Minty Pea Purée on Sourdough Toast


Pea purée on buttered wholemeal spelt sourdough bread.

Few foods can match the vivid green of puréed frozen peas. The fresh taste of the peas combines beautifully with the mint an lemon to produce a very green flavour.

Gena Hamshaw of Food52 and creator of this recipe notes: “This dish is pure springtime comfort. A flavorful, bright green purée of mint, shallots, garlic, and peas meets crispy, rustic slices of toast.

Slices of toasted wholemeal spelt sourdough bread, lathered with a generous helping of butter, served as a fitting vehicle for these peas. The result was delicious and an excellent, sophisticated looking way of serving what is quite a simple meal of peas.

Ingredients (with slightly varying ingredients from the original recipe):

  • olive oil
  • A small red onion (instead of a shallot, thinly sliced
  • A generous helping of garlic, minced
  • An eyeballed quantity of frozen green peas
  • Some lemon juice
  • Salt, to taste
  • Black pepper, to taste
  • A handful of mint leaves
  • An onion was sliced and sauteed in olive oil for a couple of minutes. A generous helping of garlic and frozen peas was added and sautéed for another few minutes until the peas are warmed through.
  • The peas, onion, and garlic was placed in a food processor and the peas, lemon juice, lemon zest, salt, pepper , and mint leaves added in. The mixture was pulse mixed continuously until it is puréed but with some texture.Finally some extra mint leaves were blended in to taste.
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Adventures in sourdough bread.


Wholemeal spelt sourdough bread with oxtail stew.

I have never baked my own bread. This is despite having had a go at cooking many different things over the years and so recently I decided to rectify this omission. Given that I have an interest in fermenting foods and historic cooking techniques the obvious choice was to attempt some sourdough bread with a fermentation of wild yeasts and bacteria.

This required both a starter and a method, as I had little knowledge on this subject. After searching around for recipes and becoming rather confused by the apparently many and various complicated methods for producing sourdough I stumbled upon an excellent article by Hugh Fearnley-Whittingstall in the Guardian newspaper. As usual Hugh manages to simplify the sometimes complicated subject of preparing  real food and make it readily understandable.

The first step was to make an active starter culture. I used Organic Wholemeal Rye Flour from Doves Farm to make the starter mixing together 100 grams of water and 100 grams of the flour in an open topped jar. The next day the same amount of flour and water were mixed in. Then each subsequent day the starter was halved and a fresh 100 grams of water and 100 grams of rye flour mixed in. The starter took a little while to get going but after a couple of weeks the culture was fermenting well and occasionally attempting to escape its jar.

Once my starter was ready it was time to move onto the bread baking. My sourdough making is complicated by the rather cool temperatures of my old granite Scottish home. With room temperatures rather lower than is normal my bread would require longer fermentation times than many recipes suggest.

Given my interest in the history of food and cooking I have so far chosen to try out a range of old varieties of wheat that I could get my hands on.


Active wholemeal rye flour sourdough starter.

The recipe

For the sponge

  • 150ml active rye flour starter
  • 250g wholemeal spelt flour

For the loaf

  • 300g wholemeal spelt flour
  • 15 olive oil
  • 10g fine sea salt


  • To cope with the cool temperatures, and the limitations of my being at work all day, I mixed the sponge in the evening after getting home from work.
  • The sponge was fermented overnight for 12 hours, by which time it had risen well and was frothy with bubbles.
  • In the morning I added in the salt, olive oil, and flour and mixed it into a dough. This was kneaded for 10 minutes and then placed in a greased bowl and covered in clingfilm.
  • After about 10 hours proving, when home from work, I punched down the dough and placed in a bowl lined with a well floured tea towel.
  • After about three hours proving again I heated the oven to 200C, sadly about he maximum my oven seems to reached judging my my oven thermometer, placing my cast iron bakestone in the oven preheat with a backing tray on the oven shelf below it.
  • The dough was turned out onto the hot bakestone and boiling water poured into the backing tray. The bread was baked for 40 minutes, topping up the boiling water at 15 minutes to maintain the humid atmosphere.

wpid-img_20150622_213425.jpgFirst sourdough bread – Spelt flour

This first loaf worked out really well and the spelt flour produced an earthy rich flavour when combined with the sourdough fermentation.


Sourdough number two – Spelt flour.

This second loaf was also made with Doves Farm Organic Wholemeal Spelt Flour. Again the method worked well with spelt and scoring the dough when placing it in the oven helped the bread rise a little more than before.


Sourdough number three – Einkorn flour.

Einkorn flour is the ancestor of all modern wheat, grown for many thousands of years since the beginnings of agriculture. The flour for this bread is Doves Farm Organic Einkorn Wholemeal Flour purchased from Real Foods in Edinburgh. Due to this it has a lower level of gluten than modern bread wheats, and the different structure of the gluten means it will never rise like a modern bread loaf. However, this current method I’m using produced a good loaf, equal in structure and shape to the spelt flour loaves. The flavour of einkorn in this bread is very distinctive, imparting a mild, almost nutty taste to the bread. This einkorn flour is also produced quite a pale light coloured loaf despite being wholemeal and the bran it contains much be light in colour.


Sourdough number four – Khorasan (Kamut) flour.

For this loaf I used another ancient flour known as Khorasan, or Kamut, flour named after in the Khorasan region of Iran. This Doves Farm Organic Khorasan Wholemeal Flour was again found at Real Foods store in Edinburgh. Using the same method this flour produced a great tasting loaf, pale in colour and with a rich flavour all of its own.


Sourdough number five – white spelt flour.

A new recent find in Aberdeen was some Doves Farm White Spelt Flour at the Grampian Health Food Store. This white flour had a lighter flavour due to the reduced bran, with a slightly more open texture to the bread.

This foray into bread baking has definitely stimulated my interest in the process of baking bread and sourdough fermentation. This method from Hugh Fearnley-Whittingstall has so far worked really well around the times I have available during the week and the cool temperatures in my home that require long proving times.

