December 2009 Blog with Durk and Sandy

[O]f those men who have overturned the liberties of republics, the greatest number have begun their career by paying an obsequious court to the people; commencing demagogues, and ending tyrants.

— Alexander Hamilton, Federalist No. 1


For the year 2006, the total health care spending (U.S.) was estimated at $2.2 trillion, while, for that same year, the total estimated out-of-pocket expenses was $302.5 billion (with the rest out of taxpayers’ pockets); spending on complementary and alternative medicine was $33.9 billion, with natural products representing $14.8 billion (est.) of the spending on complementary and alternative medicine.

— Science Stats, Science News, August 29, 2009
(sources: 2007 National Health Interview Survey,
Centers for Medicare and Medicaid Services)

Universal [health] coverage is so expensive that Congress can’t get there without taxing Democrats.

— Michael Barone, Rasmussen Reports

A nation of sheep will beget a government of wolves.

— Edward R. Murrow


Postprandial Triglycerides Reduced by Tea Catechins

Although elevated fasting levels of serum lipids can be significant risk factors for cardiovascular disease, much emphasis is now being focused on postprandial (after meal) lipid levels, which may be even more important risk factors.1

A recent paper1 reports that tea catechins attenuated the postprandial increase in plasma triacylglycerol (triglyceride) levels following a fat load in a randomized, triple-crossover design study of nine male subjects with mild or borderline hypertriacylglycerolemia (high triglycerides). A semi-purified extract of green tea was used for preparation of test beverages (10 mg tea catechins as control, 224 mg of tea catechins as moderate dose, and 674 mg as high dose). “Expressed as a percentage of control, the average reductions in IAUC [increment area under the curve] after a moderate and a high-catechin dosage were 15.1% and 28.7%, respectively. However, no significant effect on IAUC was observed between the control and the moderate dosage of tea catechins.”1

“The assumption that exaggerated lipaemia in the postprandial phase may be implicated in the early development of atherosclerosis is now widely accepted . . . .”

The authors referred to the results of other studies for possible mechanisms by which the tea catechins decreased postprandial plasma triacylglycerol in their own study. One such potential mechanism is the marked ability of green tea catechins to inhibit gastric and pancreatic lipases, thus limiting intestinal lipid absorption. Our ShapeShifter Teas Booster Caps™ contain 660 mg of green tea catechins per capsule, of which 330 mg is EGCG.

Suppression by Tea Catechins With a Galloyl Moiety on Postprandial Hypertriglyceridemia in Rats

In this study,2 a lipid emulsion was administered orally to rats along with epigallocatechin gallate (EGCG) at a dose of 100 mg/kg. The result showed that, compared to the lipid emulsion group that received placebo, there was a significant inhibition by EGCG in the plasma increase in triacylglycerol. In a second experiment, rats receiving the lipid emulsion along with 50–200 mg/kg of a tea extract comprised largely of catechins with a galloyl moiety, had suppressed increases in plasma TG (triglyceride) levels 1 and 2 hours after administration compared to those receiving distilled water. The suppression of the TG AUC (area under the curve) by the tea extract was statistically significant at 200 mg/kg. “Its plasma TG-lowering effect is thought to be produced by at least two different mechanisms, i.e., inhibition of the absorption of fat from the intestine, and activation of the catabolism of TG in the bloodstream.” In this study, the authors attribute the decrease in TG increase to the first mechanism (reduced absorption) because “the administration of catechins without the lipid emulsion had no effect on the plasma TG level.” Our ShapeShifter Teas Booster Caps™ contain 660 mg of green tea catechins per capsule, of which 330 mg. is EGCG.

Neuroprotection by Green Tea Theanine and Catechins

This review3 of neuroprotection by green tea components covers many studies, mostly in vitro mechanistic studies and animal model studies, but also a few human studies.

The author discusses the following: “An epidemiological study showed that the incidence of stroke was significantly lower in people who consume more than five cups of green tea (Camellia sinensis) per day.”

