10/13/2025
⚕️ 3 Common Medications That Quietly Increase Your Risk for Dementia and Alzheimer’s
Conventional medicine often blames “aging genes” for cognitive decline, but in reality, I believe much of it stems from drug-induced neurochemistry disruption. Even medications taken exactly as prescribed can alter neurotransmitters, lipid metabolism, and mitochondrial function in ways that accelerate neurodegeneration.
A Harvard-trained physician, Dr. Josh Hellman, recently pointed out three categories worth your attention. Let’s unpack why they matter and what’s happening physiologically behind the scenes.
1. Anticholinergic Drugs
Common examples: Benadryl (diphenhydramine), Dramamine, Unisom, certain antidepressants (paroxetine, amitriptyline), bladder medications (oxybutynin, tolterodine), and even some cold medicines and OTC sleep aids.
Mechanism: These drugs block the neurotransmitter acetylcholine (the brain chemical that helps with memory, focus, and muscle control), which is critical for memory, focus, and REM sleep (the dream-state which is integral to brain health).
Long-term blockade leads to cholinergic neuron atrophy (damage and shrinkage of brain cells that rely on acetylcholine) and hippocampal shrinkage (loss of volume in the brain’s main memory center), both hallmark findings in Alzheimer’s brains. Acetylcholine is also vital for the vagus nerve (the nerve that connects your brain and gut and keeps your body calm), meaning chronic anticholinergic use keeps your nervous system in sympathetic overdrive (fight-or-flight mode).
Research highlights:
- A 2019 study in JAMA Internal Medicine found that cumulative anticholinergic exposure increased dementia risk by up to 49% over ten years [1].
- Functional MRI studies show decreased glucose metabolism (less brain energy activity) in memory-related brain regions after prolonged use [2].
2. Benzodiazepines
Common examples: Xanax (alprazolam), Ativan (lorazepam), Va**um (diazepam), Klonopin (clonazepam), and sleeping pills like Restoril (temazepam).
Mechanism: Benzodiazepines enhance GABA-A receptor activity (boosting your main “calm down” chemical, GABA), producing sedation and anxiolysis (relief of anxiety), but with chronic use, they downregulate GABA receptors (making the brain’s calming system less responsive) and impair synaptic plasticity (the brain’s ability to learn and adapt). This leads to glutamate dominance (too much excitatory activity), neuronal apoptosis (cell death), and long-term structural brain changes seen on PET imaging. They also suppress deep sleep, where amyloid-β clearance (toxic waste removal from the brain) normally occurs via the glymphatic system (the brain’s nighttime cleaning process).
Research highlights:
- A large cohort study published in BMJ found benzodiazepine users had a 43–51% higher risk of Alzheimer’s, even after adjusting for anxiety or insomnia [3].
- GABAergic disruption (imbalanced calming neurotransmitters) alters calcium homeostasis (how brain cells regulate calcium), which accelerates tau phosphorylation (tangling of brain proteins), another key step in Alzheimer’s pathology [4].
3. Statin Drugs
Common examples: Lipitor (atorvastatin), Crestor (rosuvastatin), Zocor (simvastatin), and Pravachol (pravastatin).
Mechanism: Statins block HMG-CoA reductase (the enzyme your body uses to make cholesterol), lowering cholesterol, but the brain is cholesterol-dependent, using it to form myelin sheaths (the insulation around nerves), maintain cell membranes, and synthesize hormones and neurotransmitters. Reduced cholesterol interferes with synapse formation (how brain cells communicate), CoQ10 production (a key energy molecule for mitochondria), and glial cell energy metabolism (support-cell function that keeps neurons alive). Statins also deplete fat-soluble vitamins (like vitamin A, D, and E), and CoQ10, critical for mitochondrial and neuronal health.
Research highlights:
- Multiple analyses show a correlation between statin use and memory loss or cognitive dysfunction, especially lipophilic statins that cross the blood-brain barrier (enter the brain easily) [5].
- Animal models demonstrate that cholesterol depletion alters amyloid precursor protein processing (how the brain builds or breaks down amyloid), increasing β-amyloid plaque formation (a defining feature of Alzheimer’s) [6].
Final Thoughts
Pharmaceuticals are not inherently evil, but uninformed use is. If you or a loved one are on any of these medications long-term, it’s worth asking:
1) Are there safer alternatives to manage symptoms without compromising brain integrity?
2) Are nutrient and neurotransmitter pathways being supported properly?
3)And most importantly, is this drug addressing a root cause, or just suppressing it?
Because prevention doesn’t begin with a prescription, it begins with awareness.
Disclaimer: The information and opinions shared are for informational purposes only including, but not limited to, text, graphics, images and other material and are not intended as medical advice or instruction. Nothing mentioned is intended to be a substitute for professional medical advice, diagnosis or treatment.
References (APA format)
1. Richardson, K., Fox, C., Maidment, I., et al. (2019). Anticholinergic drugs and risk of dementia: case–control study. JAMA Internal Medicine, 179(8), 1084–1093. https://doi.org/10.1001/jamainternmed.2019.0677
2. Risacher, S. L., et al. (2016). Association between anticholinergic medication use and brain metabolism and atrophy in cognitively normal older adults. JAMA Neurology, 73(6), 721–732.
3. Billioti de Gage, S., et al. (2014). Benzodiazepine use and risk of Alzheimer’s disease: case–control study. BMJ, 349, g5205.
4. Calabrese, E. J., & Baldwin, L. A. (2018). Neuroprotective role of GABAergic modulation in neurodegenerative disorders. Pharmacological Reviews, 70(1), 88–120.
5. Wagstaff, L. R., et al. (2003). Statin-associated memory loss: analysis of 60 case reports and review of the literature. Pharmacotherapy, 23(7), 871–880.
6. Puglielli, L., Tanzi, R. E., & Kovacs, D. M. (2003). Alzheimer’s disease: the cholesterol connection. Nature Neuroscience Reviews, 4(7), 524–534.
