There is a labcorp test for Galectin 3. Levels greater than 17 are a sign of heart failure. My daughter did take this a few times (because of the cancer) and she was on MCP (heavily at times) hers was in single digits. I’m thinking it was $60. My doc would probably order it for me, but I have not bothered.
I suppose if your galectin 3 was low without the MCP, then probably there would be little benefit to taking it. It increases with age.
I’m taking it for chelation as I have found out through a routine prenatal test that I had lead exposure — although I never lived in a house with the common risk factors. It must be from 17 years of growing up in Eastern Europe in a town of heavy traffic before they had unleaded gasoline. That’s what the Chinese American OB concluded too, as he had seen the same in Chinese patients from polluted areas. Lead gets sequestered in bones and then during pregnancy it can get released (lovely ain’t it?). Anyway my daughter with whom I was pregnant at the time is now 11 and wicked smart but I always wonder if she’d be a certified genius if mom hadn’t been breathing so much car exhaust growing up. I’m sure the other kids got their fair share too, just didn’t happen to be picked up by the blood work (they only tested that one time because I lived by the WTC back then and it was standard procedure from 9/11).
Anyway. I take it, and it actually tastes delicious. I just often end up skipping because you’re supposed to be taking it on an empty stomach and it’s hard to find the right window of time, my mornings being so hectic.
I have taken MCP episodically and have been fascinated by the research around it. I wouldn’t say it’s necessarily cheap, however.
For the wimpy among us, I imagine that an organic, low sugar, chunky marmalade might give some benefit. I’m thinking that it would be lovely to snack on the dehydrated citrus slices with which they adorn craft cocktails these days. Most of us have fairly extensive stacks, so I have to think of ways to incorporate new products that also adds some pleasure.
No it’s not cheap at all.
I confess that I don’t understand the chelation thing entirely. My understanding is that there are very low levels in your blood normally. Somehow the chelators reach into your other tissues and pull it out. I don’t know if pectasol does that, I’ll believe it ties up and eliminates all that is in the blood. It’s a slow process in any case.
DMSA, which you can buy on ebay is the best lead chelator out there and per the amount removed, I’ll say it’s cheaper than pectasol. Though I admit I don’t have any proof, and only a few anecdotal reports of pectasol working. I still take it every 2 weeks and supplement copper and zinc because it takes them away even better than it removes lead.
I think the heavy metals are big negative players in longevity, particularly heart disease. Still working the problem here. Good Luck,
I didn’t know you could buy DMSA on eBay! Will look into it. Actually it’s my concern about any heavy metals being released into my milk that has kept me from using my pectasol frequently. I don’t know if it does that but in theory it’s a possibility. I’m waiting till I wean in the summer before getting serious with chelation. I agree that heavy metal toxicity is a big negative for longevity and I had forgotten for the longest time about my lead toxicity which I wouldn’t even have known about were it not for that random lead blood test 12 years ago. So lately it’s come back on my radar and my ears are pricked to make sure I address it and sooner rather than later.
The article below says PH has no effect; it is the heat.
One study noted that only heat-treated pectin powder induced apoptosis in human prostate cancer cells, while pH-modified pectin powder had no apoptotic activity.12
The abstract of the source (footnote 12)
https://academic.oup.com/glycob/article-abstract/17/8/805/612035?redirectedFrom=fulltext&login=false
says:
Commercially available fractionated pectin powder (FPP) induced apoptosis (approximately 40-fold above non-treated cells) in both cell lines as determined by the Apoptosense assay and activation of caspase-3 and its substrate, poly(ADP-ribose) polymerase. Conversely, citrus pectin (CP) and the pH-modified CP, PectaSol, had little or no apoptotic activity.
Heat treatment of CP (HTCP) led to the induction of significant levels of apoptosis comparable to FPP, suggesting a means for generating apoptotic pectic structures.
Looks like heating will do the job.
The study used human prostate cancer cells. It was not an in vivo study.
The article is very strange to me in that he acts like galectin 3 inhibition is uncertain and maybe a theory. But in the references he has these two studies:
The first sentence says “The pH-modified citrus pectin (MCP) has been demonstrated to inhibit galectin-3 in cancer progression.”
So then he cites another study that says it really doesn’t:
https://www.sciencedirect.com/science/article/pii/S0021925820394709
I really wish I had tested my galectin 3 before I started treatment. I don’t know if my daughter did, I’ll ask tomorrow. This is something that should be very easy to prove and I’m sure it has been done. The Life Extension article I quoted earlier talked all about it like it was real.
Tricky business.
For peels I only buy organic citrus and carefully scrub with a lot of flowing water. And yes, I eat the whole peel, I don’t try to separate any layers. FWIW, I have a friend who has been eating peels from conventionally grown oranges for over twenty years, and two years ago got tested for some pesticide levels in her blood. The upshot was that she didn’t have elevated levels, though spoiler alert, pretty much everyone in the US (and likely Europ?) has some pesticide exposure evident in their blood. Anecdotal n=1, but it made me feel better, lol.
