Curcumin (Curcuma longa): A Comprehensive Reference
1. Identity: Botanical and Chemical Characterization
1.1 Botanical Source and Taxonomy
Curcumin is a bright yellow chemical produced by the plant species Curcuma longa, the principal curcuminoid of turmeric, a member of the ginger family, Zingiberaceae. Turmeric (Curcuma longa) is a flowering plant in this family and is a perennial, rhizomatous, herbaceous plant native to the Indian subcontinent and Southeast Asia, requiring temperatures between 20 and 30 °C and high annual rainfall to thrive. Turmeric is believed to have originated from South or Southeast Asia, more likely in Vietnam, China, or western India, and is only identified as a domesticated plant, not found in the wild. India is the biggest producer, consumer, and supplier, but it is also cultivated extensively in Cambodia, Bangladesh, Nepal, Indonesia, Thailand, Malaysia, Madagascar, Tamil Nadu, Maharashtra, and the Philippines.
Plants are gathered each year for their rhizomes; some are used for propagation and others for consumption or dyeing. The rhizomes can be used fresh, but they are often boiled in water and dried, after which they are ground into a deep orange-yellow, shelf-stable spice powder commonly used as a coloring and flavoring agent in many Asian cuisines, especially for curries.
1.2 Chemical Identity
Curcumin (diarylheptanoid) is one member of a group of natural compounds called curcuminoids, derived from the rhizome of Curcuma longa, an East Indian plant, contained in an extract commonly called turmeric. Chemically, curcumin is a polyphenol, more particularly a diarylheptanoid. In 1910, Milobedzka and Lampe reported the chemical structure of curcumin to be as diferuloylmethane, and in 1913, the same group accomplished the synthesis of the compound.
Along with curcumin (curcumin I), the principal curcuminoid, three other curcuminoids are present in turmeric: demethoxycurcumin (curcumin II), bisdemethoxycurcumin (curcumin III), and the recently identified cyclocurcumin. Commercial curcumin is a mixture of curcuminoids containing approximately 77% curcumin, 18% demethoxycurcumin, and 3% bisdemethoxycurcumin. It is important to note that materials often referred to as curcumin are not identical to the pure, single-chemical entity.
The C. longa plant is known to possess acidic polysaccharides (which include ukonan A, B, C, and D), 4.2% volatile oils (which include turmerone, ar-turmerone, curcumene, germacrone, and ar-curcumene as main constituents), and 5.8% essential oils.
1.3 Common Forms and Preparations
Curcumin is sold as an herbal supplement, cosmetics ingredient, food flavoring, and food coloring. The most common applications are as an ingredient in dietary supplements, in cosmetics, as flavoring for foods such as turmeric-flavored beverages in South and Southeast Asia, and as coloring for foods such as curry powders, mustards, butters, and cheeses.
Rhizoma Curcumae Longae appeared in the WHO Monographs on Selected Medicinal Plants, Volume 1 (WHO, 1999); it is listed in the European Pharmacopoeia monograph #2543, and the European Scientific Cooperative on Phytotherapy (ESCOP) included it in its 2nd Edition Supplement monographs. Commercial supplement forms include standardized powdered root extracts, standardized curcuminoid extracts (typically 95% curcuminoids), phospholipid complexes (e.g., Meriva), nanoparticle formulations, and piperine-enhanced preparations, all of which have been developed to address curcumin's inherently low oral bioavailability.
2. Traditional and Historical Use
2.1 Timeline and Spread
Turmeric has been utilized by humans for nearly 6,000 years, with use in India dated back roughly 6,000 years. It probably spread to both Morocco and China by around 700 AD, reached East Africa by 800 AD and West Africa by 1200 AD. In the thirteenth century, Arab merchants brought turmeric to Europe.
The historic background of the Curcuma species begins in Far Eastern medicine and dates back 5,000 years in Ayurveda. Turmeric (Curcuma longa) maintained its cultural and therapeutic significance over centuries in Ayurveda, Unani, and Traditional Chinese Medicine.
2.2 Ayurvedic and South Asian Traditions
Curcumin, a yellow polyphenolic pigment from the Curcuma longa rhizome, has been used for centuries for culinary and food coloring purposes, and as an ingredient for various medicinal preparations, widely used in Ayurveda and Chinese medicine. Often called "Indian saffron" due to its vibrant yellow hue, turmeric is well documented in Indian traditional medicine and was customarily applied to the foreheads of Hindu girls for aesthetic purposes.
