TEA = CHAMPAGNE?

[Note: this post is an edited repeat of a Pairteas Facebook post from the past—hope you enjoy it, and hope you and yours experience fulfillment and happiness throughout 2017 and beyond!]

...Of course not exactly! 

But for those of us who, like me, can't tolerate alcohol and are thus tea-totalers, is there a tasty tea-based alternative?

Think I may have found it—try it and let me know what you think!

• Started with the question: what is the flavor profile of champagne? According to winefolly.com, champagne has flavors of citrus fruits, white peach, white cherry, almond, and toast (yeasty).
• In addition it has (of course) alcohol, which comes across on the palate as "acid." How to get a similar profile?
• Amazingly, by using white tea: white tea actually has a number of chemicals it shares with peach, cherry, almond, and bready flavors, the latter thanks to its long withering. In addition, it has about half the catechins of green tea, so is decidedly less bitter.
• Next, we need the carbonation. At first was thinking about getting a sparkling alcohol-free apple cider—there are a couple of chemicals in white tea with an apple-like flavor—but champagne isn't apple-y to me, so I nixed that idea.
• So I took myself to our local gourmet store to find a fizzy drink that wouldn't be too sweet, and found Juniper Berry DRY. To find out more about this exquisite sparkling soda, which you can get on Amazon, go to: http://www.drysparkling.com/flavors/juniper-berry/
• Remembering that champagne also has a peach aspect, and that I wanted to cut sweetness a bit (and also because white tea has about half the catechins of green tea), I also got some Fee Brothers peach bitters (http://www.feebrothers.com/products/bitters/peach_bitters.php).

Here's the recipe:
• Bring 18 oz (half liter) of water to 170ºF (I checked with a food thermometer, but you can guess the temp because little bubbles start to appear). Add the water to 8 grams of white tea, brew for 60 seconds, and remove the leaves. This yields a rather dark tea (see photo below), but it will soon be diluted!

• Either let the tea cool down or be sure to put a metal spoon in your glass, then pour equal amounts of tea (first) and sparkling soda (second).
• For each 4 ounces of the tea/soda combo, add two dashes of peach bitters (or more, to taste). 

• Enjoy!!

=>> While you can still taste the tea very gently, the overall flavor and aftertaste is remarkably like champagne, and it feels so very festive!!! 

The picture below shows the result. Note that the tea soaked up some two ounces of the starting water! Sorry it's not in a champagne glass—am in down-sizing mode, and can't reach them right now!

Oh, and the bubbles don't show up in the picture, but the tiny bubbles are there...

Injury to a leaf and the chemicals it produces

In looking for discussions of the consequences of damage on leaf volatile production—the aromatic compounds produced when leaves are damaged, came across an experiment that detailed what the intact parts of a leaf does when the leaf sustains partial damage.*

Matsui and colleagues injured Arabidopsis leaves. Arabidopsis thaliana is a favorite research plant, because it grows quickly, and because it is the first plant for which the complete genome was sequenced.

Arabidopsis thaliana, from Wikipedia

The injured part of the leaf produced a chemical, (Z)-3-hexenal. The plant produces this chemical to decrease the chances of further attack, because it is insecticidal, bacteriocidal, and fungicidal. However, this chemical can also be toxic to the plant itself. 

The question is, then, what does the uninjured part of the leaf do with (Z)-3-hexenal that reaches it. It turns out that the leaf converts the chemical into non-toxic products, (Z)-3-hexenol and (Z)-3-hexenyl acetate. As shown in the diagram below (from the article), this conversion requires an enzyme, aldehyde reductase, and a chemical called NADPH (green oval). The production of NADPH for this reaction requires energy and intact cells, so can only be carried out by the uninjured part of the plant. 

Meanwhile, as you can see in the diagram (red oval), enzymes in the injured part of the plant spontaneously transform (Z)-3-hexenal into (E)-2-hexenal, and, with oxygen from the air (red circle), into at least three other compounds. No energy is needed for these steps, so they occur spontaneously when cell compartments are broken down and enzymes are released.

In the “You can’t win” department: the non-toxic products are released into the air and attract many different predatory insects that proceed to destroy the injured plant...

Why the interest in this question? (E)-2-hexenal is one of the chemicals one of the chemicals that gives the smell to new-mown grass, and one of the chemicals that are produced in the tea leaf after plucking and during withering, and one of the chemicals we humans appreciate in the flavor of green tea!

