Obesity Drives Alzheimer's Through Fat Vesicles and Leptin

Obesity increases Alzheimer's risk by altering how fat-derived vesicles communicate with the brain, causing amyloid proteins to misfold and form toxic plaques that damage neurons and impair cognition

Specific lipids from obese individuals, including sphingolipids and ceramides, create oxidative stress in brain cells, reduce mitochondrial energy production, and accelerate the formation of sticky amyloid aggregates

Excessive fat consumption promotes Alzheimer's development, though balanced, controlled intake at lower concentrations helps inhibit amyloid aggregation and reduce disease risk

Leptin resistance from obesity prevents this protective hormone from reaching the brain, disabling the cleanup process that normally breaks down amyloid proteins while worsening inflammation and cognitive decline

Cellular health restoration requires eliminating four key factors — excess linoleic acid from vegetable oils, endocrine-disrupting chemicals, electromagnetic fields, and endotoxins in the gut