- 4 hours ago
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When a loved one is diagnosed with Parkinson’s, Alzheimer’s or motor neurone disease (MND/ALS), life suddenly feels like it’s happening in slow motion. Movements become smaller. Words arrive a bit later. Energy fades. Beneath those changes, the brain is quietly struggling with something very simple and very brutal: it cannot make enough energy from its usual fuel.
This is where the ketogenic diet steps onto the stage. It’s often sold online as a miracle: “fuel your brain with fat, fix your mitochondria, reverse decline.” The science is far more interesting, far more hopeful than click-bait headlines – and also far more complicated.
The big question is not “Is keto good or bad?”
It’s: “Can this way of eating be a friend or foe for this brain, in this body, at this stage of disease?”
Let’s walk through what we actually know – and what we definitely don’t – in plain English, but anchored all the way in hard science.
When the brain’s favourite fuel starts to fail
Under normal circumstances, your brain runs almost entirely on glucose. Think of glucose as the electricity supply for a city: constant, tightly regulated and absolutely essential. In neurodegenerative diseases, that electrical system begins to flicker.
Brain scans in Alzheimer’s disease show a drop in glucose use in key areas for memory long before severe symptoms appear (Mujica-Parodi et al., 2020). Parkinson’s disease (PD) has its own pattern of reduced glucose metabolism in the motor and frontal networks that govern movement and thinking (Krikorian et al., 2019). ALS/MND is deeply linked to dysfunction and oxidative stress – essentially, the tiny power stations inside neurones (mitochondria) are damaged and leak “sparks” in the form of reactive oxygen species (ROS), highly reactive oxygen-containing molecules that can damage cells (Tefera & Borges, 2017; Manoharan et al., 2016).
At the same time, inflammation and misfolded proteins are adding fuel to the fire. Oxidative stress and mitochondrial failure are now recognised as central features of neurodegeneration in both Alzheimer’s and Parkinson’s (Maalouf, Rho, & Mattson, 2009; Manoharan et al., 2016). Dopamine-producing neurones in Parkinson’s are especially vulnerable because they are metabolically “expensive” cells – they fire rhythmically, handle large calcium loads and sit right at the edge of energetic burnout (Tieu et al., 2003).
So we have a brain that:
• struggles to use glucose
• is flooded by oxidative stress
• and has overworked mitochondria trying to keep the lights on
This is exactly the environment where ketones start to look attractive.
What a ketogenic diet actually is – beyond internet buzzword
The ketogenic diet is often reduced online to “cut carbs, eat bacon”, but medically it means something very specific. It refers to any dietary approach that reliably raises levels of ketone bodies in the blood - particularly beta-hydroxybutyrate (β-HB) - into a range called nutritional ketosis (about 0.5–4.0 mmol/L) (Murray et al., 2016; Murray et al., 2024). Ketone bodies are molecules made from fat, and they can act as an alternative fuel for the brain when glucose is low or when the brain cannot use glucose efficiently - which is exactly what happens in many neurodegenerative diseases.
To enter this metabolic state, carbohydrate intake must be reduced enough that the liver shifts from burning glucose to burning fat. As the liver breaks down fatty acids, it produces three ketone bodies: acetoacetate, β-HB and acetone. These travel through the bloodstream and can cross into the brain through specialised transporters. Once inside neurones, ketones are converted into energy inside the mitochondria - the cell’s power stations - bypassing some of the pathways that become impaired in Parkinson’s, Alzheimer’s and motor neurone disease.
The classic therapeutic ketogenic diet used in epilepsy is extremely strict: around 90 per cent of daily calories from fat, with only 5–10 per cent from carbohydrate and the rest from protein (Włodarek, 2019; Kossoff & Hartman, 2012). This is a dramatic shift from a typical Western diet, where carbohydrate usually provides more than half of daily energy intake. Over time, newer versions were developed to make ketosis more achievable: the Medium-Chain Triglyceride (MCT) ketogenic diet, the Modified Atkins Diet (MAD) and low-glycaemic index plans. All aim to produce ketones but allow slightly more flexibility and a broader range of foods (Paoli, 2014; Włodarek, 2019).
Ketosis can also be reached without such strict restriction by using exogenous ketones -drinks or esters that supply β-HB directly to the bloodstream (Stubbs et al., 2015; Clarke et al., 2012). These do not replace dietary interventions entirely, but they can help raise ketone levels when dietary changes are difficult or medically inappropriate.