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The origins of semi-dwarf wheat


John Linnell, Wheat (1860)

The late summer landscape of 19th Century England, such as painted by John Linnell, was filled with fields of tall golden wheat ripening in the sun. Across the Atlantic the prairies of the midwest states inspired the words by Katharine Lee Bates to America the Beautiful,

O beautiful for halcyon skies,
For amber waves of grain,
For purple mountain majesties
Above the enameled plain!
America! America!
God shed His grace on thee,
Till souls wax fair as earth and air
And music-hearted sea!

In contrast today, on the prairies of the midwest or the fields of England, the wheat is unlikely to be so tall or waving in such a poetic manner. The wheat grown today is rather shorter and stockier, with stronger stems. This is a result of wheat breeding over the past hundred years to increase the yield of wheat by reducing plant height and make the plants resistant to lodging in conditions of intensive agriculture. Wheat breeders developed plants with shorter and stiffer straws, producing semi-dwarf, high-yielding varieties that were much better adapted to intensive agriculture. Before this time the traditional varieties of wheat grown were limited in the yield they could produce as adding more fertiliser resulted in the wheat stalks growing taller and weaker making them vulnerable to breaking.

The modern semi-dwarf varieties of wheat have recently come into public attention due to the publication of popular diet books blaming these new types of wheat for a plethora of modern health problems. However, rather than these alleged health issues, I was interested to know where these semi-dwarf wheats came from and the origin of the genes responsible. In an interesting article from 2005, Katarina and Ksenija Borojevic outline the history of the genes responsible for our modern dwarf wheat, with more of a focus on Europe, rather than the better known efforts in America that resulted in the Green Revolution.

The story starts further back than you might imagine, and to Korea, where naturally occurring short stemed wheat varieties were grown as far back as the third and fourth centuries A.D. The genes responsible were natural mutations rather than a production of any human intervention. These short varieties of wheat found there way to Japan as a result of the Korean-Japanese War during the sixteenth century. Semi-dwarf wheat varieties were widely grown in Japan by the 19th Century and served to provide the dwarfing genes for all our modern wheat varieties now grown around the world.

The variety Akakomugi, a 19th Century Japanese landrace of semi-dwarf wheat, provided the dwarfing genes first transferred to Europe in the early 20th Century. The Italian wheat breeder Nazareno Strampelli was to use this Japanese wheat, crossing Akakomugi with an Italian wheat by 1913 to produce a new shorter, lodging resistant Italians wheat. By 1918 a number of new semi-dwarf wheat varieties had been developed from this initial hybridisation which soon became very well known and were grown in Italy and South America, particularly in Argentina. By 1931 Nazareno Strampelli, using further hybridisations, had produced another improved variety called San Pastore that proved to be an extraordinary success and was widely grown in Italy and many other countries for more than 35 years.

These wheat breeding initiatives were supported and encouraged by the Italian government as they coincided with a drive for Italy to be self sufficient in food. This was known, as occurred during Mussolini’s time, as the Battle for Grain. These new semi-dwarf wheat hybrids enabled Italy to double its cereal production from 1922 to 1939 and and to become more or less self-sufficient in cereal production, where previously they had been heavily reliant on foreign imports.

After World War II, the Yugoslav government was also keen to encourage national self sufficiency and imported dwarf Italian wheat varieties during the 1950’s. These were widely grown, and through hybridisation with local wheats, enabled the development of new high-yielding winter wheat that were grown on a large-scale. Average yields increased from 1.36 tons of wheat per hectare up to 5.21 tones per hectare. Neighbouring countries including Hungary, Bulgaria, Romania, the former Czechoslovakia obtained similar results.

The gene responsible for reduced height originating in the Japanese Akakomugi wheat is known as Rht8 (abbreviated for reduced height 8). The function of this gene is still not clear but has been suggested to reduce sensitivity to brassinosteroids, a class of plant hormones that promote stem elongation and cell division. The identity of this Rht8 gene was only discovered at the end of the 20th Century and has been shown to have contributed its semi-dwarf characteristics of wheat across South Central Europe and the former USSR.

Semi-dwarf wheat reached the Americas via a completely separate route and through unrelated genes. Japanese wheat breeders, continuing their work on reduced height wheat, produced a new variety in 1932 that became known as Norin 10. This was produced by crossing an old Japanese dwarf landrace wheat called Daruma with American wheat varieties. Norin 10 grew to just two feet tall, instead of the usual four.

Norin 10 was never an important variety in Japan but found its way to the USA due to the occupying US army after the Second World War. S. D. Salmon, a scientist working on wheat research with the U.S. Department of Agriculture (USDA) was serving as an advisor of the occupation army when he made a  visit to the Marioka Agriculture Research Station on Honshu in Japan. He returned to the US, with wheat samples, given by Japanese scientists during his visit, Norin 10 was among these samples.  The genes making Norin 10 a short wheat  are the Rht1 and Rht2 genes that make the wheat plant insensitive to another type of plant growth hormones called gibberellins.

In 1952, an agronomist working at Washington State University called O. A.Vogel used this Norin 10 to cross with a popular wheat variety grown in Washington at the time. The resulting variety called Gaines became the predominant wheat variety in the Pacific Northwest in the late 1960s with farmers producing record wheat yields. It was from Washington State that Norin 10 was acquired by Norman Bourlag at the International Maize and Wheat Improvement Center (CIMMYT) in Mexico where new dwarf  wheat varieties were developed and later spread around the world, resulting in the Green Revolution and earning Norman Bourlag the 1970 Nobel Peace Prize. Adding the dwarfing genes in Norin 10 to their wheat breeding enabled the development of high yielding wheat varieties that could stand high levels of added fertiliser. These varieties developed at the CIMMYT dramatically increased wheat yields around the world, first enabling Mexico to become self sufficient in wheat and later countries like India and Pakistan.

