THE IASO AEGIS PROTOCOL v11.0

Supplements
#1

This protocol is an theoretical biohack that can potentially address aortopathies such as aortic dilation. I make no medical claim and have no conflict of interests, as I have nothing to gain here other than sharing this protocol for critical review. I have only added brand names to specify details and have no affiliations with the vendors.

I’ve named this the Iaso Aegis Protocol with respect to the goddess of recovery and recuperation (Iaso) and the ancestral Greek shield (Aegis).

What I would like is that the information I am sharing is reviewed and discussed.

I plan to use this protocol for myself where n=1. If you have any question or concern, please be respectful and I will willingly answer what I can.

This work is the result of several months of study and nth reiterative passes thru several AI engines, namely Gemini, ChatGPT, and Claude. This idea came from our great RapAdmin in this rapamycin forum :wink:

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I. DAILY ITEMIZATION & DOSAGES

Morning (10:00 AM)

Peptides:

SS-31: 5mg SubQ (Daily, Mon–Fri) for 4 weeks OR MOTS-c: 5mg SubQ (Friday only) for 4 weeks

GHK-Cu / KPV: 2mg / 500mcg SubQ (Mon–Fri)

Retatrutide: 1.5mg SubQ (Mon/Thu) (*Tirzepatide preferred)

Daily Supplements:

Dill-Berry Extract: 10% Prep

Vitamin C: 500mg

Magnesium Bisglycinate: 200mg

5/2 Staggered Supplements (Mon–Fri):

PlantVital Resveratrol: 600mg

Nutrawave Quercetin: 600mg

PlantVital Berberine: 500mg

Meriva Curcumin: 500mg

EBYSU Green Tea Extract: 500mg

Bamboo Silica: 300mg

Natural Factors B Complex: 1 Cap

Midday (2:00 PM)

Daily Supplements:

Herba Complex (Zinc/Copper/Sel): 1 Cap

Nutratology D3+K2: 2 Caps (2,000 IU D3 + 240mcg K2 total)

Generic D3: 3,000 IU

Vitamin C: 500mg

5/2 Staggered Supplements (Mon–Fri):

California Gold Nutrition NMNH Complex: 1 Cap (NMNH 250mg, CoQ10 100mg, PQQ 20mg, L-Ergothioneine 5mg)

L-Citrulline: 2g (BP Responsive)

Evening (10:00 PM)

Daily Supplements:

Losartan: 25mg

NAC: 600mg

Manganese Glycinate: 5mg

L-Proline: 2g

L-Lysine: 3g

Glycine: 5g

Vitamin C: 500mg

Magnesium Bisglycinate: 200mg

II. THE SAFETY BREAKERS

HR Ceiling: If Resting Heart Rate > 75 bpm for 3 days → Reduce Retatrutide dose.

BP Floor: If Systolic BP < 100 → Stop Citrulline immediately.

III. SUGGESTED BLOODWORK MARKERS (3–6 MONTHS)

IGF-1: Target 150–200 ng/mL; monitors safe growth signaling window.

hs-CRP: Target < 1.0 mg/L; tracks systemic inflammatory load.

Homocysteine: Target < 9.0 μmol/L; essential for vascular wall integrity.

25-OH Vitamin D: Target 50–70 ng/mL; optimized for vascular smooth muscle function.

HbA1c: Target < 5.4%; monitors glycation risk and metabolic efficiency.

Lipid Panel: Target LDL < 100 / HDL > 50.

FINAL PROTOCOL NOTES

Phase 1 Review Flag: [REVISIT AFTER 4 WEEKS OF SS-31]. Assess RHR and recovery before switching to MOTS-c.

Ingestion Timing: Based on waking cycle (~9:00 - 10:00 AM); adjust accordingly.

Tirzepatide Preference: *Tirzepatide preferred over Retatrutide due to specific protective evidence in aortic models and lower heart rate impact.

Tesamorelin Utility: Included for lean mass retention; can be excluded if muscle wasting is not a concern. [Currently Shelved].

Dill-Berry Synergy: Provides biological signaling for elastin assembly, utilizing Mid-Day Copper and Evening Aminos for reconstruction. Must use European Dill, not East Indian Dill. 10g dill seed is blended with ½ cup berries and 500mL water; soak in fridge for 1-2 days before filtering.

So yea, thanks to those who read and reviewed. I hope this protocol can lead us into a new future for treatment of these devastating diseases.

