Alzheimer’s is often referred to as “type 3 diabetes,” a term that reflects the brain’s impaired
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. One study found that depriving human neurons of glucose led to Alzheimer-like changes (PMID: 37037474). Brain imaging consistently shows hypometabolism in Alzheimer’s patients, even in those with genetic risk factors like APOE4.
Hypothyroidism, thiamine deficiency, magnesium and calcium depletion, heavy metal toxicity, and iron accumulation all impair glucose metabolism. Without adequate energy, neurons can’t function properly. More than anything, Alzheimer’s is an energetic / metabolic issue.
Interestingly, low energy production leads to a buildup of excitatory neurotransmitters, especially acetylcholine and glutamate. Contrary to the common belief that Alzheimer’s is caused by underactive neurons, it’s actually driven by overexcitation. Many conventional treatments have focused on raising acetylcholine, however, acetylcholine and glutamate become toxic when not properly cleared, overstimulating neurons and triggering oxidative stress and cell death (PMID: 35335180).
This may explain why many Alzheimer’s drugs have not been very successful. They amplify the very excitatory pathways. Increasing acetylcholine activity without addressing the underlying energy deficit or restoring inhibitory balance, may worsen neuronal stress rather than relieve it.
Progesterone helps buffer the brain against excitotoxicity by calming overactive neural pathways, enhancing GABA, regulating calcium influx, and supporting glucose metabolism. It also increases levels of acetylcholinesterase, the enzyme that breaks down acetylcholine. When progesterone levels decline with age, this built-in protection is lost, leaving the brain more vulnerable.
Видео Alzheimer’s is often referred to as “type 3 diabetes,” a term that reflects the brain’s impaired канала Leigh Erin Connealy MD
Hypothyroidism, thiamine deficiency, magnesium and calcium depletion, heavy metal toxicity, and iron accumulation all impair glucose metabolism. Without adequate energy, neurons can’t function properly. More than anything, Alzheimer’s is an energetic / metabolic issue.
Interestingly, low energy production leads to a buildup of excitatory neurotransmitters, especially acetylcholine and glutamate. Contrary to the common belief that Alzheimer’s is caused by underactive neurons, it’s actually driven by overexcitation. Many conventional treatments have focused on raising acetylcholine, however, acetylcholine and glutamate become toxic when not properly cleared, overstimulating neurons and triggering oxidative stress and cell death (PMID: 35335180).
This may explain why many Alzheimer’s drugs have not been very successful. They amplify the very excitatory pathways. Increasing acetylcholine activity without addressing the underlying energy deficit or restoring inhibitory balance, may worsen neuronal stress rather than relieve it.
Progesterone helps buffer the brain against excitotoxicity by calming overactive neural pathways, enhancing GABA, regulating calcium influx, and supporting glucose metabolism. It also increases levels of acetylcholinesterase, the enzyme that breaks down acetylcholine. When progesterone levels decline with age, this built-in protection is lost, leaving the brain more vulnerable.
Видео Alzheimer’s is often referred to as “type 3 diabetes,” a term that reflects the brain’s impaired канала Leigh Erin Connealy MD
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24 июня 2025 г. 23:22:29
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