Curcumin linked to deadly liver disease

[Curt]

329 - Common herbal supplement linked to deadly liver disease
Times of India Lifestyle Desk 02 June 2025 https://timesofindia.indiatimes.com/life-style/health-fitness/health-news/common-herbal-supplement-linked-to-deadly-liver-disease/articleshow/121484287.cms

The Drug Induced Liver Injury Network (DILIN has reported several cases of liver injury linked to turmeric supplements. In a study spanning from 2004 to 2012, ten cases were identified, al occurring after 2011, with a noticeable increase since 2017. Symptoms reported include fatigue, nausea, dark urine, and jaundice. In severe instances, patients required hospitalization, and one case resulted in acute liver failure.

Example: 54 year-old Robert Grafton had been taking multiple natural supplements, including turmeric but was then diagnosed with a deadly liver disease. "In March, the former radiology technologist added something new to his regimen - a turmeric based liquid supplement. He had seen it advertised for improving liver health on social media. However a week later, Grafton noticed his urine had turned dark, he felt nauseous, lost his appetite and was constantly itchy," the Daily Mail reported.

Tests revealed he had developed drug induced liver injury. He was taking turmeric pills that contained 2,250 milligrams of curcumin.
...............................................
The article recommends to be careful and follow the allowed dosages of supplements overall. Also watch out for Black Pepper (piperine) added to boost absorption but it can increase the risk of liver issues in some people, especially if taking medications.
...............................................

Comparing the side effects of excessive use of herbs vs excessive use of medicines the number of cases reported i.e. 10 case over 8 years is not significant. However, this can because of the reporting mechanism and awareness of the existence of a database that needs to be updated. The key takeaway here is that no matter how beneficial or how potent and reliable a substance is in addressing symptoms or disease conditions nothing should be taken in excess , too frequently or  too casually. Apply self-control and balance in everything.

[Richard Myers]

At first when reading the article I was concerned that something was not right. But, as I continued reading i agree with the article. It was not the amount of turmeric that was 2250mg, it was the amount of curcumin that was being taken. When concentrating a remedial agent we can expect side effects.   Having been greatly blessed by taking a moderate dose of curcumin twice, I would hesitate to say it is dangerous. It has been used for a very long time and there has not been a lot of problems reported. That does not mean all herbs being used for a long time are safe. Read the medical study being used to support the risk from using the remedial agent (curcumin) with black pepper. Curcumin is not easily absorbed. Black Pepper increases the amount of Curcumin being absorbed, thus increasing the risk of side effects when taking a large dose of Curcumin.

When experiencing the greatest  pain, Cucumin removed it completely. I took it two days and only had a small amount of the mixture which included Vit C, Vit D3, and magnesium.  The Curcumin was a very high purity level which could not be found again. Thus, I refused to use it since it was so powerful. There might be a time when it would be a great value. So, here is the study being used to support the article revealing the risk.

Clinical Research StudyVolume 136, Issue 2p200-206February 2023
Liver Injury Associated with Turmeric—A Growing Problem: Ten Cases from the Drug-Induced Liver Injury Network [DILIN]
Dina Halegoua-DeMarzio, MDa dlh004@jefferson.edu ∙ Victor Navarro, MDb ∙ Jawad Ahmad, MDc ∙ … ∙ Elizabeth Phillips, MDl ∙ Andrew Stolz, MDm ∙ Raj Vuppalanchi, MDi … Show more
Cover Image - The American Journal of Medicine, Volume 136, Issue 2