* Matsui K, Sugimoto K, Mano J, Ozawa R, Takabayashi J (2012) Differential Metabolisms of Green Leaf Volatiles in Injured and Intact Parts of a Wounded Leaf Meet Distinct Ecophysiological Requirements. PLoS ONE 7(4): e36433. doi:10.1371/journal.pone.0036433

’Tis the season…

…here in the US Northeast for sore throats, whether caused by infection, or simply too dry indoor air. Was thinking about the soothing aspect of hot toddies, and came across a recipe from Emeril Lagasse, in the Food Network website, here:

http://www.foodnetwork.com/recipes/emeril-lagasse/hot-tea-toddy-recipe.html#communityReviews

This recipe got five stars as a treat(meant) for sore throats. However, fact is for me, that I won’t ever try this recipe, because I don’t do alcohol, and I don’t even like the smell of whisk(e)y...

...so I searched some more, and came across this excellent blogpost: in it, Aparna travels to India and back, and finishes with the recipe for a non-alcoholic tea-based hot toddy for sore throats that is also good sipped cold:

https://www.mydiversekitchen.com/a-non-alcoholic-hot-tea-toddy-amp-a-photography-exercise-recipe

What these two recipes share (aside from tea) is the presence of spices that activate both TRPV1, the hot receptor and TRPA1, the cold receptor. For TRPV1, for example, it’s black pepper in Aparna’s alcohol-free version, and alcohol itself in Emeril’s version; and for TRPA1 it’s powdered dried ginger with its shogaols and lemon in Aparna’s recipe, and lemon juice in Emeril’s.

If you sip either of these two drinks, you will first feel a bite of pain, only to feel the pain quickly subside and the soreness in your throat with it. 

Why would activation of TRPV1 and TRPA1 together actually be soothing?

To untangle the answer, first a rather unusual experiment where the researchers passed cold dry air across the throats of forty-five healthy (and, I might add, somewhat foolhardy) volunteers to cause a sore throat—the kind of experience we have here in the US Northeast during these cold winter months.* 

This treatment led to inflammation. To quote the authors’ paper:

“This study shows that tonic stimulation of the pharyngeal mucosa with cold dry air causes pain, irritation, and discomfort whilst swallowing and an increase of inflammatory mediators, which is reversible.”

The inflammatory markers they measured included substance P. Its levels rose in the throat during cold air treatment, and vanished about 30 minutes after cold treatment was stopped. 

Substance P tells pain nerve endings to send pain messages to the brain, and is released with TRPA1 activation by the cold air. Release of substance P in turn leads to release of the other inflammatory mediators, which then leads to the release of more substance P, and so on in a vicious cycle.

When you activate either TRPA1 or TRPV1 alone, the associated nerve endings release substance P. However, when you activate both together, you first get a burst of substance P release, but then the two receptors mutually inhibit—to my simplistic thinking, nature made it difficult to sense both hot and cold at the same time. 

Not so simplistically, though, we do know for sure that both receptors can sit on the same cells, and that when both are stimulated simultaneously, they can cancel each other out. **

The ingredients in these hot toddies do just this—that’s why hot toddies can make your throat feel so good!

* Renner B, Ahne G, Grosan E, Kettenmann B, Kobal G, Shephard A. Tonic stimulation of the pharyngeal mucosa causes pain and a reversible increase of inflammatory mediators. Inflammation Research. 2013;62(12):1045-1051. doi:10.1007/s00011-013-0663-7.

** Barry G. Green, Betsy L. McAuliffe. Menthol desensitization of capsaicin irritation: Evidence of a short-term anti-nociceptive effect. Physiology & Behavior 68 (2000) 631–639.

 ** Takaishi, M., Uchida, K., Suzuki, Y. et al. Reciprocal effects of capsaicin and menthol on thermosensation through regulated activities of TRPV1 and TRPM8. J Physiol Sci (2016) 66: 143. doi:10.1007/s12576-015-0427-y. 

Note: menthol activates TRPA1 as well as the cool receptor TRPM8.

"The Sweet Wine Lovers' Manifesto"

Friend of Pairteas and wine genius Tim Hanni MW (= Master of Wine) is working on a new book, “The Sweet Wine Lovers' Manifesto,” and I’ve just read through a draft. It’s a bit embarrassing insofar as he mentions me a bit, but then I do prefer sweet wines, so the book does speak to my interests and preferences. 

What sweetness does, as I have mentioned before, is to cut the burn of alcohol to which I am genetically very sensitive. According to my 23andme results, I carry T at rs161364 in both of my copies of the TRPV1 gene, the hot receptor, on chromosome 17.  This means that I am exquisitely sensitive to the burn of alcohol.* This double T state is also relatively rare in people of European descent like me: while about 39% of people of European descent carry one T, only 10% carry two. The percentage of Asians and Native Americans with two T’s is even lower, between 4 and 5%, while the percentage of Sub-Saharan Africans is essentially zero.** In other words, the T is a gain-of-function genetic mutation that occurred after anatomically modern humans walked out of Africa to settle the rest of the world.