The researcher notes that the green tea component theanine (gamma-glutamylethylamide) is chemically similar to the excitatory neurotransmitter glutamic acid which, when released in excessive amounts (a condition called excitotoxicity), can cause damage such as forebrain ischemic neuronal death. The investigations of the author3 demonstrated that theanine has a neuroprotective effect in transient ischemic neuronal death.

As the author explains, glutamic acid “plays an important role in memory and learning by producing synaptic plasticity, known as long term potentiation (LTP) or long term depression (LTD).

“However, when the intracellular energy source ATP is depleted by injury such as ischemia, depolarization of the neuronal membrane leads to excessive release of glutamic acid and lack of ability to reabsorb this glutamic acid by the glutamate transporter, resulting in an excessive concentration of glutamic acid in the extracellular space.”

Since theanine may be an analog of the excitatory neurotransmitter glutamic acid, the author paid special attention to the effects of theanine as a possible competitor with glutamic acid in the binding of glutamate receptors. He discusses studies, in vitro and in vivo, showing protection by theanine against glutamate excitotoxicity. For example, he examined the neuroprotective effect of theanine against postischemic neuronal death in a transient ischemia model in gerbil hippocampus. The theanine treated animals received 50 µM, 125 µM, or 500 µM theanine before transient forebrain ischemia. “Ischemic neuronal death in field CA1 of the hippocampus was suppressed in the theanine-pretreated groups in a dose-dependent manner, with approximately 60% and 90% survival with theanine 125 µM and 500 µM, respectively.”

The author further discusses studies showing the binding of theanine to glutamate receptor subtypes, such as AMPA, kainate, and NMDA; though theanine’s binding capacity to these receptor subtypes was found to be much lower than that of glutamic acid, the author believes that theanine may still act as a glutamate antagonist. The author urges that more studies be done to clarify this.


  1. Unno et al. Effect of tea catechins on postprandial plasma lipid responses in human subjects. Br J Nutr 93:543-7 (2005). <liBiosci Biotechnol Biochem 69(7):1288-91 (2005).</li
  2. Neuroprotective effects of the green tea components theanine and catechins. Biol Pharm Bull25(12):1513-8 (2002).



Choline is found in especially large amounts in animal products, such as meat, fish, liver, and eggs, but also in a few vegetable products such as wheat germ and soybeans.1 A new study1 reports on the association between plasma choline concentrations and scores on tests for symptoms of anxiety and depression in a general population sample of both men and women ages 46–49 and 70–74 years in the Hordaland Health Study (Norway). This is interesting because, despite the fact that many papers have been published concerning the relationship between choline and cognition, far fewer have focused on its effects on emotional functioning.

In this study, a significant association was found between high anxiety levels (but not depression) and choline levels in the lowest versus the highest quintile [the Odds Ratio between those in the lowest quintile as compared to those in the highest quintile was 1.36 (95% CI: 1.06, 1.69, with p<0.007) for the model fully adjusted for potential confounding factors]. As these subjects had all been participants in a homocysteine study, the researchers also had plasma levels for betaine and dimethylglycine as well as choline, but found no significant relationship between either betaine or dimethylglycine and anxiety or depression.

The authors point out that data on the role of acetylcholine (made from choline) in mental disorders and emotional regulation in humans is sparse. They note that in rats, dorsal hippocampal cholinergic transmission mediates an anxiolytic (anti-anxiety) effect. Moreover, nicotine, which activates nicotinic cholinergic receptors, has effects on anxiety in animal and human studies. They suggest that the importance of choline in methylation reactions may play a role in choline’s anti-anxiety effects. “Stress, an anxiety component, induces an increase in adrenal catecholamines, which increases the demand for methylation reactions required in norepinephrine and adrenaline synthesis.” Nevertheless, they found no evidence that choline’s role in methylation reactions was a factor in anxiety in a previous study of the same population.