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Abstract
Background
Turmeric is a commonly used herbal product that has been implicated in causing liver injury. The aim of this case series is to describe the clinical, histologic, and human leukocyte antigen (HLA) associations of turmeric-associated liver injury cases enrolled the in US Drug-Induced Liver Injury Network (DILIN).
Methods
All adjudicated cases enrolled in DILIN between 2004 and 2022 in which turmeric was an implicated product were reviewed. Causality was assessed using a 5-point expert opinion score. Available products were analyzed for the presence of turmeric using ultra-high-performance liquid chromatography. Genetic analyses included HLA sequencing.
Results
Ten cases of turmeric-associated liver injury were found, all enrolled since 2011, and 6 since 2017. Of the 10 cases, 8 were women, 9 were White, and median age was 56 years (range 35-71). Liver injury was hepatocellular in 9 patients and mixed in 1. Liver biopsies in 4 patients showed acute hepatitis or mixed cholestatic-hepatic injury with eosinophils. Five patients were hospitalized, and 1 patient died of acute liver failure. Chemical analysis confirmed the presence of turmeric in all 7 products tested; 3 also contained piperine (black pepper). HLA typing demonstrated that 7 patients carried HLA-B*35:01, 2 of whom were homozygous, yielding an allele frequency of 0.450 compared with population controls of 0.056-0.069.
Conclusion
Liver injury due to turmeric appears to be increasing in the United States, perhaps reflecting usage patterns or increased combination with black pepper. Turmeric causes potentially severe liver injury that is typically hepatocellular, with a latency of 1 to 4 months and strong linkage to HLA-B*35:01.
Keywords

    Drug-induced liver injury
    Hepatotoxicity
    Herbal-induced liver injury
    Turmeric