It is clear the genes responsible for dwarfism in wheat plants have a long history and a complex route has taken them from ancient Korea into modern wheat plants in Europe and the rest of the world. While the work North America and the green revolution has attracted most of the attention, in Europe at least, genes introduced in the early 20th Century have also been important in the development of of modern wheat. It is also interesting that parts of Europe have been eating semi-dwarf hybrid wheat since the 1920s. Whatever the alleged health implications of these modern wheat varieties, the genes that make make them shorter have a long history and appeared spontaneously long before the work of modern genetics and crop manipulation.



Borojevic K. and Borojevic K. (2005) The Transfer and History of “Reduced Height Genes” (Rht) in Wheat from Japan to Europe. Journal of Heredity96(4):455-459.

“Wheat is the main crop and often a strategic crop in many European countries. From a historical perspective, we describe the transfer of “reduced height genes” (Rht genes) from Japanese wheat varieties to wheat varieties in Europe and their influence on the increase of the total wheat production in the last century. Historic pathways of Rht genes were influenced directly or indirectly by wheat breeders exchanging seed samples and by some governments importing large quantities of wheat during historically critical periods for their countries.”

Borojevic K. and Borojevic K. (2005) Historic Role of the Wheat Variety Akakomugi in Southern and Central European Wheat Breeding Programs. Breeding Science. 55(3):253-256

“The old semidwarf, not very attractive, Japanese wheat variety Akakomugi was the source of the dwarfing gene Rht8 and photoperiodic insensitive gene PpD1 to many semidwarf wheat varieties in South and Central Europe in the 20th century. Integrating the Rht8 and PpD1genes in wheat varieties offered the best opportunities for reducing plant height, accelerating time of flowering, improving grain fill before the onset of dry summer conditions, enhancing spikelet fertility, and consequently increasing yields. Many breeders from South and Central Europe and from the former Soviet Union were creating winter short high yielding wheat varieties without knowing at the time that Akakomugi was the donor of such important genes. At the end of the 20th century, it was discovered that dwarfing gene Rht8 and photoperiodic insensitive gene PpD1 are located on the short arm of chromosome 2D in wheat. Microsatellite analyses proved that Akakomugi is the source for the Rht8 and PpD1 genes in many short wheat varieties in South and Central Europe.”

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Bourbon, Brandy and Armagnac: Phenolics and antioxidant capacity

In a recent post I looked into the science behind the phenolic compounds found in my favorite Scottish malt whiskies, and extracted into said water of life via the action of alcohol and water on the wood of the oak barrels they are aged within. I realise this was quite neglectful of the fact that a range of other distilled spirits undergo barrel aging to produce their unique characteristics. Thankfully science has not been so negligent on this topic and a study from 1999 in the Journal of Agricultural and Food Chemistry investigated this very subject.

spirits TAS

The graph shows the mean total antioxidant status (mmol/L) of distilled spirits analysed by Goldberg et al in their 1999 study.

This study analysed both the total antioxidant capacity and the amounts of a range of phenolic and furan compounds. This included both a single malt scotch whisky and a blended whisky, although unfortunately for comparison with my previous post they do not mention the age of this whisky. Judging from the amount of ellagic acid in the table below it could be suggested to be a 10-12 year old single malt. Of more interest here is that the study also included an American bourbon, French brandy and Armagnac. This study included a few different compounds found in barrel aged spirits. The structures of these are shown below, illustrating the complexity of compounds that develop during the aging process.

spirits TAS compounds

Structural formulas of the main compounds mentioned.

Looking at the graph above and table below a particularly interesting finding is that American bourbon exceeded the Scotch malt whisky in both its antioxidant capacity and levels of individual phenolic compounds. The authors suggest some reasons for this:

“Bourbon whiskey is made by rather different procedures. Two, in particular, are worthy of note. The distillation takes place at a quite low proof, not exceeding 160; this has the effect of allowing many congeners to pass over with the ethyl alcohol. The second is the use of charred oak barrels for aging, periods of up to 8 years not being uncommon. It appears that these two processes may account for the higher phenolic and furan contents and TAS of this whiskey compared with the previous three whiskies”

Perhaps also the use of freshly made oak barrels increases the transfer of phenolic compounds into bourbon, as compared to Scotch whisky which reuses previously used barrels. Vanillic Acid, Syringaldehyde were found in the highest amounts in bourbon. The lower levels identified in the Canadian rye whisky are mostly likely to a much shorter duration of barrel ageing.

spirits TAS table

The quantities of six polyphenols in the various spirits tested.

The striking feature of this study is the high amounts of all phenolic compounds in Armagnac, which had by far the highest concentrations of gallic acid, syringic acid, vanillin, and ellagic acid, as well as the second highest of vanillic acid, syringaldehyde, coniferaldehyde, and trimethoxyphenylacetic acid. This is possibly due to the exacting and protected methods used to produce Armagnac, of which wood aging of up to 10 years in Limousin oak for cognac and black Monlezun oak, a “black oak” from the Monlezun forest in Gascony, for armagnac, is a notable feature. Of interested, the ellagic acid found in both whiskies and Armagnac, is also proposed to be responsible for some of the health benefits of fruits such as blackberries, cranberries, pomegranates,raspberries, which are the main source of ellagic acid in the diet. However, the amounts in even Armagnac are rather low in comparison.

While the evidence from my previous post showed that long aged Scottish malt whisky, aged 25 years, had a much higher level of phenolic compounds than any in this study, the age of Scotch malt whisky at which most people drink it may not quite reach the levels of phenolics found in American bourbon, and is probably rather inferior to Armagnac. As the phenolic compounds extracted from oak wood during the aging of alcohol are common to all aged spirits, any health effects mentioned in my previous post would apply to all. However, it is worth remembering any possible health benefit is going to be redundant if consumed in large quantities.

*Any spelling mistakes in the post are due to the influence of good whisky.


