December 2008 Blog with Durk and Sandy

December 25, 2008

December 2008 Blog with Durk and Sandy

elephant, n. A mouse built to government specifications. 
— Robert Heinlein

The Most Endangered Species Is Sanity

Last week, [five industry groups] filed suit in federal court to attempt to change the text of the listing [of the polar bear as a threatened species] that says business projects in Alaska—but no other state—must undergo reviews of their greenhouse gas emissions. Nature 2008 Sept 4;455:4

 

Cold in Them Thar Hills

Anchorage, Alaska is experiencing one of its coldest years on record . . . Temperatures were particularly cool during the summer. The average daily high temperature at Anchorage International Airport from June 1 to Aug. 5 was 59.3 degrees Fahrenheit, making it the second coldest summer since 1952.
— Aleks Karnick 
Environment & Climate News, October 2008
The sea ice cover minimum was 9.4% greater in the Arctic area this year compared to last, which was attributed to fewer warm days and winds blowing in different directions.
— Nature 2008 Sept 25;455:441
Congress consists of one-third, more or less, scoundrels; two-thirds, more or less, idiots; and three-thirds, more or less, poltroons.
— H. L. Mencken

(D&S: Poltroons are cheats and liars. Seems that nothing has changed.)

 

New Blades Added to the Swiss Army Knife of Preventive Medicine: Aspirin

New discoveries on the effects of aspirin (the acetylated version of the plant hormone salicylic acid) keep adding new understanding of the mechanisms for its health benefits. A newly published paper1 explains more on the source of cardiovascular protection by aspirin by revealing that aspirin induced paraoxonase 1 (PON1, a molecule that is synthesized in the liver and circulates in association with apo-A1 and HDL) and the apo-A1 gene in mice.

PON1 is a known protectant against atherosclerosis; studies have shown that people who take aspirin have increased levels of PON1. PON1-deficient mice have been shown to be more susceptible to atherosclerosis.1 Moreover, low levels of HDL are positively correlated with low levels of PON1.1 The cardiovascular protective effects of HDL depend to a great extent on its content of apoA1 and PON1. The fact that HDL becomes less protective and even proatherogenic due to oxidative- and/or nitrative-stress-induced damage to apoA1 and PON1 in those with cardiovascular disease or risk factors for it is probably one of the major reasons that it is not uncommon for people with normal levels of HDL and LDL to still have heart attacks.

In this study,1 normal C57BL/6 mice were fed 2 mg/day or not of aspirin along with an atherogenic diet for 9 days. The aspirin-fed mice had a 10-fold induction in PON1 liver gene expression and a 6-fold induction in apoA-1 gene expression compared with the controls (not receiving aspirin).

Interestingly, a number of natural substances have also been found to increase PON1, including quercetin and catechin (in both humans and mice); resveratrol was reported to induce PON1 gene expression in primary hepatocyte (liver cells) culture.1

Reference

  1. Jaichander et al. Induction of paraoxonase 1 and apolipoprotein A-1 gene expression by aspirin. J Lipid Res 49:2142-8 (2008).

 

Myeloperoxidase (MPO), a Risk Factor in Atherogenesis; 
Protective Dietary Substances

Myeloperoxidase (MPO) is an important enzyme in immune activity, such as its function as the major component of neutrophil azurophilic granules (release of which is part of the inflammatory process induced by neutrophils) and its presence in monocytes (but not macrophages).1 MPO uses hydrogen peroxide and chloride anions to produce hypochlorous acid, an important microbial killer.1

MPO in Neurodegeneration

Microglia, which are immune cells resident in the brain, also generate MPO, which is associated with the chronic inflammation of neurodegeneration in the brain.2 It was also reported2 that MPO is released by microglia during phagocytosis (of, for example, bacteria, fungi, and viruses) but that, since microglia are not very effective phagocytes for beta-amyloid, “frustrated phagocytosis” could lead to copious quantities of MPO in the extracellular milieu because the phagolysosome (where the phagocytosis of beta-amyloid is being “attempted”) does not close.