Clinical Significance
•
Turmeric is a widely used herbal product promoted as a dietary supplement for a variety of conditions.
•
Liver injury due to turmeric appears to be increasing, reflecting usage patterns and combination with black pepper, which increases its absorption.
•
The pattern of turmeric-related liver injury is typically hepatocellular, with a latency of 1 to 4 months and linkage to HLA-B*35:01.
Introduction
Turmeric is a widely used herbal product derived from the roots of Curcuma longa, a perennial plant belonging to the ginger family. Extracts of the rhizomes of turmeric contain curcuminoids, such as curcumin, which are believed to be the active components.1 Turmeric is promoted as a dietary supplement for a variety of conditions, including arthritis, respiratory infections, liver disease, aging, and more recently, for prevention of coronavirus disease 2019 (COVID-19).2 Recently, turmeric has been implicated in rare cases of clinically apparent acute liver injury.3-6
Trials of turmeric in humans have not shown toxic effects,7-10 and curcumin is reported to be safe orally at the dose of 6 grams per day for 4 to 7 weeks.11 One reason given for its safety is that curcumin is poorly absorbed orally. Indeed, it is unclear whether there is adequate systemic exposure to achieve any of the purported beneficial or adverse effects of oral turmeric or curcumin.12,13 However, recently marketed turmeric supplements often include piperine (black pepper), which can substantially increase its systemic bioavailability. For example, only 20 mg of piperine taken with turmeric is reported to increase its bioavailability 20-fold in serum.12 Conceivably, the enhanced bioavailability could potentiate liver injury.
The US Drug-Induced Liver Injury Network (DILIN) has prospectively enrolled cases of liver injury due to medications and herbal and dietary supplements since 2004.14-18 Patients with suspected drug-induced liver injury undergo testing to exclude other causes of liver injury, and expert opinion is used to assess whether the liver injury is due to a medication or herbal and dietary supplements.15 The aims of this case series were 1) to describe the clinical phenotype of turmeric-associated hepatotoxicity, 2) conduct chemical analysis of products to confirm the presence of turmeric, and 3) perform genetic analyses to identify possible human leukocyte antigen (HLA) associations.
Materials and Methods
The DILIN Prospective Study (ClinicalTrials.gov Identifier: NCT00345930) is an ongoing multicenter observational study conducted at 6 centers throughout the United States. Its design and inclusion and exclusion criteria have been described previously in detail.15 Suspected cases of drug-induced liver injury presenting within 6 months of injury onset meeting predefined laboratory criteria are prospectively enrolled in DILIN at clinical study sites. Eligibility criteria include total bilirubin ≥2.5 mg/dL or international normalized ratio (INR) >1.5 and any elevation in alanine or aspartate aminotransferase (ALT or AST) or alkaline phosphatase (Alk P) levels; or elevations of ALT or AST above 5 times the upper limit of normal (ULN) or Alk P above 2 times ULN on 2 consecutive measurements at least 24 hours apart. A systematic approach is used to exclude nondrug or nonherbal and dietary supplement causes for the liver injury.15
A standardized protocol assesses the causal relationship between the use of a medication or herbal and dietary supplements and liver injury.15 Causality is graded by expert consensus opinion as either definite (>95% likelihood), highly likely (75%-95%), probable (50%-74%), possible (25%-49%), or unlikely (<25%). The pattern of liver injury is categorized using the R-value, where R = [ALT/ULN] ÷ [Alk P/ULN]; hepatocellular being defined by an R ≥5, cholestatic ≤2 and “mixed” between 2 and 5. A 5-point scale is used to define severity, ranging from 1 (mild, anicteric), 2 (moderate, jaundiced), 3 (moderate and hospitalized), 4 (severe, evidence of hepatic failure), and 5 (death or liver transplantation due to drug-induced liver injury within 6 months of onset).
For the current study, only high confidence cases of herbal and dietary supplement-related liver injury (causality graded as definite, highly likely, or probable) were assessed for demographic, clinical, biochemical, and histologic features. Descriptive statistics were computed for demographic and patient characteristics by median (lowest, highest) for continuous variables and as frequency (%) for categorical variables.
