October 2009 Blog with Durk and Sandy

There are two ways to conquer and enslave a nation. One is by the sword. The other is by debt.— John Adams

There are 1011 stars in the galaxy. That used to be a huge number. But it’s only a hundred billion. It’s less than the national deficit. We used to call them astronomical numbers. Now we should call them economical numbers.— Richard Feynman

If I knew then what I know now, I’d be a time traveler.— Sandy Shaw

The very ink with which all history is written is merely fluid prejudice.— Mark Twain

What is the difference between a taxidermist & a tax collector? The taxidermist takes only your skin.— Mark Twain


We are back in the courts again as plaintiffs in three new Emord & Associates suits against the FDA, two involving First Amendment violations in relation to health claims for vitamins E and C and a reduction of the risk of various cancers and in relation to health claims for selenium and a reduction of the risk of various cancers. The other suit is a challenge to the FDA’s Good Manufacturing Practices which, among other things, is unconstitutionally vague (void for vagueness). It is not possible to understand specifically what it is that the regulations require you to do, yet you can be prosecuted criminally for violating them. For details on the new FDA suits, see www.emord.com.


A most unusual new study1 reports that feeding sedentary bobwhite quails a diet enriched in n-3 fatty acids DHA and EPA to the levels of that which is eaten naturally in the wild by the semipalmated sandpiper to prepare for a migration from Canada to South America results in similar improvements in oxidative enzymes in muscles. These muscular improvements are obtained in wild semipalmated sandpipers by their stuffing themselves (body mass is doubled) with marine invertebrates containing “record” amounts of EPA and DHA, which results in substitution by n-3 fatty acids in place of n-6 fatty acids in muscle cell membranes. The authors state that “[o]nly extreme regimes of endurance training can lead to increments in oxidative capacity matching those induced here by diet.” Moreover, they suggest, “[c]hoosing n-3 fatty acid doping over endurance training strikes us as a better strategy to boost aerobic capacity when rapid storage of energy is critical.”

The activity of flight muscle CS (citrate synthase, a Krebs Cycle enzyme) was significantly increased by EPA, while CPT (carnitine palmitoyl transferase, a beta-oxidation enzyme that stimulates the use of fats as fuels) was stimulated by DHA. The authors report that six weeks of n-3 fatty acid supplements “were sufficient to increase enzyme activities by 58–90% in quail flight muscles. … A survey of the literature shows that aerobic exercise training can stimulate enzyme activities by up to 42% in rats [after 8 weeks of training], 38–76% in humans [7 weeks] and 41–72% in horses [10 weeks]. Therefore, the increases in oxidative enzyme activities observed in birds eating n-3 fatty acids can surpass those reported for mammals after endurance training and they occur more rapidly.” References were included in the original quote, but are deleted here for clarity.

Different experiments were done in which EPA was administered alone, DHA administered alone, or the two administered together to the sedentary quails. Interestingly, EPA and DHA were found to work by different mechanisms. The combined treatment did not provide a metabolic advantage except possibly for an increase in cytochrome oxidase, which was increased only in the EPA + DHA group.

The researchers hypothesize that another substantial benefit of the extreme n-3 diet for the migrating birds may be because the increased ratio of n-3/n-6 fatty acids “causes chronic inhibition of inflammation pathways” that in along-distance flight causes muscle damage.

“In preparation for long migrations, some birds improve their physical fitness by eating!”1Importantly, though, over the course of their long flight, the excess fat stored in their bodies is burned as fuel. The paper didn’t discuss what happened to the sedentary quail after their n-3 eating binges (i.e., did they burn off the excess fat over time or remain fat? Of course, they might simply have been euthanized, leaving us in the dark about the fate of their fat).


  1. Nagahuedi et al. Mimicking the natural doping of migrant sandpipers in sedentary quails: effects of dietary n-3 fatty acids on muscle membranes and PPAR expression. J Exp Biol 212:1106-1114 (2009).