Traditionally, turmeric was widely used in Ayurveda medicine and traditional Asian medicine for treatment of digestive, respiratory and circulatory diseases, as well as skin diseases. The rhizome of turmeric has been used as an herbal medicine, coloring agent, spice, and food additive for thousands of years in different parts of the world particularly in Asian countries. It has been used for a range of diseases in many traditional medical schools, including Islamic traditional medicine, Chinese traditional medicine, and Ayurveda, mainly for digestive problems, as a cardio-, hepato-, and neuroprotective agent, as well as in many inflammatory conditions such as arthritis and for enhancing the immune system.
2.3 Traditional Chinese Medicine
In China, turmeric is used to treat various health conditions, including hepatitis, osteoporosis, sore throat, dermatitis, and wound healing. Historically, dried curcumin powder has been a fundamental component of traditional medicine, aiding in the treatment of numerous ailments.
2.4 Other Traditional Systems
Curcumin, a lipophilic polyphenolic antioxidant extracted from Curcuma longa, has been used for thousands of years in traditional medicine. It has been considered beneficial for health by diverse cultures and used as a dietary spice in India, Thailand, and Indonesia; Chinese traditional medicine and Ayurveda are examples of traditional schools demonstrating curcumin's health-promoting properties.
3. Key Constituents and Active Compounds
3.1 Curcuminoid Profile
The chemical composition of the turmeric rhizome is very diverse. Diarylheptanoid derivatives, also known as curcuminoids — of which curcumin, demethoxycurcumin, and bisdemethoxycurcumin are the most important representatives — are the major active constituents of the plant rhizome. These compounds exist in both keto and enol forms.
3.2 Antioxidant Properties
Curcumin has a polyphenol nature; therefore, its anti-inflammatory mechanisms may be due in part to its antioxidant properties. Many properties of curcumin — such as antioxidant, anti-inflammatory, antimicrobial, and antimutagenic effects — are attributed to the presence of hydroxyl and methoxy groups in the curcumin structure. Curcumin exhibits potent antioxidant properties by scavenging free radicals and modulating oxidative pathways to mitigate diseases associated with oxidative stress.
3.3 Anti-inflammatory Mechanisms
Curcumin exerts its core anti-inflammatory effects mainly by inhibiting the activation of nuclear factor-κB (NF-κB) signaling pathway, regulating the mitogen-activated protein kinase extracellular signal-regulated kinase (ERK) phosphorylation cascade, and regulating the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. The significant anti-inflammatory activity of curcumin stems from its regulation of multiple key signaling pathways, including NF-κB, MAPK, JAK-STAT, NLRP3 inflammasome, and Nrf2/ARE pathways.
Curcumin blocks the formation of reactive-oxygen species, possesses anti-inflammatory properties as a result of inhibition of cyclooxygenases (COX) and other enzymes involved in inflammation, and disrupts cell signal transduction by various mechanisms including inhibition of protein kinase C.
3.4 Bioavailability: A Central Challenge
The bioavailability of curcumin is poor in the body, due to low absorption, rapid metabolism, limited tissue distribution, and short half-life. Its clinical application faces significant bottlenecks, primarily manifested in its inherent extremely low water solubility, poor bioavailability, and unfavorable pharmacokinetic profile.
Piperine, an alkaloid from black pepper, inhibits hepatic and intestinal glucuronidation and can increase curcumin's bioavailability by up to 2,000%. The enhanced drug bioavailability caused by piperine is due to its potent inhibition of drug metabolism, being able to inhibit human P-glycoprotein and CYP3A4, while it interferes with UDP-glucose dehydrogenase and glucuronidation activities in liver. Various nano-formulations, including liposomes, nanoparticles, phospholipid complexes, and curcumin conjugates, have been shown to enhance solubility, stability, bioavailability, circulation time, and targeted action.
4. Scientific Evidence by Area of Use
4.1 Musculoskeletal: Osteoarthritis and Arthritis
Osteoarthritis (OA), particularly of the knee, is among the most extensively studied indications for curcumin in human clinical trials.
Eleven randomized controlled trials with a total of 1,258 participants with primary knee OA were reviewed and meta-analyzed. The meta-analysis results showed that curcuminoids were significantly more effective than comparators regarding visual analogue scale (VAS) and WOMAC pain scores. However, no significant difference in pain relief or adverse events between high-dose (daily dose ≥1,000 mg or total dose ≥42 g) and low-dose (daily dose <1,000 mg or total dose <42 g) curcuminoid treatments was observed.