MPO and Protein Modification

Myeloperoxidase is also involved in protein modifications by a process called carbamylation (in which urea-generated cyanate modifies lysine residues in protein molecules), which can lead to protein dysfunctions, as occur in several diseases.1

MPO Damage to HDL and apoA1 Increases Risk of Cardiovascular Disease

It has recently been reported in a number of papers3,4 that MPO is an important source of nitrating oxidants that damage the atheroprotective properties of HDL and apoA1. “. . . both in vitro and in vivo studies demonstrate accompanying functional impairment in ABCA1-dependent cholesterol efflux from cholesterol-laden macrophages with increasing levels of oxidation of apoA-1, suggesting that oxidative processes catalyzed by MPO may participate in the development of ‘dysfunctional’ or ‘proinflammatory’ forms of HDL.”3 “High concentrations of enzymatically active myeloperoxidase have been found in human vascular lesions, and characteristic protein and lipid oxidation products of the enzyme have been detected in LDL isolated from atherosclerotic tissue.”4

MPO and Lung Inflammation

Alveolar macrophages (polymorphonuclear leukocyte neutrophils) have also been reported to be activated by myeloperoxidase released in models of lung inflammation, as occurs in (for example) asthma and pneumonia.5

MPO and Lipid Peroxidation at Sites of Inflammation

Another paper6 reports that MPO functions as a major enzymatic catalyst for initiation of lipid peroxidation at sites of inflammation. As the authors of the paper note, “Initiation of lipid peroxidation and the formation of bioactive eicosanoids are pivotal processes in inflammation and atherosclerosis.” The authors suggest that there is a “need for development of inhibitors for MPO as a novel anti-inflammatory therapeutic.”

Natural Products that Inhibit or Reduce MPO Activity

The flavonoid quercetin is a potent inhibitor of human MPO in a system using stimulated human neutrophils.7 We include 130 mg of quercetin in the recommended 12 capsules per day of our Personal Radical Shield™.

Resveratrol has been reported to inhibit the activity of equine neutrophil MPO by a direct interaction with MPO,8 inhibiting the chlorination, oxidation, and nitration activities of MPO in a dose-dependent manner. MPO release has been associated with various inflammatory disorders of horses, including laminitis, recurrent airway obstructions, and intestinal strangulation pathologies.8 In the equine neutrophil system reported in Reference 8, 10 μM resveratrol inhibited 90% of the MPO nitration and chlorination reactions and 80% of the MPO oxidation reactions. Our Durk Pearson & Sandy Shaw’s®MealMate™ contains 20 mg of resveratrol per capsule (suggested daily dose 3–8 capsules).

Cocoa flavanols have also been reported to inhibit MPO-induced lipid peroxidation of LDL in the presence of nitrite.9 The paper reports that “Dietary flavonoids including (-)-epicatechin, a major flavan-3-ol in cocoa products, grapes, and wine, are substrates of MPO as well as potent inhibitors of LPO [lipid peroxidation] in LDL at micromolar concentrations.” As the authors also note, “More recently, it has been reported that MPO modifies not only LDL but also HDL, thereby abolishing the antiatherosclerotic actions of HDL, thus extending our picture on the role of MPO in plasma lipoprotein metabolism.” Our Durk Pearson & Sandy Shaw’s Glycemic Control LifeByChocolate™ high-fiber/high-protein/low-digestible-carbohydrates chocolate pudding mix contains lots of cocoa. A delicious new variation for our chocolate pudding mix is to sprinkle Chinese 5 spice (a fragrant combination of star anise, pepper, fennel, cloves, and cinnamon) on top. We use it generously for a really great flavor burst.

In another paper,10 which examined the effect of several flavonoids on MPO activity in a chemical assay, it was found that quercetin was the strongest inhibitor of MPO-catalyzed dityrosine formation, followed (in descending order of potency) by: kaempferol > fisetin > luteolin > taxifolin. A major metabolite of quercetin, quercetin-3-β-D-glucuronide, was also a potent inhibitor. They reported that quercetin was also the strongest radical scavenger, followed by luteolin > fisetin > taxifolin > kaempferol.

