Curcumin: benefits, dosage, contraindications

Other name(s) 

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Properties

Anti-inflammatory

Many compounds in turmeric exhibit anti-inflammatory effects primarily through volatile compounds like germacrone (sesquiterpene isolated from volatile oils). These beneficial effects are shown both in vitro and in vivo, in response to acute or chronic inflammations. In acute infections, the most frequently invoked mechanism involves prostaglandins, whose secretion is significantly reduced. Active compounds in turmeric also inhibit trypsin and hyaluronidase during inflammations, essential for the development of certain inflammations, especially joint-related. In chronic inflammation, several anti-inflammatory properties have been proposed following studies conducted in animals and humans: inhibition of phospholipases, lipooxygenases, leukotrienes, thromboxanes, prostaglandins, collagenase, elastase, hyaluronidase... as well as action on the generation of nitric oxide (NO). Regarding NO, curcuminoids inhibit the transformation of NO into peroxynitrite and nitrite, thereby avoiding the deleterious effects of these metabolites at the vascular and DNA cellular levels. Moreover, curcuminoids inhibit platelet aggregation and slow down the production of platelet thromboxane.

Antibacterial

Turmeric has antimicrobial properties. Indeed, turmeric or its curcuminoid constituents appear to have activity against certain bacteria, including E. coli, Yersinia enterocolitica, Staphylococcus aureus, Bacillus subtilis, Bacillus cereus, Helicobacter pylori, Mycobacterium tuberculosis, and Neisseria gonorrhoeae.

Antioxidant

Curcuminoids are electron donors, thus providing neutralization of free radicals and reactive oxygen species (ROS). Curcuminoids notably exert protection against lipid peroxidation. Furthermore, curcuminoids have an indirect action on ROS which operates at various levels: - Activation of protein kinase C and regulation of intracellular calcium, resulting in inhibition of ROS production. - Inhibition of 5-lipoxygenase, preventing the incorporation of ROS into polyunsaturated fatty acids. - Inhibition of the conversion of xanthine dehydrogenase/xanthine oxidase, thereby inhibiting superoxide ion production. - Modulation of superoxide dismutase expression, associated with regulation of oxidative stress at the cardiac and renal level.

Antidepressant

In humans, the antidepressant effects of curcumin were related to a decrease in inflammatory cytokine levels and an increase in brain-derived neurotrophic factor (BDNF) levels (a protein that acts on certain neurons in the central and peripheral nervous system. BDNF is involved in the survival of existing neurons and encourages the growth and differentiation of new neurons and synapses). The antidepressant effect of curcumin is also due to the decrease in cortisol levels and the role of the hypothalamic-pituitary axis. Furthermore, in vitro and animal studies suggest that the antidepressant effects of turmeric extract stem from its ability to inhibit monoamine oxidase (MAO) A and possibly MAO B, leading to an increase in serotonin, dopamine, and norepinephrine levels. Curcumin, a component of turmeric, also seems to increase adenylate cyclase activity and cyclic adenosine monophosphate (cAMP) concentration, which has been associated with antidepressant effects.

Cardiovascular

Turmeric slows down the atheromatous process in the arterial system by reducing aortic lipid deposits and in vivo blood levels of peroxidized lipids. In vitro, turmeric can protect against myocardial infarction by reducing inflammatory cytokines and extracellular matrix proteases. Furthermore, curcumin may have antithrombotic effects. Research suggests it could inhibit platelet aggregation, platelet-activating factor, and arachidonic acid, possibly by interfering with thromboxane synthesis. Other cardiovascular effects induced by turmeric in vitro include reduced blood pressure, vasorelaxation, and improved endothelial function.

Hepatoprotective

In cases of liver injury, curcumin has a major protective role by activating in the liver antioxidant enzymatic systems: superoxide dismutase, catalase, glutathione peroxidase, and transferase. Additionally, curcumin limits iron-induced oxidation.

Analgesic

It has been demonstrated that turmeric and its constituents, administered orally, alleviate pain, but the exact mechanism of action is not yet clear.

Digestive effect

With daily administration, turmeric leads to: • At the stomach level: - An increase in gastrin secretion. - Inhibition of ulcer formation induced by various stress factors: alcohol, indomethacin... • At the gallbladder level: A choleretic and cholagogue action, and prevents gallstone formation. • At the pancreas level: An increase in the activity of pancreatic lipases and amylases, trypsin, and chymotrypsin. • At the gastrointestinal tract level: An antispasmodic action.

Antiparasitic

Animal models have shown that curcumin may have activity against the protozoa Leishmania amazonensis, Toxoplasma gondii, Schistosomiasis mansoni, Giardia lamblia, and Plasmodium. In vitro evidence suggests that curcumin has antiparasitic activity against Cryptosporidium parvum.

Lipid-lowering

Through its antioxidant action, turmeric reduces lipid peroxidation induced by chemical molecules (carbon tetrachloride, paraquat, and cyclophosphamide). In humans, the ingestion of an alcoholic turmeric extract for 30 days: - Lowers LDL cholesterol (Low Density Lipoprotein) by 62% and ApoB (apolipoprotein B) by 83%. - Increases HDL cholesterol (High Density Lipoprotein) by 72% and ApoA by 25%.

Hypoglycemic

It has been found that curcumin can increase insulin sensitivity and secretion in insulin-resistant individuals. However, several clinical studies have shown that the reduction in blood glucose is minor and inconsistent overall. The decrease in blood glucose is likely significant in subjects with type 2 diabetes.