Interestingly, alcohol is also bitter. It activates at least two different bitter receptors: TAS2R13 and TAS2R38.* The latter receptor is also the one that responds to PROP (6-n-propylthiouracil) that researchers have used extensively to test for taste sensitivity. I happen to have the genetic markers that lead to high sensitivity to bitter for both of these receptors as well, but the burn I get from alcohol is so intense that bitterness takes a back seat.

Another genetic feature that I have: the most active version of a protein called gustin. This protein helps to govern the number and function of your taste papillae.*** A person can carry one or two copies of the most active (A) form of the gene for this protein, and I happen to carry two (I’m A/A at rs2274333), hence my tongue is a carpet of taste papillae and taste buds. Lest you think this is a great thing, you should know that being so sensitive means that I taste nasty stuff more strongly, too, and alcohol burns all the more.

This is my tongue, stained with blue food coloring. Taste papillae don't stain very much, which is why most of the tongue is pink, while the upper part, towards the back of the tongue, is blue. The fissures appear when there is a carpet of taste papillae, and you can also see some round papillae sticking up separately. Compare with the picture below, of a person with few papillae—most of the tongue is blue; the taste papillae are the pinkish dots that are scattered on the tongue surface.

Sweet activates TRPV5, which turns off TRPV1—that’s why I can tolerate Harvey’s Bristol Cream Sherry at 17.6% alcohol, while I cannot abide a Cabernet Sauvignon at 16% alcohol.

Though another confession is needed here, namely that I hate the taste of green peppers, which is characteristic of Cabs…but it’s the burn that gets to me first.

In any case, while genetics alters your degree of sweet wine liking (or to be more exact, your degree of high alcohol dry wine dislike), in fact more people enjoy sweet wines than really enjoy those high alcohol dry wines. According to Tim, if it weren’t for the snob appeal of the latter, people would be drinking sweet wines much more often, and not just with dessert. Keep an eye out for his book with more details!

* Alissa L. Allen, John E. McGeary, and John E. Hayes. Polymorphisms in TRPV1 and TAS2Rs associate with sensations from sampled ethanol. Alcohol Clin Exp Res. 2014 October ; 38(10): 2550–2560. doi:10.1111/acer.12527. 

** https://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?rs=rs161364. Note I used the HAPmap data for these percentages. While some people quarrel with HAPmap data, those percentages seem to correspond to my experience.

*** Melis M, Atzori E, Cabras S, Zonza A, Calò C, et al. (2013). The Gustin (CA6) Gene Polymorphism, rs2274333 (A/G), as a Mechanistic Link between PROP Tasting and Fungiform Taste Papilla Density and Maintenance. PLoS ONE 8(9): e74151. doi:10.1371/journal.pone.0074151.

The flavors of your tea: cold versus hot brewing

Have been asked to give a talk at next year’s World Tea Expo about the differences between hot and cold brewed tea. Friend of Pairteas Marzi Pecen was recently in Japan, where she especially enjoyed a cold brewed oolong—enjoyed it even more than hot brewed! — so I was curious to find out how cold brewing might affect the composition of the resulting tea.

To create a tea with cold brewing you rely on the water solubility of compounds at roughly room temperature. By contrast, many compounds that are not soluble at room temperature become more soluble and are released from the tea leaves at hot temperatures. One major group of compounds that are barely soluble at cooler temperatures are the catechins and polyphenols. Their release from tea requires near boiling to boiling temperatures, and a longer steep even then. For a cold brew to become significantly bitter, the brewing time has to be quite prolonged and the proportion of leaf to water high.*

Another compound of interest in oolong is dimethyl sulfide. That is the compound that gives the tea, whether green or oolong, a seashore/oceanic/marine flavor, and is one of the two major compounds in oolong that make people dislike the tea. It is insoluble at room temperature. The other compound is indole, which at very low concentrations is pleasantly floral, but at higher concentrations (or if you are sensitive to it) has an odor that can be politely called animalic. Interestingly, indole is barely water soluble at room temperature, so it will appear in a cold brew at very low concentrations if properly done—in other words at the concentration range where it is pleasant. 

What will appear in a cold brew are the delightfully malty, fruity, and floral compounds in oolong, for example nerolidol, which is considered the hallmark of high quality oolong, and (R)-(-)-linalool, which gives the tea a lavender and sweet basil-like aroma, together with the jasmine-related compounds that make really good oolongs so distinctive.**

Above is nerolidol — the double lines indicate double bonds between carbon molecules, with each carbon at the juncture between lines and at each end. This compound is in the form of a relatively short carbon chain, with an OH (oxygen-hydrogen) group, which help make it more soluble in water—the molecule can let go of the hydrogen, which is then "replaced" by the hydrogen of a water molecule.
Contrast this structure with indole, below, which has two linked circles of carbon atoms—these circle structures are much less soluble in water, because they tend to bond to themselves in a stack, and water can't get in between. Images from Wikipedia.

