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Does taking turmeric help, and how much of it does one have to take?

American scientists were able to show a favorable effect after feeding curcumin to mice with CF with a particular genetic defect (so-called deltaF508 – original source: “Curcumin, a major constituent of turmeric, corrects cystic fibrosis defects.” Science 2004, 304: 600-602). Curcumin is an ingredient of turmeric, a curry spice that is widely used in Asian cuisine. It causes the yellow color and the intensive flavor of the spice.

The genetic defect deltaF508 is the most frequent form of the mutation of the CF gene and is found in approximately 70 percent of all patients in Northern and Central Europe. Due to this defect, among other things, the chloride ion channel (so-called CFTR channel) is formed but not able to reach its destination within the cell. Therefore, it cannot work properly. The researchers were able to prove in mice and a hamster cell culture that the CFTR channel worked close to normal again after a turmeric treatment. To explain turmeric’s mechanism of action, the scientists, among other things, hypothesized that it blocks so-called chaperones that would usually prevent the defective CFTR channel from reaching its destination, the cell surface. Another possible explanation is that turmeric attaches itself directly to the CFTR channel and changes its features in a way that guarantees its normal function again.

It is not known in how far these results obtained from mice can actually be transferred to humans. So far, studies with CF test subjects have not been able to confirm this favorable data gained from animal experiments. Although curcumin has proven to be well-tolerated even in higher dosages, one cannot exclude relevant side effects with humans. Therefore, curcumin intake in therapeutic dosages outside of controlled studies is not to be recommended in any case.

For your information, I am including here an earlier question (from 2004) about curcumin from the German expert advice on CF, in which Prof. Wagner warns extensively about risks involved in uncritically transferring data from animal experiments to humans.

Kind regards,
Dr. TO Hirche

-----Quoting earlier question to the expert advice, dated 13.05.2004:


My son Timo is delta F508 heterozygous. Can one expect a positive effect of curcumin here, too? Is it right that this does not concern turmeric, the dietary supplement, but merely the coloring agent, i.e., E100=cucurmin? – 45mg of that per kilogram body weight?

When can one expect first research results concerning side effects and dosage? I would be very grateful for an answer – kind regards from Saarbruecken

Ilka Ebert-Roßbach and Timo


Hello Ilka and Timo!

Not so fast, please… It does not work like that! This does not have anything to do with being overly cautious, or with laws or regulations. But it is not so simple. This is a study with laboratory animals, small delta-F508-homozygous mice; depending on the respective experimental directive, 1 or 45 mg/kg were administered, but one certainly cannot just project that and do it the same way with humans. In addition, curcumin is a chemical compound used for experimental research and whose features have not been tested for innocuousness with humans. The mice were treated between three days and eleven weeks; again, this cannot be extrapolated to humans regarding effectiveness or innocuousness. In their own study, the authors themselves challenge the question whether the effect is transferable to humans: “Naturally, it has to be noted that the success achieved in the animal experiments presented here does not guarantee similar results with CF patients. Taken together, questions about the bioavailability of curcumin, about the ways in which it is being metabolized by different specie, and about the extent to which the mice model accurately emulates the significant features of CF could diminish curcumin’s ability to alter the function of delta-F508 in the situation of the disease in a human being.”

As for the other aspects of your questions: there are delta-F508 heterozygous forms that seem to have the same cellular-biological defect as the homozygous form; there are also, however, those where the biochemical effect is completely different. If the second mutation is known, one can – at least for some mutations – speculate whether the mechanism of action (if it is traceable with humans) can work with this kind of mutation, too.

We all hope that there will be a multicentric study – perhaps already beginning this fall. It is hard to tell when one can anticipate results. Presumably, such a study will comprise homozygous delta-F508 subjects as a start. However, it is a long way from such a study to an approved therapy. Considering that the substance leads to an improvement of the electrolyte disorder (with mice!!) by avoiding that the final control of cell-produced protein molecules is tricked, one can also imagine other, unwanted effects. After all, this control system is not an unnecessary luxury but vital for the complex cellular processes. Here, before one can dare to undertake such a drastic modification with a human being over years or decades (through administration of the drug over such long periods, since there are no lasting welcome effects, after all – if the active ingredient is deactivated or eliminated, no effect can be proven anymore), one has to examine as accurately as possible the promotion of tumor development or other long-term effects.

Kind regards,
Prof. Dr. T.O.F. Wagner

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