The key point is this: ketogenic therapy is not about a specific list of foods. It is about shifting the body into a different metabolic state — one where ketones, rather than glucose, become a major source of energy for the brain.
Why scientists think keto might help a degenerating brain
Once ketones circulate in the body, a series of changes unfold - and this is where the neurodegeneration story becomes especially interesting.
First, ketones give struggling brain cells an alternative fuel. One ketone in particular, beta-hydroxybutyrate (β-HB), produces energy more efficiently than glucose. It creates more ATP - the “energy currency” inside every cell - for every unit of oxygen used. For neurones that are already running on empty, this efficiency matters enormously (Maalouf et al., 2009; Włodarek, 2019).
In laboratory models of Alzheimer’s and PD, ketones can even “rescue” neurones exposed to toxins that damage their mitochondria. These toxins specifically disrupt complex I — the first “step” in the mitochondria’s energy-production line. Think of complex I as the ignition switch that starts the whole energy-making engine. When it fails, the cell stalls and produces more oxidative stress. Ketones appear to support this system, helping neurones survive longer and function better (Kashiwaya et al., 2000; Tieu et al., 2003).
Second, ketones help reduce oxidative stress - the biochemical equivalent of rust. When the body burns less glucose and shifts towards fat metabolism, more glucose is redirected into a protective side-pathway that makes nicotinamide adenine dinucleotide phosphate (NADPH). NADPH is essential for recharging glutathione, the brain’s most powerful antioxidant (Maalouf et al., 2009; Bolliri & Barreto, 2020). Studies in animals show that ketogenic diets boost glutathione and the enzymes that work with it, effectively strengthening the brain’s internal “fire brigade” (Ziegler et al., 2003).
Third, ketones are also signalling molecules - tiny messengers that switch certain inflammation pathways on or off. β-HB can calm two major inflammatory systems, NF-κB and the NLRP3 inflammasome. These function like alarm sirens inside the brain: useful when danger is present, damaging when they keep blaring. Ketones help quieten these alarms, reducing inflammatory activity in microglia — the brain’s resident immune cells (Fu et al., 2015; Murray et al., 2024). Ketones also increase levels of brain-derived neurotrophic factor (BDNF), a protein often described as “fertiliser” for neurones because it strengthens connections and supports resilience (Maalouf et al., 2009; Murray et al., 2024).
Fourth, in Alzheimer’s studies, ketogenic interventions have reduced harmful proteins — such as amyloid-β and phosphorylated tau - while improving memory in animals (Van der Auwera et al., 2005; Kashiwaya et al., 2013). These benefits likely come from the same mechanisms: steadier mitochondria, less oxidative stress and calmer inflammation.
Finally, the gut–brain axis plays a major role, particularly in PD. Many people with Parkinson’s show gut dysbiosis - fewer beneficial, short-chain-fatty-acid (SCFA) producing bacteria, more inflammatory microbes and a leakier gut lining. This imbalance can increase inflammation throughout the body and may even contribute to abnormal α-synuclein folding in the nervous system (Scheperjans et al., 2015; Sampson et al., 2016). SCFAs such as butyrate help keep the gut barrier healthy and modulate immune signalling. Ketogenic diets have been shown in animals to shift the microbiome toward a healthier balance - and astonishingly, faecal transplants from keto-fed mice can transfer some of these protective effects to other animals (Jiang et al., 2023).
So on paper - and especially in controlled laboratory settings - ketones appear to act as a multi-tool: alternative energy, stronger antioxidant defences, calmer immune activity, fewer misfolded proteins, more BDNF and a healthier gut environment.
But the real question remains: what happens in humans living with these diseases, outside the laboratory?
What human studies tell us – and what they don’t
Human evidence is growing, but it is still early days.
In Alzheimer’s disease and mild cognitive impairment, several trials of MCT drinks and modified ketogenic diets have shown small to moderate improvements in memory and global cognition, especially in people without the APOE4 gene variant (Reger et al., 2004; Henderson et al., 2009; Ota et al., 2018; Taylor et al., 2017). APOE4 is a version of a cholesterol-transport gene linked to higher risk of Alzheimer’s and cardiovascular disease. One study found that even a short, very low-carbohydrate diet improved verbal memory in adults at risk of Alzheimer’s, with higher ketone levels correlating with better performance (Krikorian et al., 2012).
