Expensive supplements… more expensive than most of the longevity drugs:
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I buy this one. I get it when there’s a 40% off Swanson products. I’m on their email list and they’re always running some kind of promotion with varying % off, so I just wait until it’s 40% off; it happens about once a month.
https://www.swansonvitamins.com/p/swanson-ultra-deltagold-tocotrienols-50-mg-60-sgels
This one is double strength:
https://www.swansonvitamins.com/p/swanson-ultra-double-strength-tocotrienols-100-mg-60-liq-caps
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A_User
#5
FYI: COI: DeltaGold, etc, is Dr. Tan’s supplement which he manufactures.
Have you noticed any change in LDL levels (as per the rabbit study)?
Modern Healthspan is skeptical
@A_User No, I haven’t noticed an effect on LDL. But my dose is low: 50mg/day.
Does the “three-double-bond” tail make tocotrienols better—and can it back-fire in an iron-rich, pro-oxidant milieu?
1. Where the double bonds sit and why it matters
| Side-chain geometry |
Tocopherols (Toc) |
Tocotrienols (T₃) |
| Length (carbons) |
16 (phytyl) |
13 (farnesyl) |
| Unsaturation |
0 |
3 all-trans double bonds at C-3′, 7′, 11′ |
| Shape |
“L-shaped”, bulky, rigid |
Shorter, straighter, kink-friendly
|
-
Membrane access & lateral mobility. Molecular-dynamics and ESR work show that the unsaturated side chain slips into phospholipid bilayers ~1.5–2 × faster, then diffuses laterally almost 10 × faster than the saturated phytyl tail. This lets a single T₃ molecule intercept more lipid-peroxyl (LOO•) radicals per unit time.
-
Recycling efficiency. The T₃ chromanoxyl radical (T₃-O•) is reduced back to its active form by ascorbate or co-Q roughly twice as fast as the tocopheroxyl radical, because the unsaturated tail keeps the head closer to the membrane interface where water-soluble reductants dwell.
-
Membrane disordering. By inserting kinks between phospholipid acyl chains, T₃ lowers the local order parameter; this “loosens” the bilayer and speeds up termination of radical chains.
Net result: in classic Fe²⁺ + ascorbate or Fe²⁺ + NADPH microsomal models T₃ quenches lipid peroxidation 40–60 × better than α-Toc at equal chromanol concentration.
2. Does that extra unsaturation make T₃ itself a peroxidation target?
Theoretical risk. Any double bond can, in principle, be attacked by alkoxyl (LO•) or hydroxyl (•OH) radicals generated in Fenton chemistry (Fe²⁺ + H₂O₂ → •OH + OH⁻ + Fe³⁺). T₃ therefore contains three “PUFA-like” positions that could form lipid-hydroperoxides (LOOH-T₃).
Why it rarely matters in practice
-
Stoichiometry & kinetics. T₃ sits in membranes at tens of µM at most, whereas bulk PUFA tails are present at 100–200 mM. Even if a T₃ double bond were hit, removing one antioxidant is negligible compared with breaking a radical chain that would otherwise oxidise dozens of PUFA molecules.
-
Self-sacrifice ends the chain. Once the chromanol head has donated H•, the resulting T₃-O• delocalises over the aromatic ring and does not propagate lipid chains. It can either be recycled or dimerise to a non-radical product.
-
Head first, tail later. Kinetic isotope–labelling shows the phenolic hydrogen of T₃ reacts with peroxyl radicals 10⁴ – 10⁵ × faster than abstraction from its own side-chain allylic position; the radical never “waits around” long enough to attack the tail.
3. What happens when free iron is abundant?
| Condition |
Observed effect of T₃ |
Notes |
| Physiologic iron (transferrin-bound) |
Robust inhibition of LDL, microsomal and mitochondrial lipid peroxidation |
T₃ ≫ Toc in Fe²⁺ + ascorbate assays |
| Pathologic labile-iron pool (hemochromatosis, ferroptosis models) |
T₃ still blunts malondialdehyde/4-HNE formation and delays ferroptotic death in cell cultures; some studies show it matches deferoxamine when combined with GPX4 co-factors |
Likely synergy between radical scavenging and mild iron-chelation by the chromanol oxygen pair |
| Very high iron, no co-antioxidants (in vitro) |
Like any tocol, T₃-O• can oxidise additional PUFA if vitamin C/ubiquinol are absent; pro-oxidant inflection appears only when [T₃] ≫ [PUFA] in liposomes—conditions far above nutritional levels |
A handful of reports document T₃ acting pro-oxidantly at ≥100 µM in iron-spiked buffers |
Key takeaway: The three double bonds do not make tocotrienols a meaningful peroxidation liability under biologic or supplemental doses (≤ 250 mg/d). Instead, they are the very reason T₃ is faster and stronger as a chain-breaker than tocopherols. Pro-oxidant behaviour shows up only in artificial systems with millimolar iron and no reductant network—exactly the same edge-case where α-Toc also turns pro-oxidant.
4. Practical tips if you’re iron-loaded or worried about pro-oxidancy
-
Stay within studied doses. 100–300 mg mixed T₃/day keeps plasma ≤5 µM—well inside the antioxidant zone.
-
Support the antioxidant network. Co-ingest vitamin C (250–500 mg) or polyphenols; they recycle T₃-O• back to its active form.
-
Mind α-Toc. >200 IU/day α-Tocopherol accelerates hepatic CYP4F2 breakdown of T₃—robbing you of its benefits and, paradoxically, raising the α/γ ratio that favours tocopherol-mediated peroxidation.
-
Check labile-iron status. If ferritin > 400 ng/mL or transferrin saturation > 45 %, consider phlebotomy or iron-chelating polyphenols alongside T₃.
Bottom line
The very unsaturation that differentiates tocotrienols is what lets them “surf” lipid bilayers and intercept radicals more swiftly than tocopherols. In physiologic settings—even those rich in redox-active iron—tocotrienols overwhelmingly act as antioxidants. Only under extreme, non-physiologic iron overload and in the absence of recycling partners can their own double bonds become a liability, and even then no more so than for conventional vitamin E.
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