So if you like your tea bitter and astringent, or if you want catechins and polyphenols for health reasons, hot brewing is the way to go, but if you want to appreciate the deliciously delicate flavors that oolongs offer, it may be best to cold-brew them!

* Sheng-Dun Lin, Joan-Hwa Yang, Yun-Jung Hsieh, En-Hui Liu, Jeng-Leun Mau. Effect of Different Brewing Methods on Quality of Green Tea. Journal of Food Processing and Preservation . 38 (2014) 1234–1243. doi:10.1111/jfpp.12084. 

** Zhu J, Chen F, Wang L, Niu Y, Yu D, Shu C, Chen H, Wang H, Xiao Z. Comparison of Aroma-Active Volatiles in Oolong Tea Infusions Using GC-Olfactometry, GC-FPD, and GC-MS. J Agric Food Chem. 2015 Sep 2;63(34):7499-510. doi: 10.1021/acs.jafc.5b02358. Epub 2015 Aug 19.

Remember the previous two posts, where I discussed an article about wine liking and the effects of cheese on liking?* There was one wine, in particular — Madiran — that had high astringency, and was relatively disliked compared with other wines used in the study, and disliked even more with each successive sip. Cheese significantly decreased the progressive dislike, and I attributed this change to the effects of fat in the cheese. Here I reconsider this proposition.

Tannat grapes used in Madiran — wines made from these grapes in France have an extra high tannin content. Image from Wikipedia.

Friend of Pairteas and wine expert Tim Hanni MW pointed out to me the other day that he had tried the experiment of evaluating wine astringency with and without olive oil, to test the notion that astringency could be diminished by fat. He found that olive oil did nothing to diminish astringency, and suggested that the effect of the cheeses on wine astringency that I discussed in last week’s post was due to other factors in the cheese, such as salt and sourness, and not due to the fat content. In fact, as he found, you can diminish wine's astringency by taking a pinch of salt and then sucking on a lemon before drinking your wine. I've seen this process in action and it really works.

This observation got me thinking about the very complex system of trigeminal and taste activation. 

First, how do tannins interact with the trigeminal receptors to create the sensation of  astringency? 

Tanninns have to bind to both bitter receptors and TRPV1, the trigeminal hot receptor, simultaneously. If they are displaced from either of these receptors by another compound your won’t sense astringency. 

So what do salt and lemon juice do in this regard?

With respect to salt, it activates a specific part of the TRPV1 receptor, and changes its conformation. The following is speculation on my part, but it is likely that the salt, by activating the TRPV1 receptor in its way, bumps the tannins off their binding site, so the can no longer cause astringency. Further, salt inhibits the ability of bitter sensitive taste bud cells to send on their message, providing another way for the sensation of astringency to be blocked.

Second, lemon juice contains compounds that interact with bitterness receptors, acid receptors, and cold receptors (TRPA1), so it can act through each of these pathways to influence astringency. By interacting with bitterness receptors, lemon juice can bump tannins off the bitter attachments they need to create the astringency sensation. Next, the pathway for bitterness sensation acts through cells that respond to citric acid. If these cells are activated by sufficient amounts of acid, the message they send will be dominated by sourness rather than bitterness, so astringency will be inhibited. Finally, when you activate TRPA1 you inhibit TRPV1, the trigeminal receptor needed for astringency sensation, so here you have yet another way in which lemon juice could decrease astringency.

Why didn’t olive oil work to decrease wine’s astringency? As we noted before, fats do inhibit TRPV1 activity, so one would expect an effect—after all, you can turn down the heat of capsaicin with some fatty food. Two possibilities come to mind. 

One possibility is that the part of TRPV1 to which tannins bind is not affected by the presence of fat. It is worth noting that there is good evidence that capsaicin binds to a different part of TRPV1 from salt—changes in the DNA of TRPV1 that increase capsaicin heat are in a different place in the resulting TRPV1 molecule from changes in the DNA that affect salt sensitivity. So the notion that tannins might bind a different site in the molecule from fat is not unreasonable.

The second possibility has to do with olive oil itself. Good quality olive oil (and Tim would be sure to use the best!!) is astringent all by itself, plus it contains bitter compounds, as well as oleocanthol, which activates another trigeminal receptor, the cold receptor TRPA1—activation of this receptor gives you the catch in your throat when you take in really good olive oil. That catch feeling may augment the aversive sensations rather than decrease them. 