Recent Scientific Reports on Turmeric and Its Major Constituents, including Curcumin and Related Curcuminoid

The scientific literature on the beneficial biological activities of turmeric and its constituents continues to rapidly increase. Here is a very small and selected sample of several of these publications (we have many more, not to speak of the far larger number in the entire scientific literature), showing an impressive diversity of health and medical benefits for turmeric root and various constituents, particularly curcumin.


Turmeric and curcumin, in a variety of animal and human studies, have been shown to be safe (at up to 8 g per day of curcumin for 3 months in humans). “Average consumption of 0.5 to 1.5 g/day/person turmeric by Asians showed no toxic symptoms. Administration of turmeric at higher doses (2.5 g/kg body weight) to male and female guinea pigs, monkeys and Wistar rats showed no changes in the appearance and weight of kidney, liver and heart. Wu (2003) reported in a phase I human trial with 25 subjects using up to 8000 mg of curcumin per day for 3 months found no toxicity. In five other human trials using 1125–2500 mg curcumin per day it was also found it to be safe.” (References deleted here, but provided in original paper.1)


“Woo et al (2007) reported that curcumin suppresses obesity-induced inflammatory responses by suppressing adipose tissue macrophage accumulation or activation and inhibiting MCP-1 release from adipocytes.” (Reference provided in paper.1)

This is very important because the accumulation of infiltrating macrophages and T-lymphocytes into adipose tissue in rodents fed high fat diets is what leads to chronic adipose tissue inflammation and metabolic syndrome.2 The researchers of this paper2sought to understand the mechanism(s) by which normal fat (adipose) tissue is converted from a lean phenotype to the obese phenotype in the diet-induced obesity model (high fat diet) in mice. By following the changes in the interaction of immune cells and adipose tissue as fat accumulated during the high fat diet, they discovered that obese adipose tissue stimulates CD8+ T-cells which, in turn, induce the recruitment and differentiation of macrophages, resulting in the initiation and maintenance of adipose tissue inflammation along with insulin resistance. As noted in the paragraph above, curcumin has been shown to inhibit this process.

Blood Glucose

In a mouse model of type 2 diabetes, curcuminoids and sesquiterpenoids in turmeric suppressed an increase in blood glucose level.3 One method of treating human type 2 diabetes is to administer drugs that increase the activity of PPAR-gamma, a nuclear receptor that induces fat cell differentiation. The differentiation of pre-adipocytes to adipocytes increases insulin sensitivity by causing the creation of small new adipocytes (inherently more insulin sensitive than large old adipocytes) from the pre-adipocytes. In this paper,3 curcuminoids (curcumin, demethoxycurcumin, bisdemethoxycurcumin) and a sesquiterpenoid (ar-turmerone), all found in turmeric, were found to have hypoglycemic effects (reduced blood sugar) by activating PPAR-gamma as one of the mechanisms.

Cancer Prevention/Treatment

A recent review of the anticancer potential of curcumin8 reported that cell and animal studies have shown antiproliferative effects against a variety of cancers including breast carcinoma, colon carcinoma, renal cell carcinoma, hepatocellular (liver) carcinoma, T cell leukemia, B cell lymphoma, acute myelogenous leukemia, basal cell (skin) carcinoma, melanoma, and prostate carcinoma. Mechanistic studies have shown that curcumin can downregulate transcription factors involved in the development and progression of cancer, including NF-kappaB, AP-1, and Egr-1, and down-regulate the expression of other factors involved in cancer including COX2, LOX, NOS, MMP-9, µPA, TNF, chemokines, cell surface adhesion molecules and cyclin DI; it can also down-regulate growth factors that affect cancer including EGFR and HER2; and inhibits the activity of c-Jun-terminal kinase, protein tyrosine kinases and protein serine/threonine kinases.

