November 2013 Blog with Durk and Sandy

by

APPETIZERS

In an honest search for knowledge you quite often
have to abide by ignorance for an indefinite period.
— Erwin Schrodinger

Being a scientist requires having faith in uncertainty, finding
pleasure in mystery, and learning to cultivate doubt. There is no surer
way to screw up an experiment than to be certain of its outcome.
— Stuart Firestein, Ignorance: How It Drives Science (Oxford Univ. Press, 2012)

When you’re over the hill, you pick up speed.
— Satchel Paige (D&S: But that’s only true if you’re not too far over the hill.)

Any man who thinks he can be happy and prosperous by letting the
Government take care of him better take a closer look at the American Indian.
— Henry Ford

Governments specialize in creating problems that they then generously solve for the people, creating yet more serious and more systemic problems in the process.
— George Gilder, Winter 1989 Cato Journal

Libenter homines id quod volunt credunt.
(People easily believe that which they want to believe.)
— Julius Caesar

I wondered why the baseball was getting bigger. Then it hit me!
— from the Casey Daily Dispatch (Doug Casey, not Casey at the Bat)

I know a guy who’s addicted to brake fluid. He says he can stop any time.
— from Casey Daily Dispatch

HYDROGEN THERAPY – HYDROGEN PROTECTS AGAINST LIPID
METABOLISM DISORDERS AND ATHEROSCLEROSIS

One of the signaling pathways that causes excessive fatty acid uptake in obesity results from the scavenger receptor CD36. Platelet quantities of CD36 are found at elevated levels in the plasma of hyperlipidemic mice and in the plasma of humans with low levels of HDL. These higher levels of CD36 were found to promote platelet activation and, hence, the risk of blood clot-induced heart attacks.1 “Thus, interactions of platelet CD36 with specific endogenous oxidized lipids play a crucial role in the well-known clinical associations between dyslipidemia, oxidant stress, and a prothrombotic phenotype.”1 “CD36 is implicated in a variety of pathological conditions, including atherosclerosis, diabetes and innate immunity.”1

It was known that oxidized LDL increased platelet activation but the mechanism was not understood. The authors of paper #1 found that oxidized choline glycerophospholipids, generated as a result of LDL oxidation and then bound to the scavenger receptor CD36 in platelets caused the increased platelet activation. Moreover, these oxidized choline glycerophospholipids promote foam cell formation, which are key factors in the development of atherosclerotic plaques.2

A new paper in the developing field of hydrogen therapy3 has reported that molecular hydrogen treatment of HepG2 human liver cells downregulated the protein expression of CD36 and decreased the cellular uptake of fatty acids and decreased lipid accumulation in the cells. “Our results suggest that downregulation of CD36 expression by hydrogen pretreatment may be the primary mechanism against hepatic steatosis [fatty liver] in this in vitro model.”3

As we have written before, certain prebiotics can be converted by hydrogen-producing gut microbiota into gaseous hydrogen, a very selective antioxidant that is mostly active against the highly toxic hydroxyl radical and the oxidant peroxynitrite. Hydrogen then diffuses throughout the body (even into mitochondria) before being exhaled from the lungs or passing out of the body via the skin or as farts. (See “Hydrogen Therapy” in the June 2012 issue of Life Enhancement).

Hydrogen Reported to Downregulate CD36

As this new paper3 shows, hydrogen is also able to downregulate CD36 and this may be a new way to prevent platelet hyperactivity that can lead to blood clot-induced heart attacks and strokes.

References

  1. Podrez et al. Platelet CD36 links hyperlipidemia, oxidant stress and a prothrombotic phenotype. Nat Med. 13(9):1086-95 (2007).
  2. Jackson & Calkin. The clot thickens—oxidized lipids and thrombosis. Nat Med.13(9):1015-1016 (2007).
  3. Iio et al. Molecular hydrogen attenuates fatty acid uptake and lipid accumulation through downregulating CD36 expression in HepG2 cells. Med Gas Res. 3:6 (2013).