That said, one thing is quite clear: if you don’t like bitterness and astringency in your wine or your tea, add a tiny bit of salt and some lemon juice, and violà — deliciousness prevails!

* Mara V. Galmarini, Anne-Laure Loiseau, Michel Visalli, and Pascal Schlich. Use of Multi-Intake Temporal Dominance of Sensations (TDS) to Evaluate the Influence of Cheese on Wine Perception. Journal of Food Science Vol. 81, Nr. 10, 2016. doi: 10.1111/1750-3841.13500. 

Wine and Cheese Pairing: 2 - wines with cheeses

In my previous post, I discussed a fascinating paper by Galmarinin and her colleagues, where French study participants tried four different wines with and without cheese.* In that post, I noted that the participants preferred the sweet white wine (Pacherenc) over the drier white wine (Sancerre); the two white wines over the Pinot Noir (Bourgogne); and all of these wines over the wine with the highest level of alcohol and of tannins and therefore astringency, Madiran (a blend of Cabernet Sauvignon and Tannat).

In this post, we will look at the effects of the cheeses consumed before sips of the wine. The researchers used four cheeses, as shown in the following table:

Note: all the cheese contained between 73 and 75% fat.

This diagram shows the effect of the four cheeses on wine liking:

As you can see, none of the cheeses had any effect on liking of the Pacherenc, still the preferred wine overall. These cheeses had only a slight effect on Sancerre liking. Where we see a difference is with the Bourgogne and the Madiran. With respect to the Bourgogne, the cheeses eliminate the slight decrease in liking from sip 1 to sip 3. With the Madiran, the decrease in liking with successive sips in the absence of cheese is notable, but when the cheeses are consumed between sips there is actually an increase in liking. Overall, Madiran still wasn’t liked as much as the other wines, but the difference among them was minimized.

What is the cheese doing? 

The first graph below shows the results on astringency when the cheeses are consumed. I didn’t include Pacherenc in this graph because it is not astringent, even when sipped alone. 

As you can see, cheese decreases the astringency of each of the other wines. Sancerre has relatively little astringency, so the decreases are minor and the effect of the cheeses on Sancerre liking is minor as well. As astringency in the absence of cheese rises, the effect of the cheeses is more dramatic. In the case of Bourgogne wine, cheese brings the perceived astringency down to levels comparable to those of Sancerre without cheese; in the case of the Madiran it brings the levels to slightly below those of Bourgogne without cheese. These results parallel the results for those of liking, suggesting that that 1) astringency is aversive for this group of tasters; and 2) that these cheeses have an effect on astringency. 

How do cheese affect astringency? 

In two linked ways: first, the fat in cheese turns off TRPV1, the hot receptor and one of the two receptors necessary for astringency to be perceived; second, by turning off TRPV1, TRPA1 (the cold receptor) can be activated. TRPA1 is also activated by the pungency in the cheese, further turning off TRPV1. The net effect is a decrease in astringency, so dislike of the wines is decreased.

What about the relative increase liking that we see with the Madiran when coupled with cheese?

The graph below shows what happens with three significant characteristics of the Madiran:

As you can see, with the cheeses' sourness—another aversive characteristic—decreases, while the perception of the wine’s red fruits increases. In other words the cheeses allowed the pleasant flavors hidden in the wine to come forward. Note that Roquefort is least effective at decreasing astringency and sourness and also least effective in increasing red fruit perception.

Incidentally, the red fruit flavors are perceived with the help of another receptor, TRPV3, a warm receptor. TRPV3 is also inhibited by activation of TRPV1. If TRPV1 is inactivated, then the red fruit chemicals that activate TRPV3 have a chance to be perceived. 

My take-homes from this paper are: 

• First, it important to consider the effects of wines and foods over time, such as in successive sips—these authors are among the first to take a serious look at this all important feature of our normal consumption, and to develop a method for recording and identifying the changes people perceive as they work their way through a meal.
• Second, as my friend Tim Hanni** points out, “Big Reds,” such as the Madiran used in this study, are generally not as much liked as the less astringent wines—this observation makes me think that liking a “Big Red” is as much a macho thing of reveling in the aversive, as it is about diminished sensitivity to the effects of TRPV1 activation—something like eating super hot chili peppers to show off. We must remember, however, that the pain induced by activation of TRPV1 by chili peppers declines the more you eat them. It may then be true that the more Big Reds you drink, the more inured and eventually insensitive you are to their astringency.
• Finally, these data strongly suggest that the biology of TRPV1, TRPA1, and TRPV3 as I have outlined in previous posts holds true.