Incidentally, you may be surprised (or not) to know that the FDA will not permit as a health claim for a dietary supplement that it “may reduce the risk of developing a disease” on the basis that it is able to treat that disease. In other words, even if a large clinical trial convincingly demonstrated that turmeric extract or curcumin was effective in treating colorectal cancer (such a study hasn’t been done yet), that would not suffice to support a health claim that turmeric/curcumin “may reduce the risk of colorectal cancer.” It seems to us that if you can get rid of abnormal cells that are part of a disease process, you are both preventing and treating the disease. But of course the FDA thugs have big guns; the agency continues to censor most truthful health information on foods and dietary supplements, refusing to obey the Constitution’s command that “Congress shall make no law … abridging the freedom of speech, or of the press …”

In a very small human clinical study,8a 15 patients with advanced colorectal cancer refractory to standard chemotherapies were treated with turmeric extract in proprietary capsule form at doses between 440 and 2200 mg/day, containing 36-180 mg of curcumin. “One third of the patients in this study experienced stable disease for 3 months or longer, and in one additional patient, Curcuma [turmeric] extract may have been linked to a decrease in venous tumor marker level and abatement of progression of the primary colon tumor without a cytostatic effect on liver metastases. The possibility that patients with colorectal cancer may benefit from consumption of Curcuma [turmeric] extract merits evaluation at higher dose levels and ultimately within the framework of larger studies incorporating control groups.”

Each capsule used in the study contained 20 mg of curcumin plus 2 mg of desmethoxycurcumin suspended in 200 mg of essential oils derived from turmeric. Typical constituents of the Curcuma (turmeric) essential oils include tumerone, atlantone, and zingiberene8a After at least a 2 hour fast, patients consumed 2, 4, 6, 8, or 10 capsules once daily with water (translating to doses of 440, 880, 1320, 1760, and 2300 mg of Curcuma extract per day containing 36, 72, 108, 144, and 180 mg of curcumin, respectively. Treatment was continued until disease progression was established or consent was withdrawn.8a

Chemotherapeutic effect of oral curcumin extract was described: “All patients enrolled exhibited radiological evidence of progressive malignant disease before recruitment. Levels of the tumor marker CEA [carcinoembryonic antigen] in venous blood were above the normal range in all patients, and those of CA19.9 were abnormal in 80% of patients. In one patient, who received 440 mg of Curcuma extract (equivalent to 36 mg of curcumin) daily, venous blood CEA levels decreased from a pretreatment value of 310 ± 15 to 175 ± 9 µg/liter after 2 months of treatment. This patient experienced stabilization of disease in the colon but progression in the liver, as demonstrated on CT scan. … Five patients exhibited stable disease on CT scan [three (on 440, 880, and 1760 mg of Curcuma extract) for 3 months and two (on 880 and 1320 mg of Curcumaextract) for 4 months of treatment.]

Alzheimer’s Disease

Several compounds isolated from turmeric have been shown to protect PC12 neuronal cells from beta-amyloid damage.9 One of the pharmacological approaches to treating Alzheimer’s disease (AD) is to administer drugs that interfere with beta-amyloid formation and deposition and drugs that attenuate beta-amyloid toxicity. The researchers doing this study used a methanol extract of turmeric to protect PC12 cells from beta-amyloid insult. They found five turmeric constituents that were particularly effective.

In a separate paper,10 researchers tested the effects of curcumin for protecting aging female rats from cognitive dysfunction after receiving a brain infusion of both the more soluble amyloid-beta(1-40) and the more rapidly aggregating amyloid-beta(1-42) with a lipoprotein chaperone. In one experiment, aging rats were placed either on a control diet or the same diet but also containing 2,000 ppm curcumin or 375 ppm ibuprofen for two months before being administered the infusions. (2,000 ppm curcumin in the rat’s diet is probably very roughly equivalent to 1 to 2 grams per day for a human.) Unlike ibuprofen (to which it was compared), treatment with dietary curcumin completely suppressed the elevated (2.3-fold increased) levels of isoprostanes (a product of oxidative stress) found in the amyloid-beta treated animals.