References

  1. Rader & Ischiropoulos. ‘Multipurpose oxidase’ in atherogenesis. Nature Med13(10):1146-7 (2007).
  2. Lefkowitz & Lefkowitz. Microglia and myeloperoxidase: a deadly partnership in neurodegenerative disease. Free Rad Biol Med 45:726-31 (2008).
  3. Zheng et al. Apolipoprotein A-1 is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease. J Clin Invest 114(4):529-41 (2004).
  4. Pennathur et al. Human atherosclerotic intima and blood of patients with established coronary artery disease contain high density lipoprotein damaged by reactive nitrogen species. J Biol Chem 279(41):42977-83 (2004).
  5. Grattendick et al. Alveolar macrophage activation by myeloperoxidase. Am J Respir Cell Mol Biol 26:716-22 (2002).
  6. Zhang et al. Myeloperoxidase functions as a major enzymatic catalyst for initiation of lipid peroxidation at sites of inflammation. J Biol Chem277(48):46116-22 (2002).
  7. Pincemail et al. Human myeloperoxidase activity is inhibited in vitro by quercetin. Comparison with three related compounds. Experientia 44:450-3 (1988).
  8. Kohnen et al. Resveratrol inhibits the activity of equine neutrophil myeloperoxidase by a direct interaction with the enzyme. J Agric Food Chem55:8080-7 (2007).
  9. Schewe & Sies. Myeloperoxidase-induced lipid peroxidation of LDL in the presence of nitrite. Protection by cocoa flavanols. BioFactors 24:49-58 (2005).
  10. Shiba et al. Flavonoids as substrates and inhibitors of myeloperoxidase: molecular actions of aglycone and metabolites. Chem Res Toxicol 21:1600-9 (2008).

 

Oleic Acid Responsible for the Blood Pressure-Reducing Effect of Olive Oil

Although numerous studies have reported that high intake of olive oil reduces blood pressure, the mechanism has remained unclear, with some proposing that olive oil’s high oleic acid content is largely responsible while others believe that the polyphenols in olive oil may play a large role.

A new study1 now reports evidence that strongly supports the hypothesis that it is oleic acid, through its effects on membrane lipid content and certain aspects of cell signaling (G protein-mediated signaling), that causes the reduction in blood pressure from consuming a diet (such as the Mediterranean diet) enriched in olive oil.

The authors of the new paper cite earlier work of theirs in which they showed that oleic acid, but not its structural analogs elaidic and stearic acid, regulates the activity of the alpha2A/D adrenoceptor (one of the types of the receptor that responds to adrenaline and noradrenaline)/G protein/adenylyl cyclase-cAMP/pKA system by modulating the structure of plasma membrane lipids.1 The authors note that “altered levels and function of G proteins have been reported in both hypertensive humans and experimental models of hypertension. . . . Indeed, a rise in the expression of inhibitory G1 proteins in the aorta of hypertensive animals precedes the development of high BP, which is probably a major contributory factor in the pathogenesis of hypertension.”

Remarkably, the authors demonstrate that oleic acid could cause an acute and significant reduction of blood pressure in Sprague-Dawley rats after both acute (2 hours) and chronic yet short (2 weeks) administration. The rats received an oral dose of 1 g/kg one time for the acute determination and once each 12 hours for 14 days for the chronic determination. (This scales to a human dose—as a percentage of food—of about 5–10 g twice per day.) “Although the hypotensive effects of acute (single dose) olive oil were transient (with a peak at 2–4 hours after treatment), reductions in BP were not only marked but they were also stable after 3 or 4 days of high olive oil intake. This rather rapid effect after acute intake of free fatty acids and related lipids is most likely caused by their easy transfer from the small intestine to blood vessels, where they can regulate cell signaling in vascular cells.”