Goldberg DM, Hoffman B, Yang J, Soleas GJ. (1999) Phenolic constituents, furans, and total antioxidant status of distilled spirits. Journal of Agricultural and Food Chemistry. 47(10):3978-85


“The concentrations of 11 phenols and 5 furans were measured in 12 categories of distilled spirits by HPLC methodology, together with the total antioxidant status (TAS) of the same beverages. Ellagic acid was the phenol present in highest concentration in all beverages. Moderate amounts of syringaldehyde, syringic acid, and gallic acid, as well as lesser amounts of vanillin and vanillic acid, were measurable in most samples of whiskey, brandy, and rum but were largely undetectable in gin, vodka, liqueurs, and miscellaneous spirits. 5-(Hydroxymethyl)furfural was the predominant furan in the former three beverages, notably cognac, with 2-furaldehyde the next highest, but these were undetectable in most of the latter beverages. Highest TAS values were given by armagnac, cognac, and bourbon whiskey, all three of which tended toward the highest concentrations of phenols. Negative TAS values were exhibited by rum, vodka, gin, and miscellaneous spirits in line with the low or undetectable phenol concentrations in these beverages. Wood aging is the most likely source of phenols and furans in distilled spirits. Those beverages exposed to this treatment contain significant antioxidant activity, which is between the ranges for white and red wines, with the potential to augment the antiatherosclerotic functions attributable to the ethanol that they contain.

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Oat Avenanthramides

Oats are one of the quintessential foods of the traditional Scottish diet. In terms of health benefits they are best known for their fibre content, particularly their beta-glucan content. Less well known is that this humble grain contains a unique class of more than twenty polyphenols known as avenanthramides, not found in any other foods. In recent years evidence has been emerging that these avenanthramides potentially have a wide range of beneficial effects on our health.




Structure of avenanthramides

As well as being a staple food in Scotland and other regions of northern Europe, oats also have a long history in medicine. They have been used to treat various conditions such insomnia, anxietyand skin conditions, including eczema, and burns in various forms such as food, tea, or in baths. The use of wild oats (Avena sativa) has apparently been recorded for use in skin care as far back as 2000 BCE in Egypt and the Arabian peninsula and various skin conditions were often treated with oatmeal baths in the 19th and early 20th centuries. In 1989 the FDA recognised colloidal oatmeal as a safe and effective over the counter skin protectant drug and later in 2003 it was approved as an ingredient to be used as a skin protectant, one of the few botanical ingredients considered an effective skin protectant (Kurtz and Wallo 2007).

Until comparatively recently little thought had been given to the compounds in oats responsible for these anti-inflammatory activities of oats until the discoverly of avenanthramides in the late 1980’s (Collins 1989). These avenanthramides are a unique, group of soluble phenolic compounds which are not present in other cereal grains. These compounds are antipathogens (phytoalexins), meaning they are produced by the plant in to defend against plant pathogens such as fungi. While more than 20 different forms of avenanthramides are present in oats, three of these known as A, B, and C, make up the majority (Meydani 2009). These avenanthramides are now considered to form the active ingredients in oats responsible for their beneficial effects when applied to the skin.

Beyond the skin evidence is also emerging that these avenanthramides can have a range of beneficial effects within the body (Meydani 2009) . They have potent antioxidant properties potentially preventing the oxidation of cholesterol transporting low-density lipoproteins, at least in the lab (Chen 2004). Their anti-inflammatory effects may be able to help reduce inflammation in the cells lining our arteries (Liu 2004). Another interesting biological effect of avenanthramides is on nitric oxide (NO)-dependent vasodilation, a process that relaxes blood vessels leading to better circulation and reduced blood pressure (Nie 2006). Avenanthramides in very low concentrations have been shown to reduce inflammatory responses in skin cells and so mediate the anti-itch properties of oats when used on the skin, indicating that very little avenanthramides may be required to produce an effect (Sur 2008). Avenanthramides have been shown to be bioavailable in humans, being absorbed into the circulation, and to increase the antioxidant capacity of the blood in healthy older adults when fed enriched enriched oat products (Chen 2007). Even avenanthramides that are not absorbed could have an beneficial effects in our gut, given their anti-inflammatory effects when applied to the skin, this is speculative though.

Little information is currently available on the concentration of these avenanthramides present the oats used for our food, or the various oat products produced from them. One study that investigated the effects of processing on oats found that the avenanthramides content was much reduced in rolled oats, due to the effects of drum drying (Bryngelsson 2002). Rolled oats are steamed before being rolled flat, and require drying afterwards to remove the moisture added during the steaming process. The same study found that similar treatments to oatmeal, oats that had been heated and then then ground, had little on the avenanthramide content (Bryngelsson 2002). An earlier study found that the avenanthramides in products with added oatmeal such as bread, fresh pasta, muffins, and macaroni, survived well into the final products and end had an increase in free avenanthramides (Dimberg 2001). The amounts of avenanthramides can vary between different varieties of oats and survive storage and heating quite well (Dimberg 1996). A new method has even been proposed, using a process of “false malting” wherein selected or pre-treated grain is conventionally malted but does not germinate, that can dramatically increase the avenanthramide content of oats (Collins 2010). This suggests that the avenanthramides in the oats do survive into the food we eat, although there are still many unknowns about all the effects of oat varieties and processing techniques.

While little research has been carried out on the influence of avenanthramides in the amounts found in the oats we eat, they are an interesting group of compounds that potentially provide some extra benefits to eating oats and contribute to the healthfulness of oats as a part of the diet.