In herbal and dietary supplement suspected cases, attempts were made to retrieve the product taken by the patient for inclusion in a supplement repository. Products were then sent to the National Center for Natural Products Research (University of Mississippi, University Park), where they were tested using high-performance liquid chromatography and mass spectroscopy to verify that the ingredients matched the product label, and to search for contaminants and common hepatotoxins. In patients who gave consent for genetic testing, DNA was extracted from whole blood at a central sample repository and aliquots were sent to the Vanderbilt University Medical Center Immunogenomics, Microbial Genetics, and Single Cell Technologies core for high resolution HLA Class I and II gene sequencing. Available liver biopsies were sent to and reviewed by a single expert hepatic histopathologist (DEK). The biopsies were scored for multiple histological features as well as an overall pattern of liver injury without knowledge of the clinical information.19
Descriptive statistics were computed to describe the study cohorts, using median and range for continuous variables and frequency and percentage for categorical variables. Comparisons of the allele or carriage frequency of HLA-B*35:01 between groups were assessed by Fisher's exact test. All analyses were carried out in SAS version 9.4 (SAS Institute Inc, Cary, NC). All authors had full access to the study data and reviewed and approved the final manuscript.
The DILIN Prospective Study was registered with ClinicalTrials.gov (NCT # 00345930). All patients provided written informed consent for enrollment, and all details of the study protocol were reviewed and approved by institutional review boards at each site as well as by a Data Safety and Monitoring Board appointed by the National Institute of Diabetes and Digestive and Kidney Diseases.
Results
A total of 2392 cases of suspected drug-induced liver injury were enrolled in the DILIN Prospective Study between September 2004 and March 2022. Of this total, 2278 had undergone formal adjudication for causality and 1798 were scored as definite, highly likely, or probable (high confidence). Of the high confidence cases, 345 (19%) were attributed to an herbal and dietary supplement, 10 (3%) of which were attributed to turmeric. All turmeric cases were enrolled during or after 2011, and 6 since 2017 (Figure 1).
Figure 1
Figure 1 Year of presentation of 10 cases of turmeric liver injury. Shown are the years of the clinical presentation of 10 cases of turmeric liver injury reported in the Drug-Induced Liver Injury Network Prospective Study. Cases with turmeric exposure only are shown in blue; those with combined turmeric and piperine exposure (based upon product label and chemical analysis) are shown in orange.
The 10 cases included 8 female and 2 male patients; 9 were White and 1 was Black (Table 1). The median age was 56 years (range 35 to 71), and median BMI 26.7 kg/m2 (range, 14.7 to 39.5). Seven patients used alcohol, but none to excess, and none had a history of underlying liver disease.
    Total (N = 10)
Median age/years (range)   56 (35-71)
Sex: female/male   8/2
Race: White/African American   9/1
Median BMI kg/m2 (range)   26.7 (14.7-39.5)
Alcohol use/abuse   8/0
    Onset   Peak
Median ALT, U/L (range)   1140 (328-2245)   1392 (470-2521)
Median Alk P, U/L (range)   164 (41-441)   168 (88-538)
Median total bilirubin, mg/dL (range)   2.5 (0.7-13.9)   4.0 (0.8-26)
Median INR (range)   1.0 (0.9-1.2)   1.1 (1.0-2.5)
ANA +   5 (50%)
ASMA +   2 (20%)
Median IgG, mg/dL (range)   1070 (769-1840)
Median days from starting turmeric to symptoms (range)   84 (16-410)
Median days from starting turmeric to DILI onset (range)   86 (38-429)
Median days from onset to peak bilirubin   8 (0-19)
Median days from peak bilirubin to <2.5 mg/dL   10.5
Enzyme pattern at onset   
Cholestatic (R ≤2)   0 (0%)
Mixed (R >2 and <5)   1 (11%)
Hepatocellular (R >5)   9 (89%)
Median R value at onset (range)   13.9 (3.4-42.
Severity score   
Mild   5 (50%)
Moderate   1 (10%)
Moderate-hospitalized   3 (30%)
Severe   0 (0%)
Fatal   1 (11%)
Chronic liver injury   0 (0%)
Table 1
Clinical Features of 10 Patients with Acute Liver Injury Attributed to Turmeric
Alk P = alkaline phosphatase; ALT = alanine aminotransferase; ANA = antinuclear antibody; ASMA = anti-smooth muscle antibodies; BMI = body mass index; IgG = immunoglobulin G; INR = international normalized ratio.

