February 2007 Blog with Durk and Sandy


A new rat study of caloric restriction (CR) of late-middle-aged animals1 breaks new ground by using a diet in which fat calories and protein calories are the same in the restricted diet as for the ad libitum-fed rats; only carbohydrates (sucrose and cornstarch) are restricted. The beneficial results reported are very exciting because they point to an emphasis on a reduced-carbohydrate but high-protein (as a percentage of calories) diet for better long-term health.

In the usual CR diet, all sources of calories (carbohydrate, proteins, and fat) are restricted (vitamins and minerals are, however, fed at control levels), and, although CR has been shown to delay the onset of age-related mitochondrial abnormalities, it does not prevent the decline in ATP productivity needed to sustain muscle-protein fractional synthesis rate and contractile activity.1 The authors of this new study hypothesized that a limited ATP production during the usual CR is associated with a reduction in mitochondrial protein turnover and that maintaining protein intake during CR would stimulate mitochondrial protein turnover and improve mitochondrial protein oxidation and function. They looked at the effect of the carbohydrate-only CR (which we’re calling CarbCR) on the effect of mitochondrial function, as well as on muscle mass and function. The researchers looked at two types of muscle—soleus (a slow-twitch type) and tibialis anterior (a fast-twitch type)—because they exhibit different patterns of change with aging.

Increased ATP Production in CarbCR Rats

Carbohydrates in the CarbCR rats were restricted to about half of those consumed by the rats eating ad libitum, while fats and protein were the same as in the ad libitum diet. Wistar rats (21 months old) were fed either an ad libitum, 40% protein energy-restricted diet (which we’re calling AllCalCR for “all calories restricted,” the usual caloric restriction regimen) or a 40% CarbCR diet for 5 months. The weight loss observed in the CarbCR rats was the same as in the AllCalCR rats. However, there were no modifications of mitochondrial ATP production in either soleus or tibialis muscles in the AllCalCR group, whereas the CarbCR group had increased ATP production (by 30% in the soleus, P=0.07, and by 27% in the tibialis, P<0.05). Oxygen consumption in mitochondrial state 3 in the soleus decreased by 25% (P<0.05 vs. ad libitum) in the AllCalCR group but was maintained in the CarbCR rats.

In the tibialis, AllCalCR rats had the lowest mitochondrial-protein FSR (fractional synthesis rate) on synthesis of mitochondrial and myofibrillar proteins (e.g., myosin and actin, major contractile proteins) as compared to CarbCR and ad libitum. The reduction in muscle mitochondrial protein synthesis was significantly attenuated (P<0.05) in the CarbCR rats. Thus, maintaining protein intake significantly reduced the negative impact of an “all calories restricted” diet on muscle protein synthesis in the tibialis (a type II fiber).

Carbohydrate-Calorie-Restricted Rats Were Stronger

The authors report that absolute muscular force (grip force) was significantly increased in the CarbCR rats as compared with both the AllCalCR rats (7% greater, P<0.01) and ad libitum (18% greater, P<0.0001). The muscular force-to-body mass ratio was significantly increased in the AllCalCR rats (by 30%, P<0.0001, compared to ad libitum), but was increased even more in the CarbCR rats (by 49%, P<0.0001, compared to ad libitum and by 13%, P<0.01, compared to AllCalCR rats). The CarbCR rats exhibited a significant increase in the synthesis rates of myosin and actin, the major contractile proteins, as compared to the AllCalCR rats.

Reducing Carbohydrate Calories with a High-Fiber, High-Protein Whole Grain

One way to reduce carbohydrate calories while maintaining high protein levels is to substitute a high-fiber, high-protein, reduced-starch whole grain (such as our Glycemic Control™ line of extrahigh-beta-glucan, high-protein barley) in place of regular carbohydrates. The barley flour can be used in place of high-digestible-carbohydrate, lower-protein, and lower-fiber flours. The barley thick (not quick) flakes look like rice when cooked and have a nutty taste. We use them in cooked foods in place of rice. It makes a great barley pilaf, too—see recipe at the end of this newsletter. The barley quick flakes are great as a morning cereal, either with or without other cereals. Sandy mixes a little Go Lean Crunch®, a high-protein, high-fiber, low-sugar cereal (for extra crunch) along with 3 or 4 tablespoons of barley quick flakes for a snack or even a meal.

