Many people believe that Alzheimer’s, dementia, and cognitive decline are caused by a lack of neural activity – that the brain simply isn’t firing enough.
However, these conditions are actually driven by overexcitation.
The common conventional treatments, drugs like cholinesterase inhibitors and NMDA receptor antagonists, are designed to boost excitatory neurotransmitters acetylcholine and glutamate and stimulate nerve activity. Both acetylcholine and glutamate can become toxic when not properly cleared, overstimulating neurons and triggering oxidative stress and cell death.
This may explain why many Alzheimer’s drugs have not been very successful. They amplify the excitatory pathways that are already overactive in people with the disease.
More than anything, Alzheimer’s is a metabolic and energetic issue. Brain imaging consistently shows hypometabolism in Alzheimer’s patients, even in those with genetic risk factors like APOE4.
Alzheimer’s is often referred to as “type 3 diabetes,” a term that reflects the brain’s impaired ability to metabolize glucose. Unlike other tissues, the brain depends almost entirely on glucose for energy; it cannot use fat. In Alzheimer’s, glucose uptake declines sharply, especially in memory-related areas like the hippocampus.
Studies have found that depriving human neurons of glucose led to Alzheimer-like changes. (PMID: 37037474)
Low energy production can actually lead to overexcitation. Poor glucose metabolism in the brain deprives neurons of the fuel they need to produce ATP. Without enough ATP, the energy-dependent systems that clear excitatory neurotransmitters like glutamate and acetylcholine fail. This causes these stimulatory signals to linger in the synapse, leading to chronic overexcitation and oxidative damage. Over time, this contributes to the neurodegeneration seen in Alzheimer’s.
When the energy supply is insufficient, excitatory processes aren’t terminated properly, leading to chronic stimulation and cellular exhaustion or death. In other words, it’s not a lack of stimulation causing neuronal death — it’s too much, without the energy to shut it off.
So, anything that interrupts glucose metabolism and energy production in the brain is a potential driver of Alzheimer’s, dementia, and cognitive decline:
- hypothyroidism
- heavy metal toxicity
- thiamine deficiency
- low intake of calcium & magnesium
- iron overload in brain tissue
- low progesterone
- high intake of PUFAs
- traumatic brain injury
A more effective approach would be to address these factors and improve energy metabolism in the brain.
To support glucose metabolism:
- Ensure adequate thyroid hormone levels (supplementation with T4 and T3 is sometimes needed).
- Ensure adequate intake of thiamine and B vitamins. Riboflavin (B2), niacinamide (B3), pantothenic acid (B5), and biotin all play roles in mitochondrial energy production.
- Ensure adequate intake of magnesium and potassium.
- Prioritize regular meals and avoid prolonged fasting if you’re metabolically compromised. Skipping meals can cause blood sugar dips and stress the brain’s ability to access fuel efficiently.
- Avoid high intake of PUFAs which interfere with glucose transport and mitochondrial efficiency.
To prevent metal overload:
- Maintain balanced mineral intake, especially calcium, magnesium, sodium, potassium, and zinc. These minerals compete with toxic metals (like lead, mercury, and aluminum) for absorption and binding sites in tissues.
- Ensure adequate dietary calcium and magnesium, which can block the absorption and retention of toxic metals and buffer against excitotoxicity.
- Support liver detox pathways with nutrients like taurine and glycine to help eliminate stored metals and reduce their burden on the brain.
- Be mindful of environmental exposures—use filtered water, minimize aluminum-containing products, and avoid mercury-containing seafood.
- Avoid processed foods and grains with fortified iron.
To prevent overexcitation:
- Ensure adequate progesterone levels. Progesterone has a natural calming effect on the brain. It enhances GABA activity (the brain’s main inhibitory neurotransmitter) and reduces excessive glutamate stimulation. Low progesterone is associated with anxiety, poor sleep, and neuronal overstimulation.
- Consider pregnenolone supplementation. Pregnenolone is the precursor to progesterone and other neurosteroids. It supports GABAergic tone, protects against excitotoxicity, and promotes neuroplasticity.
- Support GABA synthesis. Nutrients like vitamin B6, magnesium, and taurine help produce and regulate GABA, reducing neural excitability.
- Avoid excess glutamate intake. MSG (monosodium glutamate) and other sources of free glutamate can overstimulate the brain. This excitatory overload is why some people experience symptoms like headaches, brain fog, or anxiety after consuming foods high in MSG.