Bryngelsson, S. et al. (2002) Effects of commercial processing on levels of antioxidants in oats (Avena sativa L.). Journal of Agricultural and Food Chemistry50:18901896.
“The effects of various commercial hydrothermal processes (steaming, autoclaving, and drum drying) on levels of selected oat antioxidants were investigated. Steaming and flaking of dehulled oat groats resulted in moderate losses of tocotrienols, caffeic acid, and the avenanthramide Bp (N-(4′-hydroxy)-(E)-cinnamoyl-5-hydroxy-anthranilic acid), while ferulic acid and vanillin increased. The tocopherols and the avenanthramides Bc (N-(3′,4′-dihydroxy-(E)-cinnamoyl-5-hydroxy-anthranilic acid) and Bf (N-(4′-hydroxy-3′-methoxy)-(E)-cinnamoyl-5-hydroxy-anthranilic acid) were not affected by steaming. Autoclaving of grains (including the hulls) caused increased levels of all tocopherols and tocotrienols analyzed except beta-tocotrienol, which was not affected. Vanillin and ferulic and p-coumaric acids also increased, whereas the avenanthramides decreased, and caffeic acid was almost completely eliminated. Drum drying of steamed rolled oats resulted in an almost complete loss of tocopherols and tocotrienols, as well as a large decrease in total cinnamic acids and avenanthramides. The same process applied to wholemeal made from groats from autoclaved grains resulted in less pronounced losses, especially for the avenanthramides which were not significantly affected.
Chen, CY. et al. (2004) Avenanthramides and phenolic acids from oats are bioavailable and act synergistically with vitamin C to enhance hamster and human LDL resistance to oxidationJournal of Nutrition. 134(6):1459-66
“The intake of phenolic acids and related polyphenolic compounds has been inversely associated with the risk of heart disease, but limited information is available about their bioavailability or mechanisms of action. Polyphenolics, principally avenanthramides, and simple phenolic acids in oat bran phenol-rich powder were dissolved in HCl:H(2)O:methanol (1:19:80) and characterized by HPLC with electrochemical detection. The bioavailability of these oat phenolics was examined in BioF1B hamsters. Hamsters were gavaged with saline containing 0.25 g oat bran phenol-rich powder (40 micromol phenolics), and blood was collected between 20 and 120 min. Peak plasma concentrations of avenanthramides A and B, p-coumaric, p-hydroxybenzoic, vanillic, ferulic, sinapic, and syringic acids appeared at 40 min. Although absorbed oat phenolics did not enhance ex vivo resistance of LDL to Cu(2+)-induced oxidation, in vitro addition of ascorbic acid synergistically extended the lag time of the 60-min sample from 137 to 216 min (P < or = 0.05), unmasking the bioactivity of the oat phenolics from the oral dose. The antioxidant capability of oat phenolics to protect human LDL against oxidation induced by 10 micromol/L Cu(2+) was also determined in vitro. Oat phenolics from 0.52 to 1.95 micromol/L increased the lag time to LDL oxidation in a dose-dependent manner (P < or = 0.0001). Combining the oat phenolics with 5 micromol/L ascorbic acid extended the lag time in a synergistic fashion (P < or = 0.005). Thus, oat phenolics, including avenanthramides, are bioavailable in hamsters and interact synergistically with vitamin C to protect LDL during oxidation.
Chen, CY. et al. (2007) Avenanthramides Are Bioavailable and Have Antioxidant Activity in Humans after Acute Consumption of an Enriched Mixture from Oats . The Journal of Nutrition137(6): 1375-1382
“The consumption of polyphenols is associated with a decreased risk of cardiovascular disease. Avenanthramides (AV), alkaloids occurring only in oats, may have anti-atherosclerotic activity, but there is no information concerning their bioavailability and bioactivity in humans. We characterized the pharmacokinetics and antioxidant action of avenanthramide A, B, and C in healthy older adults in a randomized, placebo-controlled, 3-way crossover trial with 1-wk washout periods. Six free-living subjects (3 mol/L, 3 F; 60.8 ± 3.6 y) consumed 360 mL skim milk alone (placebo) or containing 0.5 or 1 g avenanthramide-enriched mixture (AEM) extracted from oats. Plasma samples were collected over a 10-h period. Concentrations of AV-A, AV-B, and AV-C in the AEM were 154, 109, and 111 μmol/g, respectively. Maximum plasma concentrations of AV (free + conjugated) after consumption of 0.5 and 1 g AEM were 112.9 and 374.6 nmol/L for AV-A, 13.2 and 96.0 nmol/L for AV-B, and 41.4 and 89.0 nmol/L for AV-C, respectively. Times to reach the Cmax for both doses were 2.30, 1.75, and 2.15 h for AV-A, AV-B, and AV-C and half times for elimination were 1.75, 3.75, and 3.00 h, respectively. The elimination kinetics of plasma AV appeared to follow first-order kinetics. The bioavailability of AV-A was 4-fold larger than that of AV-B at the 0.5 g AEM dose. After consumption of 1 g AEM, plasma reduced glutathione was elevated by 21% at 15 min (P ≤ 0.005) and by 14% at 10 h (P ≤ 0.05). Thus, oat AV are bioavailable and increase antioxidant capacity in healthy older adults.”
Collins F. (1989) Oat phenolics: avenanthramides, novel substituted N-cinnamoylanthranilate alkaloids from oat groats and hulls. Journal of Agriculture and Food Chemistry37(1),:60–66
“Fractionation of methanolic extracts of oat groats and hulls by anion-exchange chromatography revealed the presence of a series of anionic, substituted cinnamic acid conjugates, trivially named avenanthramides. Two-dimensional thin-layer chromatography (TLC) showed groat extracts contain more than 25 distinct avenanthramides, while hull extracts contained about 20. Some 15 were common to both groat and hull preparations. The substances were purified by repeated column chromatography on Sephadex LH-20, using TLC to monitor purity, and crystallized from aqueous acetone. The complete structures of 10 avenanthramides have been elucidated using ‘H and 13C nuclear magnetic resonance (NMR), mass spectroscopy (MS), ultraviolet absorption spectroscopy (UV), and hydrolytic techniques and confirmed by total synthesis. The physicochemical properties, potential biological activity, and distribution within the oat grain are discussed.”
Collins, FW. (2010) Avenanthramides in oats: A new method of producing whole oats and oat ingredients with greatly elevated avenanthramide levels. Online. AACC International Cereal Science Knowledge Database.
“Avenanthramides, of which over 35 distinct components have been found to date, represent the major readily-bioavailable, soluble phenolics present in the oat kernel These hydroxycinnamoyl alkaloids are found only in oats and have been shown to not only act as antioxidants but also to inhibit the pro-inflammatory processes associated with atherosclerotic disease progression. Based on recent in vivo pharmacokinetic results in humans and in vitro human vascular cell culture models, effective concentrations of avenanthramides required to influence vascular antioxidant status and the inflammatory response can be provisionally projected. Threshold response levels (approximately 30 to 60 mg from a dietary source delivery system such as a 50 g serving of oat bran) would require an oat product with at least 600 to 1,200 ppm total avenanthramides. This is a significantly higher concentration range than those currently recorded for existing oat varieties or existing whole grain oat products. Recently a process has been found that significantly increases the levels of avenanthramides in native oat kernels. Levels ranging from about 900 to 2,000 ppm in the whole groat, representing an enrichment factor of about 25- to 40-fold have been achieved by this process, without significantly altering the milling quality of the product. The process involves the concept of “false malting” wherein selected or pre-treated grain is conventionally malted but does not germinate. The selected oats refer to “dormant oat” varieties, i.e. varieties exhibiting secondary dormancy and preferably hulless, while non-dormant varieties can be made dormant using a simple dry heat process. In-depth HPLC analyses of avenanthramides from oats treated by this patent-pending process show little if any qualitative differences relative to untreated oats. Abrasion bran fractions show levels as high as 3,500 ppm total avenanthramides.”
Dimberg, LH. et al. (1996) Variation in Oat Groats Due to Variety, Storage and Heat Treatment. I: Phenolic Compounds. Journal of Cereal Science. 24(3):263–272.
