though GLP-1’s do affect atherosclerotic heart disease and alcohol addiction, they fail in three studies to slow dementia.

This is a link to the (disgraced) Peter Attia site.  I had resisted subscribing to his content because I disagreed with his approach and thought he was too extreme.  I finally subscribed and within weeks, it was revealed that he was a client of Epstein.  Bah…  But I’m linking to this because I think it’s something that people are asking about.

I, unlike many in the biohacking world like Attia, don’t agree that it’s a great idea to prevent illness with drugs if there isn’t hard, uncorrupted, science behind it.

GLP-1 receptor agonists—drugs like semaglutide (Ozempic/Wegovy)—were originally designed for type 2 diabetes but have revealed a surprisingly broad range of effects. Beyond lowering blood sugar and promoting weight loss, these medications have been shown to reduce cardiovascular risk, improve kidney outcomes, and even decrease addictive behaviors. Early data also suggested a potential role in preventing dementia, raising significant excitement in the medical community.

However, when this hypothesis was tested directly in clinical trials, the results were disappointing. Large randomized trials (EVOKE and ELAD) found that GLP-1 drugs did not slow cognitive decline or improve function in patients who already had mild cognitive impairment or Alzheimer’s disease. Even though the drugs clearly affected biology—reducing inflammation markers and influencing some brain biomarkers—these changes did not translate into meaningful clinical benefit.

Several explanations help reconcile this disconnect:

• Too late to intervene: These drugs may not reverse established neurodegeneration. Once structural brain damage occurs, modest metabolic or anti-inflammatory effects are unlikely to restore function.
• Too small an effect: Biomarker improvements were modest (~10%), far below the magnitude seen with treatments that successfully alter disease progression.
• Wrong target at the wrong time: Inflammation plays a complex, sometimes protective role in Alzheimer’s. Suppressing it too late may be ineffective—or even counterproductive.
• Different patient populations: Earlier positive data came from metabolically unhealthy individuals (obesity, diabetes), whereas trial participants were often leaner and healthier.

The key takeaway is not that GLP-1 drugs are ineffective—but that timing and context are everything. Current evidence suggests they may still hold promise as preventative tools, particularly in at-risk individuals with metabolic dysfunction, rather than as treatments for established dementia.