Hydrogen, a Selective Antioxidant, May Interfere Less with
Physiological Radical Signaling Than Other Antioxidants Do

One of the things we explained about hydrogen acting as a selective antioxidant is that it is a potent scavenger of the toxic hydroxyl radical, not known to be a radical engaged in physiological signaling, but to be much less of a scavenger of those radicals that ARE known to act in physiological signaling, such as superoxide or nitric oxide. Here is an example recently reported in the journal Free Radical Biology And Medicine1 that shows how hydrogen, acting as a selective antioxidant, could, hypothetically, not interfere with the physiological signaling of very low dose superoxide radicals, while still scavenging undesired hydroxyl radicals and peroxynitrite, the potent oxidant resulting from the chemical reaction between superoxide radicals and nitric oxide.

The new paper1 reported that very low doses of superoxide (acting at the picomolar level) can stimulate angiogenesis after the induction of ischemia (reduced blood flow) in a mouse model of peripheral artery disease. Under these conditions, angiogenesis is a beneficial compensatory mechanism for restoring blood flow in the ischemic area. An antioxidant that blocked the signaling of the very low dose superoxide would interfere with the induction of angiogenesis and, hence, be undesirable. As the authors1 said, the induction of angiogenesis by VEGF (vascular endothelial growth factor) observed in this study, “verif[ied] that slightly elevated levels of ROS [reactive oxygen species] restore blood flow by stimulating endothelial cell proliferation through a VEGF-dependent pathway.” Hydrogen is an antioxidant that would not be expected to interfere with these slightly elevated levels of physiological radical signaling.

Reference

  1. Bir et al. Control of angiogenesis dictated by picomolar superoxide levels. Free Rad Biol Med. 63:135-142 (2013)

More Beneficial Effects Reported for Increased Intake of Oleic Acid
 

Two new papers report additional beneficial effects of dietary intake of oleic acid (a monounsaturated fat) as a substitute for saturated fat. (Though olive oil is an excellent source of oleic acid, high oleic sunflower oil contains 85% oleic acid, a far higher percentage.) The first paper1 reports that substituting monounsaturated fats (oleic acid) for saturated fats (palmitic acid) in the diet of 12 human volunteers increased daily physical activity, increased resting energy expenditure, and (very interestingly) was associated with LESS ANGER AND HOSTILITY.

The subjects participated in a cross-over design in which they received for three weeks a high palmitic acid diet similar to a Western diet that contained 40.4% of calories as fat (palmitic acid, 16.0% calories, oleic acid 16.2% of calories), followed (separated by a another week of the control diet) a diet similar to the Mediterranean diet in fat composition (40.1% of calories as fat with 2.4% of calories as palmitic acid and 28.8% of calories as oleic acid). The oils were provided at room temperature as blends that were not used for cooking, but were mixed with food. There were two cohorts of 18 and 14 young adults as subjects.

The second paper2 reports that oleic acid, but not other long chain fatty acids, signals to the SIRT1-PGC-1alpha complex to increase rates of fatty acid oxidation, thus improving the mitochondria energy metabolism of skeletal muscle cells. In this way, oleic acid provides protection against inflammation, dyslipidemias, and insulin resistance.2Subjects took a Profile of Mood States questionnaire to assess mood. Ten of 12 men and women exhibited a significantly lower anger-hostility score with the HOA (high oleic acid) than with the HPA (high palmitic acid). The authors note that they could not tell from their data if this result was due to increased oleic acid or decreased palmitic acid. They also found that 27 of 29 subjects in the 2 cohorts increased their physical activity during the low saturated fat (reduced palmitic acid) diet. (Reduced physical activity while consuming more saturated fat could be a result of increased inflammatory activity induced by consuming saturated fats, such as increased secretion of TNF-alpha (tumor necrosis factor alpha) associated with saturated fats as compared to monounsaturated fats.)

References

  1. Kien et al. Substituting dietary monounsaturated fat for saturated fat is associated with increased daily physical activity and resting energy expenditure and with changes in mood. Am J Clin Nutr. 97:689-97 (2013).
  2. Lim et al. Oleic acid stimulates complete oxidation of fatty acids through Protein Kinase A-dependent activation of SIRT1-PGC1alpha complex. J Biol Chem.288(10):7117-26 (2013).