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The 3 most common reasons reported by patients for turmeric use were arthritis, pain relief, and general health or well-being. Turmeric was used for a median of 86 days prior to onset of injury with laboratory abnormalities (range 38-429 days). At presentation, 9 patients were symptomatic, and the most common symptoms were jaundice, nausea, and abdominal pain. None had fever or rash noted on presentation, and itching was not prominent. Initial median ALT was 1140 U/L (range 328-2245), Alk P 164 U/L (41-441), total bilirubin 2.5 mg/dL (0.7-13.9), and INR 1.0 (0.9-1.2). Five patients developed jaundice, and median serum total bilirubin peaked at 4.0 mg/dL (0.8-26) and INR 1.1 (1.0-2.5). Liver injury pattern was initially hepatocellular in 9 patients and mixed in 1 patient (median R = 13.9; range 3.4-42.. Five patients were hospitalized, and one patient died of acute liver failure. No patient underwent liver transplantation, and none of 9 patients had evidence of chronic liver injury when seen 5 or more months after onset.
Five patients had antinuclear antibody (1:160 to 1:640), and 2 had low levels of smooth muscle antibody (1:20 and 1:80). However, immunoglobin levels were normal or only modestly elevated (immunoglobulin G 769-1840 mg/dL) in the 7 patients in whom they were measured, and only one patient was treated with corticosteroids (and for 6 days only). Extrahepatic manifestations such as rash, thrombocytopenia, neutropenia, or other manifestations of acute drug hypersensitivity were not seen. A history of drug allergies was reported by 7 patients, but none had a history of liver injury from a medication.
Five patients underwent liver biopsies, 4 of which were available for central review (Figure 2). Three biopsies were obtained within 30 days of injury onset, while the fourth was done approximately 8 months later. Of the 3 biopsies performed within 30 days of onset, 2 showed acute hepatitis with moderate to severe inflammatory activity and the third showed a cholestatic hepatitis with mild inflammation and moderate cholestasis in zone 3. The cases showing acute hepatitis histologically both had increased numbers of eosinophils. One of the cases with severe hepatic injury also had clusters of plasma cells and both confluent and bridging necrosis, mimicking autoimmune hepatitis. All 3 cases showed duct injury and varying degrees of hepatocyte apoptosis. No biopsy had advanced fibrosis, although the one case with severe hepatic injury did show portal fibrotic expansion. Two had mild macrovesicular steatosis. The biopsy taken at 8 months after onset showed minimal hepatitis with eosinophils and no fibrosis.
Figure 2
Figure 2 Histological changes associated with turmeric liver injury. (A) Case 3: Severe acute hepatitis with bridging necrosis spanning between a portal area and a central vein (hematoxylin & eosin [H&E] 200×). (B) Case 3: Higher magnification shows clusters of plasma cells at the portal-parenchymal interface (H&E 600×). (C) Case 4: Canalicular cholestasis (arrow) with mild lobular hepatitis (H&E 400×). (D) Case 5: Moderate hepatitis with increased numbers of eosinophils (arrows) in the portal area (H&E 400×).
The turmeric products consumed by patients and implicated in injury were obtained from 7 patients. Chemical analysis confirmed the presence of turmeric in all 7; 3 also contained piperine (black pepper), and none contained green tea (Camellia sinensis), Garcinia cambogia, or Polygonum multiflorum (Fo-ti). Piperine was noted on the label of an additional patient's product that was not available for testing. No other common hepatotoxins were detected.
All 10 patients underwent HLA sequencing, and 7 were found to carry HLA-B*35:01, a class I HLA allele previously implicated in green tea, Garcinia cambogia, and Polygonum multiflorum hepatotoxicity.20,21 Two patients were homozygous, so that the allele frequency was 0.450 and carrier frequency 70%. The published allele frequencies of HLA-B*35:01 in a large US population is 0.056 in Whites of European ancestry and 0.069 in Americans of African ancestry (allelefrequenices.net: accessed August 11, 2022). There were minor differences in clinical and biochemical features of the 7 patients with HLA-B*35:01 and the 3 without this allele, but the numbers of cases were too few to make any firm conclusions (Table 2). The 3 subjects without HLA-B*35:01 included the single Black patient (Case #2), the single case with mixed rather than hepatocellular liver injury (Case #7), and the single case of acute liver failure, which also was unusual in having a latency to onset of more than 1 year (Case #10).
Feature   HLA-B*35:01 Positive (n = 7)   HLA-B*35:01 Negative (n = 3)
Female sex   5 (72%)   3 (100%)
White race   7 (100%)   2 (67%)
Age [years], median (range)   55 (35-71)   62 (37-63)
Latency to symptom onset [days]   52 (16-99)   104 (76-410)
Latency to lab onset   70 (38-107)   109 (83-429)
Initial ALT [U/L]   1425 (328-2245)   581 (470-1230)
Initial Alk P [U/L]   125 (41-250)   329 (164-441)
Initial bilirubin [mg/dL]   0.8 (0.5-13.9)   2.5 (1.6-6.0)
Initial R value   13.7.1 (9.3-42.   8.5 (3.4-13.9)
Peak ALT [U/L]   2014 (1140-2521)   581 (470-1360)
Peak Alk P [U/L]   138 (88-306)   333 (164-538)
Peak bilirubin [mg/dL]   1.9 (0.8-26.0)   6.0 (1.6-23.6)
Peak INR   1.1 (1.0-1.4)   1.1 (0.9-2.5)
ANA or SMA positivity   5 (71%)   1 (33%)
Enzyme pattern       
Hepatocellular   6 (100%)   2 (67%)
Mixed or cholestatic   0   1 (33%)
Severity       
Mild (1+)   4 (57%)   1 (33%)
Moderate (2+ and 3+)   3 (43%)   1 (33%)
Severe or fatal (4+ and 5+)   0 (0%)   1 (33%)
Table 2
Clinical Features of Patients with Turmeric Induced Liver Injury With or Without HLA-B*35:01
Median (range) for continuous variables and frequency (%) for categorical variables.
Alk P = alkaline phosphatase; ALT = alanine aminotransferase; ANA = antinuclear antibody; INR = international normalized ratio; SMA = smooth muscle antibody.