So if you are stuck with a wine that you don't like because of its astringency, by all means ask for some cheese to go with it!

* Mara V. Galmarini, Anne-Laure Loiseau, Michel Visalli, and Pascal Schlich. Use of Multi-Intake Temporal Dominance of Sensations (TDS) to Evaluate the Influence of Cheese on Wine Perception. Journal of Food Science Vol. 81, Nr. 10, 2016. doi: 10.1111/1750-3841.13500.

** http://www.winesandvines.com/template.cfm?section=columns_article&content=84604&columns_id=24&ctitle=Big%2C%20Dry%20Reds%3A%20Just%20a%20Fad%3F

Wine and cheese pairing: I - the wines

My attention was called to a fascinating paper about the effects of pairing cheeses with wines, by a French group at the Centre des Sciences du Goût et de l’Alimentation, CNRS, INRA, Univ. Bourgogne, Franche-Comté, in Dijon, France.* In the next set of posts I will review this paper in detail, because it illustrates very clearly several points that I have been making in this blog.

First, about the wines themselves (am saving the discussion of cheese effects for the next post):

The four wines chosen for the study were Pacherenc, Sancerre, Bourgogne, and Madiran. Pacherenc is a sweet white wine, Sancerre is a dry one, Bourgogne is a Pinot Noir, and finally Madiran is a combination of Cabernet Sauvignon and Tannat grapes, with a high alcohol (15.2%) and tannin content. 

The consumers in the study—31 local Dijonnais who drank wine and ate cheese regularly, and who had participated in at least one previous sensory study—evaluated the wines initially and then after a second and a third sip. Evaluation consisted of a measure of liking and measures of sensory characteristics such as sweetness, astringency and sourness, as well as fruitiness.

These consumers definitely preferred the sweet Pacherenc wine to the others, and particularly to the Madiran—initial liking scores were double for the Pacherenc compared to the Madiran!  Furthermore, with each succeeding sip, liking for the Pacherenc remained the same or even increased slightly, while liking scores for the Madiran decreased significantly as astringency came to dominate the sensory impression. 

These results fall perfectly in line with the biology of sweetness and astringency: sweetness is perceived at the beginning of a sip and tends to fade a little bit as the sip progresses, but can return in full force with subsequent sips. By contrast, astringency takes a few “beats” to kick in before it starts to dominate a flavor profile.

The difference lies in the function of the receptors and their second messengers. In the case of sweetness, the process of perception involves a series of reactions in the taste cell that occur quite rapidly. The receptors for sweet compounds grab their respective molecules, and send the message through a series of coupled reactions to TRPM5, the second messenger, which in turn enables the cells to send the “sweet” message to the brain. TRPM5 turns on quickly, and then turns off quickly, so you sense a decrease in sweetness over time after the sip. Here are the results for the Pacherenc:

This figure was extracted from Figure 3 of the article, and shows the results for there successive sips of the Pacherenc wine. The thickness of the bars is proportional to the intensity of the sensation, and the length refers to the duration. "The x-axis of each graph represents standardized time between 0 and 1. Different letters on liking scores represent significant differences among sips for each wine according to LSD test. "

By contrast, astringency activates TRPV1, the hot receptor, which is activated by alcohol as well. TRPV1 is a “slow-on slow-off” receptor, so the effect builds. Think of your first bite of a food liberally sprinkled with hot peppers. You may say, “Oh it isn’t that hot!” only to experience a burst of pain milliseconds later. And as you keep eating the food, the effect gets stronger and stronger, and lingers long after you have stopped eating. This is what happens with astringency as well—by the third sip, the astringency is there all the time, and pretty much dominates the picture, as you can see in the diagram below.

This figure was extracted from Figure 3 of the article, and shows the results for three successive sips of the Madiran wine. Note the significant decrease in liking, the slower onset of astringency with the first sip, its quicker onset by the second sip, and its greater overall intensity with the third sip.

It’s worth noting that the alcohol perception for the Madiran wine was slight to non-existent, despite the wine's high alcohol content. In the presence of high tannins, astringency is sensed in preference to the alcohol burn, because astringency involves coupled signals with bitter receptors; the result is that our brains tend to choose astringency as the overall sensation. In addition, all the other possible flavors are virtually drowned out by astringency, and red fruits only have a chance to be perceived when the person actively switches from sensing astringency to sensing the fruit flavors.

Wine Wizard and Friend of Pairteas Tim Hanni MW (= Master of Wine) has been trying to promote the notion that many sophisticated consumers actually prefer the sweeter wines, and that this preference is especially pronounced for people whose palates are more sensitive—in other words whose palates may be more affected by strong sensations such as astringency.** 

Here is a group of French people who agree with him!