  1. Bjelland et al. Choline in anxiety and depression: the Hordaland Health Study. Am J Clin Nutr 90:1056-60 (2009).



Here is another way to increase HDL, at least in rats.1 As rodents handle cholesterol differently than humans, humans might not get exactly the same effects, though we would expect that the changes would be in the same direction. The results of this study are particularly interesting, as the feeding of a high cholesterol diet as a way to increase serum cholesterol levels would suggest cholesterol absorption as the main source for the increased serum cholesterol. As noted in the next article in this issue, increased cholesterol absorption and decreased cholesterol synthesis may be important changes in cholesterol homeostasis that increase the risk of cardiovascular disease. Hence, if curcumin can decrease cholesterol absorption in humans as this study suggests it does in rats; that would point to an anti-cardiovascular disease effect.

Male Swiss albino rats were fed a high cholesterol diet for seven days. Another group received the same diet but enriched with 0.5% w/w curcumin. A third group received peanut oil orally as a vehicle and served as controls. Unsurprisingly, the rats getting the high cholesterol diet (HCD) developed hypercholesterolemia, with high serum total cholesterol; serum HDL-C decreased by 21% as compared to controls. There was a 12-fold increase in serum LDL-C and a 16-fold increase in the LDL-C/HDL-C risk ratio compared to controls.

Supplementation with 0.5% curcumin had significant effects on serum lipids. Serum total cholesterol decreased by about 21% compared to rats fed the HCD alone. (The total cholesterol in the HCD-curcumin rats still had an increase of 122% compared to controls.) The most remarkable effect, however, was a 50% increase in serum HDL levels in the HCD-curcumin rats as compared to the rats getting the HCD diet alone. The researcher notes that the serum level of HDL-C actually exceeded normal values by 19%. The LDL-C/HDL-C ratio was lowered by 52% following curcumin intake compared to animals fed HCD alone.

As the author suggests, “[t]aken together, one could argue that the hypolipidemic effect of curcumin observed in the current study could possibly be ascribed to an effect on the absorption of cholesterol in the gut, especially [as] curcumin was admixed with the HCD.”

  1. Curcumin attenuates diet-induced hypercholesterolemia in rats. Med Sci Monit 11(7):BR228-34 (2005).



A randomized, double blind placebo controlled trial was conducted to test the efficacy of curcumin as maintenance therapy for patients with quiescent ulcerative colitis (UC), e.g., to determine whether curcumin could prevent relapse.1

Ulcerative colitis is a type of chronic, relapsing inflammatory bowel disease. In this study, 45 patients with quiescent ulcerative colitis received curcumin, 1 gram after breakfast and 1 gram after the evening meal, plus sulfasalazine or mesalamine, while another 44 patients received placebo plus sulfasalazine or mesalamine for six months. Of 43 patients who received curcumin, 2 relapsed during the six months of treatment (4.65%), while 8 of 39 patients (20.51%) receiving placebo relapsed (P = 0.040). The authors attribute the beneficial effects of curcumin in this study, at least in part, to the inhibition of the pro-inflammatory transcription factor NF-kappaB (nuclear factor kappa B) that has been reported in other studies.

The researchers report: “In our study, both the clinical and endoscopic evaluation scores were significantly improved by curcumin therapy. Especially the endoscopic score was substantially improved compared with the placebo.”

  1. Hanai et al. Curcumin maintenance therapy for ulcerative colitis: randomized, multicenter, double-blind, placebo-controlled trial. Clin Gastroenterol Hepatol4:1502-6 (2006).



A new paper1 reports on the association between Vitamin D and cognition in 3,369 men aged 40–79 years from eight centers enrolled in the European Male Ageing Study. Tests for different aspects of cognition were included. There was no significant difference between those with high levels of 25(OH)D and those with lower levels except in the DSST test. The DSST test is described in the paper as a “subtest adopted from the Wechsler Adult Intelligence Scales and provides a reliable measure of psychomotor speed and visual scanning. Participants were asked to make as many correct symbol-for-digit substitutions as possible within a 1 minute period.”

The authors conclude: “Although we were unable to specifically explain this observation [the significant association between 25(OH)D levels and DSST scores], the DSST appears robust . . . .” However, note that the association between 25(OH)D and DSST score was only significant among the older men, that is, those aged 60–69 and 70–79.