TIL lemon peel is more palatable than orange peel. it might have been meyer lemon b/c it didnt seem like a pure lemon…
Short version: the big post-harvest citrus fungicides you’ll bump into on peels — imazalil, thiabendazole (TBZ), and sometimes fenhexamid — aren’t infamous neurotoxins, but they’re not exactly spa water either. Risk-wise, they’re mainly managed by how much peel you eat and how high the residues are on that batch of fruit.
Here’s the no-nonsense readout, using typical toxicology guardrails (ADI = tolerable daily intake over a lifetime; ARfD = one-day “don’t exceed” number):
Imazalil
- Toxicology guardrails: JMPR sets ADI ≈ 0–0.01 mg/kg/day and ARfD = 0.05 mg/kg. That’s the conservative, global reference many regulators lean on.
- Residues on peels: Surveys routinely find peel levels in the ~0.1–4 mg/kg band for oranges and similar citrus. Peel holds far more than pulp.
- Back-of-mouth math: Say you eat ~60 g of peel from one orange. At 2–4 mg/kg imazalil, that’s about 0.12–0.24 mg total, or ~0.0026–0.0051 mg/kg body weight if you weigh ~47 kg. That’s 5–10% of the ARfD for a single day, but 25–50% of the ADI if you did it daily at the high end. Translation: a one-off is well inside acute limits; making zest your main course every day edges toward the long-term line.
- Side-note on “scariness”: EPA once labeled imazalil “likely to be carcinogenic” in older assessments, though later reviews tightened methods and still judged typical dietary exposure acceptable under current limits. Nuance matters, headlines don’t.
Thiabendazole (TBZ)
- Toxicology guardrails: EU/EFSA commonly uses ADI = 0.1 mg/kg/day and ARfD = 0.1 mg/kg for TBZ; JMPR has also used a higher ARfD in some contexts, but the EU values are stricter.
- Residues on peels: Widespread on citrus peels; mg/kg-level residues are normal after waxing.
- Dose ballpark: Using 3 mg/kg on peel and the same 60 g peel serving yields ~0.18 mg total, or ~0.0038 mg/kg bw, which is ~4% of the ARfD and ~4% of the ADI. In other words, TBZ is usually the less exciting one risk-wise at typical levels.
Fenhexamid
- Toxicology guardrails: EFSA ADI = 0.2 mg/kg/day; no notable neurotox red flags in peer review.
- Residues on peels: Mostly a grape/berry fungicide, but lemon-peel studies have found very high outliers, e.g. ~30 mg/kg average, max ~66 mg/kg in some datasets. That’s lemons, not usually oranges, but still relevant if you snack on mixed citrus peels.
- Dose ballpark: At 30 mg/kg in 60 g peel you’d ingest ~1.8 mg total, or ~0.038 mg/kg bw — about 19% of the ADI for one day. At a freakish 66 mg/kg, you’d be at ~42% of the ADI. Not panic time, but not nothing if you do it often.
Peel vs pulp, and why your habit matters
Citrus peels concentrate residues; pulp tends to show a ~0.07 “processing factor” relative to whole fruit, so peel-eaters are the ones getting the full brunt. Regular washing peels helps a bit, but it’s not magic.
Neurotoxicity specifically
- None of these three are classic acute neurotoxins at dietary levels. Regulatory endpoints for imazalil and TBZ come from systemic or developmental studies rather than frank neurotox. EFSA’s cumulative neuro groups focus on different pesticide classes; these three aren’t leading characters there. Practical meaning: dietary neuro risk from peels is considered low at legal residues, but imazalil carries broader toxicology baggage that keeps regulators conservative.
If you’re still eating whole oranges like they wronged you
- Prefer organic or peel-untreated citrus when you plan to eat the rind. Post-harvest fungicides target the peel by design.
- Soak + scrub: a baking-soda wash or thorough soap-free scrub under running water reduces surface residues; it won’t touch what’s already diffused in.
- Rotate fruit and source: residue profiles vary wildly by lot and country. Variety is your friend.
Bottom line: for orange peels specifically, imazalil/TBZ are the main riders. A single whole-peel orange typically lands well below acute toxicity thresholds, but a daily, high-peel habit can start nibbling at long-term intake limits, especially at the high-residue end. If you want the bitter-pith aesthetic without the chemical garnish, go organic or peel-untreated when you plan to eat the rind, and clean like you mean it.
Short version: if you eat the peel, oranges usually carry more pesticide on the peel than apples do. Citrus rinds soak up post-harvest fungicides like imazalil and thiabendazole; apple skins have residues too, but the peel levels reported for citrus are often higher. Sorry, zest gobblers.