PEPPERMINT OIL CAN IMPROVE EXERCISE PERFORMANCE IN HUMAN ATHLETES

A couple of issues ago in this newsletter we reported on a study of menthol1(administered by subcutaneous injection in young mice). Treatment with menthol for 10 successive days improved spatial memory (as reflected in the animals’ performance in the dreaded Morris water maze. In addition, pre-treatment with menthol in both young and old mice reversed the amnesia induced in the animals by treatment with beta-amyloid on the tenth day. In other studies cited in the paper, menthol exhibited acetylcholinesterase inhibitory activity, thus increasing cholinergic nervous system activity, which may explain at least in part the improvement in memory in the Morris water maze and in response to beta-amyloid-induced amnesia.

Here, we report on another new study,2 showing that functional parameters of exercise significantly improved in 12 healthy male students after receiving peppermint oil treatment (one bottle of 500 ml. of mineral water per day containing 0.05 ml peppermint oil for ten days). Tests were administered after treatment for ten days and compared to the initial test results before receiving peppermint oil. The results strongly supported the effectiveness of peppermint oil on exercise performance, respiratory function variables, systolic blood pressure, heart rate, and respiratory gas exchange parameters.2 There were significant differences exhibiting improved performance between pre- and post-test results for resting heart rate, maximum heart rate, systolic blood pressure, diastolic blood pressure, chest circumference at maximum inhale, and chest circumference at maximum exhale. There have been inconsistencies in the results shown by peppermint oil in other studies, which the authors attribute at least in part to lack of good-quality evidence.

References

  1. Bhadania et al. Protective effect of menthol on beta-amyloid peptide induced cognitive deficits in mice. Eur J Pharmacol. 681:50-4 (2012).
  2. Meamarbashi and Rajabi. The effects of peppermint on exercise performance. J Int Soc Sports Nutr. 10:15 (2013) Open Access.

EAT LESS BY PAYING ATTENTION TO YOUR FOOD
YUP, IT’S OK TO PLAY WITH YOUR FOOD

A new paper1 suggests that paying more attention to your food as you eat it will increase the neurological activity that signals satiety and awareness of food intake, thus having a beneficial effect on limiting how much you eat. The only will power required here is to pay attention to your food as you eat. You don’t try to force yourself to limit your intake, but to increase the focus your brain has on what you’ve eaten and, with that information, your brain will regulate your intake without any effort on your part.

The authors reviewed 24 papers of “neurologically intact” adults 18 years of age or older that took part in studies of the effect of distractions, awareness, or attention to food intake and food memory. (Food memory is important because it is generally recognized that in assessing food intake from memory, it is common to underestimate how much was eaten.)

Interestingly, the scientists found evidence that distraction produced a larger increase on later food intake than it did on immediate food intake. The six studies examining distractions while eating and later food intake were all performed by the same group.

The overall findings suggested four principles for reducing food intake:

  1. Eat while avoiding distracting stimuli, such as watching television.
  2. Prepare for eating by remembering similar meals before beginning the meal. Imagine reruns of similar meals.
  3. Pay attention to the food you’re eating.
  4. Remember the parts of the meal as you eat.

The authors suggest, for example, that food wrappers and other cues of eating (such as empty plates) not be removed from the eating area until the meal is completed, so as to constantly remind you of what and how much you’ve eaten. Forgetting all the food you’ve eaten impairs the brain’s ability to maintain a running total of all that you’ve consumed and hence to generate the proper regulatory signals.

  1. D&S: We would also add to these other suggestions that playing with your food, as in “sculpting” carrots into shapes with your teeth and tongue as you eat the carrots, may be a good way to interact with the food, increasing the attention you pay to the sensory stimuli as you eat. Remember when your mother admonished you not to play with your food? Maybe, in that case, her advice was not so good. (It probably had more to do with your mother’s concern that you would dawdle and end up wasting food. Way back then, there were actually a lot of children starving in China.)

References

  1. Robinson et al. Eating attentively: a systematic review and meta-analysis of the effect of food intake memory and awareness on eating. Am J Clin Nutr. 97:728-42 (2013).

BUT WHEN YOU’RE NOT EATING—OR ABOUT TO EAT,
IT MAY BE BEST NOT TO PAY ATTENTION TO FOOD

To get the most out of food and possibly eat less as a result, you should try to increase the signals that the food induces in your nutrient-sensing systems by paying close attention to your food when eating and avoiding distractions. However, as reported in an article in the December 28, 2007 Cell, Drosophila melanogaster (fruit flies) that are on a regime of dietary restriction but exposed to food-derived odorants don’t get the full benefit from the life extending effects of the diet restriction (DR). The food odorants alone decrease the expected lifespan increase, attenuating the longer lifespan the flies would otherwise derive from DR. This effect is not observed in fully fed flies.