  1. Lee et al. Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men.J Neurol Neurosurg Psychiatry 80:722-9 (2009).



Sudden death heart attacks constitute about half of all heart attacks. Omega-3 fatty acids are known to provide powerful protection against the cardiac arrhythmias responsible for sudden death heart attacks. However, a new study1 also reports very powerful protection against ischemia/reperfusion (IR)-induced cardiac arrhythmias by the flavonone hesperidin. Hesperidin is hydrolyzed by intestinal microflora to create its major active metabolite hesperitin.1

Ischemia/reperfusion causes damage to tissues whenever blood flow (and oxygen supply) is temporarily interrupted and then resumes. While some of the damage is caused by the reduced oxygen supply resulting from the initial interruption of blood flow, more damage occurs when the blood flow resumes due to the creation of reactive oxygen species (ROS) that takes place at that time. As the authors of the new study point out, “I/R-induced arrhythmias have been shown to be ameliorated in animal models by many free radical scavengers or antioxidants, such as mannitol, superoxide dismutase, catalase, ascorbate, allopurinol [inhibitor of the ROS-generating enzyme xanthine oxidase], methionine, glutathione, and desferoxamine [an iron chelator].”

The authors of the new paper indicated that they knew of no prior evidence that treatment with hesperidin could suppress I/R-induced arrhythmias, but carried out this study in an in vivo rat model to test this possibility.

The rats were divided into four groups. Group 1 were sham operated. They had the same surgical procedures as the experimental rats, but did not have their coronary artery ligated (no ischemia). Group 2 were subjected to 30 minutes of coronary artery ligation (ischemia) and 60 minutes reperfusion. Group 2 were the I/R controls since they did not receive hesperidin, the active treatment. Group 3 were treated the same as Group 2 but received hesperidin (100 mg/kg/day, p.o.) for 15 days before being subjected to the ischemia and reperfusion. Group 4 were treated like Group three but received vitamin E (100 mg/kg/day, p.o.) rather than hesperidin for 15 days before being subjected to ischemia/reperfusion.

The results showed, among other things, reduction by hesperidin in incidences of arrhythmia as compared to the I/R control group. Vitamin E also reduced the incidence of arrhythmia but not as effectively as hesperidin. Moreover, the I/R control group had a significant increase in the severity of arrhythmias as compared to the sham operated group. In the hesperidin treated I/R group, there was a significant reduction in severity of arrhythmias as compared to the I/R controls.

I/R resulted in a significant decrease in the tissue level of nitrite (an important source of nitric oxide) as compared to sham operated controls (135.5 ± 4.38 nmol/g tissue, p<0.05, n=6 vs. 157.3 ± 6.22), but the hesperidin treated I/R group had a significant increase in tissue nitrite level as compared to the I/R control group (160.2 ± 3.37 nmol/gm tissue, p<0.05, n=6 vs. 135.5 ± 4.38 nmol/g tissue, p<0.05, n=6). Vitamin E also improved nitrite levels but not as significantly as hesperidin.

Other results included that hesperidin protected the tissue levels of superoxide dismutase in I/R animals, almost maintaining the same level as the sham operated animals. Vitamin E was slightly less effective than hesperidin.

There are many conditions besides cardiovascular disease in which tissues can be exposed to ischemia/reperfusion, such as sleep apnea (intermittent hypoxia), emphysema and COPD, and clogged carotid arteries (TIA or stroke), where hesperidin (and omega-3 fatty acids) supplementation would appear to be a very good idea. We get our hesperidin (in addition to dietary sources) from Personal Radical Shield™; the recommended 12 capsules a day contain 120 mg hesperidin, as well as 800 mg of vitamin E.

  1. Gandhi et al. Protection against in vivo focal myocardial ischemia/reperfusion injury-induced arrhythmias and apoptosis by hesperidin. Free Rad Res43(9):817-27 (2009).