One Bayesian network meta-analysis included 23 studies from 7 countries, comprising 2,175 knee OA patients and 6 interventions. The results showed that compared with placebo, curcumin significantly reduced the visual analogue scale pain score (MD = −1.63, 95% CI: −2.91 to −0.45) and total WOMAC score (MD = −18.85, 95% CI: −29.53 to −8.76).
In a further systematic review and meta-analysis including fifteen studies with 1,670 patients, curcuminoids were significantly more effective than placebo in improvements of VAS for pain (WMD: −1.77, 95% CI: −2.44 to −1.09) and WOMAC total score (WMD: −7.06, 95% CI: −12.27 to −1.84).
Meta-analyses of eight randomized controlled trials with more than 800 participants with primarily knee OA found scientific evidence supporting the efficacy of turmeric extract (about 1,000 mg/day of curcumin) in treating OA. Curcumin may have some beneficial effects on knee pain and quality of life in patients with knee OA; although curcumin is less effective at relieving pain than ibuprofen, it appears safe for short-term use and may reduce the need for rescue medication.
For broader arthritis, a meta-analysis of 29 RCTs involving 2,396 participants covering five types of arthritis — including Ankylosing Spondylitis, Rheumatoid Arthritis, Osteoarthritis, Juvenile idiopathic arthritis, and gout/hyperuricemia — found that curcumin and Curcuma longa extract, administered in doses ranging from 120 mg to 1,500 mg for a duration of 4 to 36 weeks, generally showed safety in all studies and improved the severity of inflammation and pain levels. However, the authors noted that more RCTs are needed.
Evidence strength: Moderate-to-good for knee OA pain outcomes. Multiple meta-analyses of RCTs consistently show statistically significant, though modest, pain reduction. Evidence for other arthritis subtypes is more limited and preliminary.
4.2 Metabolic Syndrome, Type 2 Diabetes, and Lipid Profile
A systematic review published in 2016 reviewed the effects of curcumin on chronic diseases including cancer, inflammatory diseases, metabolic diseases, cardiovascular diseases, neurological disease, and skin diseases. More recent clinical studies and systematic review/meta-analyses regarding metabolic syndrome show some heterogeneity; Tabrizi et al. reported that curcumin reduced fasting glucose, HbA1c, triglycerides, and total cholesterol in metabolic syndrome patients, although no changes in LDL and HDL levels were observed.
Accumulating clinical evidence demonstrates that curcumin has good therapeutic potential and a low number of side effects for type 2 diabetes mellitus, obesity, and non-alcoholic fatty liver disease. It can lower blood glucose and lipid levels, improve insulin resistance, and reduce inflammation and oxidative stress. However, more high-quality clinical trials are still required to verify its efficacy and determine its molecular mechanisms and targets.
On lipid outcomes specifically, results are mixed. One meta-analysis of randomized controlled trials did not indicate a significant effect of curcumin on any of the lipid parameters studied (total cholesterol, LDL-C, HDL-C, or triglycerides), and a subgroup analysis of studies in patients at cardiovascular risk also showed no significant effect. The authors concluded that further RCTs with longer supplementation duration, and bioavailability-improved formulations of curcumin, are warranted in dyslipidemic subjects.
By contrast, a review focusing specifically on bioavailability-enhanced formulations found more positive signals: curcumin supplementation significantly reduced at least one lipid profile index in 15 of 22 eligible studies, and improved more than one index in five studies. Curcumin had no effect on any lipid index in seven studies. Overall, studies using a bioavailable formulation of curcumin had a better impact on the lipid profile.
A meta-analysis of nano-curcumin supplementation found associations with improvements in glycemic profile by decreasing fasting blood glucose, insulin, and HOMA-IR, and increases in HDL. In terms of other lipid markers, subgroup analyses showed that nano-curcumin had more favorable effects on lipid profiles in individuals with dyslipidemia at baseline. Nano-curcumin supplementation also showed favorable anti-inflammatory effects by decreasing CRP and IL-6, and a hypotensive effect evidenced by a decrease in systolic blood pressure.
Evidence strength: Preliminary-to-moderate for metabolic outcomes. Effect sizes and significance vary considerably by formulation and baseline disease status. Bioavailability-enhanced forms produce more consistent signals. Results should be considered hypothesis-generating pending larger, more rigorous trials.
4.3 Inflammatory Bowel Conditions
Pharmacological studies have confirmed the therapeutic value of curcumin in a variety of inflammation-related diseases, including inflammatory bowel disease. Studies have shown that curcumin can intervene in the occurrence and development of chronic inflammatory diseases by regulating key inflammatory signaling pathways such as NF-κB, MAPK, and JAK-STAT, including in inflammatory bowel disease.