“Low molecular weight phenolic compounds present in heat processed oats (Avena sativaL) were analysed. The oat grains were of three varieties (Kapp, Mustang and Svea), stored at different relative humidities (30, 55 or 80%) and periods (3·5 or 15·5 months) and processed with or without hulls. Eleven UV-absorbing compounds detected by High Performance Liquid Chromatography were subjected to univariate and multivariate statistical analysis. The selected compounds included caffeic acid,p-coumaric acid, ferulic acid, vanillic acid,p-hydroxybenzaldehyde, vanillin, coniferyl alcohol, three avenanthramides and one unidentified substance. The levels of vanillic acid, vanillin and, especially,p-coumaric acid,p-hydroxybenzaldehyde and coniferyl alcohol increased significantly in samples processed with hulls, but not in samples processed without hulls. Ferulic acid increased in both processes, while caffeic acid and the avenanthramides were found to decrease during processing. Storage of unprocessed samples for 1 year generally increased the levels of phenolic acids and aldehydes. For the phenolic acids (except ferulic acid), this increase was most pronounced after storage at high relative humidity (80%). The avenanthramides were present at their highest levels in Mustang, caffeic acid in Svea and Mustang, the unidentified compound in Svea, while all the other compounds studied were present predominantly in the variety Kapp.”
Dimberg, LH. et al. (2001) Stability of Oat Avenanthramides. Cereal Chemistry. 78(3): 278-281
“The three main oat avenanthramides, N-(4′-hydroxy)-(E)-cinnamoyl-5-hydroxyanthranilic acid (Bp), N-(4′-hydroxy-3′-methoxy)-(E)-cinnamoyl-5-hydroxyanthranilic acid (Bf), and N-(3′,4′-dihydroxy)-(E)-cinnamoyl-5-hydroxyanthranilic acid (Bc), and their corresponding cinnamic acids, p-coumaric (P), ferulic (F), and caffeic (C), were investigated for stability to pH, temperature, and UV-light treatment. The retention of the avenanthramides after processing of oat-based food products was also analyzed. The avenanthramide Bc and the cinnamic acid Cwere sensitive to alkali and neutral conditions, especially in combination with heat treatment, whereas the other compounds studied were more stable. The cinnamic acids but not the avenanthramides were isomerized when irradiated with UV-light. The avenanthramides were restored after processing of oat-based products.”
Kurtz ES and Wallo W. (2007) Colloidal oatmeal: history, chemistry and clinical properties. Journal of Durgs in Dermatology. 6(2):167-70.
“Oatmeal has been used for centuries as a soothing agent to relieve itch and irritation associated with various xerotic dermatoses. In 1945, a ready to use colloidal oatmeal, produced by finely grinding the oat and boiling it to extract the colloidal material, became available. Today, colloidal oatmeal is available in various dosage forms from powders for the bath to shampoos, shaving gels, and moisturizing creams. Currently, the use of colloidal oatmeal as a skin protectant is regulated by the U.S. Food and Drug Administration (FDA) according to the Over-The-Counter Final Monograph for Skin Protectant Drug Products issued in June 2003. Its preparation is also standardized by the United States Pharmacopeia. The many clinical properties of colloidal oatmeal derive from its chemical polymorphism. The high concentration in starches and beta-glucan is responsible for the protective and water-holding functions of oat. The presence of different types of phenols confers antioxidant and anti-inflammatory activity. Some of the oat phenols are also strong ultraviolet absorbers. The cleansing activity of oat is mostly due to saponins. Its many functional properties make colloidal oatmeal a cleanser, moisturizer, buffer, as well as a soothing and protective anti-inflammatory agent.”
Meydani M. (2009) Potential health benefits of avenanthramides of oats. Nutrition Reviews. 67(12):731-5
“Oats are known to be a healthy food for the heart due mainly to their high β-glucan content. In addition, they contain more than 20 unique polyphenols, avenanthramides, which have shown strong antioxidant activity in vitro and in vivo. The polyphenols of oats have also recently been shown to exhibit anti-inflammatory, antiproliferative, and anti-itching activity, which may provide additional protection against coronary heart disease, colon cancer, and skin irritation.
Nie L. et al (2006) Avenanthramide, a polyphenol from oats, inhibits vascular smooth muscle cell proliferation and enhances nitric oxide production. Atherosclerosis186:260266.
“The proliferation of vascular smooth muscle cells (SMC) and impaired nitric oxide (NO) production are both crucial pathophysiological processes in the initiation and development of atherosclerosis. Epidemiological data have indicated that diets rich in whole grain foods are associated with a reduced risk of developing atherosclerosis. Avenanthramides are polyphenols found exclusively in oats (Avena sativa L.). The present study was conducted to examine the effect of synthetically prepared avenanthramide-2c on the proliferation of SMC and NO production by SMC and human aortic endothelial cells (HAEC). Avenanthramide-2c significantly inhibited serum-induced SMC proliferation. At a concentration of 120 microM, avenanthramide-2c inhibited more than 50% of SMC proliferation, as measured by [3H] thymidine incorporation, and increased the doubling time of rat SMC line (A10) from 28 to 48 h. Treatment of human SMC with 40, 80, and 120 microM avenanthramide-2cinhibited cell number increase by 41, 62, and 73%, respectively. In addition, avenanthramide-2c treatment significantly and dose-dependently increased NO production in both SMC and HAEC. At a concentration of 120 microM, avenanthramide-2c increased NO production by three-fold in SMC, and by nine-fold in HAEC. These increases were in parallel with the up-regulation of mRNA expression for endothelial NO synthase (eNOS) in both vascular SMC and HAEC. These results suggest that the avenanthramides of oats may contribute to the prevention of atherosclerosis through inhibition of SMC proliferation and increasing NO production.
Sur R. et al. (2008) Avenanthramides, polyphenols from oats, exhibit anti-inflammatory and anti-itch activity. Archives of Dermatological Research300:569574
“Oatmeal has been used for centuries as a soothing agent to relieve itch and irritation associated with various xerotic dermatoses; however few studies have sought to identify the active phytochemical(s) in oat that mediate this anti-inflammatory activity. Avenanthramides are phenolic compounds present in oats at approximately 300 parts per million (ppm) and have been reported to exhibit anti-oxidant activity in various cell-types. In the current study we investigated whether these compounds exert anti-inflammatory activity in the skin. We found that avenanthramides at concentrations as low as 1 parts per billion inhibited the degradation of inhibitor of nuclear factor kappa B-alpha (IkappaB-alpha) in keratinocytes which correlated with decreased phosphorylation of p65 subunit of nuclear factor kappa B (NF-kappaB). Furthermore, cells treated with avenanthramides showed a significant inhibition of tumor necrosis factor-alpha (TNF-alpha) induced NF-kappaB luciferase activity and subsequent reduction of interleukin-8 (IL-8) release. Additionally, topical application of 1-3 ppm avenanthramides mitigated inflammation in murine models of contact hypersensitivity and neurogenic inflammation and reduced pruritogen-induced scratching in a murine itch model. Taken together these results demonstrate that avenanthramides are potent anti-inflammatory agents that appear to mediate the anti-irritant effects of oats.
Liu L. et al. (2004) The antiatherogenic potential of oat phenolic compoundsAtherosclerosis. 175(1):39-49
“Avenanthramides are phenolic antioxidants, which are present in oats. Avenanthramides A, B, and C are the major constituents of the total soluble antioxidant phenolic compounds in oats. We tested the potential antiatherogenic activity of partially purified avenanthramides from oats by examining their effects on adhesion of monocytes to human aortic endothelial cell (HAEC) monolayers, expression of adhesion molecules, and production of proinflammatory cytokines and chemokines by HAEC. The oat avenanthramides mixture was prepared and partially purified by column chromatography. This avenanthramide-enriched mixture (AEM) had no toxicity to HAEC as tested up to 40 ng/ml. The pre-incubation of HAEC with 4, 20, and 40ng/ml AEM for 24h significantly decreased adhesion of U937 monocytic cells to interleukin (IL)-1beta-stimulated HAEC in a concentration-dependent manner. Pre-incubation of HAEC with AEM at 20 and 40 microg/ml, but not at 4 microg/ml, for 24h significantly suppressed IL-1beta-stimulated expressions of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin and the secretion of proinflammatory cytokines IL-6, chemokines IL-8 and monocyte chemoattractant protein (MCP)-1. These data provide evidence for the potential anti-inflammatory and antiatherogenic effects of antioxidant avenanthramides present in oats.
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Whisky polyphenols and their potential health effects