This study suggests that if you plan to reduce caloric intake or to select a different proportion of calorie sources in your diet, it is important to maintain your consumption of protein. Reduce carbohydrates, not protein. Eat fats in moderation, preferably monounsaturated and omega-3 polyunsaturated. Saturated fats should be eaten sparingly, as studies have shown, for example, that palmitic acid, a saturated fat found in fatty meats, butter, cream, etc., has negative effects on insulin sensitivity2 and promotes inflammation in adipose (fat) tissue.3 Moreover, another study4 reported that the ratio of oleic to palmitic acid content of the diet determines the thrombogenic (clot-promoting) and fibrinolytic (clot-busting) factors during the postprandial state in men. Increases in postprandial concentrations of tissue factor (prothrombotic) and plasminogen activator inhibitor-1 (antifibrinolytic), both of which increase the risk of clots, were observed when the ratio of oleic (monounsaturated fat) to palmitic acid (saturated fat) decreased. The same study also reports that n-3 LCPUFAs (DHA and EPA) may partially reduce the thrombotic potential of a fat-rich meal.


  1. Zangarelli et al. Synergistic effects of caloric restriction with maintained protein intake on skeletal muscle performance in 21 month old rats: a mitochondria-mediated pathway. FASEB J 20:2439-50 (2006).
  2. Solinas et al. Saturated fatty acids inhibit induction of insulin gene transcription by JNK-mediated phosphorylation of insulin-receptor substrates. Proc Natl Acad Sci USA 103(44):16454-9 (2006).
  3. Ajuwon and Spurlock. Palmitate activates the NF-kappaB transcription factor and induces IL-6 and TNFalpha expression in 3T3-L1 adipocytes. J Nutr 135:1841-6 (2005).
  4. Pacheco et al. Ratio of oleic to palmitic acid is a dietary determinant of thrombogenic and fibrinolytic factors during the postprandial state in men. Am J Clin Nutr 84:342-9 (2006).



There is a growing body of evidence that glucose ingestion causes a number of proinflammatory changes in normal as well as in diabetic humans. One of its effects is the production of superoxide radicals by leukocytes and an increase in plasma thiobarbituric acid-reacting substances (TBARS, lipid-peroxidation products). A recent paper1 reports that hyperglycemia is a major predictor of morbidity and mortality in acute heart attack, stroke, and in patients undergoing coronary artery bypass graft surgery. “Mortality in AMI [acute myocardial infarction, heart attack], stroke, and intensive care unit (ICU) patients increases by 100% with significant hyperglycemia and by more than 6 times in patients with hyperglycemia without a prior diagnosis of diabetes.”

The authors1 investigated whether glucose intake activates the key proinflammatory transcription factor, NF-kappaB (nuclear factor-kappa B) and whether this leads to an increase in the transcription of another major proinflammatory signaling molecule, the cytokine TNF-alpha (tumor necrosis factor-alpha). NF-kappaB activation is associated with many types of human cancers.

Eight healthy human subjects participated [5 males and 3 females; 31–39 years old; weight 56.7 to 90.7 kg; mean body mass index (body weight in kilograms divided by height in meters squared) was 25.6 ± 3.1 kg/m2]. The subjects were given 75 g of glucose dissolved in 300 ml of water (whimsically called Glucola) to drink over 5 minutes. Four weeks later, as a comparison, the same subjects were given a drink of 300 ml of water containing saccharine.