In another experiment,10 middle aged rats were evaluated for spatial memory in a standard Morris water maze after being fed a control diet or a control diet plus 500 ppm curcumin followed by amyloid-beta infusion. The animals that received the curcumin enhanced diet and the infusion showed reduced path length and latency in finding the hidden platform in the water maze, with their performance restored to the levels found in the vehicle-infused (no amyloid-beta) controls. Moreover, the 500 ppm curcumin treated animals had markedly reduced total amyloid-beta plaque numbers: 80% compared to control diet fed animals.

For more on Alzheimer’s disease, see the next paper below (under “neurogenesis”).


Another paper11 reported on the effect of curcumin on cultured mouse neural progenitor cells (PC12) and adult hippocampal neurogenesis (creation of new neurons in the hippocampus, an important brain area for learning and memory). Low concentrations (0.1 µM, 0.5 µM) of curcumin stimulated neural progenitor cell proliferation, while high concentrations (≥10 µM) inhibited neural progenitor cell growth and were cytotoxic. They also found that curcumin promotes hippocampal neurogenesis in adult mice; 500 nmol/kg body weight of curcumin was administered intraperitoneally which, the authors estimate, resulted in roughly 1–2 µM concentration in the brain. The researchers identified the neurogenic effect as being mediated by an ERK and p38 MAPK mechanism.

The researchers11 conclude that: “relatively low doses of curcumin can stimulate hippocampal neuroplasticity, a finding with important implications for preventative and therapeutic approaches for a range of neurological disorders that involve impaired neurogenesis, including depression, diabetes, and AD [Alzheimer’s disease].” Uncontrollable stress is another inhibitor of neurogenesis.11

Lifespan Extension in Fruit Flies

A recent paper1a reports that fruitflies grown on media containing 1.0 mg of curcumin/gram of media had a lifespan extension of about 15% as compared to controls (same media but without added curcumin). The fruitflies grown on media containing 0.5 mg of curcumin/gram of media had a nonsignificant increase in lifespan compared to controls. 1.0 mg/g of media is probably very roughly equivalent to 2 g/day for a human.

The mechanism of curcumin life extension appears to involve protection against superoxide radicals, as the addition of disulfiram (a superoxide dismutase inhibitor) along with the curcumin in the media prevented the lifespan extending effect of the curcumin.1a

Autoimmune Diseases

“According to Bright (2007), curcumin inhibits autoimmune diseases by regulating inflammatory cytokines such as IL-1beta, IL-6, IL-12, TNF-alpha and IFN-gamma and associated JAK-STAT, AP-1, and NF-kappaB signalling pathways in immune cells.” (Reference provided in paper.1)

In another study,1b researchers using a widely utilized animal model of experimental rheumatoid arthritis (in female Lewis rats), found that administration of a complex turmeric extract depleted in its essential oils and containing less than 50% curcuminoids prevented joint inflammation. The authors warn that the use of anti-TNF (tumor necrosis factor, an inflammatory cytokine) to treat rheumatoid arthritis can reactivate latent granulomatous infections in RA patients with latent tuberculosis. The warning is presumably because a sufficiently potent anti-inflammatory could dangerously decrease the immune system response to bacterial or viral infections. However, no such response has, to our knowledge, been reported with the use of turmeric extracts or curcumin in animal or human studies.

COPD & Asthma: Curcumin Restores Corticosteroid Sensitivity

One of the many problems in COPD (and asthma) is that corticosteroids, which are ordinarily potent anti-inflammatories, are not effective in reducing the chronic inflammation in the lungs of COPD patients. Hence, corticosteroids cannot be used to treat the disease. An exciting new study4 reports that curcumin at nanomolar (!) concentrations specifically restores corticosteroid sensitivity in cigarette smoke extract or oxidative stress exposed cells (monocytes). It does this by increasing levels of histone deacetylase 2, depleted in lungs with COPD; the decrease in histone deacetylase 2 activity is correlated with COPD severity. Histone deacetylase 2 is critical for corticosteroid anti-inflammatory activity. The researchers report that curcumin at concentrations up to 1 µM “acts at a post translational level by maintaining both HDAC2 [histone deacetylase 2] activity and expression, thereby reversing steroid insensitivity induced by either CSE [cigarette smoke extract] or oxidative stress in monocytes. Curcumin may therefore have potential to reverse steroid resistance, which is common in patients with COPD and asthma.” (Emphasis added.)