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Discussion
The experience in DILIN reported here with turmeric-associated liver injury suggests that this phenomenon may be increasing in the United States, at least since 2017. Additionally, a reliable description of the clinical presentation, laboratory features, liver histology, and outcomes of turmeric-associated liver injury are provided from these prospectively enrolled and well-characterized cases. Of note, no other drug or herbal and dietary supplement product was implicated in these cases. Specifically, the typical injury occurs in women using turmeric for arthritis, pain relief, or general health. Patients present with a hepatocellular pattern of injury after a latency of 1 to 4 months. Autoantibodies such as antinuclear antibody and smooth muscle antibody are frequent but with normal immunoglobulin levels. Most cases are self-limited, with rapid improvement in liver tests on discontinuing turmeric. Rarely, the injury can be severe and result in death.
Like many herbal products, turmeric has a long history of safe use in traditional medicine, and as a culinary ingredient (curry). Turmeric has been claimed to be beneficial for multiple conditions, from aging to arthritis, and for prevention or amelioration of COVID-19.2,7-10 The increasing popularity of turmeric over the last 5 years appears to mirror the increase in reported cases collected in the DILIN Prospective Study.21-23
Chemical analysis confirmed the presence of turmeric in all 7 products tested. Moreover, the detection of piperine in several of the more recent cases raises the possibility that it increased bioavailability, and thus, toxic exposure was the cause of hepatotoxicity. However, no cases of hepatotoxicity secondary to piperine ingestion alone have been reported, making the latter possibility less likely. Thus, it stands to reason that the addition of piperine could enhance direct toxicity of the turmeric product. Other approaches to increase bioavailability have also been adopted recently, including use of lecithin and packaging turmeric in nanoparticles.
The small sample size of this case series limited the genetic analysis. However, it is notable that 7 of the 10 patients carried HLA-B*35:01, a class I HLA allele previously implicated in green tea (Camellia sinensis), Garcinia cambogia, and Polygonum multiflorum hepatotoxicity.18,20,21 Genetic studies performed by our group and others suggest that there is a common susceptibility link in persons carrying HLA-B*35:01, making them sensitive to multiple polyphenols.20,21 Therefore, carriage of this allele may be a risk factor for liver injury from several herbal components.
Consumers in the United States spent an estimated $11.261 billion on herbal and dietary supplement sales in 2020, according to the American Botanical Council's 2020 Herb Market Report, marking the first time total annual sales surpassed $10 billion.22 Turmeric was noted to be one of the top 10 ingredients in sold herbal and dietary supplements.23,24 Despite broad claims for potential benefits of turmeric to treat multiple conditions, clinical trials published so far have not yet produced evidence of significant efficacy and it is not an approved therapeutic agent.13,24
The small number of cases and DILIN's non-population-based approach to enrollment limit confidence in a statement that the frequency of turmeric-associated liver injury is increasing. Yet, the observation of increased frequency in the DILIN cohort coupled with the growing popularity of the product and its being touted as a treatment or prevention from COVID-19 lead to a reasonable presumption of a growing incidence of attributable hepatotoxicity. Therefore, practitioners should be aware of the risk of liver injury associated with turmeric. Studies of the potential for additive or synergistic hepatotoxicity of turmeric when combined with piperine are needed to better understand the potential mechanism of liver injury.
Acknowledgment
The authors acknowledge with thanks the invaluable help of Hoss Rostami, BSMSE for identifying product labels.
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[rahab]