In the Cell article,1 flies with severe olfactory defects are reported to live significantly longer than wild-type flies. They are of normal size and have a normal metabolic rate but increased triglyceride storage and are resistant to both starvation and hyperoxia.2

What the fly results might mean for humans is that constant exposure to the sights and smells of food could induce the signals of nutrient-sensing systems that interfere with the “stop eating” metabolic pathways that would otherwise be active. Or, as hinted at in the article,1 reducing sensory responses to food when one is not eating might be a way to mimic DR. The commentary authors point out that there is a “‘cephalic phase response’ which is an assemblage of physiological changes elicited by the sight, smell and taste of food, a sort of small scale “preview” of the full eating program. It involves preabsorptive release enzymes and hormones including pancreatic polypeptides, insulin, and glucagon and is generally viewed as a mechanism to optimize nutrient absorption and metabolism. A study of how this preview program is initiated and how it is terminated in the absence of actual eating might reveal some clues on how the nutrient-sensing pathways regulate the drive to eat.

References

  1. Libert and Pletcher. Modulation of longevity by environmental sensing. Cell.131(7):1231-4 (2007).
  2. Libert et al. Regulation of Drosophila life span by olfaction and food-derived odors. Science. 315:1133-37 (2007).

LIFE EXTENDING NATURAL PRODUCTS CAN GIVE DIFFERENT RESULTS WHEN FED OVER AN ANIMAL’S ENTIRE LIFETIME AS COMPARED TO FED AT JUST SPECIFIC PARTS OF THE LIFESPAN

The researchers report that there is significant change (~23%) in genome wide transcript profiles with age in Drosophila, suggesting that gene-induced changes by treatments with putative life extending materials may not have the same effects at all life stages.1 They found that curcumin had beneficial effects in the normal lived Ra strain of Drosophila in that it increased longevity when administered in the developmental or health span stages, which (they suggest) could be due to systemic effects on the TOR complex, where reduced expression has been associated with life extending effects in studies with model organisms, but that curcumin had a negative effect on lifespan when administered over the entire adult lifespan or over the senescent stage only. They propose that this could be due to “an apparent curcumin-dependent accelerated neuromuscular degeneration observed in the legs of mid- and late-life treated animals.”A new study1 reports that curcumin acts as a dietary restriction mimetic by increasing lifespan when administered during specific periods of the lifespan of Drosophila but find that whole life intervention is not always the most effective intervention. Basically, they report here1 that 4-phenyl butyrate (4PB), a life extending natural product, administered during the first 12 days of the adult lifespan was not as effective as feeding during the time period from 12 days to the end of life. The researchers identified the first 12 days as including a portion of the adult healthspan, while the period of 12 days to the end of life included the transition and senescent periods. The results of this and other studies looking at treatment with life extending materials at only specific periods of the lifespan are pointing to additional complications in interpreting how increases in lifespan are produced.

The authors conclude that life-time feeding may be responsible for the failure of curcumin to significantly extend the healthspan and delay the onset of senescence by studies in other labs.

In a different paper,2 researchers found that increased oxidative resistance induced in human MEF cells and in Drosophila by exposure to acute, chronic, and repeated oxidative stress had different effects on lifespan. “Regrettably, regimens of adaptation to both repeated and chronic stress that were successful for short-term survival in Drosophila nevertheless also caused significant reduction in life span for the flies.”2

The authors sum up their findings: “repeated MEF cell oxidant exposures seem to prevent adaptive stress responses if the interval between exposures is too short and/or if each exposure is at too high an oxidant level. In contrast, repeated cell exposures at 12-h intervals, especially at lower oxidant concentrations, seem to potentiate positive stress adaptations and extend the period of protection. Chronic oxidant exposure at low oxidant levels can actually potentiate and extend adaptive responses, but chronic exposure to higher oxidant levels prevents adaptation.” For the Drosophila melanogaster, repeated oxidative stress adaptation at intervals of 1 or 3 days is toxic but intervals of 7 days are tolerated in terms of [improved] short-term survival. Life span however, seems to be negatively influenced by all repeated stress adaptation regimens. Short-term survival is also negatively influenced by chronic oxidative stress adaptation at all levels.”2 “All repeated treatments appeared to have a negative long-term effect, because flies that were repeatedly exposed to H2O2 [hydrogen peroxide] had a shorter life spans than untreated flies. We also observed a progressive decline in Drosophila life span with frequency of H2O2 treatment.”2

These results indicate that there is a great deal yet to learn about the dose and timing of hormesis that results not only in short term resistance to stresses such as oxidative stress but increased lifespan, which would appear to require different processes that work over a long period of time.