That the blood pressure-reducing effect was caused by oleic acid was supported by the finding that “. . . the correlation between the reduction of BP [blood pressure] and the dose of cis-MUFAs [oleic acid moieties] administered to animals was highly significant (r = 0.94; P < 0.001; n = 8).”1 Blood pressure was also reduced similarly by virgin olive oil and triolein (the major constituent of virgin olive oil, consisting of a triglyceride with three oleic acid moieties).

The authors conclude that the increased concentration of cis-MUFA (oleic acid, a monounsaturated fatty acid) in lipid membranes “regulates the localization, activity, and expression of important signaling molecules in the adrenergic receptor pathway, enhancing the production of vasodilatory stimuli (e.g., cAMP and PKA) and restricting vasoconstriction pathways (inositol-triphosphate, Ca2+, diacylglycerol, and Rho kinase).”

Another paper2 reports finding similar changes in G proteins as well as in PKCalpha activity in plasma membrane lipids from elderly persons with type 2 diabetes after consuming a diet rich in sunflower oil (not the high-oleic acid variety that we use) followed by a diet enriched in virgin olive oil for 4 weeks. The authors believe that these changes “probably account for the positive effects of VOO [virgin olive oil] on glycemic homeostasis.”

While olive oil contains an average of about 85% oleic acid,3 our high-oleic sunflower oil contains about 96% oleic acid. Hence, we would expect it to have similar (or perhaps greater) effects on blood pressure in comparison to olive oil. We prefer the high-oleic sunflower oil because it contains much less of the atherogenic palmitic acid,4 which comprises reportedly 10.9% of fatty acid content of virgin olive oil.2

References

  1. Teres et al. Oleic acid content is responsible for the reduction in blood pressure induced by olive oil. Proc Natl Acad Sci USA 105(37):13811-6 (2008).
  2. Perona et al. Consumption of virgin olive oil influences membrane lipid composition and regulates intracellular signaling in elderly adults with type 2 diabetes mellitus. J Gerontol A Biol Sci Med Sci 62A(3):256-63 (2007).
  3. Wahle et al. Olive oil and modulation of cell signaling in disease prevention. Lipids 39(12):1223-31 (2004).
  4. Olefsky. Fat talks, liver and muscle listen. Cell 134:914-6 (2008).

 

White Wine Has Cardioprotective Effects by Activating a Cell Survival Pathway, Including the Longevity-Associated Gene FOXO3a

White wine, though lacking in polyphenols (plentiful in red wine) has been shown in a new study1 to protect against heart injury in myocardial ischemic-reperfusion (heart attack, where blood flow is first blocked and then restored) in rats. This protection was provided by a different set of natural constituents, including caffeic acid (twice as much in white wine as in red), tyrosol, and shikimic acid.

The authors report that “In human case control studies, red and white wine demonstrated equal effects on fibrinolytic [clot-busting] factors and collagen-induced platelet aggregation.” Moreover, tyrosol and caffeic acid have been found to modulate oxidative stress and inflammatory reactions.1 Previous work by these scientists reported white wine reduced heart cell death (infarct size) during experimental heart attacks. The researchers conducted this new study of myocardial ischemic-reperfusion injury in rats to determine the effects of white wine under these conditions on protective signaling from Akt, FOXO3a, eNOS, and the redox transcription factor NFkappaB. The experimental animals (subject to ischemia-reperfusion) received white wine by gavage (pumped into their stomachs). A wine sham group received white wine by gavage but did not receive the ischemia-reperfusion treatment.

The results showed that white wine decreased the infarct size to approximately 21% as compared to 39% in the control IR (ischemia-reperfusion) group. There was a significant decrease in the apoptosis (programmed cell death) of cardiac cells and of endothelial cells in the treated group vs. the untreated. “On the whole, white wine treatment has demonstrated progressive, significant increase in left ventricular function as compared to the untreated group.” The results for the biochemical pathways included finding that white wine significantly increased the phosphorylation (i.e., activation) of Akt (1.5-fold in the wine shams and 2.6-fold in the wine ischemia-reperfusion experimental group), significantly increased eNOS (in both the wine shams and the wine ischemia-reperfusion groups), and increased levels of phosphorylated FOXO3a in both wine shams and wine ischemia-reperfusion groups, while significantly increasing the DNA binding of NFkappaB in both wine sham and wine/ischemia-reperfusion groups as compared to controls.

