism in the hippocampus and cortex is now documented to appear decades before symptoms. Some researchers describe Alzheimer's as "type 3 diabetes" — insulin resistance that has reached the brain. In Parkinson's disease, the dopaminergic neurons that die first have exceptionally high energy demands and are particularly vulnerable when energy production is impaired.
Ketones cross the blood-brain barrier through a different mechanism than glucose. They can fuel neurons that can no longer use glucose efficiently — bypassing the transport failure at the root of the problem.
This is not a fringe theory. It is a mechanistic explanation supported by a growing body of research — and, in the case of epilepsy, by a century of clinical use.
Research into MCTs and ketone supplementation shows short-term cognitive improvements in some patients with early to moderate disease. Dr. Dale Bredesen's work identifies up to 36 contributing factors — and documents cases where early intervention has reversed symptoms entirely.
A pilot study by VanItallie et al. showed significant reductions in tremor and motor symptoms in patients on a ketogenic diet for 28 days. Mitochondrial dysfunction in dopaminergic neurons is the proposed mechanism.
MS involves the progressive destruction of the myelin sheath surrounding nerve fibres. Neuroinflammation is central to this process — and ketogenic nutrition has documented anti-inflammatory effects on the central nervous system. Early intervention, before myelin damage becomes irreversible, is where the evidence is most promising.
The ketogenic diet has been used as a treatment for drug-resistant epilepsy since the 1920s. The strongest and longest-established evidence base — proof of concept for ketone-based neurological intervention.
Neurological decline is not binary. It is a continuum. The metabolic dysfunction that characterises Alzheimer's and Parkinson's does not appear at diagnosis — it builds over decades beforehand.
This means the relevant question is not only whether ketosis can help people who already have these conditions. It is whether maintaining ketosis over time reduces the risk of developing them.
The epidemiological evidence is not yet definitive. But the mechanistic case is coherent: reduced neuroinflammation, improved mitochondrial function, reduced oxidative stress, and an alternative fuel source for neurons that are under metabolic stress before they visibly fail.
If you have a family history of neurological disease, or are simply paying attention to what healthy ageing actually requires, the brain health dimension of the NKFB protocol is worth understanding.
Read: Why Age-Related Disease Is Not Inevitable →The pharmaceutical industry operates on a one-cause, one-solution model. Identify a target, develop a drug, run a trial. For infectious disease, this works well. For chronic neurological conditions — which are multi-factorial, metabolic, and develop over decades — it consistently fails.
Dr. Dale Bredesen, author of The End of Alzheimer's, has documented up to 36 distinct factors that contribute to and determine the type of dementia a person develops. His ReCODE protocol addresses these factors systematically — and has documented cases where patients with early-stage Alzheimer's have recovered measurable cognitive function. This does not fit the silver-bullet model, so most neurologists trained in conventional medical schools do not engage with it. Bredesen created the Apollo Health organisation specifically to train the doctors and health coaches who are willing to.
The same pattern repeats in multiple sclerosis. The dominant medical approach manages symptoms and slows progression. Alternative hypotheses — including the role of underlying infections in triggering and sustaining the autoimmune response that destroys the myelin sheath — are largely dismissed by establishment neurology, regardless of the evidence. I have followed this area closely, in part because of a friend I have known since childhood who has been severely affected by MS for years, living in a care facility where the neurologists in charge have no interest in alternatives.
The common thread is not conspiracy. It is institutional inertia. Doctors trained in one model have careers invested in that model. The patients who pay the price are the ones who run out of time before the model catches up.
Read: What the Research Actually Shows →Epilepsy: Ketogenic diet in clinical use since 1921. Mechanism well-documented. Established proof of concept for ketone-based neurological effect.
Alzheimer's: Henderson et al. (2009) — MCT supplementation showed significant cognitive improvement vs. placebo in ApoE4-negative patients. Mary Newport case studies and subsequent trials. Ongoing RCTs in multiple centres.
Parkinson's: VanItallie et al. (2005) — 5 patients, 28-day ketogenic diet, significant reduction in UPDRS motor scores. Followed by larger observational studies.
Gut-brain axis: Emerging research shows microbiome changes on ketogenic diets may contribute to neurological effects independent of ketone levels — potentially relevant across all three conditions.
If you are caring for someone with Parkinson's or dementia, or supporting a family member through a diagnosis, the available evidence is sufficient to justify exploring a ketogenic or modified ketogenic protocol as part of a broader management approach — with appropriate medical supervision for anyone on medication, given the interactions that can occur as metabolic status changes.
The Parkinson's Alternative Approaches booklet — written from both a pharmacological and personal perspective — goes into practical implementation, drug interactions to monitor, and how to adapt the protocol for people who may have difficulty with standard dietary changes. Currently available in German; English translation in progress.
This work is personal. My father died with serious diabetic neuropathy. The neurological consequences of metabolic disease are not abstract to me.