- Citrus peels: residues concentrate in the rind; pulp is much lower. Reported peel levels include imazalil around ~0.1–4 mg/kg in oranges, with other fungicides sometimes higher; one dataset even found lemon-peel fenhexamid averaging ~30 mg/kg and up to 66 mg/kg. Peeling cuts residues by ~80–100% because most of it’s in the peel.
- Apple peels: also higher than apple flesh, but typical peel concentrations for many pesticides show ranges like 0.02–1.38 mg/kg across surveys; washing in plain water doesn’t do much, while peeling drops residues substantially.
- Big-picture safety: routine monitoring finds residues on produce are usually below legal limits, which is nice, but “below limit” still isn’t “none,” especially if you chew the whole rind.
If you’re determined to eat the whole orange anyway
I admire the commitment to chaos. Do a few harm-reduction moves:
- Prefer organic or “unwaxed/untreated peel” citrus when you plan to eat the rind, since those post-harvest fungicides target the peel.
- Soak and scrub: a 1% baking-soda solution (10 g per liter) for 12–15 minutes, then rinse. This removes a lot of surface residues like TBZ/phosmet on apples; it won’t touch what’s diffused deeper, but it helps for rinds.
- Heat steps (blanching/boiling) can further reduce some residues, if you’re candying or cooking the peel.
Bottom line: orange peel ≳ apple peel for residue load, mainly because of citrus fungicides living on the rind. If you’re eating peels, clean aggressively or go organic; if not, your mitochondria can unclench a little.
Nobiletin Exhibits Neuroprotective Effects against Mitochondrial Complex I Inhibition via Regulating Apoptotic Signaling
IMO they’re super healthy. Every phytonutrient from citrus peel I’ve researched shows amazing benefits.
A new study:
Sirtuin 1 (SIRT1) has long been a foundational focus in longevity science due to its role as an NAD-dependent enzyme regulating metabolic health, DNA repair, and cell survival. Early enthusiasm for natural sirtuin-activating compounds (STACs) like resveratrol faced heavy academic skepticism when it was revealed that standard fluorescent testing assays frequently produced false positives caused by accidental interactions with the fluorescent tags themselves. To cut through this experimental noise, a research team developed a highly reliable, non-fluorescent screening method utilizing mass spectrometry. By applying this pristine testing framework to peel extracts from 28 distinct citrus cultivars, the researchers mapped out an entirely new class of potent, natural SIRT1 activators: polymethoxyflavonoids (PMFs).
The standout discovery centered on three specific cultivars—kara mandarin, shiikuwasha, and dekopon—whose hydrophobic peel fractions robustly drove SIRT1 activity in a clear, dose-dependent fashion. When the team isolated the individual active molecules, they discovered that a compound called 3’,4’,3,5,6,7,8-heptamethoxyflavone (HMF), found prominently in kara mandarin, completely outshone resveratrol. Mechanistically, HMF acts as a direct allosteric accelerator. It binds to a flat hydrophobic patch on the sirtuin enzyme’s regulatory domain, reshaping its architecture so that it binds its natural protein targets with nearly double the normal affinity.
This find provides a compelling structural explanation for how simple dietary components can act as molecular switches for longevity pathways. While typical plant polyphenols struggle with poor bioavailability due to rapid degradation during digestion, the heavy methoxylation on these citrus PMFs shields them, enabling better membrane permeability and tissue distribution. However, the paper adds a strict warning to over-optimistic biohackers: structural nuance dictates function. A minor shift in the position of these methoxy groups can completely flip the molecule’s utility; for instance, the closely related isomer isosinensetin was found to actively shut down SIRT1 activity. This study successfully elevates citrus waste byproducts into high-value targets for longevity optimization.
To effectively leverage these findings for healthspan extension, focus must shift from standard citrus juices to targeted peel components. Traditional citrus flavonoids like hesperidin and narirutin, which dominate the white inner albedo and juice, show absolutely zero SIRT1 activation. Instead, the therapeutic compounds are strictly localized within the flavedo—the thin, colored outer layer of the peel. To capture the most potent molecular matrix, select specific cultivars like Kara Mandarin, Shiikuwasha (Okinawan flat lemon), and Dekopon.
Because unstandardized whole peel contains a complex mixture of compounds, including the SIRT1 inhibitor isosinensetin, clean extraction protocols matter. Ethanol-based extractions are highly effective at liberating the highly hydrophobic polymethoxyflavonoids like HMF, nobiletin, and tangeretin that drive enzyme optimization. Furthermore, because PMFs lack exposed hydroxyl groups, they feature superior stability against phase II digestive conjugation compared to standard polyphenols like quercetin or resveratrol, making them highly efficient targets for oral delivery strategies intended to boost systemic sirtuin performance.