What I found out not to long ago was that any turmeric manufacturered in India contains lead.  They use it to enhance the color.  I can only imagine how much I consumed.
Fortunately garlic helps rid the body of lead.

I now purchase from a company in Georgia that has 3rd party testing to prove no metals in their product.

[Curt]

"When experiencing the greatest  pain, Cucumin removed it completely."

Aaaamen Brother Rchard. Happy to hear of your experience with it.

Yes, extracts are more prone to abuse. It is not easy for anyone to assess he amount of an ingredient used i an extract. I spoke to someone just recently who bought a bottle of Golden Seal and in a week it was finished. The individual was saying they were going to buy another bottle. Absolutely no idea of the strength of the first bottle. Because there is a long dropper sometimes the dropper is filled and two or three dropper fuls is very easy to squeeze into water.

We must remember this statement from Mnistry of Healng pg 127.3
The use of natural remedies requires an amount of care and effort that many are not willing to give. Nature's process of healing and upbuilding is gradual, and to the impatient it seems slow.

Nature is slow because our absorption rate is slow, the body uses small amounts gradually and dosages should follow that pattern, small over a longer duration than concentrated to get fast results.

Summary... Temperance (self control) in everything

[Richard Myers]

Amen Brother Curt.

Yes, many want a pill to remove the pain right away. And they want a cure via the pill. But, the problem is not just impatience, few want to change their lifestyle which is often the reason why there is an illness. We must deal with the cause of the illness else we are only putting on a bandage.

Rahab, thanks for the warning about lead. I did a little research and found that much of the lead was coming from


How to Test Turmeric for Lead

The easiest way to avoid this issue is to use fresh turmeric. If you buy it fresh, and local, you’re much closer to the source and you control the process. Whole and unpeeled turmeric is less likely to be contaminated or adulterated. You can easily slice, grate, or dry it — and it stays good in your fridge for a long time.

To test if the powder in your cupboard may contain lead, mix a teaspoon of turmeric powder with water. If there is lead, it will instantly leave streaks of water-soluble colour in the water.

We tested our own turmeric in a recent Ask Julie Anything – check it out!

You can also test the turmeric for adulteration in a few other ways:

1. The Water Test: Take a glass of warm water and add a teaspoon of your turmeric powder to it. Let it sit for 10-15 minutes. If the turmeric powder settles down, it is pure. If it doesn’t settle to the bottom and leaves a dark yellow colour, it is adulterated.

2. The Palm Test: Take a pinch of your turmeric powder and rub it into the palm of your hand for a few seconds, then turn your palm over. Pure turmeric will stick to your palm and leave a yellow stain, whereas adulterated turmeric will mostly fall off.

While this may not be a common issue, it’s an important one. Always check the source of your turmeric and test if you’re unsure of purity. No amount of lead is safe, so you need to avoid it for yourself and your pets!

[Richard Myers]

Turmeric is not the only spice being contaminated by lead.   It is a serious danger that many are not aware of.  The FDA ought to be more concerned about these foods which are contaminated with lead.

Here is a study from PubMed that reveals the danger from lead in Turmeric.   source

[rahab]

Thank you Richard for the research

[Curt]

Six post back Bro Richard provided information on Liver Injury. Here are references for the sources of lead. I ran a check with the built-in AI in my browser to summarize the available information and retrieved the following. Remember that the built in AI tool is a reasonable assistance for quick searching and the informaton should be checked/verified as best as possible.

..............................................
AI Overview
Lead can be found in herbal products due to contamination during the growing, processing, or transport of the herbs, or from therapeutic addition. Lead can be present in soil and water where herbs are grown, from airborne pollutants, fertilizers, or from grinding machinery. Some herbal products may also be adulterated with lead to enhance color or increase weight, and certain folk medicines, like Greta and Azarcon, are known to contain lead.

Here's a more detailed breakdown of the sources:

1. Naturally Occurring Lead:
Lead is a naturally occurring element and can be found in trace amounts in soil and water.
Herbs grown in soil or exposed to contaminated water can absorb lead.
Lead can also be deposited in soil and water from airborne pollutants, fertilizer application, and grinding machinery.

2. Contamination During Processing:
Lead can be introduced during the processing of herbal products, from contaminated equipment or packaging.
Spices, in particular, may be adulterated with lead to improve their appearance or weight.

3. Therapeutic Addition (Folk Medicines):
Certain folk medicines, like those used in Ayurveda and traditional Chinese medicine, may contain lead as part of the preparation.
Examples include Greta, Azarcon, and Pay-loo-ah, which are used for various ailments.