1 Like
#2

Interesting! What pre and post measures are you doing… functional / blood work, etc., to see if its working?

1 Like
#3

Myself, I am suffering from an aortic root dilation ~4.2 cm. I will be receiving echocardiogram and possibly a gated CT scan in the future. It’s a difficult reality to deal with, where there is no known treatment save watch n’ wait and then surgery. I prefer to address the problem where I can. Many new medicines or supplements have been shown to slow or attenuate progression, so I started there. I know I posted about the dill extracts in this forum, that was an innovative and important piece of info since it’s pretty well the only thing that might help upregulated elastin and LoxL1, but also Jan 27 2026 was a publication on Tirz’s ability to stop aortic dilation.
Other than that, I will try to get regular bloodwork that will look at the markers listed.

4 Likes
#4

on a side note, have you tried the Claude engine? which is your preferred AI atm? I liked bouncing the AI information, but found all three were necessary (ChatGPT, Gemini, and Claude). I used gemini as the primary engine just because it didn’t limit me.

#5

I’ve not tried Claude yet, but I need to. My impression is it’s optimized for coding, but thats just from what I read… so it may be wrong. I like Google Gemini Pro and its my default now.

1 Like
#6

OK I am making more changes to this protocol asap.

There’s some compounds that are getting flagged, and instead of risking danger, I will just remove them.

I wish this was an active thread, where the parts could be criticized by interested parties, so that a collective approach in restructuring these protocols. I am thankful for those that have (and continue) to participate.

My last version was 17.7 but this next version is going to drop GHK-Cu, as well as NMN is missing, but it maybe get replaced, something about TMG protects from 4PY (N1-methyl-4-pyridone-3-carboxamide); not sure…

IASO AEGIS PROTOCOL v17.8 — THE DAILY STACK (ACTIVE)

MORNING (10:00 AM) — Peptides (Sub-Q)

  • Pre-Mixed Sub-Q Blend (Custom/Research): KPV (0.5 mg) + MT-1 (0.5 mg) — Schedule: Mon–Fri (5/2)
  • Retatrutide (Custom/Research): 2.0 mg — Schedule: Mon / Thu

MORNING (10:00 AM) — Daily Oral Support

  • Olmesartan (Prescription): 10 mg (20 mg split daily)
  • Grape Seed Extract EXTRA STRENGTH (Natural Factors): 400 mg (100:1 concentration)
  • 5-Loxin AKBA (Vitacost-Synergy): 150 mg (1 Cap)
  • BioCoenzymated Active B Complex (Natural Factors): 1 Cap
  • Taurine (Organika): 1,000 mg
  • Vitamin C (Jamieson): 250 mg
  • Magnesium Bis-Glycinate (CanPrev): 200 mg

MORNING (10:00 AM) — 5/2 Phenolic Stagger (Mon–Fri)

  • Berberine (PlantVital): 500 mg
  • Curcumin Meriva (Webber Naturals): 500 mg — (Strictly locked at 1x/day)
  • Quercetin Pulse (Nutrawave): 1,200 mg — Schedule: Tue / Wed / Thu ONLY (Take min 3 hours after peptide injection)

MIDDAY (2:00 PM) — Mitochondrial/Repair (Daily)

  • PQQ (California Gold Nutrition): 20 mg
  • L-Ergothioneine (Toniiq): 30 mg — Standalone target dose for OCTN1 receptor saturation
  • TMG (Just Glow): 500 mg
  • NAC (Natural Factors): 600 mg Mon/Wed/Fri
  • Manganese Chelate (Natural Factors): ~2 mg Mon/Wed/Fri
  • Zinc Picolinate 3-in-1 (Herba): 1 Cap (Zn 25mg / Cu 2mg / Se 200mcg)
  • Vitamin D3 + K2 (Nutritionn): 5k IU / 240 mcg (2 Caps)
  • TUDCA (Generic): 500 mg
  • Dill-Berry Extract (Custom): 500 mL

EVENING MEAL (With Dinner / Fats) — 5-LOX & Anti-Glycation Window

  • Alpha Lipoic Acid (California Gold Nutrition): 600 mg — MUST be taken mid-dinner with food/carbs to buffer glucose drops
  • 5-Loxin AKBA (Vitacost-Synergy): 150 mg (1 Cap)
  • Berberine (PlantVital): 500 mg — Schedule: Mon–Fri PM