In PD, the picture is similar but more nuanced. An early feasibility study using a very strict 4:1 ketogenic diet for four weeks saw 5 of 5 completers improve their Unified Parkinson’s Disease Rating Scale (UPDRS) scores, but the study was small, unblinded and difficult to interpret (Vanitallie et al., 2005). A better-designed randomised trial compared a low-fat diet with a more moderate ketogenic diet in 47 people over eight weeks. Both groups improved overall, but the ketogenic group had a much larger reduction in non-motor symptoms – things like urinary urgency, pain, cognitive fog and daytime sleepiness (Phillips et al., 2018). Motor scores, however, did not differ significantly between groups.
A separate trial in people with Parkinson’s and mild cognitive impairment found that a low-carbohydrate, ketone-producing diet improved working memory and verbal fluency, again without clear motor changes (Krikorian et al., 2019). Another small study showed that nutritional ketosis over 12 weeks reduced anxiety scores and improved non-motor experiences of daily living, alongside better blood sugar markers (Tidman et al., 2021). More recently, a short inpatient study combining a modified ketogenic diet with MCT oil found that most participants could tolerate the diet for three weeks, reported improved non-motor symptoms and achieved stable ketosis, but objective motor outcomes changed little over that time (Choi et al., 2024).
In ALS/MND, evidence is mostly pre-clinical, but ketogenic diets and ketone esters have shown neuroprotective effects in animal models of motor neurone degeneration, improving survival and motor performance while reducing oxidative damage (Zhao et al., 2006; Bolliri & Barreto, 2020). Human data here are still extremely limited.
The pattern that emerges is this:
Ketogenic approaches seem particularly good at lifting non-motor symptoms, cognitive function and metabolic health, but we have far less proof that they slow disease progression or meaningfully improve long-term motor outcomes.
Trials have been short (4–12 weeks), small and sometimes non-blinded. That doesn’t mean ketogenic strategies don’t help; it means we must hold both hope and humility at the same time.
When keto becomes a foe: risks in a vulnerable brain and body
The same mechanisms that make ketogenic diets powerful can also make them risky – especially for older adults and those already losing weight.
High-fat ketogenic diets often suppress appetite and reduce overall calorie intake. In children with epilepsy this can be useful; in someone with Parkinson’s, dementia or ALS/MND who is already struggling to maintain weight, it can be dangerous. Weight loss, loss of muscle mass (sarcopenia) and frailty are all linked to faster decline and poorer outcomes in neurodegenerative disease (Włodarek, 2019; Bauer et al., 2013).
Classical ketogenic diets and their variants have well-documented side effects: nausea, vomiting, constipation, abdominal pain, diarrhoea, dehydration, kidney stones, dyslipidaemia (unfavourable cholesterol changes), micronutrient deficiencies, reduced bone mineral density and, in some cases, liver or pancreatic stress (Nazarewicz, 2007; Paoli, 2013; Włodarek, 2019). In Parkinson’s, constipation and gut dysmotility are already major problems; a high-fat, low-fibre diet can easily make them worse. Many patients in PD ketogenic trials report transient worsening of tremor, fatigue, headaches and “keto flu” symptoms in the first weeks (Phillips et al., 2018; Tidman et al., 2021).
There is also a medication angle. Levodopa absorption and transport into the brain compete with other amino acids from protein. Some ketogenic protocols deliberately lower protein to improve levodopa effectiveness, but if this is taken too far, it risks accelerating muscle loss and worsening frailty (Vanitallie et al., 2005; Phillips et al., 2018). On the flip side, a high-protein keto diet could interfere with levodopa’s action and undermine symptom control.
And then there is the question: what are you leaving out to make room for all that fat? Strict keto often displaces wholegrains, legumes, many fruits and some vegetables - all rich in fibre, B-vitamins, magnesium, polyphenols and prebiotics that feed the gut microbiome. Given that gut health and SCFAs like butyrate are strongly linked to inflammation, barrier integrity and even brain function, this is not a trivial cost (Scheperjans et al., 2015; Jiang et al., 2023).
For a robust, metabolically healthy 40-year-old, these trade-offs may be manageable. For an 80-year-old with Parkinson’s, weight loss, swallowing difficulties and osteoporosis, they may not be.
Why one-size-fits-all keto fails: the case for nutrigenomics
Not all bodies burn fat, handle ketones or manage cholesterol in the same way. Our genes quietly shape how we respond to any diet - and ketogenic diets are no exception.