“Moreover, given that curcumin is considerably more efficacious in restoring HDAC2 in ROS [reactive oxygen species]-stressed cells at low nanomolar levels, this in turn would help to restore the HAT/HDAC [histone acetylation/deacetylation] imbalance that exists under oxidative stress, curtailing the magnitude of any inflammatory response. Consequently, this might help to explain, in part, why curcumin is considered to [be] more efficacious as an anti-inflammatory under conditions of oxidative stress.”4

Peroxynitrite Scavenging by Curcuminoids: Atherosclerosis and Ischemia/reperfusion

A structure/function study5 reports on the study of three curcuminoids isolated from turmeric (Curcuma longa L.) that were tested for their ability in a chemical test to scavenge peroxynitrite, a potent oxidative product resulting from the chemical interaction between nitric oxide and superoxide radicals, as occurs in such conditions as atherosclerosis and ischemia/perfusion. One turmeric-derived molecular form of curcumin (shown in a molecular diagram) that contained two feruloyl groups had potent peroxynitrite-scavenging ability.

Peroxynitrite Scavenging and Pain

Interesting new work has been published on the development of tolerance to the pain-reducing effects of morphine. It has been proposed that peroxynitrite is involved in the development of this tolerance and the subsequent loss of pain suppression by morphine.6 As the researchers explain, “Besides its role in the development of morphine-induced antinociceptive [anti-pain] tolerance that will be reviewed herein, peroxynitrite is also implicated in the development of hyperalgesia [increased pain] associated with acute and chronic inflammation …” Peroxynitrite scavengers such as certain curcuminoids, thus, may offer the possibility of reducing the development of tolerance to morphine as well as reducing inflammatory pain.


A recent paper7 reports that constituents of turmeric inhibit sortase A (a bacterial surface protein anchoring transpeptidase) and Staphyloccus aureus cell adhesion to fibronectin. As the authors explain, “[g]ram-positive pathogenic bacteria display surface proteins that play important roles in the adhesion to specific organ tissues, the invasion of host cells, or the evasion of host-immune responses. These virulent-associated proteins are covalently anchored in bacterial cell wall peptidoglycan through a general sorting mechanism catalyzed by a superfamily of membrane-associated transpeptidases termed sortases.” Preventing the adhesion of bacteria to cells is similar to what is done by certain compounds in cranberry juice in the prevention of bladder infections.


  1. Niranjan and Prakash. Chemical constituents and biological activities of turmeric(Curcuma longa L.)— A review. J Food Sci Technol 45(2):109-116 (2008).
    1a. Suckow and Suckow. Lifespan extension by the antioxidant curcumin in Drosophila melanogaster. Int J Biomed Sci 2(4):401-4 (2006).
    1b. Funk et al. Turmeric extracts containing curcuminoids prevent experimental rheumatoid arthritis. J Nat Prod 69:351-5 (2006).
    2. Nishimura et al. CD8+ effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity. Nat Med 15(8):914-20 (2009).
    3. Nishiyama et al. Curcuminoids and sesquiterpenoids in turmeric (Curcuma longa L.) suppress an increase in blood glucose level in type 2 diabetic KK-AY mice,” J Agric Food Chem 53:959-63 (2005).
    4. Meja et al. Curcumin restores corticosteroid function in monocytes exposed to oxidants by maintaining HDAC2. Am J Respir Cell Mol Biol 39:312-323 (2008).
    5. Kim et al. In vitro peroxynitrite scavenging activity of diarylheptanoids from Curcuma longa. Phytother Res 17:481-484 (2003).
    6. Salvemini. Peroxynitrite and opiate antinociceptive tolerance: a painful reality. Arch Biochem Biophys 484:238-244 (2009).
    7. Park et al. Curcuma longa L. constituents inhibit sortase A and Staphyloccus aureus cell adhesion to fibronectin. J Agric Food Chem 53:9005-9009 (2005).
    8. Aggarwal et al. Anticancer potential of curcumin: preclinical and clinical studies. Anticancer Res 23:363-98 (2003)
    8a. Sharma et al. Pharmacodynamic and pharmacokinetic study of oral Curcuma extract in patients with colorectal cancer. Clin Cancer Res 7:1894-1900 (2001).
    9. Park and Kim. Discovery of natural products from Curcuma longa that protect cells from beta-amyloid insult: a drug discovery effort against Alzheimer’s disease. J Nat Prod 65(9):1227-31 (2002).
    10. Frautschy et al. Phenolic anti-inflammatory antioxidant reversal of Abeta-induced cognitive deficits and neuropathology. Neurobiol Aging 22:993-1005 (2001).
    11. Kim et al. Curcumin stimulates proliferation of embryonic neuiral progenitor cells and neurogenesis in the adult hippocampus. J Biol Chem 283(21):14497-505 (2008).