We use CLA only at a low dose for its anti-carcinogenic properties because at the higher doses needed for anti-obesity effects, CLA has been reported to cause inflammation, insulin resistance, and endoplasmic reticulum stress in mice, humans and cell cultures of adipocytes.1 The authors of a new paper1 hypothesized that resveratrol, a known anti-inflammatory and antioxidant molecule, would attenuate the inflammation and insulin resistance caused by 10,12 CLA in human adipocytes (fat cells). The researchers used 50 µM resveratrol in human adipocytes cultured with 10,12 CLA and found that at this dose resveratrol prevented inflammation and attenuated the activation of ERK1/2 and induction of the genes for the inflammatory cytokines IL-6, IL-8, and IL-1beta within 12 hours. Resveratrol also blocked 10,12 CLA induction of the inflammatory prostaglandin pathway (PLA2, cyclooxygenase-2 (COX-2), and PGF2alpha).

The authors report: “Indeed, 10,12 CLA treated cultures co-supplemented with 50 µM RSV [resveratrol] had higher levels of insulin-stimulated glucose uptake, compared with cultures treated with 10,12 CLA alone. Consistent with these data, RSV blocked 10,12 CLA induction of SOCS-3, a protein that causes insulin resistance through serine phosphorylation of IRS-1.”

The only downside of these beneficial effects of resveratrol on CLA supplementation was that resveratrol attenuated some of the desired anti-obesity effects of CLA; “RSV co-supplementation attenuated delipidation and suppression of FA [fatty acid] uptake by 10,12 CLA.”

Nevertheless, if you are going to be using CLA at doses high enough for anti-obesity effects and want to avoid the adverse effects of CLA, we would suggest you also take resveratrol along with it. We get our daily resveratrol from dietary sources (mostly from the 1 or 2 glasses of red wine we drink per day) as well as from MealMate™, our weight maintenance help formulation (two capsules provides 40 mg of resveratrol).

  1. Kennedy et al. Conjugated linoleic acid-mediated inflammation and insulin resistance in human adipocytes are attenuated by resveratrol. J Lipid Res50:225-32 (2009).



Al-Quaeda has been appointed editor-in-chief of
Yale University Press.

.— Flemming Rose, Danish editor behind
the published Mohammed cartoons

Flemming Rose comments above on the fact that Yale University Press published a book called The Cartoons That Shook the World but decided to remove all the images of Mohammed, including both historical images and the recently published “controversial” cartoons, from the book against the desires of the book’s author Jytte Klausen. This is a really pathetic example of a university wanting to profit from a controversial subject but too cowardly to actually let you see what was so controversial. Rose points out: “… we and other Danish newspapers have republished Westergaard’s cartoon dozens of times without any reaction, so why on earth anticipate violence because of a reproduction of the newspaper page?”

See the whole, very interesting interview with Flemming Rose at, website for the Foundation for Individual Rights in Education, a group very effectively defending First Amendment rights of students and professors at publicly funded universities across America.



BHT, butylated hydroxytoluene, has been used for decades as a food antioxidant additive for preservative purposes (as well as a material for experimental studies of life extension in animals). Many people, however, stay away from anything containing BHT because of a concern about its synthetic nature. Recently, however, a group of researchers discovered that four freshwater phytoplankton, including a green alga and three cyanobacteria, produce BHT as an antioxidant:1 the researchers found that the quantity of cellular BHT displayed a positive correlation with the antioxidant activity of the tested species. The scientists suggested that “these species constitute a potential source for producing natural BHT.” True, but a molecule of natural BHT is the same as a molecule of synthetic BHT, so it really doesn’t matter who produced it, man or phytoplankton.

  1. Babu and Wu. Production of natural butylated hydroxytoluene as an antioxidant by freshwater phytoplankton. J Phycol44:1447-54 (2008).



We always take our Ineffable Essence™ (combination of monosodium glutamate and disodium inosinate, two natural flavor molecules) with us whenever we travel so that we can enhance food flavors (we call it “replacement therapy for food,” as the natural levels of these molecules decrease rapidly as food ages) and of course we use it at home. You may be surprised to learn that many foods contain substantial amounts of natural glutamate, which is an important part of their savory (called umami) flavor. For example, the table below shows the natural glutamate content of various foods.