Variants in genes that govern lipid transport, fatty acid desaturation, insulin sensitivity, mitochondrial function, detoxification and inflammatory signalling can all change how safe or effective a high-fat, low-carb pattern will be. APOE4, for example, is associated with altered lipid handling and higher cardiovascular and Alzheimer’s risk. Some studies suggest that people who carry APOE4 respond less consistently to MCT-based ketogenic therapies for cognition (Henderson et al., 2009). Other polymorphisms may affect how well someone generates ketones, recycles glutathione or regulates inflammatory pathways like NF-κB.
This is the realm of nutrigenomics - understanding how nutrition interacts with an individual’s genetic landscape. It doesn’t mean genes are destiny; it means they provide a map of where the road is smooth and where it might be full of potholes.
At You Nutrition Clinic, this is exactly where we start. We look at each person’s story: their diagnosis, medications, weight history, gut function, blood markers and, when available, their genetic data. We ask not, “Can you do keto?” but, “Is a ketogenic or ketone-supported strategy appropriate for you – and if so, in what form, at what intensity, and for how long?”
Sometimes the answer is a carefully supervised classical ketogenic protocol. Sometimes it is a softer, metabolically mindful pattern: lower in refined carbohydrates, higher in fibre and healthy fats, using MCTs or exogenous ketones to gently raise β-HB without severe restriction. Sometimes, ketogenic strategies are not appropriate at all – and the focus shifts to Mediterranean-style, anti-inflammatory nutrition, optimising blood sugar, micronutrients and the gut–brain axis instead.
Ketotarian: borrowing the best of keto without losing the plants
This is where the idea of ketotarian eating becomes especially interesting for neurodegenerative conditions.
Instead of centring the diet on meat, butter and cream, ketotarian approaches are largely plant-based or plant-forward. They aim to keep carbohydrates low enough to allow mild ketosis, but they do it with:
• abundant non-starchy vegetables
• olive oil and other extra-virgin plant oils
• nuts, seeds and avocados
• fermented foods, herbs and spices
• and – depending on the individual – modest amounts of eggs, fish or other carefully chosen animal products
From a science perspective, this allows you to harness some of the metabolic benefits of ketones - alternative fuel, reduced glycaemic load, improved insulin sensitivity - while still feeding the microbiome with fibre and polyphenols, supporting SCFA production, and providing folate, magnesium, vitamin K and other micronutrients that can be lost on very low-plant ketogenic diets (Paoli, 2013; Jiang et al., 2023).
For someone with Parkinson’s who has constipation, early weight loss and a family history of heart disease, a strict 4:1 ketogenic pattern might be too blunt an instrument. A personalised, ketotarian pattern, possibly layered with time-restricted eating or gentle overnight fasting where appropriate, might deliver a more balanced combination of brain fuel and long-term safety.
Again, there is no universal answer - but there is a spectrum of options between “standard Western diet” and “full medical keto”, and that is where many people with neurodegeneration may find their sweet spot.
How You Nutrition Clinic can help you navigate this
Trying to do all of this alone - while caring for someone you love, or while living with symptoms yourself - is overwhelming. The internet will happily offer you extremes. Real life requires nuance.
At You Nutrition Clinic, our role is to sit in that nuanced middle with you. To translate complex research into practical, compassionate plans. To use your biochemistry and, where appropriate, your nutrigenomic data to decide:
• whether a ketogenic, ketotarian or non-ketogenic metabolic approach is right for you
• how to protect weight, muscle and bone while experimenting with fuel sources
• how to support the gut–brain axis, antioxidant systems and inflammation alongside any dietary changes
The story of ketogenic diets and neurodegeneration is still being written. Early chapters suggest real promise, especially for non-motor symptoms, cognition and metabolic health. Later chapters will need to answer the harder questions: long-term safety, true disease modification and who benefits most – or not at all.
Those are exactly the questions we’ll explore in the next instalment.
💬 Stay Connected
If you’d like personalised, evidence-based guidance on whether a ketogenic, ketotarian or alternative metabolic approach is right for you or a loved one living with Parkinson’s, Alzheimer’s or ALS/MND, our practitioners at You Nutrition Clinic can help you navigate the science safely and compassionately.
We combine clinical assessment, biochemistry and nutrigenomic insights to create plans that protect weight, support gut health and stabilise energy — without the risks of a one-size-fits-all diet.
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