While we are discussing cystatin (see article above), it is interesting to note that cystatin D is a member of the cystatin superfamily of endogenous inhibitors of endosomal/lysosomal cysteine proteases.1 This particular cystatin may be a tumor suppressor, as it is an endogenous inhibitor of cysteine cathepsins that have been proposed to be major players in tumor progression as they are proteases that break down matrix components and adhesion proteins. A new paper1 reports that cystatin D RNA expression is increased by vitamin D (1alpha, 25(OH)2D3) treatment in colon cancer cells, which inhibits proliferation, invasiveness, migration and increases cell adhesiveness.


  1. Alvarez-Diaz et al. Cystatin D is a candidate tumor suppressor gene induced by vitamin D in human colon cancer cells. J Clin Invest 119(8):2343-58 (2009).


Hypertriacylglycerolemia (high levels of triglycerides), especially following a meal (postprandial) is a prominent risk factor for cardiovascular disease in diabetics (possibly even more important than high blood sugar levels1) and in non-diabetics, too.

A new paper2 reports that black tea polyphenols (BTP, derived from an ethanol extract of dried black tea leaves) administered to 8 week old male Wistar rats reduced the blood level of triacylglycerols (triglycerides) following an infusion into the stomach of a fat emulsion (immediately after the BTP) as compared to another group of rats that received the fat emulsion but not the black tea polyphenols (BTP). In fact, the high-BTP group of rats had triacylglycerol levels following the fat emulsion that remained almost at basal levels (e.g., there was practically no increase).

Further investigation found that the BTP dose-dependently inhibited pancreatic lipase in vitro, which is probably the mechanism responsible for BTP reduction of blood triacylglycerols in the rats, though no test for an effect of pancreatic lipase in the rats was done. Though the researchers note that they used relatively high amounts of black-tea components in order to obtain a “conspicuous” difference, they “consider that the effective dose of BTP in humans can be lower than that used in rats.” As they explained, they had done an earlier study that showed that green tea catechins suppressed postprandial hypertriacylglycerolemia in rats. In that study, they gave the rats 100 mg/kg of body weight of green tea catechins. But in a human study, they found that the green tea catechins suppressed postprandial hypertriacylglycerolemia at 215 mg per person, much less than that given the rats (Unno et al. Suppressive effects of tea catechins on elevation of postprandial serum triglycerides. Jpn J Nutr Assessment [in Japanese] 22:207-12 (2005).)

The components of black tea that were effective in inhibiting pancreatic lipase activity were theaflavins with galloyl moieties (theaflavin-3,3’-digallate was more effective than epigallocatechin gallate [EGCG], epicatechin gallate, and a mixture of EGCG and epicatechin gallate).