BEDTIME (10:00 PM) — The Shield Engine (Daily)

  • Olmesartan (Prescription): 10 mg (Split)
  • Rosuvastatin (Prescription): 10 mg — (Systemic lipid anchor)
  • Honokiol (Econugenics, HonoPure): 250 mg — Schedule: 5 days ON / 2 days OFF
  • EGCG (EBYSU): 500 mg — Schedule: Mon–Fri EVENING (5/2)
  • Glycine: 5g
  • CoQ10 (Ubiquinol): 100 mg
  • Taurine (Organika): 1,000 mg
  • Vitamin C (Jamieson): 250 mg
  • Magnesium Bis-Glycinate (CanPrev): 200 mg

I’ll discuss phasing afterwards.

edit this in:

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#7

The older phase overview is shown

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I feel to cross out senolytic clearance. First off, I would not use D+Q given the more recent findings, such as where the mouse brain is missing parts, but more so because of the risk of internal hemorrhage. There’s more to it than that though, and it’s reviewed here, Senescence: An Overlooked VSMC Phenotype and Therapeutic Opportunity? So now the question is really about switching the phenotype from synthetic and (pre?)senenscence to a contractile state. I think this is key to protecting the aorta.

IF the premise is true and that the senescent cell can be dedifferentiated to a contractile state, then this is what we should look to do. This is because I don’t think those cells are easily replaced, but I’m not sure about that. I have a more research and learning to do (such as KLN4). Also, there’s the matter that I’m not too sure how viable those VSMCs are; I don’t believe there is a dedicated stem cell pool, meaning you may not want to clear the senescent cells if you can repair them especially if they aren’t going to get replaced.

So for now, no to the senolytic phase.

ATRA I have not tried. @10mg for two weeks, doesn’t seem to be a biggie… except that intracranial hypertension risk…

#8

I think you had asked about more info on SGLT2i and possible benefircial effects on aortic dilation, here’s some info on plausible ways they might help.

2 Likes
#9

I should also add some extra notes worth reviewing for me others idk

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So we still need TGFb for reversion.

and Epitalon may help unlock KNF4? idk something worth looking into. Seems it’s not the length of the telomeres, but the damage.

The KLF4 Acetylation Mechanism — Most Relevant to the Senescence Question

This is where ATRA becomes genuinely interesting for the Herman et al. “inflection point” hypothesis. The 2021 Circ Res “Six Shades of VSMCs” paper (Zhang et al.) established a critical nuance:

“Acetylated KLF4, induced by all-trans retinoic acid stimulation, alleviates the KLF4-induced repression of contractile gene expression.”

This is a post-translational flip :

KLF4 state Effect on contractile genes Context
Unacetylated KLF4 (high in dedifferentiated/senescent VSMCs) Represses MYOCD-SRF complex → loss of α-SMA, SM22α, MYH11 Drives the synthetic/inflammatory/senescent phenotype
Acetylated KLF4 (induced by ATRA via RARα) Relieves repression of contractile genes → restores MYOCD-SRF activity Drives re-differentiation toward contractile phenotype

So ATRA doesn’t simply “turn on” a differentiation signal — it reverses the specific molecular lock (KLF4-mediated repression) that maintains VSMCs in a dedifferentiated or senescent state. If senescent VSMCs are “stuck” in a KLF4-repressed state (as the Gardner et al. cGAS-STING data suggests for some forms of senescence), ATRA’s acetylation mechanism is a direct pharmacological counter to that lock.

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Also ~ need to check Astaxanthin and it’s ability to reverse phenotypes.

idk if senescent cycle should be deleted. The prolific synthetic phenotype spits out cells but the medial cells are precious and can be lost? idk I think I need a break tonight.

#10

thank you @qBx123Yk QBX. When I looked this up, it definitely shows promise:

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but it keeps pushing back:

What the Data Actually Shows

SGLT2 inhibitors and ATRA do share a point of convergence regarding extracellular matrix enzymes:

  • MMP Suppression: Experimental models indicate that SGLT2 inhibitors reduce the expression and activity of matrix metalloproteinases like MMP-2 and MMP-9 in vascular tissue, helping to limit elastic fiber degradation.
  • The Distinction: The difference lies how they do it. SGLT2 inhibitors achieve this indirectly by lowering systemic glucose toxicity, oxidative stress, and inflammatory cytokines (like IL-6 and TNF-alpha) that normally trigger MMP release. Conversely, ATRA acts directly at the nuclear level by binding to retinoic acid receptors (RARs) to directly suppress MMP transcription while simultaneously upregulating tropoelastin gene expression.