Nevertheless, the results of these studies must be reconciled with others that found mild stresses to have anti-aging hormetic effects and appeared to show an effective approach to modulate aging.3 For example, in paper #3. researchers reported that a single heat-shock early in life extended longevity by 20% or more in C. elegans by decreasing initial mortality only, with the rate of increase of subsequent mortality (the Gompertz component) being unchanged. Worms were also exposed to multiple heat shocks3 in the study with each heat shock having a hormetic effect on lifespan but with the magnitude of each additional single heat-shock decreasing as the age of the animal increased.

References

  1. Soh et al. Curcumin is an early-acting stage-specific inducer of extended functional longevity in Drosophila. Exp Gerontol. 48:229-39 (2013).
  2. Pickering et al. Oxidative stress adaptation with acute, chronic, and repeated stress. Free Radic Biol Med. 55:109-18 (2013).
  3. See, for example, Wu et al. Multiple mild heat-shocks decrease the Gompertz component of mortality in Caenorhabditis elegans. Exp Gerontol. 44:607-12 (2009).

DETERMINING WHETHER CLIMATE CHANGE IS CAUSED BY HUMANS, THE EASY WAY

A study reported in the 1 Feb Science reveals that, when asked whether humans are causing climate change, Demo­crats were likely to say yes, Republicans likely to say no, but Independents were likely to say yes on unseasonably warm days but to say no on unseasonably cold days. No surprise but it just goes to show that very short term events rather than consideration of the totality of the evidence can be a deciding factor in how people perceive the reality of human-induced global warming (or probably anything else, for that matter). This is an excellent way for those looking for the “right” response to a survey to plan when to ask people if they think humans are causing climate change to get the answers they want.

EPIGENETIC CHANGES IN EXPRESSION
OF GENES VIA DNA METHYLATION PART II

In the May 2013 issue of this newsletter, we published an article on “Methylation, a major mechanism regulating gene expression, changes with age, revealing dynamic landscape.” We continue that here with new data. In our May article, we discussed how methyl donors (such as s-adenosylmethione (SAMe), folic acid, choline, and methionine) are part of a system that, under the regulation of DNA methyltransferases either adds a methyl group to or removes a methyl group from a specific site on DNA histones which controls whether a gene can be transcribed (turned on) or silenced (turned off). With the discovery of this process, much exciting new research has already been and continues to be published.

Changes in Age-dependent Epigenetic Parameters by Exercise in Rat Hippocampus

New research on the effect of exercise on DNA methylation are being published. One paper1 reports on the effects in male Wistar rats at ages 3 and 20 months old of engaging in two exercise protocols on a treadmill, one for a single session of 20 minutes of exercise and the other chronic treadmill exercise (20 minutes running each day for 2 weeks). The results showed that the 20 month old (and 20 months qualifies as aged if you’re a rat) had lower histone H3-K9 methylation levels (about 50%) as compared to the 3 month old rats. Also, the levels of DNMT1 (DNA methylatransferase 1) were significantly diminished in the aged animals by about 25%. The level of DNMT3b (DNA methyltransferase 3b) was not modified by age.

These results are consistent with the data from other studies as noted by the authors.1They explain that there is a “genome-wide tendency to DNA hypomethylation in multiple vertebrate organs during aging process. In addition, the age-related global hypomethylation is related to DNMT1 deficits in senescent human fibroblasts. However, studies reporting DNMT content in the brain during aging process are lacking.”