Food Glutamate (mg/100 g)
Parmesan cheese 8,210
chedder cheese 6,090
walnuts 658
fresh tomato 310
beans 880
steak >2,000
white mushrooms 400
salmon 3,840
broccoli 950
(These data from Ajinomoto Co., which manufactures and
sells MSG and sodium inosinate.)

Scientists recently published a paper1 asking the question: can supplementation with glutamate be used to improve health?

As the researchers explained, there is a decrease in sensitivity to and preference for L-glutamate (the umami taste) in elderly Japanese and Western as compared to middle-aged individuals. They report that “umami taste sensitivity is correlated with the protein preference score.” Not surprising, as amino acids contribute to umami taste. Favorable effects of MSG on palatability and appetite were reported in elderly patients with reduced sodium intake and in those who had lost body weight as a result of disease. Salivary secretion was reported to be increased after ingesting food containing MSG as compared to the same food without MSG. Thus, the authors suggest, umami may help “increase salivary flow” and, therefore, “have clinical potential in the elderly, who frequently experience dry mouth and its complications [e.g., tooth decay, difficulty swallowing].”

Another group was reported by the authors to find an improvement in immune function in the elderly after the enhancement of the flavors of “typical” institutionalized diets, while MSG supplementation (0.5% MSG added to the staple diet of elderly patients) in a different study resulted in a significant increase in peripheral lymphocyte concentrations (a possible improvement in immune function), as well as improvements in speech, facial expression, and eye opening.

  1. Yamamoto et al. Can dietary supplementation of monosodium glutamate improve the health of the elderly? Am J Clin Nutr 90(Suppl.):844S-9S (2009).



Another paper1 reported on the effects of glutamate consumption on various aspects of energy homeostasis. The researchers reported that chronic, ad lib ingestion of a palatable solution of monosodium L-glutamate (1% wt:vol) by rats “has also been found to reduce weight gain, fat deposition, and plasma leptin concentrations compared with rats that ingest water alone.” There was no difference in food intake. The authors1suggest that these effects may be mediated by the vagal nerve signaling from the gut to the brain. As they explain, “[s]timulation of these [L-glutamate] receptors [in gut epithelial cells] by luminal L-glutamate activates vagal afferent nerve fibers and subsequently parts of the brain targeted directly or indirectly by these vagal inputs [e.g., the cerebral cortex, basal ganglia, limbic system, and hypothalamus].” In addition, the chronic, elective ingestion of a palatable solution of monosodium L-glutamate (MSG) by rats has been found to reduce the development of obesity, fat deposition, and elevated plasma leptin concentrations through an enhancement of energy expenditure.

The natural flavor molecules in Ineffable Essence can add a lot to the taste of meals containing foodstuffs that normally contain significant amounts of them, such as meats, dairy products, eggs, and vegetables. It won’t make awful food taste good (though it won’t make it worse), but it can make make good food taste great.

  1. Kondoh et al. Activation of the gut-brain axis by dietary glutamate and physiological significance in energy homeostasis.Am J Clin Nutr 90(Suppl.):832S-7S (2009).



We include this special report because it is a shocking revelation of little-known aggressive new rules issued by the IRS to loot the incomes of anybody anywhere in the world who owns a U.S. stock or bond. As a result of these rules, they can declare the incomes of non-U.S. citizens to be subject to U.S. estate taxes (at 45% with new tougher rules coming from the Obama Administration), income taxes, and corporate taxes if they own a single share of stock of a U.S. company or if they own a single U.S. Treasury bond.

The result is what might be expected. As the following report from Wegelin & Co., Swiss private bankers since 1741, explain in their Investment Commentary No. 265 (Aug. 24, 2009), they are advising non-U.S. citizens to flee U.S. stocks and bonds. The first section is technical and a little hard to comprehend because it is an attempt by Wegelin & Co. to explain the IRS’s sweeping rules for what constitutes a “U.S. person” (anywhere in the world) who is subject to all U.S. taxes. If you want to get to where the bank explains how they see these IRS rules affecting the U.S., skip to section 5 (“The USA’s Achilles’ Heel”) and read from there.