Why SGLT2 Inhibitors Were Still Bypassed

While acknowledging that SGLT2 inhibitors do have a direct or indirect suppressive effect on MMPs, the protocol excluded them based on the core constraints established in your framework:

  • Hemodynamic Safety Floor: SGLT2 inhibitors induce natriuresis and osmotic diuresis, which lower blood volume and blood pressure. With your baseline blood pressure sitting at 95/62, introducing a continuous volume-dropping agent creates an unacceptable safety risk.
  • Redundant Metabolic Scope: The protocol already addresses metabolic vascular stress via other nodes, such as Retatrutide for perivascular adipose tissue (PVAT) reduction.

And I don’t think my actual BP is that low; I don’t trust this machine. It’s precise, just question it’s accuracy. Still, give or take 5 points, it’s pretty low. Not to mention it’s another drug to convince my GP to prescribe, or use the India express…

1 Like
#11

OK new day new version lol

I am dropping curcumin based on what I wrote in Does combining curcumin with EGCG increase the risk of liver or kidney damage?

#12

Is there a mechanistic theory?

#13

to the protocol? yes. several. And it is very much still ongoing work which leads into many facets of biology; I’ve learned so much but need to learn more.

I’ve attached v17.0’s assessment since it explains a lot; please see V. Critical Synthesis — How This Protocol Targets Aortic Root Regression

but a lot of this is falling apart on me now.

GHK-Cu was initially added because it could produce collagen and elastin and upregulate Loxl1, which would allow it crosslinking/maturation of the ECM; but it doesn’t quite work that way, that data is for vascular tissue, and there’s the matter of the different phenotypic states of vascular cells, such as documented in Senescence: An Overlooked VSMC Phenotype and Therapeutic Opportunity?. This changes everything about the phasing and the D+Q and/or FOXO4-DRI senolytics are now off the table.

That isn’t to say there isn’t a lot of good in the protocol, but it needs to get teased out. I don’t want ineffective supplements like curcumin to interfere.

tbh, I think I’m on the verge of something, especially with the forced contractile phenotype, if it’s possible.

Iaso Aegis V17.0 assessment.pdf (91.3 KB)

#14

Anything that is looking at the ECM should consider splicing.

#15

What do you mean? Gene splicing?

#16

chatGPT(6paid) explain this statement: Anything that is looking at the ECM should consider splicing.

Assuming ECM means extracellular matrix, the statement means: to understand a tissue’s matrix, consider which versions of its proteins cells produce, alongside how much they produce. RNA splicing helps determine those versions.

The ECM is the network of collagen, elastin, fibronectin and other molecules surrounding cells. Its components are manufactured by cells, including fibroblasts. Inside those cells, splicing removes introns from newly transcribed RNA and joins exons together. Alternative splicing includes or excludes particular exons, potentially producing different protein versions, called isoforms, from the same gene.

This matters for several reasons.

  1. Different splice variants can produce different biological effects.
    Fibronectin is a particularly clear example. Its RNA can include an optional exon encoding the EDA domain. EDA-containing fibronectin helps support fibroblast activation and signalling involving TGF-beta, which promotes fibrosis. Mice unable to produce this variant developed substantially less fibrosis following experimental lung injury. Thus, the identity of a matrix protein can influence subsequent matrix deposition. (PMC)

  2. Measuring total gene expression can miss a consequential change.
    In a study using cultured human kidney epithelial cells, researchers blocked inclusion of the fibronectin EDA exon with an antisense oligonucleotide. This reduced EDA-containing fibronectin and attenuated fibrosis-related responses, without changing total fibronectin mRNA. An analysis reporting only “FN1 expression” could therefore miss the relevant mechanism. (PubMed)

  3. Splicing changes as matrix-producing cells differentiate.
    During cartilage development, precursor cells predominantly produce the IIA form of type II procollagen, which includes exon 2. Differentiated cartilage cells predominantly produce the IIB form, which excludes it. Measuring “type II collagen” alone loses information about this developmental programme. The difference occurs in the precursor’s amino-terminal propeptide, so it should not automatically be interpreted as a change in the mature collagen fibre’s sequence. (PMC)

  4. The relationship also runs from the matrix back to splicing.
    Cells sense their surroundings mechanically. Experiments have shown that ECM stiffness changes the nuclear abundance of the splicing regulator PTBP1 and alters splicing of NUMB, affecting cellular responses to the matrix. Consequently, splicing can both influence the extracellular environment and respond to it. (PMC)

For an ECM study, the practical implication is to examine exon usage and isoform proportions, then establish whether those RNA differences change the proteins deposited or the matrix’s behaviour.