Further results1 showed that “[w]hen measured 1 h after [single] session ended, young adult exercised rats exhibited lower levels of DNMT3b (about 30%) when compared to its sedentary group [young adult rats not exercised] (p=0.042); while no delayed (18 h) effects of exercise were observed.” This change was not observed in the aged rats. There were no changes in DNMT3b as a result of chronic exercise in all groups. Likewise for DNMT1, the acute (single session) of exercise acutely diminished this DNA methyltransferase by about 45% in the hippocampi of 3 month old rats (p<0.001) without any changes 18 hours after exercise. Again, this change was not observed in the aged rats. Meanwhile, there was no significant effect of the chronic exercise regimen on DNMT1 in either young adult or aged rats.

The transient effect of decreased DNMT3b after acute exercise implies that, as suggested by the authors of a different (earlier) study,2 DNA hypomethylation is an early event in contraction-induced gene activation. The second study2 also found that the promoter of genes with exercise-induced increased expression (PGC-1alpha, PDK4, PPAR-delta) were hypomethylated (had decreased methylation after as compared to before exercise) in human healthy sedentary subjects following acute exercise. Hypo­methylation supports the notion that there was greater expression of those genes. Note that PGC-1alpha is a “master” gene that controls mitochondrial biogenesis.

The results1 also support the idea that there is a decrease in histone methylation in many genes with an increase in others occurring as part of the aging process.

DNA Methylation Deficits in Memory with Age Can Be Reversed by Increasing a DNA Methyltransferase

A recent paper3 reports that aged mice have decreased expression of a DNA methyltransferase (DNMT3a2) that results in memory deficits and that restoration of the expression of this enzyme can reverse the memory deficits.

One of the tests used by the researchers to detect the memory defect was by exposing the mice to a tone followed by a foot shock. When exposed to the tone in a different context 24 hours later, the old mice froze with fear much less often than the young mice, indicating that the memory of the old mice functioned less well (e.g., they were less likely to remember the warning tone). Using a recombinant adeno-associated virus to deliver the gene for DNMT3a2, the scientists were able to restore the memory of the old mice.

The authors3 hypothesized that the loss of the DNA methyltransferase resulted in decreased methylation of and less expression of the enzyme’s target genes. (In this case, the DNA methylation acted as a transcriptional activator, increasing gene expression, although DNA methyl­ation can in other circumstances act as a transcriptional suppressor, decreasing gene expression—yup, it’s complicated.) See also reference #4, which is the commentary on paper #3.

Methylation Changes Found in Night Shiftworkers

Finally, we have another new paper5 that reports on a study of DNA methylation changes in 10 randomly selected women from an initial group of 17 with long histories of night shiftwork that were compared to 10 female dayworkers. The researchers found widespread methylation changes at imprinted genes in the night shiftworkers. (Imprinted genes are the alleles of genes, which are expressed depending upon the parent of origin. “Loss of monoallelic expression at imprinted genes, known as loss of imprinting (LOI), has been associated with various cancer types and may play a role as an early driver in tumor development.”5) Among the genes with methylation changes, the paper reported, were many with roles in circadian clock pathways that have been linked to cancer risk.

The authors propose that, although it has not been proven, long-term shiftwork may induce changes in methylation by perturbing the normal circadian exposure to light. “Interestingly, the magnitudes of methylation changes observed are comparable to methylation changes which have been attributed to occupational exposures to low-dose benzene and polycyclic aromatic hydrocarbons.” Such exposures can be carcinogenic at high enough doses.

Hypomethylation to Resensitize Diffuse Large B-Cell Lymphoma to Chemo­therapy; Restores Tumor Suppressor Gene Activity

We have written about the exciting new finding that DNA hypomethylation has been shown in some cancers to restore the activity of tumor suppressor genes that have been silenced by hypermethylation.6 Hypomethylating drugs such as azacytidine are being used in early trials to restore the sensitivity of cancers that have become chemotherapy resistant. In a new paper,6 researchers used diffuse large B-cell lymphoma cell lines to study the use of the hypomethylation drug azacytidine to reactivate the SMAD1 gene that resensitized the cells to standard chemotherapeutic treatment after they had become resistant.

In another very recent paper,7 the authors review the new work on DNA hypermethylation that silences tumor suppressor genes and the discovery of agents that can reactivate these silenced genes, such as drugs (for example, azacytidine) or natural compounds acting via different mechanisms to inhibit DNA methyltransferases, thus decreasing methylation, that includes curcumin, EGCG, resveratrol, parthenolide, and others).