Scapa, one of my current Scottish whiskies

Scottish malt whisky, unlike other beverages such as red wine, tea or coffee, has received little attention with regards to its phenolic plant phytochemicals.

In the production of malt whisky the pure distilled spirit is aged in oak barrels for a number of years. During this aging constituents that make up the wood gradually dissolve into the spirit determining its flavour, colour and taste (Tanaka 2010). The wood of American white oak used to make many of the barrels used to age whisky contains significant amounts of an oak wood polyphenols called ellagitannins. The processing stages of making barrel for whisky production, including seasoning and toasting, results in various chemical changes in the ellagitannins of the wood resulting in the phenolic compounds in the whisky being rather different than the original oak wood polyphenols (Cadahia 2001). The original tannins decompose during toasting or charring of the barrels and then during the aging process oxygen molecules are absorbed through the wood further oxidising the dissolved phenolic compounds. The polyphenols in whisky are a mixture of products resulting from a complex chemical process (Tanaka 2010). These non-volatile components of whisky are known are whisky congeners, they are not found in the freshly distilled spirit but rather are a result of the long aging of good whisky. A range of these phenolic compounds were isolated from commercially bottled Japanese whisky including carboxyl ellagic acid, gallic acid, ellagic acid, brevifolin carboxylic acid, among others (Fujieda 2008). In another study ellagic acid, gallic acid, and lyoniresinol were found to be the principle polyphenols in a range of whiskies of both Japanese and Scottish origin. However, these three compounds only made up 20% of the antioxidant capacity of the whisky tested, suggesting there are a range of other polyphenols involved (Koga 2007).

Whisky graph 3

Levels of gallic acid, ellagic acid, and lyoniresinol in whisky of different ages (Fujieda 2008).

Unlike other popular beverages whisky has been rather lacking in study regarding the potential effects of these plant phytochemicals when ingested by humans. One of the few studies on the subject, carried out at my own Rowett Institute, examined the concentration of phenolic compounds and antioxidant capacity of volunteers blood after drinking 100 millilitres, (3.5 ounces) of either red wine, a 12 y old malt whisky which had been matured in oak wood casks, or a `new make’ whisky which is the newly-distilled whisky spirit prior to maturation. Surely one of the more arduous nutrition studies ever carried out (Duthie et al. 1998).

whisky graph 1

Concentration of total phenols in volunteers blood after drinking whisky or red wine (Duthie 1998).