Increases in Inflammatory NF-kappaB after Glucose Ingestion

Results showed that plasma glucose concentrations after Glucola increased from 93.5 ± 6.4 to 128.6 ± 21.0, 109.0 ± 20.1, and 94.1 ± 10.1 mg/dL, respectively at 1, 2, and 3 hours (P<0.05). Plasma insulin concentration increased from 9.6 ± 1.9 to 50.4 ± 12.6, 20.6 ± 7.1, and 10.6 ± 4.2 μU/mL, respectively, at 1, 2, and 3 hours (P<0.01). Importantly, the NF-kappaB binding increased by 215.0 ± 36.9%, 206.1 ± 24.3%, and 244.7 ± 65.7% of the basal level at 1, 2, and 3 hours, respectively (P<0.05). There was no significant change in NF-kappaB binding activity after water challenge. The concentration of I-kappaB-alpha protein, which inhibits NF-kappaB migration to the nucleus, where it binds to DNA, was decreased significantly at 1, 2, and 3 hours (P<0.05).

There was a concomitant increase after Glucola in messenger RNA expression of TNF-alpha and of p47phox (a protein that is part of NADPH oxidase, an enzyme involved in inflammation that, for example, increases generation of superoxide radicals).

Anti-Inflammatory Effects of Insulin

Interestingly, insulin has been found to have anti-inflammatory effects,1–3 counteracting the proinflammatory effects of glucose, by suppressing NF-kappaB binding, increasing I-kappaB-alpha protein, and decreasing reactive oxygen species generation. Insulin also suppresses the prothrombotic tissue factor and plasminogen activator inhibitor-1 genes, as well as inhibiting matrix metalloproteinase-9 (MMP-9) and VEGF (vascular endothelial growth factor, responsible for angiogenesis, among other things). It is clear, therefore, that insulin resistance is a recipe for unopposed glucose inflammation.

The authors also note that IKK-beta, which regulates NF-kappaB expression, has been shown to mediate insulin resistance caused by fatty acids and that aspirin, an inhibitor of IKK-beta, prevents the induction of insulin resistance in mice.1

These same authors, in a separate paper,4 report that circulating peripheral blood mononuclear cells in the obese are in a proinflammatory state, as compared to the same cells from normal-weight subjects. They found increases in NF-kappaB binding to DNA and the inhibitor of NF-kappaB-beta (I-kappaB-beta) was significantly lower. There were elevated levels of proinflammatory migration inhibitor factor (MIF), IL-6, TNF-alpha, MMP-9, and C-reactive protein. In endothelial cells, TNF-alpha causes a reduction in the expression of the insulin receptor.4 Thus, the authors propose, the inflammatory mediators may contribute to insulin resistance.


  1. Aljada et al. Glucose ingestion induces an increase in intranuclear nuclear factor kappaB, a fall in cellular inhibitor kappaB, and an increase in tumor necrosis factor alpha messenger RNA by mononuclear cells in healthy human subjects. Metab Clin Exp 55:1177-85 (2006).
  2. Aljada et al. Insulin inhibits NFkappaB and MCP-1 expression in human aortic endothelial cells. J Clin Endocrinol Metab 86(1):450-3 (2001).
  3. Dandona et al. Insulin inhibits intranuclear nuclear factor kappaB and stimulates IkappaB in mononuclear cells in obese subjects: evidence for an anti-inflammatory effect? J Clin Endocrinol Metab 86(7):3257-65 (2001).
  4. Ghanim et al. Circulating mononuclear cells in the obese are in a proinflammatory state. Circulation 110:1564-71 (2004).



A very recent paper1 (whose authors included Nobel Prize winner Louis J. Ignarro, who won the prize for codiscovery of NO, nitric oxide) reported the results of experiments testing the hypothesis that increasing NO production by endothelial cells [either by genetically transfecting human umbilical venous epithelial cells with eNOS (endothelial nitric oxide synthase) or by treating the cells with NO donors or L-arginine or L-citrulline or antioxidants or a combination of the last three] could delay or prevent the endothelial cell senescence that results from exposure to high glucose levels.