References

  1. Elsner et al. Exercise induces age-dependent changes on epigenetic parameters in rat hippocampus: A preliminary study. Exp Gerontol. 48:136-9 (2013).
  2. Barres et al. Acute exercise remodels promoter methylation in human skeletal muscle. Cell Metab. 15:405-41 (2012).
  3. Oliveira et al. Rescue of aging-associated decline in Dnmt3a2 expression restores cognitive abilities. Nat Neurosci. 15(8):1111-3 (2012).
  4. Su & Tsai. DNA methylation in cognition comes of age. Nat Neurosci. 15(8):1061-2 (2012).
  5. Jacobs et al. Jacobs et al. Methylation alterations at imprinted genes detected among long-term shiftworkers. Environ Mol Mutagen. 54:141-6 (2013).
  6. Clozel et al. Mechanism-based epigenetic chemosensitization therapy of diffuse large B-cell lymphoma. Cancer Discov. 3(9):1-18 (2013).
  7. Singh et al. DNA methyltransferase inhibitors as epigenetic therapy for cancer. Curr Cancer Drug Targets. 2013 Mar. 18 [Epub ahead of print].

YOU’RE INVITED TO A PARTY! NOT JUST ANY PARTY—
HOW THE TASTE OF FOOD IS AFFECTED BY THE WEIGHT, SIZE, SHAPE,
AND COLOR OF THE CUTLERY USED TO EAT IT AND THE PLATES IT IS SERVED ON.

Taking a break from the usual health oriented contents of this newsletter, we found a new open access journal called Flavour at @FlavourJournal which contains a wide variety of papers on the scientific basis of flavor with ideas tested on improving the taste and flavor or limiting the amounts of food eaten by changing the shape and weight of cutlery and the color of plates food is served on. Sounds like a great source of information for the small restaurant trying to get a one-up on the competition without spending much money or for people who like to throw parties and want to have attendees really remember your party.

How Mere Cutlery—the Weight, Size, Shape, and Color of It—Can Change How You Perceive Your Food

This new paper1 tested variations on the cutlery people were given to eat food on the ratings people gave on various flavor components of that food. For example, yogurt was perceived as denser and more expensive when tasted from a light colored plastic spoon as compared to a spoon made to appear heavier (with artificial weights). Food was rated as tasting saltiest when eaten from a knife as compared to a spoon, fork, or a toothpick. In their description of other studies, the authors1 mentioned that drinking from a “cold” colored glass (a dark color as compared to a yellow, orange, or red color) may result in the perception that the drink is more thirst-quenching. In another study they described, researchers found that food eaten from bowls artificially weighted to make them appear heavy resulted in food perceived as thicker and denser (e.g., heavier), which people preferred to the same food eaten from a light bowl. (Do you suppose this could improve the eating quality of stone soup?) In yet another study (the results haven’t been published), cheddar cheese was reported to taste “sharper” when sampled after viewing pointy figures as compared to that tasted after viewing round images. (We aren’t making this up, folks.)

The researchers brought up the issue of the expectations of food consumers and suggested that food would taste better when cutlery met tasters’ expectations based on the sort of cutlery that tasters had previously used in eating better quality food.

Other nifty little tidbits reported in this paper1 include: a blue colored bowl resulted in unsalted popcorn that tasted salty. (The researchers1 mentioned that in the UK blue packaging is often associated with salty snack products.) White yogurt tasted more expensive when tasted from a white spoon as compared to a black spoon. Strawberry mousse was perceived as sweeter when sampled from a white plate as compared to a black one. In a separate study, researchers found that people would eat less when a snack was served on a red plate or a drink that has a red label.

Merely Changing the Color of a Plate Can Give People a New Taste Perception

Another paper2 reported on the effects of the color of a plate on how people perceive the taste of a dessert.

You are at a disadvantage here because, although pictures of these lovely desserts are provided in the paper, obviously you cannot see them (unless you download the free paper). They were listed as dessert A (fraisier), dessert B (fraicheur of raspberry and vanilla) and dessert C (vacherin glace with vanilla, raspberry, and basil), presented on white or black plates.