The use of a derivative of curcumin with high bioavailability and greater absorption, known as Theracurmin, showed promising results in patients with Crohn's disease by inhibiting NF-κB and thereby decreasing inflammatory cytokines.
Evidence strength: Preliminary. Human clinical data exist but are limited in scale and quality. Most evidence is mechanistic or early-phase. Findings cannot yet support clinical recommendations.
4.4 Cardiovascular Health
One pilot randomized, double-blind, placebo-controlled trial investigated curcumin efficiency on cardiovascular risk factors in 33 patients with coronary artery disease (CAD). Patients received curcumin 500 mg capsules four times daily for 8 weeks. Serum levels of triglycerides, LDL-cholesterol, and VLDL-cholesterol significantly decreased in the curcumin group compared to baseline, but in all laboratory parameters, a significant difference between curcumin and placebo groups was not detected.
A meta-analysis of nano-curcumin studies suggests that nano-curcumin supplementation may decline cardiovascular disease risk by improving glycemic and lipid profiles, inflammation, and systolic blood pressure. Future large-scale investigations with longer durations are needed to expand on these findings.
Evidence strength: Weak-to-preliminary in humans. Individual trials show internal signal, but head-to-head comparisons between curcumin and placebo across multiple well-powered RCTs have not consistently demonstrated cardiovascular benefit. The evidence base is insufficient to make clinical recommendations.
4.5 Neurological Health, Cognitive Function, and Depression
Curcumin supplementation has been shown in preclinical models to restore brain-derived neurotrophic factor (BDNF) levels while regulating monoaminergic neurotransmission and mitigating multiple pathological processes including oxidative stress, neuroinflammation, β-amyloid aggregation, tau pathology, and aluminum-induced neurotoxicity in both Alzheimer's disease and depression models.
Curcumin has displayed, in a number of studies, a potency in modulating neurotransmitter concentrations, inflammatory pathways, excitotoxicity, neuroplasticity, hypothalamic–pituitary–adrenal disturbances, insulin resistance, oxidative and nitrosative stress, and the endocannabinoid system, all of which can be involved in major depressive disorder (MDD) pathophysiology. To date, a handful of clinical trials have been published and suggest a benefit of curcumin in MDD. With evidence that is progressively growing, curcumin appears as a promising alternative option in the management of MDD.
For cognitive disorders, the picture is less clear. The results of published clinical trials (five for curcumin) are disappointing and do not allow definitive conclusions about the therapeutic or neuroprotective potential of curcumin. These compounds, being capable of interfering with several processes implicated in the early stages of dementia, could be useful in preventing or slowing down the pathology, but the potential preventive activity of curcumin should be evaluated in long-term exposure clinical trials using preparations with high bioavailability that are well standardized.
Curcumin is a polyphenol with strong antioxidant and anti-inflammatory effects that has been shown to be effective in ameliorating cognitive decline in animal studies. However, its clinical effectiveness is inconclusive, and relevant gastrointestinal adverse events have been reported.
Despite promising in vitro, in vivo, and in silico evidence, clinical translation is hindered by curcumin's low oral bioavailability, rapid metabolism, and limited central nervous system penetration. Nevertheless, preclinical and early clinical studies report beneficial effects on cognitive function, neuroinflammation, and neuronal survival across multiple neurodegenerative models.
Evidence strength: Preclinical evidence is strong and mechanistically diverse. Clinical evidence for depression is preliminary but suggestive. Evidence for cognitive/neurodegenerative disease in humans is currently weak and inconclusive, limited substantially by bioavailability challenges and small trial sizes.
4.6 Cancer: Preclinical Data and Early Clinical Trials
Extensive research over the past two decades suggests that curcuminoids interfere with multiple cell signaling pathways, providing support for the potential role of curcumin in modulating cancer development and progression. Curcumin has been shown to possess anti-angiogenic properties, and its angioinhibitory effects manifest due to downregulation of proangiogenic genes such as VEGF and angiopoietin and a decrease in migration and invasion of endothelial cells. One of the important factors implicated in chemoresistance and induced chemosensitivity is NF-κB, and curcumin has been shown to downregulate NF-κB and inhibit IKB kinase, thereby suppressing proliferation and inducing apoptosis.
