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I get what you’re saying, but even so, a HEALTHY person should never inject this kind of crap into their body. 9 times out of 10, it simply comes down to a lack of discipline and willpower. And these are usually the same people who go for the highest dose because they’re impatient and want “quick results.”
You’re assuming that someone has to be unhealthy to benefit from a pharmacological intervention, and that’s simply not true.
GLP-1 receptors regulate far more than just appetite, and research continues to explore their effects on metabolic function, inflammation, and cardiovascular health.
Being healthy doesn’t automatically eliminate the potential benefits of a compound. I agree that lifestyle interventions should be foundational, but the idea that someone must exhaust every natural option before considering pharmacology is arbitrary.
There’s a difference between using a tool responsibly and depending on it because you refuse to make lifestyle changes.
@Biohacker_Jake@rorynotsorry@BowTiedHRT@FitDadRx@tonymission
I disagree. Reducing obesity and metabolic dysfunction to a lack of discipline or willpower ignores decades of research into appetite regulation, insulin resistance, and the hormonal mechanisms governing body weight.
GLP-1s aren’t JUST shortcuts for people who lack self-control. They’re pharmacological tools that target legitimate biological pathways.
And being otherwise healthy doesn’t automatically make someone a poor candidate for GLP-1 therapy.
There’s also a significant difference between responsible, evidence-based use and someone recklessly escalating doses for faster results.
I agree that the latter is problematic, but that’s an argument against misuse, not against the entire class of medications.
We don’t dismiss blood pressure medications because someone could improve their blood pressure through lifestyle changes. Why should metabolic health be treated differently?
For decades, HDL has been called the “good cholesterol.”
Higher HDL levels are associated with lower cardiovascular risk.
So why have nearly every major pharmaceutical intervention designed to raise HDL failed to prevent heart attacks?
This is one of the most fascinating examples of the difference between correlation and causation in medicine.
Let’s examine the clinical evidence.
Torcetrapib — ILLUMINATE (2007)
Torcetrapib dramatically increased HDL cholesterol.
Unfortunately, the trial was terminated early after researchers observed increased cardiovascular events and mortality.
The drug improved the biomarker while worsening clinical outcomes. Off-target effects, including increased blood pressure, complicated interpretation.
Dalcetrapib and Evacetrapib
Both successfully increased HDL.
Neither demonstrated meaningful reductions in cardiovascular events in their major outcome trials.
Both programs encountered trials stopped for futility.
Niacin — AIM-HIGH and HPS2-THRIVE
Niacin increases HDL and improves several traditional lipid measurements.
Yet neither major trial demonstrated additional cardiovascular protection when added to contemporary lipid-lowering treatment.
HPS2-THRIVE also identified increased serious adverse events.
Anacetrapib — REVEAL
Anacetrapib finally demonstrated a modest reduction in coronary events.
However, researchers attributed much of the benefit to reductions in non-HDL cholesterol rather than increased HDL itself.
Now consider the genetic evidence.
A 2012 Lancet Mendelian randomization study examined genetic variants associated with naturally elevated HDL.
One variant increased HDL without producing the expected reduction in myocardial infarction risk.
That finding challenged the assumption that simply increasing HDL cholesterol should reduce cardiovascular events.
So what does this actually tell us?
HDL cholesterol is associated with cardiovascular health, but its concentration doesn’t necessarily reflect the functionality of HDL particles.
Higher HDL frequently accompanies favorable metabolic characteristics, including lower triglycerides and improved insulin sensitivity.
It may serve partly as a marker of metabolic health rather than a direct therapeutic target.
That doesn’t mean HDL biology is irrelevant.
HDL participates in reverse cholesterol transport, inflammation regulation, and other potentially protective processes.
But increasing the number on a laboratory report doesn’t automatically improve those functions.
My takeaway:
This is why I find pharmacology and drug development so fascinating.
A mechanism can make perfect biological sense.
A medication can successfully manipulate its intended biomarker.
And the clinical outcome can still be completely different from what researchers predicted.
It’s also why ApoB and the burden of atherogenic lipoproteins deserve so much attention in cardiovascular risk assessment.
Improving a biomarker isn’t necessarily the same as improving health outcomes.
Sometimes the marker is associated with protection without being the mechanism responsible for it.
Research: ILLUMINATE (2007), AIM-HIGH (2011), HPS2-THRIVE (2014), REVEAL (2017), Lancet Mendelian Randomization (2012).
Not medical advice.
#HDL #Cholesterol #ApoB #CardiovascularHealth #LipidResearch #Pharmacology #Longevity #MetabolicHealth
@LongevityTech The old warnings came from WHI where the average woman was about 63, years past menopause. starting age seems to change the risk picture a lot
@longevitymediaa correlating with a clock and actually aging slower aren't the same thing though. people who eat a ton of veg usually do a bunch of other stuff right too
@DoctorTro Putting metabolic syndrome first makes sense since vitamin D gets stashed in fat tissue. curious if you see levels come back up after weight loss on its own
@SBakerMD The part of that one that stuck with me was low fitness looking as bad as smoking or diabetes for mortality. and they never found a ceiling, the elite group still did best
injecting cerebrolysin only sounds crazy to the ones who dont know the benefits but after hearing the benefits it becomes quite obvious why everyone is using it.
You see them in the hospital usually due to dehydration and malnutrition, usually because they’re taking too high of a dose. The key is lowest effective dose to lose a certain percentage, then again the lowest dose to maintain that percentage lost effectively. Everyone doesn’t NEED to stay on them long term, but many will have to. A lot of that is doctors prescribing the medications without any support, nutritional guidance, physical activity plan. These drugs have many many benefits.
Yeah you’re right about the association between low HDL, elevated triglycerides, and increased MI risk. I’d maybe argue the bigger concern is the underlying metabolic dysfunction, insulin resistance, and ApoB-containing lipoproteins rather than HDL itself. HDL is a useful marker, but not always necessarily the therapeutic target.
For further context, I’m not flat out saying you can’t morning dose, but as I commented once below, it appears a lot of GHRH logic bled into HGH logic on YouTube, Reddit, X, etc when it’s completely different and timing is WAY less important for the food intake, as long as your not eating awhile after (strictly for the small edge of lipolysis HGH offers) alongside its plethora of other benefits.
Again, a small fake edge is the pointed out argument here, not an overall you can’t do this*