The authors note in their introduction that “Senescent cells from aged animals express increased levels of proinflammatory molecules, suggesting that cellular senescence in vivo contributes to the pathogenesis of human atherosclerosis.” They point out that NO “is a widespread signaling molecule in the cardiovascular system, which functions in multiple ways to protect against the initiation and progression of atherosclerosis. NO prevents the adhesion and aggregation of blood cells and inhibits vascular smooth muscle cell proliferation.”

Exposure of cells to high glucose levels for 24 hours resulted in decreased expression of eNOS, the enzyme responsible for generating NO in blood-vessel walls. “Treatment with L-arginine, L-citrulline, and antioxidants (vitamin C and E) alone or in combination showed a significant recovery of the decreased nitrite [a measure of NO] level under high glucose conditions. When L-arginine, L-citrulline, and antioxidants were given together, the recovery of nitrite production was more marked.”

Moreover, high glucose exposure for 72 hours resulted in increased cellular senescence as indicated by increased beta-galactosidase and decreased telomerase. The number of senescent cells (by the above measures) was significantly decreased when L-arginine, L-citrulline, and antioxidants were given together. The authors report an earlier paper2 in which coadministration of antioxidants with L-arginine and L-citrulline produced an enhanced antiatherosclerotic effect in advanced atherosclerosis in high-cholesterol-fed rabbits.

Treatment with the NO donor drug DETA-NO or transfecting the cells with eNOS decreased cell senescence (as indicated by reduced levels of the senescence-associated enzyme beta-galactosidase and increased levels of the senescence-reduced levels of telomerase). “Treatment with L-arginine or L-citrulline of eNOS-transfected cells partially inhibited, and combination of L-arginine and L-citrulline and antioxidants strongly prevented, high-glucose-induced cellular senescence.”

L-Arginine is converted by eNOS (and also by neuronal NOS, nNOS, and inducible NOS, iNOS) into NO and L-citrulline. This process is now believed to take place in membrane structures called caveolae, where L-arginine supplies may be limited. L-Citrulline is converted back to L-arginine in caveolae by a salvage pathway and thus supplies additional L-arginine for use by eNOS, nNOS, and iNOS.

The authors conclude, “In the present study, high-glucose-induced endothelial dysfunction, oxidative stress, and cellular senescence were reversed with the administration of L-arginine, L-citrulline, and antioxidants.”

Our InnerPower Plus™ and improved InnerPower™ contain L-arginine, L-citrulline, and antioxidants. We developed these formulations for our own daily use to help maintain healthy NO production in blood vessels and thus to help prevent atherosclerosis.


  1. Hayashi et al. Endothelial cellular senescence is inhibited by nitric oxide: implications in atherosclerosis associated with menopause and diabetes. Proc Natl Acad Sci USA 103(45):17018-23 (2006).
  2. Hayashi et al. L-Citrulline and L-arginine supplementation retards the progression of high-cholesterol-diet-induced atherosclerosis in rabbits. Proc Natl Acad Sci USA 102:13681-6 (2005).



A meal’s ability to diminish the glucose response to carbohydrates eaten during the following meal is known as the “second-meal effect.”1 Low-glycemic-index foods reduce blood glucose in response to a first meal, and this has been suggested to be the mechanism for a second-meal effect. However, as the authors of a recent paper on indigestible carbohydrates1 point out, low-glycemic-index foods often increase colonic fermentation because of the presence of fiber and resistant starch. (For example, our Glycemic Control barley products are very low-glycemic—with about the same glycemic index as lentils—and increase colonic fermentation.) The authors designed a study using ten healthy volunteers to study the effect of fermentation on the second-meal effect independently of its effects on glycemic index.

The volunteers ate three different breakfast meals consisting of sponge cakes made with rapidly digestible, nonfermentable amylopectin starch plus cellulose (the high-glycemic-index meal) or rapidly digestible, nonfermentable amylopectin starch plus the fermentable disaccharide lactulose (high-glycemic-index + Lac), or slowly digestible, partly fermentable amylose starch plus cellulose (the low-glycemic-index meal). Five hours later, the subjects were given a standard lunch containing 93 grams of digestible carbohydrates.