  1. Unger RH. Reinventing Type 2 diabetes. JAMA 299(10):1185-7 (2008). “[T]he novel lipocentric view depicts the hyperglycemia of type 2 diabetes, and the underlying insulin resistance and beta cell loss, as being secondary to the metabolic trauma caused by ectopic lipid deposition [abnormal fat accumulation taking place outside of adipose tissue] or lipotoxicity. If this is the case, hyperglycemia should be corrected by eliminating the lipid overload.” A recent study [Dixon et al. Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial. JAMA 2993:316-23 (2008).] “[P]rovides support for this lipocentric hypothesis, by demonstrating that weight loss that follows gastric banding is accompanied by remission of diabetes in 73% of obese patients with type 2 diabetes.”
  2. Kobayashi et al. “Black tea polyphenols suppress postprandial hypertriacylglycerolemia by suppressing lymphatic transport of dietary fats in rats,” J Agric Food Chem 57:7131-6 (2009).


Lung diseases such as emphysema, pulmonary fibrosis, and lung cancer are believed to be caused by an imbalance between proteases (that break down proteins) and their natural inhibitors.1 A new study1 examined the effect on the function of cysteine proteases by modifications induced by nitrosative stress (excessive production of nitric oxide, as occurs in chronic/acute lung inflammation) and the ability of quercetin and curcumin to protect lung proteins from these effects.

In humans, the lung protease inhibitor alpha-1 antitrypsin provides important protection against the breakdown of lung proteins that contribute to the development of emphysema and COPD. This new study examined the effects of nitrosative stress on the structure and function of cystatins, noncovalent competitive inhibitors of cysteine proteinases (known as cathepsins B, H, I, and S), that are ubiquitously present in mammalian tissues1 and prevent excessive proteolysis (protein breakdown) that occurs in diseases such as bronchitis, rheumatoid arthritis, osteoporosis, Alzheimer’s disease, cancer metastasis, and microbial invasion.1

The new study reports on protective effects of curcumin and quercetin against nitrosative stress-induced dysfunction of the goat lung version of cystatin. The researchers found that “[t]he treatment of cystatin from goat lungs with the NO-generating compound SNP [sodium nitroprusside, which releases NO] causes concentration and time-dependent loss of enzyme [cystatin] activity.” This may be caused by the nitrosation of active amino acid sites in the cystatin molecule or the oxidation of critical tryptophan residues in the molecule.

Curcumin and quercetin provided significant protection against the functional and structural damage to goat lung cystatin, thus helping protect the molecule’s activity against excessive protein breakdown. Curcumin (50 µM) prevented this damage to cystatin, whereas for protection to a similar extent, quercetin at 5 times that concentration was required.1

The authors conclude: “The results of the study are of great significance. Proteins are the major targets of reactive species. … modification of proteins by reactive species (ROS, NO, RNS, etc.) render them more susceptible to enhanced proteolysis, inactivation and denaturation. The present study documents the suppression of NO-induced inactivation of GLC-1 [goat lung cystatin] by curcumin and quercetin. Also, structural changes in SNP-treated GLC-1 are minimized by curcumin and quercetin.” The authors suggest that curcumin and quercetin (as well as many other polyphenols) could provide “a rather inexpensive therapeutic option against oxidative injury.”

Food sources naturally rich in quercetin include black tea, apples, and tomatoes, while about 40% of the polyphenol content of the spice turmeric root powder consists of curcumin. We take turmeric root powder itself as a source of curcumin (rather than curcumin alone) as the whole root powder contains other related molecules (called curcuminoids) that have similar or even stronger protective effects. It is available in capsules (600 mg/capsule), which is nice because the taste of turmeric root powder by itself (not as it is found prepared in food) is rather unpalatable. Quercetin is also found in our new V-Shield™ (1000 mg in the recommended 2 capsules three times a day) and in our Personal Radical Shield™ (130 mg in the recommended 12 capsules per day).


  1. Shahnawaz et al. Preventive effect of curcumin and quercetin against nitric oxide mediated modification of goat lung cystatin. J Agric Food Chem 57:6055- 6059 (2009).

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