The activation of Akt has been shown in other studies to inhibit cardiomyocyte apoptosis and also to preserve function in surviving cardiomyoctes.1 The authors note that “Recently, we have demonstrated that bromelain [a pineapple proteolytic enzyme] induces cardioprotection against ischemia-reperfusion injury through the Akt/FOXO3a pathway in rat myocardium.” [Emphasis added] Increased eNOS activity has also been shown to have cardioprotective effects, reducing cardiomyocyte apoptosis and infarct size in a rat model of ischemia-reperfusion injury.1 Induction of NFkappaB has been shown to occur under conditions where eNOS is low (as occurs during ischemia-reperfusion) and provides cytoprotection to cardiomyocytes.

FOXO3a Genotype Strongly Associated with Human Longevity

In a new paper2 scientists report finding that “genetic variation within the FOXO3a gene was strongly associated with human longevity. . . . Long-lived men also exhibited several biological markers indicative of greater insulin sensitivity, and this was associated with homozygosity [two copies of the same version of the gene] for the FOXO3A GG genotype. . . . two copies of the G allele conferred about twice the protective effect (suggesting an additive effect), roughly tripling the odds of living close to a century.” It would be interesting to see what effect the human FOXO3a genotype would have had on the protective effects of white wine if the above experiment had been done in transgenic rats. Another possible study is to examine the prevalence of the FOXO3a GG genotype in human heart attack survivors as compared to nonsurvivors.

References

  1. Thirunavukkarashu et al. White wine-induced cardioprotection against ischemia-reperfusion injury is mediated by life-extending Akt/FOXO3A/NFkappaB survival pathway. J Agric Food Chem 56:6733-9 (2008).
  2. Willcox et al. FOXO3A genotype is strongly associated with human longevity. Proc Natl Acad Sci USA 105(37):13987-92 (2008).

 

A man can never have too many 
books, too much red wine, or too much ammunition.
— Rudyard Kipling

 

As long as I don’t read the newspapers, I feel fine.
— Otto Hahn, received Nobel Prize in Chemistry, 1944

You’d Be Depressed Too If You Were Suspended by Your Tail—
Relief of Depression with SSRIs and 5-HTP

The ability of humans to make serotonin from tryptophan may determine who can benefit from selective serotonin reuptake inhibitors (SSRIs), which are antidepressant drugs, and who cannot. Many depressed people are resistant to drug treatment, including SSRIs such as fluoxetine (generic name for Prozac®). The same is true for mice. C57BL/6 mice, but not NMRI mice, respond to SSRI treatment in the tail-suspension test with decreased immobility (an antidepressant effect). A new study identified the reason why: unlike the C57BL/6 mice, the NMRI mice have a version of the tryptophan hydroxylase 2 (TPH2) gene—tryptophan hydroxylase is the rate-limiting enzyme in the synthesis of serotonin from tryptophan—that results in low levels of brain serotonin.1 “This is analogous to the finding that low TPH2 function is associated with poor responses to SSRIs in depressed patients.”1

The tail-suspension test is used in mice to test antidepressants because the ability of a compound to decrease immobility in this and the forced swimming test are predictors of antidepressant potential in humans.

TPH2 catalyzes the conversion of tryptophan to 5-hydroxytryptophan (5-HTP), the rate-limiting step in the synthesis of serotonin. The researchers1 thus tested the effects of supplementing the NMRI mice with 5-HTP as well as treating them with an SSRI on immobility in the tail-suspension test. They found that serotonin levels were higher in the frontal cortex (but not the hippocampus) after treatment with 12.5 mg/kg of 5-HTP. In tail-suspension tests where the mice received the same dose of 5-HTP as a cotreatment with either of the SSRIs citalopram or paroxetine, the formerly SSRI-unresponsive NMRI mice became significantly less immobile compared to either 5-HTP alone or the SSRI alone. For example, the maximal effect for 5-HTP and paroxetine was found for 5-HTP plus 20 mg/kg paroxetine, which resulted in a 59% decrease in immobility as compared to 5-HTP alone.