The results showed that both the high-glycemic-index + Lac meal and the low-glycemic-index meal improved glucose tolerance at lunch. In the case of the high-glycemic-index + Lac meal, the effect was associated with low nonesterified fatty acids and delayed gastric emptying. The authors concluded that “Fermentable carbohydrates, independent of their effect on a food’s glycemic index, have the potential to regulate postprandial responses to a second meal by reducing nonesterified fatty acid competition for glucose disposal and, to a minor extent, by affecting intestinal motility.” [Note: A big difference between the low-glycemic-index meal used here and our Glycemic Control barley is that the fiber added to the resistant (amylose) starch was nonfermentable purified cellulose, which is an insoluble rather than soluble fiber such as beta-glucan; beta-glucan increases viscosity, unlike cellulose, and also has immune-stimulating effects that cellulose does not have.]

In their discussion, the authors mention an earlier study by Robertson et al.2 in which amylose-resistant starch enhances carbohydrate processing even 12 hours in the postprandial period, which suggests that the effect could be due to colonic fermentation. It has been reported that low-glycemic-index meals containing nondigestible fiber eaten at night can improve the glucose response to a morning meal.3


  1. Brighenti et al. Colonic fermentation of indigestible carbohydrates contributes to the second-meal effect. Am J Clin Nutr 83:817-22 (2006).
  2. 2. Robertson et al. Prior short-term consumption of resistant starch enhances postprandial insulin sensitivity in healthy subjects. Diabetologia 46:659-65 (2003).
  3. Nilsson et al. Effects of GI and content of indigestible carbohydrates of cereal-based evening meals on glucose tolerance at a subsequent standardised breakfast. Eur J Clin Nutr 60(9):1092-9 (2006).



For those with lactose intolerance (of whom Sandy is one; she developed it in her late 50s), it is a condition of inconvenience (since it limits consumption of milk, cheese, and other dairy products) and annoying symptoms (bloating and flatulence). It had occurred to Sandy recently that undigested lactose reaching the large intestine might serve as a prebiotic that causes gas (primarily hydrogen and carbon dioxide) and bloating as a result of fermentation by microbes, just as other undigested carbohydrates (such as resistant starches) do. A 2006 paper1 proposes the same, suggesting that the differential response to dairy products between those with lactose tolerance and those without it could explain discrepancies in studies of the protective effects of dairy products against the development of colorectal cancer.

Since data concerning the status of individual subjects’ lactose tolerance was not available, the authors estimated the impact of this factor by using national prevalences of lactose intolerance, data available from several sources. They divided countries into three subgroups: those countries with low lactose-intolerance status [≤20%; North America (except Mexico), Northwest Europe, some Eastern European countries, and Australia]; those with high lactose-intolerance status [≥80%; included only Asians (China, Japan, Thailand, and their descendants who were singled out in studies coming from North America)]; and middle lactose-intolerance status (21–79%; included southern Europe, the Middle East, some western European countries, such as France, and South America).

The results of their analysis of 80 studies (27 cohort, 53 case-control) showed that in the high lactose-intolerance Asian populations, there was low dairy intake but a generally protective effect (RR = 0.84, 95% CI = 0.73–0.97) of dairy consumption on colon and rectal cancer (several papers were cited). In studies of areas with low lactose intolerance and high dairy consumption (North America, Australia, and northwest Europe), there was again a protective effect of dairy food consumption (RR = 0.80, 95% CI = 0.73–0.88). The authors’ meta-analysis of the mixed populations (which included both high and low lactose-intolerance groups, thus giving an overall middle lactose-intolerance level), resulted in a nonsignificant protective effect of dairy consumption (RR = 0.92, CI = 0.79–1.06).