* Mara V. Galmarini, Anne-Laure Loiseau, Michel Visalli, and Pascal Schlich. Use of Multi-Intake Temporal Dominance of Sensations (TDS) to Evaluate the Influence of Cheese on Wine Perception. Journal of Food Science Vol. 81, Nr. 10, 2016. doi: 10.1111/1750-3841.13500. 

** http://www.winesandvines.com/template.cfm?section=columns_article&content=84604&columns_id=24&ctitle=Big%2C%20Dry%20Reds%3A%20Just%20a%20Fad%3F

Sleep and odor memory

Was searching for something quite different when I came across a paper discussing how sleep helps with odor memory.*

In one part of this study, the participants (who were all male, btw) learned to recognize six different odors (though not name them). Then they slept, and the next day were asked to identify which odors they had or had not experienced the night before from among a set of twelve odors. 

By administering certain drugs or placebo just before sleep, the researchers were able to determine that the participants consolidated their memory for the odors during slow-wave deep sleep. 

The graph below shows the results of one part of the study. In the wake condition (on the left), participants were kept awake through the night. While their recognition ability under this condition was good, it was not as good as their ability after a period (3 hours) of slow-wave sleep, followed by staying awake (compare Placebo/Wake to Placebo/Sleep). The drug clonidine obliterated the effect of slow-wave sleep on recognition. 

Was fascinated to observe that the odors they used included several that are typical in tea, such as linalool oxides, damascenone, and 2-hexenal.** 

Conclusion: if you want to learn to recognize (and eventually name, of course) different odors in tea, it helps to get a good night’s sleep!

* Gais S, Rasch B, Dahmen J, Sara S, Born J. The Memory Function of Noradrenergic Activity in Non-REM Sleep. Journal Of Cognitive Neuroscience [serial online]. September 2011;23(9):2582-2592. Available from: Academic Search Premier, Ipswich, MA. Accessed October 26, 2016.

** Incidentally, the authors qualified these odors as being “unfamiliar”— but they probably are familiar to those of you who have been studying tea aromas.

Tea and cardiovascular disease

The edition before the last of World Tea News talks about an article in the American Journal of Medicine that suggests that consumption of tea may help prevent both calcium deposition in coronary arteries and cardiovascular events.*

Interesting news, so I thought I should take a look at the original article, which was published on line September 15, 2016.** In this post, I will talk about the baseline data, with follow-up data discussed in future posts.

The article is based on data from the Multi-Ethnic Study of Atherosclerosis (MESA). This study was prospective, which means that it followed a sample of 6814 men and women aged 44 to 84, at 6 different U.S. medical centers. It  began in 2000, finished recruiting participants in 2002, and ended on December 31st, 2013. For the present analysis, data from 6508 people were used.

Participants provided dietary information when they entered the study and every 9 to 12 months thereafter. Computed tomography scans of the degree of coronary artery calcification were done at the beginning of the study and at 4 times thereafter. Not everyone participated at each scan, and it is not clear from the write-up whether everyone was actually scanned twice. That said, the analysis took into account the time between the first and the second scan in order to obtain information about changes over time. 

Another feature of the study was the attempt to take into account a multitude of factors that are known to contribute to cardiovascular disease (CVD), for example smoking, in order to tease out the contributions of tea, coffee, and total caffeine consumption to CVD.*** On the other hand no effort was made to distinguish among types of tea consumed or between caffeinated and decaf coffee.

So what do the baseline results tell us? 

First, it is striking, though not too surprising, that the people who had calcification in their arteries at baseline were older and more likely to be white and male than people who had none, and for the most part they were experiencing the known predictors of cardiovascular disease, such as hypertension, diabetes, and family history of coronary heart disease, “good” and “bad” cholesterol levels, and exercise time per week. Notable exceptions: there was no association with body mass index, though the mean was on the high side at 28.2±5.4; the people with no calcification actually ate slightly more fat, and other dietary measures, such as vegetable and fruit consumption, had a minor effect if any—hard to tell from the data given.

CT scan of the chest in cross section (the person's back is below the bottom of the picture), showing calcification in a coronary artery, from https://www.dic-kc.com/blog/2016/heart-health-ct-coronary-calcium-score. This link leads to another  from the Mayo Clinic that discusses how calcification is scored and what it means.

Now for the relationship with tea:

First, 58% of the participants did not drink tea at all, and another 29% drank less than a cup a day—only 13% drank tea on a daily basis…why this huge difference is not explained, of course, but the authors suggest that there may be other unmeasured differences, possibly lifestyle differences, that contribute to both the choice to drink tea and any results concerning arterial calcification and CVD. 