Because of the abundance of in vitro and preclinical studies in the past two decades, there has been a significant increase in the number of clinical trials investigating the therapeutic potential of curcumin-containing products. These clinical trials have used varying formulations and doses of curcuminoids for the prevention and treatment of cancer and to ameliorate symptoms of cancer treatment. With varying formulations and doses tested in phase I clinical trials, there is evidence of bioavailability of curcumin and curcumin conjugates in plasma, urine, and tissue. Results from early-phase trials of curcumin-containing products in the chemoprevention of colon, oral, and hepatic carcinoma appear promising. However, the findings from these early trials have to be confirmed in well-powered trials evaluating safety and effectiveness as indicated by modulation of clinical outcomes.
While these reports can possibly provide support for the potential role of curcumin-containing products in modulating carcinogenesis, definitive conclusions cannot be made, especially in light of the widespread confusion regarding the chemical nature of curcumin-containing products.
Evidence strength: Preclinical evidence is extensive and mechanistically compelling. Human clinical trial data are limited to early-phase (Phase I/II) pilot studies, which show bioavailability and preliminary signals, but do not establish efficacy. No phase III trials have demonstrated clinical benefit to date. The NCI characterizes the evidence as preliminary.
4.7 Respiratory Conditions (COPD and Asthma)
In COPD, macrophages, eosinophils, and neutrophils can trigger NLRP3 inflammasome and NF-κB signaling. The increase in immune and inflammatory responses can cause neutrophil influx, airway inflammation, mucus hypersecretion, and lung damage. In asthma, immune cells can activate Th2 and Th17 responses, leading to hypersensitivity, airway remodeling, and chronic inflammation. Curcumin inhibits these pathways by modulating immune cell activation and blocking NF-κB and NLRP3 signaling, resulting in reduced inflammation and tissue damage in both COPD and asthma.
Evidence strength: Primarily mechanistic and preclinical. Human clinical evidence in respiratory disease is very limited. Studies are small, and robust RCT data are lacking.
4.8 Summary of Evidence Across Areas
Among the most studied disease categories in clinical trials of curcumin — metabolic syndrome, osteoarthritis, neurocognitive disorders, gastrointestinal disorders, and cancer — the preponderance of current evidence for several highly studied diseases (metabolic syndrome, osteoarthritis) is suggestive of clinical benefits. Additional research is needed, including systematic evaluation of diverse curcumin formulations and doses in larger, well-designed randomized controlled trials.
5. Body Systems and Health Areas Associated with Curcumin
Curcumin possesses a wide spectrum of pharmacological and biological properties including antioxidant, anti-inflammatory, neuroprotective, anticarcinogenic, antibacterial, antidiabetic, chemoprotective, and immunomodulatory actions. It has beneficial effects on cardiovascular disease, gastrointestinal tract, and skin as well. Curcumin regulates numerous cytokines, transcription factors, adhesion molecules, protein kinases, redox status, and enzymes related to inflammation, which plays a principal role in most chronic illnesses.
- Musculoskeletal system: Osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, gout
- Metabolic system: Type 2 diabetes mellitus, metabolic syndrome, obesity, non-alcoholic fatty liver disease (NAFLD)
- Cardiovascular system: Lipid profiles, blood pressure, atherosclerosis
- Nervous system: Neuroinflammation, Alzheimer's disease, Parkinson's disease, major depressive disorder
- Gastrointestinal system: Inflammatory bowel disease (Crohn's disease, ulcerative colitis), irritable bowel syndrome
- Respiratory system: COPD, asthma
- Integumentary system: Atopic dermatitis, psoriasis, wound healing
- Oncological: Chemoprevention research (colon, oral, hepatic) and adjunctive cancer therapy investigation
6. Dosage Forms and Doses Reported in Clinical Studies
Curcumin is administered in a wide variety of doses across clinical research, and no single universally established therapeutic dose exists. The following reflects doses as reported in the cited primary and review literature:
- Meta-analyses of randomized controlled trials in knee osteoarthritis have studied approximately 1,000 mg/day of curcumin as a commonly evaluated dose.
- In arthritis trials, curcumin and Curcuma longa extract were administered in doses ranging from 120 mg to 1,500 mg for a duration of 4–36 weeks.
- In a cardiovascular pilot trial in coronary artery disease patients, the dose used was 500 mg capsules four times daily (2,000 mg/day) for 8 weeks.
- A systematic review defined "low dose" as a daily dose under 1,000 mg or total dose under 42 g, and "high dose" as a daily dose of 1,000 mg or more or total dose of 42 g or more, finding no significant difference in pain relief between the two dose ranges in knee OA.