The authors propose that calcium from dairy consumption may not be consumed in large enough amounts in the high lactose-intolerant and middle lactose-intolerant populations to provide protection but that, in the high lactose-intolerant populations, protection is achieved by low dairy consumption because the lactose “. . . is not digested, reaches the colon, and therefore is a potential prebiotic. If true, it would promote the growth of bacteria (lactobacilli, bifidobacteria) that have been linked in experimental studies with colorectal cancer protection. There is at least one study that reports favorable bacterial promotion by lactose in 22 LNP [lactose-intolerant] Japanese subjects.* Further, there is evidence that regular modest intake of lactose in LNP subjects results in an inverse dose response of breath hydrogen [produced by gut bacteria] on lactose challenge testing.” The authors therefore propose that lactose-tolerance status is an effect modifier rather than a confounder and that future studies of the effects of dairy consumption in mixed populations would be expected to show a protective effect of dairy consumption if they adjust for individual lactose tolerance.


*Ito and Kimura. Influence of lactose on faecal microflora in lactose maldigesters. Microbiol Ecol Health Dis 6:73-6 (1993). For example, the ingestion of 15 g of lactose (as would be found in 330 ml, a little over 1 1/3 cup, of milk) per day for 6 days resulted in significantly increased numbers of lactobacilli, and the numbers of C. perfringens, an important human and animal pathogen, decreased from 81% to 45% of total microflora.




  1. Szilagyi et al. The effect of lactose maldigestion on the relationship between dairy food intake and colorectal cancer: a systematic review. Nutr Cancer55(2):141-50 (2006).



The Food and Agriculture Organization of the United Nations has released a report (“Livestock’s Long Shadow”) claiming that farm animals emit (bhhhrrrzzzt) nearly 20% of all greenhouse gases. They warn that by 2050 meat production will double, with a similar increase in dairy production, leading to increased flatulence accompanied by flatulence-induced global warming. Their figures show livestock responsible for 9% of carbon dioxide production, 40% of methane production, and 65% (gasp) of nitrous oxide emissions.

These figures are unreliable at best, attempts to incite fear and hasty international global controls (with the UN at the helm, of course) at worst. As sources of greenhouse gases and other factors affecting climate keep on being discovered,1–3 even if these were actually snapshot figures from some time ago (we have not seen their references and cannot comment), they are not snapshots of the current picture, which keeps changing dramatically.

Of course, ignoring inconvenient facts about published data on purported global warming is a cottage industry (a government-subsidized political agenda masquerading as science), dispensing to favored scientists billions of dollars a year in taxpayers’ money. Although a recent paper4 reported that there was a substantial cooling in the tropical Andes that coincided with glacial advances in Europe during the Little Ice Age (1250 to 1810), we keep reading news reports on climate research in Science and Nature that continue to refer to the Little Ice Age as a European (therefore, not global) phenomenon.

A final note on the supposed danger of livestock farts: When the American plains were covered by tens of millions of buffalo, there would have been the same gaseous emissions. Do you suppose those environmentalists now in an uproar at the UN about livestock would be as livid about wild animal parks or rewilded American plains filled with gas-emitting herbivores?


  1. Meskhidze and Nenes. Phytoplankton and cloudiness in the southern ocean. Science 314:1419-23 (2006). Phytoplankton blooms release large quantities of isoprene, which changes cloud condensation nucleation and acts as an organic aerosol, producing cooling.
  2. Methane quashes green credentials of hydropower. Nature 30 Nov 2006. Tropical hydroelectric dams shown to release large quantities of methane, some scientists argue greenhouse gas impact worse than that of a fossil-fuel power plant. (“The problem lies with the organic matter in the reservoir. Large amounts are trapped when land is flooded to create the dam . . . this matter decays to form methane and carbon dioxide.”) The article cites an energy policy expert (Danny Cullenward at Stanford University) suggesting that, if these estimates are correct, annual global methane emissions (which don’t include dams) need to be increased by one-fifth.
  3. The methane mystery. Nature 17 Aug 2006. Work by Frank Keppler, a geochemist at the Max Planck Institute for Nuclear Physics in Heidelberg, Germany, and his colleagues, suggests that plants could account for up to 40% of total global methane emissions. Keppler promises further surprises, according to the article. Unpublished data from experiments carried out last year in Brazil revealed that some plant species release 4000 times more methane than others. Ed Dlugokencky, an atmospheric chemist with the U.S. National Oceanic and Atmospheric Administration in Boulder, Colorado, who oversees the methane part of a global air-sampling network, calls for more measurements and says, “You need to understand the entire greenhouse budget before you can start thinking about mitigating climate change.”
  4. Polissar et al. Solar modulation of Little Ice Age climate in the tropical Andes. Proc Natl Acad Sci USA 103(24):8937-42 (2006).