4. Other Sources:
Lead-containing gasoline and point source pollution from smelters, battery manufacturing plants, and mines can contaminate the environment and affect herbs grown in those areas, according to the National Institutes of Health (NIH).
Lead dust, even from older lead-based paint, can contaminate soil and be tracked into homes, potentially affecting herbs grown in gardens.

5. Specific Herbal Products:
Some studies have found that certain herbal remedies, spices, and ceremonial powders have high levels of lead, particularly in those imported from or made in countries with environmental lead contamination.

Spices like thyme and oregano, and products like Ba-baw-san and Daw Tway, have been identified as potential sources of lead.

In summary, lead contamination in herbal products can stem from natural sources, processing and manufacturing, or deliberate adulteration. Consumers should be aware of the potential risks associated with certain herbal products, especially those from traditional medicine practices, and opt for products with proper labeling and quality control.

Other Reference Links -
CDC Morbidity & Mprtality Weekly Report: Lead in Spices, Herbal Remedies, and Ceremonial Powders Sampled from Home Investigations for Children with Elevated Blood Lead Levels — North Carolina, 2011–2018 | MMWR Nov 23, 2018
Kim A. Angelon-Gaetz, PhD; Christen Klaus; Ezan A. Chaudhry; Deidre K. Bean, MPH
https://www.cdc.gov/mmwr/volumes/67/wr/mm6746a2.htm

"What is already known about this topic?
No national limit exists for lead contamination in spices. Ingested lead is absorbed quickly by children and causes developmental delays."


Sources of Lead - New York State Department of Health
Some folk medicines contain lead. They often are imported from the Middle East, Southeast Asia, India, the Dominican Republic, or ...

New York State Department of Health: Sources of Lead
Revised 2010
https://www.health.ny.gov/environmental/lead/sources.htm#:~:text=Some%20folk%20medicines%20contain%20lead,and%20Surma%20also%20contain%20lead.


Consumer Report: Your Herbs and Spices Might Contain Arsenic, Cadmium & Lead
Lisa L. Gill Nov 9, 2021 —
https://www.health.ny.gov/environmental/lead/sources.htm#:~:text=Some%20folk%20medicines%20contain%20lead,and%20Surma%20also%20contain%20lead.
Heavy metals can show up in food if the water or soil where food is grown contains them naturally or is contaminated be...
CR tested 126 products from McCormick, Trader Joe's, Whole Foods, and other popular brands. Almost a third had heavy metal levels high enough to raise health concerns.

[rahab]

Indeed!

We have to be careful.

Best advice is to grow your own. 

[rahab]

Not sure where this fits but here goes…..

While we all know high fructose corn syrup is bad for our liver it seems like there is even more danger lurking in this sweetener!

It has mercury in it put there in the manufacturing process and sometimes on purpose.

I see young children eating candies loaded with this stuff!!  What is the future for them?

[Curt]

Hi Rahab. Brother Richard  will separate the discussion accordingly. In the mean time I will add some information on High Fructose Corn Syrup derived Fructose.

[Curt]

First off, it is HIGH Fructose, its Corn SYRUP. Those words already say its not nautral, its manufactured and was introduced in 1970 so it is old tech in the food industry as well.

High fructose corn syrup (HFCS) is made from corn starch, which is first processed into corn syrup containing glucose. Enzymes are then added to convert some of the glucose into fructose, resulting in HFCS, which typically contains either 42% or 55% fructose.

There are two main types of sugars in food: naturally occurring sugars, which are found in fruits, vegetables, and dairy (like fructose and lactose), and added sugars, which are included during processing or preparation (like sucrose and high-fructose corn syrup). Both types are metabolized similarly by the body, but naturally occurring sugars come with additional nutrients and fiber, while added sugars provide extra calories without nutritional benefits. But fructose needs to be turned to Glucose to be used for energy by the body and is metabolized in the Liver.

[rahab]

Thank you