Next, to the calcification results: of the 800 people who drank tea daily at the time of enrollment into the study, about half had no measurable calcification in their arteries and half had some. For further analysis, the authors used a cut-off score which divided people into those who had relatively little to no calcification and those who had significant calcification.

While 13% of the participants drank tea each day, they accounted for slightly more of the participants (at 14%) who did not have significant calcification in their arteries according to their cut-off, and slightly fewer (at 11%) of those with significant calcification at baseline. The big finding is that when the authors took into account (= controlled for) all the cardiovascular risk factors, including age, drinkers of a daily tea had a lower risk of having the larger amount coronary artery calcification. 

Finally, people who drank tea daily at enrollment had fewer cardiovascular events during follow-up—12.3 events per thousand person-years for those who didn’t drink tea at all versus 7.7 events for those who drank tea every day. The difference is slight, but perhaps meaningful, but clearly drinking tea does not . Note that for this analysis, people of Chinese descent were excluded, because they consumed large amounts of tea…and also had fewer cardiovascular events! Which makes one wonder…was their advantage dietary or genetic or both?

When you think about these results, remember how few people drank tea on a daily basis in this study, and remember that those who drink tea may be doing a lot of other things differently or may be different genetically as well. 

So drink your tea for enjoyment—and just maybe you’ll get some cardiovascular benefits as well.

* http://worldteanews.com/tea-health-education/moderate-tea-consumption-shows-heart-benefits?NL=WTM-001&Issue=WTM-001_20161004_WTM-001_988&sfvc4enews=42&cl=article_4_b

** Miller PE, Zhao D, Frazier-Wood AC, Michos ED, Averill M, Sandfort V, Burke GL, Polak JF, Lima JAC, Post WS, Blumenthal RS, Guallar E, Martin SS, Associations between Coffee, Tea, and Caffeine Intake with Coronary Artery Calcification and Cardiovascular Events, The American Journal of Medicine (2016), doi: 10.1016/j.amjmed.2016.08.038. 

*** Here’s the complete list: age, sex, race/ethnicity, education, smoking (never, former, current), physical activity, total fat, alcohol consumption, fruits quartiles, vegetables quartiles, red meat quartiles, systolic and diastolic blood pressures, use of antihypertensive medications, lipid-lowering medication, anti-diabetic medication, BMI, family history of CHD, diabetes, HDL-cholesterol, total cholesterol, and triglycerides, C-reactive protein and fibrinogen.

 

Pudina chai and mint as digestif

The Daily Tea has a fine article on chai, with links to different approaches—chai with black tea, of course, but also green tea chai, with origins in Kashmir, and white tea chai.* The author, Carrie Keplinger, also described variations of black tea chai, including pudina chai. 

Pudina** chai “is black tea steeped with mint leaves in milk and water, sweetened to taste… Pudina chai makes a wonderful after-dinner digestif or a soothing remedy for an upset stomach.” Which is one great way to have an after-dinner mint!

Mentha arvensis, from Wikipedia

But why do we have an after-dinner mint as a “digestif?”

I believe the answer lies in mint’s ability to activate TRPA1, the cold receptor. You can find this receptor not just in the mouth and nose, where we sense the cold, but also all the way through the gut. In the gut TRPA1 is attached both to the gut lining cells and to specialized cells, enteroendocrine cells, that regulate gut motility.

When TRPA1 receptors attached to gut lining cells are activated, blood flow to the gut increases.*** When TRPA1 receptors on the enteroendocrine cells are activated, these cells release the hormone serotonin, which in turn causes the gut to start moving what you have eaten down the tract.****

Consequence? your digestion proceeds more quickly and smoothly, and you feel less over-filled! 

* http://www.thedailytea.com/taste/chai-style-delving-worlds-popular-spiced-tea/#prettyPhoto

** Despite the best efforts of my spell-check system, this word is not “pudding.” Pudina is the Hindi/Urdu name for a wild mint, Mentha arvensis, also know as corn mint and field mint.

*** Toru Kono, Atsushi Kaneko, Yuji Omiya, Katsuya Ohbuchi, Nagisa Ohno, Mas.ahiro Yamamoto. Epithelial transient receptor potential ankyrin 1 (TRPA1)-dependent adrenomedullin upregulates blood flow in rat small intestine. American Journal of Physiology - Gastrointestinal and Liver Physiology Feb 2013, 304 (4) G428-G436; DOI: 10.1152/ajpgi.00356.2012.

**** Nozawa K, Kawabata-Shoda E, Doihara H, et al. TRPA1 regulates gastrointestinal motility through serotonin release from enterochromaffin cells. Proceedings of the National Academy of Sciences of the United States of America. 2009;106(9):3408-3413. doi:10.1073/pnas.0805323106.