Safety dosage

Adults from 18 years: 100 mg - 300 mg

Interactions

Médicaments

Antiplatelet/Anticoagulant: moderate interaction

In vitro, turmeric shows antiplatelet effects. However, human research results are contradictory. Indeed, an increase in INR (international normalized ratio, a number that describes the effectiveness of anticoagulant treatment of the vitamin K antagonist family). Furthermore, another study showed that using a dietary supplement containing broccoli powder, turmeric powder, whole pomegranate powder, and green tea extract for 6 months does not influence the INR in patients taking warfarin. Similarly, combining 500 mg of curcumin with 100 mg of aspirin does not seem to increase antiplatelet effects.

Anticancer: moderate interaction

Research results are contradictory. Indeed, a study showed that curcumin in vitro inhibits up to 71% of breast cancer cell apoptosis induced by camptothecin, and up to 65% of breast cancer cell apoptosis induced by doxorubicin. However, other in vitro research indicates that curcumin might enhance the cytotoxic effects of camptothecin and doxorubicin. This discrepancy may be linked to the curcumin dose and exposure time. In humans, the effect of curcumin on the cytotoxicity of camptothecin and doxorubicin is unknown. On the other hand, using an in vivo model of human breast cancer, it was discovered that dietary supplementation with curcumin significantly inhibited tumor regression induced by cyclophosphamide. Yet, other research has shown that curcumin might increase the cytotoxicity of cyclophosphamide.

Antidiabetic: mild interaction

Some animal research suggests that curcumin can lower blood sugar and hemoglobin A1c in diabetic patients. On the other hand, pharmacokinetic studies showed that taking 475 mg of curcumin daily for 10 days then 5 mg of glyburide showed a 12% increase in glyburide blood concentration 2 hours after the dose, but the peak blood concentration did not change. Furthermore, the combination of curcumin and glyburide slightly reduced postprandial blood sugar for up to 24 hours compared to glyburide alone. Antidiabetic medications include: glimepiride (Amaryl*), glyburide (DiaBeta*, Glynase PresTab*, Micronase*), insulin, pioglitazone (Actos*), rosiglitazone (Avandia*), chlorpropamide (Diabinese*), glipizide (Glucotrol*), tolbutamide (Orinase*), and others.

CYP450 Substrates: moderate interaction

In vitro and in animals, turmeric inhibits cytochrome P450 3A4. Literature has reported a case of a patient who underwent a transplant and was taking tacrolimus (an immunosuppressant used primarily in organ transplants, taken orally and injectable), who experienced acute nephrotoxicity with an increased tacrolimus level at 29 mg/l (even though she had therapeutic range levels), following the intake of turmeric powder with 15 tablespoons or more per day. It was thought that turmeric increased the tacrolimus level by inhibiting cytochrome P450 3A4. Theoretically, turmeric may increase the levels of other drugs that are metabolized by cytochrome P450 3A4. Drugs metabolized by CYP3A4 include calcium channel blockers (diltiazem, nicardipine, verapamil), anticancer agents (etoposide, paclitaxel, vinblastine, vindesine), antifungals (ketoconazole, itraconazole), fentanyl (Sublimaze), lidocaine (Xylocaine), losartan (Cozaar), fexofenadine (Allegra), midazolam (Versed), and others.

Estrogens: minor interaction

In vitro research has shown that curcumin competitively displaces estrogen binding to its receptors. Thus, theoretically, the use of large amounts of curcumin may affect hormone replacement therapy.

P-glycoprotein substrates: minor interaction

In vitro and animal research has shown that curcuminoids and other constituents of turmeric can inhibit P-glycoprotein activity (a protein that acts as a pump capable of expelling specific substrates, which can be endogenous molecules or exogenous xenobiotic substances, using energy provided by ATP), thus promoting the absorption of P-glycoprotein substrates. These substrates include certain chemotherapeutic agents (etoposide, paclitaxel, vinblastine, vincristine, vindesine), antifungals (ketoconazole, itraconazole), protease inhibitors (amprenavir, indinavir, nelfinavir, saquinavir) and calcium channel blockers (diltiazem, verapamil), digoxin, corticosteroids, erythromycin, cisapride (Propulsid), fexofenadine (Allegra), cyclosporine, loperamide (Imodium), quinidine, etc.

Talinolol: moderate interaction

Preliminary research in humans shows that taking curcumin for 6 days before taking a single 50 mg dose of talinolol can reduce its bioavailability.

Sulfasalazine: moderate interaction

Clinical evidence has shown that curcumin taken at therapeutic doses in humans can increase blood levels of sulfasalazine by 3.2 times.

Plantes ou autres actifs

Curcumin: minor interaction

In vitro and animal studies suggest that curcumin or turmeric may bind to iron and prevent its absorption. This does not seem to occur in humans when turmeric is used at doses commonly found in food. However, theoretically, high doses of curcumin or turmeric may decrease iron absorption.

Precautions

Breastfeeding Woman: avoid

Data are insufficient to assess the safety of turmeric during breastfeeding, so avoid its use.

Gallstones: use with caution

Turmeric causes gallbladder contraction. Use with caution in patients with gallstones.

Bleeding Disorder: use with caution

Turmeric may increase the risk of bleeding and bruising due to its antiplatelet effects. Use with caution in patients with a bleeding disorder.

Iron Deficiency: use with caution

Using turmeric at commonly found dietary levels does not appear to reduce iron absorption. However, animal and in vitro studies show that high levels of curcumin might chelate iron and reduce its absorption. Use with caution in cases of anemia caused by iron deficiency.

Contraindications

Surgical Intervention: prohibited

Turmeric can slow blood clotting. This may lead to increased bleeding during and after surgery. Stop taking turmeric at least two weeks before surgery.

Pregnant Woman: prohibited

When used orally at medicinal doses during pregnancy, turmeric might trigger menstruation or stimulate the uterus, thus affecting the pregnancy.

Conseil scientifique