Interestingly, the authors cite a paper by other researchers who found, in two other citalopram-insensitive mouse strains, that tryptophan increased citalopram response in the forced swim test. However, in that study, a tryptophan dose of 300 mg/kg was effective, as compared to 12.5 mg/kg of 5-HTP in the new study.1

5-Hydroxytryptophan, a Potent Hydroxyl Radical Scavenger

Also of interest are the findings of another paper,2 in which the researchers compared the hydroxyl radical scavenging ability of 5-hydroxytryptophan to melatonin and vitamin C. “5-HTP showed highest hydroxyl radical scavenging effects with a 50% inhibition concentration (IC50) of 1.8 µM. For vitamin C an IC50 of 12.7 µM was measured, whereas melatonin in pure demineralized water was much less efficient (IC50 = 724 µM).”2

This is interesting because the hydroxyl radical is the most potently damaging radical, able to attack any macromolecule, including lipids, protein, and DNA. Radiation damage is largely caused by the massive creation of hydroxyl radicals. (Another good scavenger for hydroxyl radicals is ethanol, though we do not recommend it for depression.)

We use our 5-hydroxytryptophan-containing formulations (Serene Tranquility™ Night with 5-HTP, which also contains melatonin, and Serene Tranquility Day with 5-HTP), with 75 mg of 5-HTP per serving.

References

  1. Jacobsen et al. Insensitivity of NMRI mice to selective serotonin reuptake inhibitors in the tail suspension test can be reversed by co-treatment with 5-hydroxytryptophan. Psychopharmacology 199:137-50 (2008).
  2. Keithahn & Lerchi. 5-Hydroxytryptophan is a more potent in vitro hydroxyl radical scavenger than melatonin or vitamin C. J Pineal Res 38:62-6 (2005).

 

Scrumptious and Good-For-You Cranberry Sauce for the Holidays

Ever wish you could get a really delicious, non-sugar-containing cranberry sauce rather than what they offer you at the supermarket? Sandy ran into this wonderful recipe for a curried cranberry sauce in the September 2008 Gourmet magazine. It was in an advertising section supplied by Spice Islands (for more recipes, see SpiceIslands.com). Sandy was particularly delighted with the flavorful selection of ingredients and the fact that it is easy to substitute erythritol for the called-for sugar. (Store cranberry sauces are loaded with sugar.) She also added a pinch or two of cloves to the original recipe. This is great for turkey or ham and really jazzes up your leftovers! Also great on hamburgers and meat loaves. Plus you get potent antioxidant and antiglycation (prevents the formation of AGEs) activity from the cranberries, oranges, cinnamon, wine, currants, cloves, and spices in the curry powder.

Curried Cranberries

Preparation time: about 10 minutes 
Start to finish, including cooking time: 70–85 minutes

You’ll need: 

1 cup

erythritol

1/2 cup

cider vinegar

1/2 cup

port wine

3/4 cup

orange marmalade (we use sugar-free)

1/3 cup

red or black currants (or raisins)

2 tsp

ground cinnamon

1–2 pinches

ground cloves

1 1/2 tsp

curry powder

1/4 tsp

salt

12 oz

fresh cranberries

Preheat oven to 325ºF. Combine erythritol, vinegar, port, marmalade, currants, cinnamon, cloves, curry powder, and salt in a large bowl. Add cranberries and mix well. Use a nonstick 2-quart baking dish (or spray with nonstick cooking spray). Pour in cranberry mixture and cover with foil. Bake for 50–60 minutes, until cranberries are soft. Before serving, let sit for 10–15 minutes to thicken slightly.

Enjoy!




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