By Sandy Shaw*
Don’t touch your thermostat.
Just sit there.
We control the climate.
We control the air you breathe.
Yes, We are the Scientists
Who have figured it all out
And who will see to it that you are protected
By our superior knowledge and our Plan.
For the next hour, this will be a test.
Do not touch your thermostat.
We will control All.


*With thanks to “The Outer Limits”




The FDA rejected a petition by the Japanese company Ito En Ltd. and its US subsidiary Ito En, Inc., which produce and market green tea, for a qualified health claim that daily consumption of at least 5 fluid ounces of green tea may reduce a number of risks associated with cardiovascular disease. Though the consumption of a mere 5 ounces of tea seems a bit small on which to base a claim, the FDA’s “review” of the data on the potential beneficial effects of tea on cardiovascular disease was ludicrous: the FDA claimed “that there is no credible evidence to support a relationship between consumption of green tea or green tea extract and a reduced risk of CVD [cardiovascular disease].” [Emphasis added]

We do not intend to do a review of the literature here, nor a complete analysis of the FDA’s methodology. We would simply like to note that the agency first threw out all data derived from cell-culture, mechanistic, and animal-model studies. They also threw out meta-analyses and government reports. (!) The agency winnowed down the body of data to only four human observational studies and four human intervention studies. The claim that there is “no credible evidence” is simply a lie, as the agency conveniently ignored most of the scientific literature on tea.

There was, for example, credible evidence in one very large epidemiological (observational) study published in the Journal of the American Medical Association.1 In the Ohsaki National Health Insurance Cohort Study, a study of 40,530 Japanese adults aged 40 to 79 years, without a history of stroke, coronary heart disease, or cancer at baseline, subjects were followed for up to 11 years for all-cause mortality and for up to 7 years for cause-specific mortality.

Green tea consumption was inversely associated with mortality due to all causes and due to cardiovascular disease. The strongest inverse association was found for stroke mortality. Cancer mortality was not significantly different from 1.00 (that is, from no tea consumption) in all green tea categories.

A few other examples include: habitual tea consumption for a year or more significantly reduced the risk of developing hypertension in 1507 Chinese men and women;2 green and black teas inhibited atherosclerosis in a hamster model by improving levels of LDL, lipid peroxides, and fibrinogen;3 there was reversal of endothelial dysfunction in patients with coronary artery disease or risk factors;4,5 and green tea EGCG induced programmed cell death in proliferating bovine aortic vascular smooth muscle cells (a mechanism for the development of atherosclerotic plaques).6 The search for mechanisms has resulted, as is often the case, in contradictory results. For example, a recent paper did not find changes in plasma antioxidant capacity or reductions in 8-hydroxy-2′-deoxyguanosine or urinary 8-isoprostane levels of human consumers of black tea.7 However, in the latter paper, the authors concluded that tea consumption has a strong beneficial effect on endothelial function and “we must consider the possibility that noncatechin components of tea may account for the observed benefit.” They suggest looking further at the polymeric polyphenols found in black (and also green) tea, as they may more potently increase endothelial nitric oxide synthesis compared to polyphenol monomers.