Doses as high as 12 g/day have been reported as well tolerated by human subjects in certain studies.
Regarding pharmacopeial standards, the European Food Safety Authority identified 5 mg/kg per day as the no observed adverse effects level (NOAEL).
The literature includes more than 11,000 scientific articles describing curcumin's properties. In the last three decades, various surveys by the U.S. Food and Drug Administration (FDA) concluded that curcumin, the most active ingredient of turmeric, is a "generally safe" compound with strong antioxidant effects.
7. Safety Considerations and Notable Interactions
7.1 General Tolerability
Adverse reactions associated with oral intake of turmeric are listed as frequent bowel movements and mild gastric discomfort. Other reported side effects of turmeric include upset stomach, acid reflux, diarrhea, constipation, and dizziness.
The American Herbal Products Association's Botanical Safety Handbook lists turmeric as Class 1 (herbs that can be safely consumed when used appropriately) and Interaction Class A (herbs for which no clinically relevant interactions are expected). Turmeric in culinary amounts is broadly considered safe. Although turmeric in culinary amounts is considered safe, the use of supplements often containing enhanced bioavailability agents like piperine may increase systemic exposure to curcumin.
7.2 Hepatotoxicity Signal
Several reports from various global surveillance systems on the safety of plant products have pointed out cases of hepatotoxicity linked to consumption of food supplements containing powdered extract and preparations of Curcuma longa. The latest trend is the use of Curcuma longa as a weight-loss product in combination with piperine. While only a few cases of hepatotoxicity, assessed using the Roussel Uclaf Causality Assessment Method (RUCAM), from prolonged intake of piperine and curcumin have been reported, it would be reasonable to speculate that the suspected toxicity of Curcuma longa could be due to the concomitant presence of piperine itself.
Piperine may raise systemic curcumin levels by acting as an inhibitor of cytochrome enzymes, allowing reactive metabolites to accumulate. High or sustained concentrations of curcumin can shift its activity from antioxidant to pro-oxidant, generating reactive oxygen species (ROS) that induce mitochondrial dysfunction and hepatocyte apoptosis. This effect underscores the fine balance between curcumin's protective and potentially harmful effects. Together, these pharmacokinetic and biochemical factors suggest that piperine and high-dose curcumin can synergistically increase susceptibility to liver injury.
7.3 Drug Interactions
The enhanced drug bioavailability caused by piperine is due to its potent inhibition of drug metabolism, being able to inhibit human P-glycoprotein and CYP3A4, while it interferes with UDP-glucose dehydrogenase and glucuronidation activities in the liver. This means piperine-containing curcumin preparations have the potential to elevate plasma concentrations of many drugs metabolized by CYP3A4.
There is a theoretical pharmacodynamic interaction with turmeric and anticoagulant medications; participants on anticoagulant therapy have been excluded from clinical trials as a precaution. Curcumin could theoretically inhibit CYP2C9 and CYP3A4; individuals taking medications considered to be sensitive substrates for either of these should be monitored carefully.
Some sources advise against combining amounts greater than 15 g turmeric powder per day with antiplatelet or anticoagulant medications.
Consuming large doses of turmeric supplements can increase urinary oxalate levels, increasing the risk of kidney stone formation.
7.4 Gallbladder and Biliary Considerations
Turmeric preparations are contraindicated in cases of obstruction of the biliary tract, and caution is advised in individuals with gallstones.
7.5 Pregnancy and Lactation
Animal studies have demonstrated that curcumin can negatively affect the blastocyst stage, implantation, and post-implantation embryo development in healthy animals; thus, the use of curcumin in pregnancy must be carefully evaluated, and it should be avoided as self-medication until further studies are carried out to define the real safety and effectiveness during pregnancy.
Reviews focused on the possible use of curcumin during pregnancy to prevent and/or reduce pregnancy-related complications such as gestational diabetes mellitus, hypertension, and preeclampsia found that the information currently available is still limited and fragmentary, mainly coming from in vitro and animal studies.
7.6 Key Summary of Safety Points
- In the last three decades, various surveys by the U.S. FDA concluded that curcumin is a "generally safe" compound with strong antioxidant effects.
- The potentiation of curcumin absorption by piperine may elevate the risk of hepatotoxicity, as reported in several recent cases involving turmeric-piperine combinations.
- Turmeric and cinnamon both increase anticoagulation and should be used with caution or monitored closely when combined with anticoagulant medications.
- The European Food Safety Authority identified 5 mg/kg per day as the no observed adverse effects level (NOAEL).
References
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