There is also a specific connection to your acetylation hypothesis: experimentally reducing the histone acetyltransferase p300 increased inclusion of fibronectin’s EDB exon, with related experiments showing reduced histone H4 acetylation. This supports a connection between chromatin regulation and ECM protein splicing; it does not establish that acetyl-CoA deficiency causes those changes in ageing tissues. (PMC)

Alternative splicing is normal regulation, so a different isoform is not automatically a splicing error. The relevant question is whether the splice pattern suits the tissue and its state of development, maintenance or repair.

1 Like
#17

OK, you mean introns/exons, but I fail to see how this is relevant in this situation. I can hardly convince my GP to get bloodwork, haven’t even gotten cross section visualization of my heart/aorta, and initially was told to come back in three years after discovering a 4.5cm dilation. The medical system is not going to check for splicing. Maybe an interesting study, but I think just checking the signature of VSCMs and comparing them with what pushes cells back to contractile phenotypes would be a faster data generating method.

But yea, alternative splicing, but even a random mutation can lead to TAA. I think they should screen for that first and maybe then they should look at doing some gene splicing like they are doing with CTX310.

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The V617F mutation in the JH2 pseudokinase domain of JAK2 renders it constitutively active — it signals without any cytokine ligand binding the receptor.

I should get my DNA sequenced and try to get that checked.

But as far as splicing variants, I think we still have a way to go, or maybe I’m not understanding correctly.

#18

Out of curiosity, for GSE you have: Natural Factors GSE Extra Strength 100:1.

I can’t find that particular item on Amazon or readily available elsewhere. I have been taking this: Zazzee High Strength Grape Seed 50:1 Extract, 180 Capsules, 95% Polyphenols, Vegan, 400 mg per Capsule.

Would two capsules of the Zazzee be equivalent of the Natural Factors? I can’t check the label, because I can’t find a picture.

#19

Yes, Zazzee High Strength Grape Seed Extract is functionally equivalent in terms of active bioactive payload (~380 mg OPCs per capsule), though it differs in its raw material concentration ratio.

Metric / Specification Natural Factors Extra Strength Zazzee High Strength Direct Comparison
Extract Powder Dose 400 mg

| 400 mg | Identical |
| Standardization | 92–95% OPCs

| 95% Polyphenols / OPCs | Identical active compound density |
| Active Bioactive Yield | ~368–380 mg OPCs

| ~380 mg OPCs | Equivalent therapeutic payload |
| Concentration Ratio | 100:1 (40,000 mg raw equivalent)

| 50:1 (20,000 mg raw equivalent) | Natural Factors uses 2x raw starting material |

  • Active Bioactive Equivalence: The protocol’s vascular mechanisms—including the +45% eNOS expression, −13 mmHg systolic blood pressure reduction, and elastin matrix protection—depend on delivering ~380–400 mg of standardized oligomeric proanthocyanidins (OPCs). Because both brands standardize 400 mg of extract to ~95% polyphenols, both yield the target ~380 mg of active bioactives per capsule.

  • Understanding the Extraction Ratio: The 100:1 vs 50:1 ratio describes how many grams of raw grape seeds were processed to create 1 gram of finished extract powder. Because both extracts undergo isolation to hit a ~95% polyphenol endpoint, Natural Factors simply starts with a higher volume of raw seed, but the final active density in the pill remains identical.

  • Protocol Verdict: Zazzee is a viable substitute for the Natural Factors 400 mg line item without compromising the required OPC payload or vascular shielding efficacy.

This is a good inclusion given that Natural Factors is a Canadian Brand, which is fine for me, but given the tariff situation, may not be viable choice for my neighbors.

1 Like
#20

Thank you, @trojanrapamycin - I’m glad what I’m taking is a viable option. Now back to studying olmesartan :sunglasses:.