Section 6 (“Rats leaving the sinking ship”) emphasizes the bank’s view that the U.S.’s greed to seize wealth by immense global expansion of U.S. tax law is accompanied by anti-capitalist, anti-market, and anti-entrepreneural policies at home that discourage investment, both foreign and domestic. The report closes with these words: “… we are well advised to take a general farewell of America. This will be painful, for the USA was once the most vital market economy in the world. But for now, it’s time to say goodbye.”

For their unparalleled greed to seize the wealth of anyone in the world, thereby driving away foreign investment in America, we might someday want to thank the Obama Administration because this may be a tipping point (or perhaps a trip wire) in which large numbers of Americans realize that “their” government is destroying all that has made America great and prosperous and, indeed, to realize what it is that has made America great and prosperous.

You can obtain the entire report here as a PDF:

It is well worth reading.



This interesting recent study1 reports on the relationship in apparently healthy men (472 men free of coronary heart disease and diabetes and taking no blood pressure-, lipid-, or uric acid-lowering medication) of various measures of liver function and insulin sensitivity. This could be a useful way to help evaluate one’s insulin sensitivity with simple blood tests.

Insulin sensitivity S1 was determined using “the minimal model of glucose disappearance.” The insulin sensitivity was found to correlate independently with serum gamma-glutamyl transferase (GGT), aspartate transaminase, and alkaline phosphatase activities; blood pressure; leukocyte count; and erythrocyte sedimentation rate.

The authors explain that there is a difference between correlation and clustering of risk factors. “For example, dyslipidemia and hypertension may both be associated with insulin resistance, but processes underlying their associations could be shared or separate. Evaluation of simple correlation will not discriminate which alternative predominates, whereas this can be achieved by an assessment of co-association. Co-association will be present when high or low levels of a particular combination of risk factors show a strong tendency to be present together [clustering] in individuals.” “In apparently healthy men, blood pressure and indices of subclinical inflammation do not cluster with other insulin resistance-related risk factors, despite correlating with insulin sensitivity. In contrast, both GGT activity and uric acid concentrations correlated with insulin sensitivity and co-associated with insulin resistance-related risk factors and are therefore components of a true risk factor cluster.”

“Among inflammation-related variables, S1 was a significant independent negative determinant of serum globulin concentration, ESR, and WBC.” “Among liver function-related variables, S1 was a significant independent negative determinant of GGT, AST, and ALP activities and of uric acid concentrations and was an independent positive determinant of serum bilirubin concentration.”

  1. Godsland and Johnston. Co-association between insulin sensitivity and measures of liver function, subclinical inflammation, and hematology. Metab Clin Exp57:1190-7 (2008).



A new study published in the Journal of Lipid Research1 has examined the relative importance in cholesterol homeostasis of cholesterol synthesis and cholesterol absorption from the gastrointestinal tract in a sample of 3,532 men and women who were offspring of the original participants in the Framingham Heart Study and their spouses. The results are somewhat different than we would have expected.

Of the 3,532 participants, the researchers identified 155 cases (51 female, 104 male) who had documented cardiovascular disease (n=117) and/or ≥50% carotid stenosis (blockage)(n=38) who were not taking lipid lowering medications. They then compared cholesterol homeostastis factors between the cases and 414 control subjects. (Mean age of cases was 67.5 ±0.7 years and of controls was 66.4 ±0.4 years.)

The authors note that “data from several clinical trials suggest that although LDL cholesterol lowering was highly efficacious, the reduction in the relative risk of major coronary events was poorly associated with baseline serum lipid concentrations.” They thus compared cholesterol absorption (using plant sterols and stanols as proxy indicators: campesterol, sitosterol, and cholestanol) in cases compared to controls. After controlling for standard risk factors, they found cholestanol, sitosterol, desmosterol, and lathosterol to be significantly associated with CVD (cardiovascular disease) risk. Thus, the effectiveness of cholesterol absorption by the GI tract is, based on these data, an important risk factor for cardiovascular disease. Of course, this varies from person to person.

