There’s no one-size-fits-all cure for Alzheimer’s—but could small shifts in food and movement help slow things down?
In this honest and hope-filled episode, Janna and Larry share what they’ve personally tried in the areas of diet and exercise, and how those changes have impacted Janna’s inflammation, energy, and daily outlook. From anti-inflammatory foods to brain-boosting walks, they offer no medical claims—just real results, told straight from lived experience. (Be sure to check the links to our research on our site at alzheimersthriver.org)
You’ll discover:
This isn’t about perfect plans—it’s about practical, encouraging steps toward thriving. And if you’ve been feeling discouraged, Janna’s message at the end will give you the boost you didn’t know you needed.
Links to research regarding this episode:
Diet-Induced Brain Insulin Resistance
“Induction of Brain Insulin Resistance and Alzheimer’s Molecular Changes by Western Diet”
Rodents fed a Western-style diet (high simple sugars + fats) developed insulin resistance in brain regions critical for Alzheimer’s. This led to increased amyloid precursor processing and tau pathology over time NIH
Human Data: Diet and Amyloid Accumulation
“High Glycemic Diet Is Related to Brain Amyloid Accumulation Over One Year in Preclinical Alzheimer’s Disease”
In cognitively-normal older adults, higher intake of high-glycemic foods (including sugars) correlated with increased amyloid PET signal over 12 months—especially in the precuneus, a region vulnerable to amyloid buildup NIH
Mechanistic Reviews: Insulin Resistance → Amyloid
· A mechanistic review outlines how insulin resistance promotes amyloidogenic APP cleavage, Aβ aggregation, and tau hyperphosphorylation—and how aggregated Aβ further disrupts insulin signaling, forming a vicious positive feedback loop PubMed
· In models, insulin resistance alters the blood–brain barrier, reducing insulin uptake and increasing Aβ entry and retention in the brain AlzheimersJournalss.
Additional Mechanisms: Glycation & Inflammation
· Elevated sugar leads to advanced glycation end-products (AGEs) that bind RAGE receptors, amplifying Aβ production, tau phosphorylation, neuroinflammation, and insulin resistance frontersin.org.
🧩 Synthesis: The Pathogenic Cycle
1. High sugar → insulin resistance (peripheral and central).
2. Brain insulin resistance → enhanced amyloidogenic APP processing and tau pathology.
3. Aβ aggregates → disrupt insulin receptor signaling, worsening insulin resistance.
4. Hyperglycemia & AGEs → aggravate oxidative stress, inflammation, and blood–brain barrier dysfunction, further increasing Aβ deposition.
5. E
Be sure to go to our website at alzheimersthriver.org to learn more about Larry and Janna's adventures.
