👨🏫 A month ago, my father — a leading expert in Ancient Roman literature — turned 80. I asked what advice I should pass to the next generation. He gave me 3:
Most people have no idea what's possible over the next 18 months.
- Obesity could be solved:
retatrutide already produces 30% bodyweight loss, bariatric surgery results from a weekly injection
- Low testosterone could stop being written off as "just aging":
new data shows GLP-1s alone raise T levels and nearly double normal sperm shape in low-T men
- Balding could become optional:
AI-designed hair loss drugs already show dramatically different, more favorable behavior in the blood than anything on the market
- Fatty liver disease could get its first real cure:
DT-109 already reversed it in animal studies by repairing the gut
- Solid tumors could be eliminated without chemo:
a single-dose bacterial therapy already wiped out colorectal cancer in mice with one treatment
- Infertility could stop being permanent:
two companies are already growing human sperm and eggs from a patient's own skin or blood cells in a lab
- The "undruggable" mutation behind half of all cancers could finally get a drug:
p53 has been the holy grail for decades and the tools are finally catching up
Most of these are already showing results in real trials.
We are watching the future get approved.
Bio/acc.
A new Nature study just identified the only trace element deficient in both mild cognitive impairment and Alzheimer's disease, and it's detectable years before diagnosis.
Researchers measured 27 metals in brain tissue from people with cognitive impairment and Alzheimer's. Only one was significantly reduced in both conditions: lithium.
Serum lithium levels were normal. The problem was brain-specific. Lithium in the prefrontal cortex was reduced in people with mild cognitive impairment, the earliest stage before full Alzheimer's develops.
The mechanism: amyloid plaques trap lithium. Using laser ablation to map lithium concentrations in brain tissue, researchers found that plaques concentrate lithium at 3-4 times the level of surrounding tissue.
The plaques sequester lithium, pulling it out of circulation where neurons need it.
When tissue was separated into plaque and non-plaque fractions, lithium in the bioavailable fraction was significantly lower in Alzheimer's patients. Lower bioavailable lithium correlated with worse memory scores.
This creates a vicious cycle. Amyloid plaques sequester lithium → lower lithium accelerates more amyloid formation → more plaques trap more lithium → bioavailable lithium drops further.
To test whether lithium deficiency drives pathology, researchers fed mice a diet that reduced brain lithium by 50%, matching the reduction seen in human cognitive impairment.
The results in both normal mice and Alzheimer's models:
• More amyloid-β deposits
• More phospho-tau accumulation
• Inflammatory microglia activation
• Loss of synapses and myelin
• Faster cognitive decline
Pathology appeared within five weeks and worsened over time.
Lithium inhibits GSK3β, a kinase that phosphorylates tau and drives neuroinflammation. When lithium drops, GSK3β activity rises, accelerating tau pathology and inflammation.
RNA sequencing showed lithium deficiency altered gene expression across neurons, astrocytes, microglia, and oligodendrocytes, producing changes that matched the transcriptome signature of human Alzheimer's disease.
The solution tested: lithium orotate. Standard lithium salts bind to amyloid, which creates the same sequestration problem. Lithium orotate has reduced amyloid-binding and remains bioavailable even when plaques are present.
Lithium orotate prevented memory loss and pathology in Alzheimer's mouse models. It also prevented age-related cognitive decline in normal aging mice.
Most Alzheimer's research targets amyloid removal after plaques form. This study shows lithium deficiency may occur upstream, before pathology accumulates.
Lithium deficiency is detectable in mild cognitive impairment, years before Alzheimer's diagnosis. That makes it a potential early intervention target.
The intervention isn't a new drug. It's restoring a trace element that's already supposed to be there, using a formulation that avoids the sequestration problem.
The decisions about whether to measure brain lithium bioavailability in midlife, and whether to intervene before irreversible damage occurs will depend on whether lithium replacement can actually prevent progression from cognitive impairment to dementia in humans.
The Longevity Industry Just Got Its Franchise.
Ultimate Longevity Center Sells 200 Territories in Four Months.
Now the question is...
Is your market still available?
Corporations posted record profits during the inflation they blamed on your wages. They raised prices because they could and pointed at you to take the heat. That is not the market. That is a margin grab with a cover story.
WTF!!! Disgusting!
Remember companies like $META are ASO (administrative services only) with whatever insurance company they use. They pay the healthcare bills. THIS should be illegal to first have access to workers health info HIPPA violation then use it to lay the most vulnerable off!
POS @finkd@Meta
One rarely-discussed part of GLP-1s is that the skin appears to have its own GLP-1 biology.
Receptors have been identified in hair follicles, keratinocytes, and immune cells inside inflamed skin.
Could dermatology be the next major GLP-1 frontier?
Off topic- can you establish a relationship with imaging centers so we can order full
body MRI’s from SuperPower? I saw that Functional by Dr Hyman has special deals with imaging centers for the scans and you
can order right off of his app.
I want to do a yearly full body MRI and I want to do CLEERLY when I do cardiac testing (CCTA’s) when needed. Thanks!
Thank you!
An MRI scan of a 33-year-old woman demonstrates the actual persistence of facial fillers she has received over the years.
Contrary to the common belief that hyaluronic acid fillers naturally break down and disappear within a few months, the imaging reveals that substantial amounts of the injected material remain even after six years, with incomplete absorption. This prolonged presence and potential migration of fillers can contribute to tissue expansion, lymphatic obstruction, and distortion of facial contours.