The FDA is holding foods and dietary supplements to the same standards as prescription drugs, despite their lack of statutory authority to do so. An editorial in a recent American Journal of Clinical Nutrition8 included this enlightening analysis of the difficulty with the FDA’s approach to judging nutrients by drug standards:

The randomized controlled trial (RCT), which has become the gold standard for establishing the efficacy of pharmacologic agents, is poorly suited to the evaluation of nutritional effects, a fact that I believe many have been reluctant to acknowledge. Several important differences between nutrients and drugs lead to this conclusion. In addition to long latency and multifactorial causation for the diseases concerned, nutrients and drugs differ in three crucial respects. First, whereas a drug-free state exists that can be contrasted with a drug-added state, with respect to nutrients, the only contrast can be between different intakes, both usually well above zero. [Comment:Even if you drink no tea, you will still be ingesting catechins and other constituents of tea from other foods.] Second, most nutrients have what is known as threshold behavior, i.e., some physiologic measure improves as intake rises up to a level of sufficiency, above which higher intakes produce no additional benefit. Third, most nutrients have beneficial effects on multiple tissues and organ systems, and thus a focus on a single or ‘primary’ outcome measure, which is favored by RCTs, is often procrustean. As a consequence of the second point, investigators using the RCT design must contrast two groups of subjects, at least one of which has a distinctly inadequate intake of the nutrient concerned. Failure to do that, as occurred in the calcium arm of the Women’s Health Initiative (WHI), constitutes an invalid test of the corresponding hypothesis. However, the assignment of subjects to an intake that is inadequate by current standards, for the span of time required to produce the necessary difference in serious outcomes, raises significant and probably insurmountable ethical problems.

From the FDA’s point of view, however, the RCT can be used as a convenient and stealthy way to discount nearly all studies of likely beneficial effects of nutrients until some hypothetical future certainty, a certainty that will never arrive; hence, this allows the FDA to reject all nutrient health claims other than those few by favored “clients” or as forced by very expensive lawsuits in a legal climate where courts are likely to defer to agencies.


  1. Kuriyama et al. Green tea consumption and mortality due to cardiovascular disease, cancer, and all causes in Japan: the Ohsaki Study. JAMA 296(10):1255-65 (2006).
  2. Yang et al. The protective effect of habitual tea consumption on hypertension. Arch Intern Med 164:1534-40 (2004).
  3. Vinson et al. Green and black teas inhibit atherosclerosis by lipid, antioxidant, and fibrinolytic mechanisms. J Agric Food Chem 52:3661-5 (2004).
  4. Duffy et al. Short and long term black tea consumption reverses endothelial dysfunction in patients with coronary artery disease. Circulation 104:151-6 (2001).
  5. Hodgson et al. Regular ingestion of black tea improves brachial artery vasodilator function. Clin Sci 102:195-201 (2002).
  6. Hofmann and Sonenshein. Green tea polyphenol epigallocatechin-3-gallate induces apoptosis of proliferating vascular smooth muscle cells via activation of p53. FASEB J Feb 5 2003.
  7. Widlansky, Duffy, et al. Effects of black tea consumption on plasma catechins and markers of oxidative stress and inflammation in patients with coronary artery disease. Free Rad Biol Med 38:499-506 (2005).
  8. Heaney. Nutrition, chronic disease, and the problem of proof. Am J Clin Nutr84:471-2 (2006).



1/8 cupolive oil
2 cupsonion, chopped
1 cupDurk Pearson & Sandy Shaw’s® Glycemic Control Nuggets™
1 can (15 oz)chicken broth, low-fat
1/2 cupblack or red currants
2 tbspfresh lemon juice
1/8 tspallspice, ground
1/2 cuppine nuts
1 tbspfresh mint (either spearmint or peppermint), chopped
1 tbspfresh dill, chopped
Heat olive oil in a largish saucepan over medium heat. Add onions, and sauté for 5 minutes. Mix in barley, then chicken broth, currants, lemon juice, and allspice. Bring to a boil, reduce heat to simmer, and cook until barley is tender and liquid is absorbed, about 15 minutes. Mix in pine nuts, mint, and dill. Season with salt and pepper. Enjoy!


*Adapted from the recipe for Rice, Raisin, and Herb Pilaf in Bon Appétit, December 2006, p. 180.

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