Just came across this multi-center retrospective case series (Jan 2026) on high-viscosity 2-hydroxypropyl-β-cyclodextrin (Cavadex) for regression of atherosclerotic plaque.**
Key points from the study:
Documented CAC reductions up to 320 points over ~12 months
One patient reversed from +27–28% annual progression to –10.5% regression
Includes cases of stenosis dropping from 70% to 27%
Rectal formulation—reports no hearing loss (unlike IV/IT routes)
Published in Cardiology Research and Cardiovascular Medicine (Gavin Publishers), not yet PubMed-indexed
I’m considering adding this to my own N-of-1 protocol (LAD calcification, ApoB 152, Lp(a) 176 9 (down 41%).
Curious if anyone here has
Read the full paper?
Tried Cavadex themselves?
Thoughts on the mechanistic plausibility or real-world traction?
Happy to share my full protocol and data if helpful. Just trying to get smarter before committing.
While the research around cyclodextrin is interesting as a starting point, from talking with researchers here in the SF Bay Area focused on this area, the current strategy by this company/researcher (Cavadex) is not believed to be effective. The current molecules have very poor bioavailability and short Half-Life. I forget the number but the researcher told me you would have to take some insane dose … Like 300 grams a day, several times a day to get even marginal benefits. It’s just me or feasible or effective.
I spoke to the founder/scientist of a company here called Cyclarity, focused on developing a custom molecule that overcomes the problems of the native cyclodextrin molecule. His thoughts on the Cavadex product:
See more on Cyclarity here - they look like our best bet for reversing plaque. They’ve finished phase 2 clinical trials in Australia recently and are moving on to phase 3 clinical trials:
I ran the case study paper you identified, through my Google Gemini research paper analysis prompt and here is what it says about the case studies:
Critical Limitations [Confidence: High]
Conflict of Interest: The lead author, Kyle Hodgetts, is the founder of the company (Cholrem) selling the intervention. The study is essentially a self-published white paper disguised as a clinical study.
Regulatory Red Flags: Cholrem and its products are currently the subject of warning letters from the TGA (Australia) and FDA regarding unapproved therapeutic claims. The paper mentions “customs seizures” as a “confounding variable,” which confirms the product is being imported via grey-market channels.
Methodological Weakness:
No Control Group: Without a placebo arm, the “symptomatic relief” is highly susceptible to the placebo effect, especially in a self-selected group of biohackers/early adopters.
Selection Bias: The cohort consists of patients who actively sought out an experimental therapy (n=50). Non-responders or those who dropped out early (excluded if <30 days) are not fully accounted for.
Data Standardization: Imaging data came from various independent clinics using different scanners/protocols, making quantitative comparison (e.g., “51 to 29.4” plaque volume) unreliable.
Safety Signals: While the paper claims no ototoxicity (a known risk of HPβCD in Niemann-Pick disease treatment), the monitoring for this specific side effect appears anecdotal rather than audiometrically rigorous.
Verdict: This paper presents a compelling hypothesis backed by legitimate mechanistic plausibility (Zimmer et al.), but the clinical data is anecdotal and commercially compromised. It serves as a signal for “N-of-1” experimentation rather than proof of efficacy.
Part 3: Claims & Verification
Claim 1:HPβCD induces rapid regression of established atherosclerotic plaque.
Evidence Level:Level D (Valid Preclinical) → Level E (Human Anecdote)
Verification: The foundational mechanism is supported by high-quality mouse data in Science Translational MedicineZimmer et al. (2016). However, the human efficacy data relies entirely on the self-published observational series by Hodgetts et al. in a predatory journal (Gavin Publishers appears on multiple watchlists). There are no independent Level A or B human trials confirming plaque regression.
Status:Translational Gap. Valid in mice; unproven in humans.
Verification:Source unverified in live search. No independent pharmacokinetic (PK) studies exist for “RemChol” or “Quad Strength” formulations in PubMed or reputable databases. Standard rectal bioavailability of cyclodextrins is historically low (<5%) and variable. The claim of superior bioavailability due to “viscosity” is theoretically plausible but empirically unsupported outside the author’s own non-peer-reviewed assertions.
Claim 3:The therapy has a clean safety profile with “no ototoxicity” (hearing loss).
Evidence Level:Level E (Anecdotal) vs. External Refutation (Level B/C)
Verification:FALSE / DANGEROUS. External high-quality data explicitly identifies permanent sensorineural hearing loss as a primary risk of systemic HPβCD. In Niemann-Pick Type C trials, high-dose HPβCD caused permanent high-frequency hearing loss in humans and animals by destroying outer hair cells. The Hodgetts study likely failed to detect this because they did not perform high-frequency audiometry.
Claim 4:HPβCD acts via “bimodal” mechanisms: rapid anti-inflammatory (NLRP3) and delayed structural regression.
Evidence Level:Level D (Mechanistic Plausibility)
Verification: Supported by Zimmer et al. (2016). HPβCD was shown to solubilize cholesterol crystals, downregulating the NLRP3 inflammasome and IL-1β production in macrophages. This mechanism is scientifically sound in vitro and in vivo (mice), but the clinical timeline (“days” for symptom relief) is speculative extrapolation.
Claim 5:The “Quad Strength” formulation is superior due to enhanced mucosal retention.
Evidence Level:Level E (Marketing/Proprietary)
Verification:Source unverified in live search. No external comparative studies exist. This is a proprietary claim by the manufacturer (Cholrem).
Participants self-administered HPβCD (Cavadex) via rectal micro-enemas, with a sub-cohort utilizing a “Quad Strength” high-viscosity formulation. Primary endpoints included annualized changes in Coronary Artery Calcium (CAC) scores, quantitative angiographic stenosis reduction, and modifications in lipid profiles.
Patient ID
Age/Sex
Baseline CAC
Follow-up CAC
Duration
Absolute Change
Annualized Rate of Change (Actual)
Expected Annual Change (+20%)
Net Benefit vs Expected
M.M.
54 M
2726
2406
12 Months
-320
-11.7%
+545 (3271)
-865 units
T.J.A.
Male
Trend
Trend
12 Months
N/A
-10.5%
+27.2% (Historical)
-37.7% divergence
H.G.
Female
591
521
9 Weeks
-70
-11.8% (in 2 mo)
+2% (pro-rated)
Significant Reversal
J.L.
Male
398
368
12 Months
-30
-7.5%
+80 (478)
-110 units
A.D.
51 M
51
29.4
9 Months
-21.6
-42.3%
+10 (61)
-31.6 units
G.R.
Female
100
60
3 Months
-40
-40.0%
+20 (120)
-60 units
Only six were scanned, from a study population of 50? Renders the evidence anecdotal.
Also the “company” selling RemChol/ Cavadex out of Australia developed a terrible reputation for taking peoples money and not shipping the product and ghosting the customer. Very shady stuff. There’s a Facebook page dedicated to it.