The researchers also examined cholesterol synthesis. Surprisingly, markers of cholesterol synthesis (using cholesterol precursors as surrogate markers of cholesterol synthesis) were significantly lower for cases as compared to controls. Thus, this study reports lower synthesis of cholesterol and higher absorption marker concentrations for cholesterol “are highly significant independent predictors of prevalent CVD in this study population.” Interestingly, the authors report that studies by different researchers (see, for example, 2,3) found that, in the absence of CHD (coronary heart disease), diabetics or those with metabolic syndrome had a low cholesterol absorption and high cholesterol synthesis profile, suggesting (the authors1 propose) that “shifts in the balance of whole-body cholesterol homeostasis may predispose individuals to the development of CVD.”

“Specifically, the cholesterol absorption markers campesterol, sitosterol, and cholestanol were associated with a 5.98-, 3.16-, and 2.57-fold increase in CVD risk (highest vs. lowest tertile), respectively. In contrast, the cholesterol synthesis marker lathosterol was associated with a 0.29-fold decrease in CVD risk, respectively highest vs. lowest tertile (all P-values <0.05).” “Additionally, the cholesterol homeostasis markers appear to be better predictors of disease than traditional lipid risk factors in this study population.”


  1. Matthan et al. Alterations in cholesterol absorption/synthesis markers characterize Framingham Offspring Study participants with CHD. J Lipid Res50:1927-35 (2009).
  2. Gylling and Miettinen. Cholesterol absorption, synthesis and LDL metabolism in NIDDM.Diabetes Care 20:90-5 (1997).
  3. Simonen et al. Introducing a new component of the metabolic syndrome: low cholesterol absorption. Am J Clin Nutr 72:82-8 (2000).



As we have noted before, it is more difficult to increase HDL than it is to decrease LDL; a few ways to increase HDL include niacin,1 orange juice,2 cocoa,3phosphatidylinositol.4 moderate alcohol, and exercise.

Here we report a new paper5 that describes the effects on HDL of a placebo or a supplement of 160 mg twice a day of anthocyanins for 12 weeks in 120 dyslipidemic subjects (age 40–65 years). Anthocyanins are naturally colored molecules that give fruits (such as berries) and vegetables (e.g., purple carrots and potatoes) their red, blue, and purple colors. The anthocyanin supplement was a proprietary mixture of 17 different natural purified anthocyanins from bilberry and black currant. A possible mechanism for the effect of the anthocyanins was also investigated by examining the effects of the anthocyanin cyanidin 3-O-beta-glucosides in the human HepG2 (liver cell) line.

Results showed that, after 12 weeks, the serum HDL-cholesterol concentration increased significantly more in the anthocyanin group than in the placebo group (13.7% (95% CI: 10.4%, 16.9%)) vs. 2.8% (95% CI: –1.6%, 7.2%)), respectively; P<0.001). Moreover, serum LDL cholesterol decreased by 13.6% (95% CI: 10.1%, 17.1%) in the anthocyanin group and increased by 0.6% (95% CI: –4.1%, 5.2%) in the placebo group by the end of the intervention, which was significantly different between the two groups (P<0.001).

A possible mechanism was identified in the in vitro study in HepG2 cells. The anthocyanin cyanidin 3-O-beta-glucosides suppressed CETP activity in a dose dependent manner. CETP is cholesterol ester transfer protein, which modifies HDL particles. It has been reported that in humans, plasma CETP activity is inversely correlated with HDL cholesterol levels (the higher the CETP level, the lower the HDL level).6


  1. Zhang et al. Niacin inhibits surface expression of ATP synthase beta chain in HepG2 cells: implications for raising HDL. J Lipid Res 49:1195-1201 (2008).
  2. Kurowska et al. HDL-cholesterol-raising effect of orange juice in subjects with hypercholesterolemia. Am J Clin Nutr 72:1095-1100 (2000).
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