This text is a consideration of the unusual properties of T3/tocotrienolsn through the transcription factor NF-κB(pronounced: en-ef-kappa-be).
NF-κB(nuclear factor kappaB)is a transcription factor, it then does not control the activation of genes. NFkappaB plays a key role in
- inflammatory reactions,
- Apoptosis etc
- aging.
NF-κB is also called a redox-sensitive transcription factor because it is activated by hydrogen superoxide and blocked by some antioxidants.
Block tocotrienolsNF-kappaB, which like theum is active in a number of diseases, including cancer, arthritis, chronic inflammation, neurodegenerative diseases and heart diseases ("active in a number of disease states, including cancer, arthritis, chronic inflammation, asthma, neurodegenerative diseases, and heart disease" [ref]).
A number of studies link the benefits of tocotrienolsn to their influence on NF-kappaB.T3 -> less NF-kappaB -> health advantage.
Overview of NF-kB influence
The NF-kB control system (in every cell of every higher living being)
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Normal state “Gesand”
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→ → →
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Alarm state "everything-or-nothing"
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← ← ←
tocotrienols
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inflammatory processes
Studies have shown that tocotrienols (especially delta-T3, gamma-T3 and TRF) block important inflammatory factors. Namely iNOS, COX-2, TNF-alpha and IL-1beta. All of these factors are controlled by NF-kappaB, so it is reasonable to assume that T3 lowers these inflammatory factors through its influence on NF-kappaB.
This control via the key genes works much more elegantly and completely than the mechanisms of action of the anti-inflammatory agents, which only block a few of these factors (such as only COX-2 through ibuprofen).
The mechanism of exactly how the anti-NF-kappaB effect of T3 works has not yet been researched, but the anti-inflammatory effects do not appear to occur directly (via iNOS, COX) or indirectly via NF-κB. As with all anti-inflammatory drugs, it must be borne in mind that the useful aspects of inflammation (defense against pathogens) must not be blocked. So far it has been documented that the strong inflammatory stimulus, such as that which occurs due to an infection or a Verlettong, can definitely override the general inhibition of inflammation through NF-kappaB blocking.
Anticancer through apoptosis
This mechanism protects against tumour formation by degenerated cells.
However, there are anti-apoptosis factors (e.g. survivin) that prevent apoptosis. Cancer cells increasingly produce such factors, presumably through NF-kappaB. NF-kappaB thus prevents cancer protection through apoptosis.
Since tocotrienol reduces NF-kappaB, this enables the cell's own protection against cancer-like degenerations. This could explain the “strong anticancer effect” of tocotrienols.
Dead cells remain unaffected, the apoptosis only affects cells that recognize their own degeneration via the "abnormality sensor", or which are stimulated by a killer T cell from the outside via a special death receptor (DR, death receptor) (see here a 4-minute animation to date).
More to dateHowT3 act against cancer through apoptosis
More to datethesT3 work against cancer
Aging
In older people, NF-kappaB tends to be more and more chronically elevated. This leads to a chronic inflammatory status and a higher susceptibility to cancer.
Body cells can enter a state of “senescence,” a type of age-related rigidity that is also related to NF-kappaB. Some very serious texts see T3 as a kind of rejuvenation opportunity against aging processes (for skin cells this was recently confirmed).
I would like to take the liberty of quoting the final word of the text discussed and translating it into German (you can find the full text in English here(link renewed to archive) ).
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"An area where T3s may effectively inpact human physiology is the chronic inflammatory state that is seen in the elthely. Systemic elevation of inflammatory cytokines such as TNF-α, IL-6, and IL-1 has been involved in the induction of age-associated frailty and correlates well with morbidity and death [32]. NF-κB dysregulation accompanies human aging [33,34]. It is possible that regulated consumption of T3s may counter this form of chronic NF-κB dysregulation without seriously inpacting acute NF-κB responses that are essential for immune responses and thereby improve the quality of life of the elthely." |
"One area where T3 can effectively influence human physiology is the chronic inflammatory state observed in the elderly. Systemic elevation of inflammatory cytokines such as TNF-α, IL-6, and IL-1 is associated with age-related frailty and correlates with disease and death[32]. it is widely hypothesized that the dysregulation of NF-κB is a side effect of aging in humans [33,34].
"It is possible that the controlled consumption of T3 against these forms of chronic dysregulation of NF-κB acts without affecting the acute responses of NF-κB that are necessary for the immune system, and so can improve the quality of life of older people." |
Other NFkappaB inhibitors
Tocotrienols are inhibitors of NFkappaB, which can explain a large part of their beneficial properties. There are other natural inhibitors of NFkB, for example:Resveratrol, Allicin, curcumin, genista,Quercetin, Gingko biloba, EGCG. They explain the anti-inflammatory properties of turmeric, garlic, red grapes, red clover, ginko and green tea and suggest that these plants such as T3 can also have an effect against cancer and slowing down aging.
The main health benefits of turmeric, grapes, garlic, ginkgo and green tea are also expected in tocotrienolsn, and vice versa.
The advantages of T3/tocotrienol in comparison to these substances are:
- T3 can be extracted relatively easily from common cooking oils
- T3 penetrates the skin very well and can therefore be used topically
- T3 is a very good antioxidant (factor 40 to 60 in comparison to alpha-tocopherol) and is relatively effective (NFkB is called a "redox-sensitive transcription factor")
- aige the plant-based alternatives have questionable properties (e.g. mutagenicity in quercetin)
- As a natural vitamin, T3 is known to have harmful side effects, especially in the low concentrations in which it becomes effective
Synergies of T3 with other natural substances to reduce NF-kB against cancer
For some of the natural substances mentioned, especially the turmeric, there is research that goes in the same direction as tocotrienolsn (anti-cancer and anti-inflammatory) Since they are NF-kB inhibitory, this is obvious. However, these substances are currently not easily available (except in food) and there are no good studies on the dosage as in tocotrienolsn.
However, we encourage the use of the mentioned natural substances at the same time as tocotrienolsn.
Turmeric (the main ingredient in Indian curry) also has a high level of research activity. Turmeric is available everywhere as a spice now also available for IV and oral use.
Of course, garlic is also available everywhere - the question is how to use it well.
EGCG (epigallocatechin gallate) is the main active ingredient in green tea and is contained in up to 1/3 weight of the dried tea leaves.
There is no reliable information about effective concentrations and bioavailability. However, these substances are promising and can easily be added to food.