A few of the results: participants in the low-contrast condition (white pasta sauce on a white plate or red pasta sauce on a red plate) served themselves significantly more pasta than those in the high contrast situation (white pasta sauce on a red plate or red pasta sauce on a white plate). Diners rated the lunch desserts uniformly more appetizing when served on a white plate while the dinner desserts were found to be similarly appetizing no matter what the color of the plate. As to overall liking of the desserts (rated after desserts had been tasted), desserts A and C resulted in similar scores no matter what the color of the plate while the pattern for dessert B was said to be the “reverse. though the meaning of “reverse” here is unclear. No hypothesis is offered for why these differences between the desserts were seen, but there is certainly something there that requires explanation since it was a consistent effect.

So the next time you go to a party, remember that your taste might be affected by a number of different tricks for serving food without actually changing the food. If you think that your latest party had some of the best food you ever had at a party, don’t be TOO impressed, it may be somewhat illusory (though still fun) and, once you innocently walked in the door, you didn’t stand a chance!

Or, the next time you give a party, consider the use of some special effects to bring out a larger WOW effect in your party crowd when they eat your food.

WE ATE AND WE ATE
WHILE WE TASTED THE PLATE
AND THE NEXT COURSE THEY BROUGHT
THE SPOONS WERE PART OF THE PLOT.
YOU WEREN’T SUPPOSED TO GUESS
WHY THE FOOD WAS A SUCCESS
AND THE PARTY SURE TO IMPRESS.
THE SCIENCE WAS THERE
BUT YOU DIDN’T KNOW WHERE
AND THE NEXT STUDY WE DO
WILL BE INSIDE OF YOU:
CAN YOUR GUT
TASTE THE DIFFERENCE, TOO.3,4

Oh, and one other thing, if you serve alcoholic drinks at your party, be sure to also serve Party Pill.™ We never go to a party without it!

References

  1. Harrar and Spence. The taste of cutlery: how the taste of food is affected by the weight, size, shape, and colour of the cutlery used to eat it. Flavour. 2:21 (2013). https://www.flavourjournal.com/content/pdf/2044-7248-2-21.pdf
  2. Piqueras-Fiszman, Giboreau, and Spence. Assessing the influence of the color of the plate on the perception of a complex food in a restaurant setting. Flavour.2:24 (2013). https://www.flavourjournal.com/content/pdf/2044-7248-2-24.pdf
  3. Surprisingly, taste buds that can literally taste sweet and bitter via the same receptors as the taste buds on your tongue have been found in gastrointestinal cells (and also elsewhere, such as in the lungs). See, for example, Mayer, Gut feelings: the emerging biology of gut-brain communication. Nature Reviews Neuroscience. 12:453-466 (2011).
  4. Untitled poem by Sandy Shaw.

WHY ARE THE NUMBERS OF INDIVIDUALS RENOUNCING
THEIR AMERICAN CITIZENSHIP INCREASING SO FAST?

We don’t think there is any great mystery about why people might be interested in renouncing their American citizenship when the costs imposed upon citizens (taxes and regulations) are increasing so rapidly. Like everything else, citizenship provides benefits and imposes costs, and there is a limit to what people are willing to accept as a reasonable “deal.” The numbers are not yet large, but the rate of increase is pointing in a steeply upward direction. These numbers are for the last quarter, data that will be shortly officially released but has been obtained and publicized by a reliable media figure. Last quarter, 1,131 individuals renounced their U.S. citizenship as compared to the same quarter last year in which 188 people renounced their U.S. citizenship.

Incredibly, the government is now charging an exit tax to prevent some high net worth individuals from taking their wealth with them. This applies to anyone whose average U.S. tax liability over the last five years was about $150,000 (roughly $500,000 in taxable income in 2012 dollars) and/or has a net worth of at least $2 million on the date of their expatriation. The net worth figure is NOT adjusted with inflation. Compare this exit tax outrage with the “Act of July 27, 1868” in which the U.S. Congress declared that “the right of expatriation is a natural and inherent right of all people, indispensable to the enjoyment of the rights of life, liberty, and the pursuit of happiness.”

We are fed up with the incredible GREED of the government. An average taxable income of $150,000 over the last five years is hardly enough to consider someone rich. In fact, this is well under the $250,000 that Obama promised was an income level that would not, under his Administration, be subject to higher taxes. Just another LIE in a growing output of government communication that is almost all LIES. Don’t get used to it, folks, then they’ve really gotcha.

References

https://www.sovereignman.com/expat

https://s3.amazonaws.com/public-inspection.federalregister.gov/

See also:

https://www.sovereignman.com/expat

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