Both the whisky and red wine produced a similar rise in total phenols in the blood of volunteers, suggesting the phenolic compounds in whisky are rapidly absorbed after drinking. The ‘new make’ whisky did not cause any rise in blood phenols. Although the levels in the blood were similar between red wine and whisky, in fact proportionately more of the phenolic compounds were absorbed from the whisky than the wine. This may be due to the higher alcohol content enhancing their absorption, and different bioavailability of the compounds in wine and whisky. New made whisky did not result in any increase in phenols in the volunteers’ blood (Duthie et al. 1998).

Whisky graph 2

Antioxidant capacity of volunteers blood after drinking whisky or red wine (Duthie 1998).

Drinking whisky or red wine increase the antioxidant capacity of the volunteers’ blood to a similar degree. Unexpectedly the ‘new make’ whisky caused a decrease in antioxidant capacity of the blood, possibly due to increased oxidative stress caused by the alcohol itself, or as suggested by the authors, the greater content of copper in the ‘new make’ whisky. This suggested that the phenolic compounds in whisky are absorbed and can influence the antioxidant capacity of the blood in a similar way to red wine, and that the aging process of whisky in oak barrels in key to these effects.

The phenolic compounds in whisky appear to be absorbed into the blood and a few small studies from Japan now hint at what effects these compounds may have in the body. Single malt whisky showed the ability to neutralise free radicals and there was a positive correlation between this activity and the how long the whisky had been aged (Koga 2007).  This antioxidant ability of whisky has been found to protect E. coli bacteria from oxidative damage caused by hydrogen peroxide, compared to the same amount of pure alcohol (Aoshima 2004). The specific compounds isolated from whisky have been shown to have a range of interesting effects. Isolated whisky phenolic compounds including ellagic acids suppressed allergic reactions to allergens in both isolated cells and in mice. These findings suggest that the phenolic compounds from whisky seemed to be beneficial to ameliorate allergic reactions (Itoh 2010). The isolated phenolic compounds from whisky were found to reduce the inflammation in isolated immune cells and in mice. These whisky phenolic compounds may be beneficial for the treatment of inflammatory disease (Itoh 2012). Ellagic acid prevented alcohol induced development of fatty liver in mice, although these were higher doses than found in whisky. These results provide a molecular basis for the prevention of alcohol-induced stress by the polyphenols in alcoholic beverages (Yao 2014). In human epithelial cells, the cells that line the blood vessels of the body, the activity of the enzyme heme oxygenase-1 was increased by the phenolic compounds isolated from whisky.  This effect only emerged in whisky aged in oak barrels. This heme oxygenase-1 enzyme is thought to protect the lining of the blood vessels from damage. Various epidemiological reports suggest a moderate consumption of alcoholic beverages appears to reduce some health risks in relation to human health. The, up-regulation of this enzyme in the cells lining the blood vessels by whisky might possibly contribute to the maintenance of blood vessel function (Suzuki 2010). These effects are interesting but should however be taken with some caution as the relevance of the potential effects, in the concentrations found in whisky, are unknown to human health.

The phenolic compound ellagic acid may have a direct effect in the gut ameliorating some of the harmful effects of alcohol on the lining of the gut. It has been shown that whisky is less irritating to the delicate lining of the gut, as compared with pure ethanol. This effect of whisky may be explained by ellagic acid, one of major polyphenols contained in whisky, and its radical scavenging action (Iino 2001). A later study confirmed that ellagic acid is able to directly protect the lining of the gut from damage and explains the less damaging effect of whisky on the stomach than pure alcohol (Iino 2002).  This is hardly to suggest that whisky is good for the gut, but at least its potential negative effects are mitigated by its polyphenols compared to pure alcohol.

The effect of whisky of uric acid levels in the blood has also been investigated. Alcohol generally increases the level of uric acid in the blood, both by increasing the production of uric acid in the liver and reducing how much is excreted in urine. This a concern for people with high blood uric acid levels who are at risk of gout, for which alcohol consumption is an important risk factor. However, unlike other alcoholic drinks, it has been found that whisky tended to lower the levels of uric acid in the blood (Nishioka 2002). This tendency was suggested to be partly due to the inhibition of xanthine oxidase, the enzyme that produces uric acid. The longer the whisky had been aged in oak casks the greater effect it had on reducing the activity of the xanthine oxidase enzyme. It was also found that whisky stimulated an increase in the amount of uric acid excreted in the urine by 27%. This improved excretion of uric acid seemed to be mainly responsible for the reduced uric acid after drinking whisky and showed that at a moderate level of drinking, whisky have different effects on uric acid than other types of alcohol (Nishioka 2002). More recently it has been suggested that the decreased serum urate level after whisky consumption may be mainly due to inhibition the uric acid transporters in the kidneys by the phenolic congeners in whisky. This would result in more uric acid being lost into the urine (Lu 2014). While this may make whisky a better choice than other drinks to those with  high blood uric acid levels or gout who wish to drink alcohol, caution should be applied, as the research on this subject is rather limited.

While these phenolic compounds may be appearing rather good now, there is a possible downside to their presence in whisky. Some older research (Damrau 1960), suggests that the same whisky congeners absorbed from the oat barrels can slow the metabolism of alcohol. This could explain the increased hangover symptoms reported by volunteers in the study, at least in comparison to vodka.

It is clear that aged malt whisky does contain phenolic compounds, originating from the oak wood barrels, and shaped by the long maturing of the whisky. These compounds, such as ellagic acid, do have the potential to beneficially affect the health of those imbibing of these spirits, above that pure alcohol would have on its own. These various phenols can potentially have a range of effects on our physiology, although it is still unclear how relevant these may be to our health. To quote one of the papers on this topic,

“We do not recommend drinking whiskey or wine as a method of antioxidant intake, since other beverages such as green tea and oolong tea also include many antioxidants such as catechin derivatives. However, you can think of the antioxidative activity of whiskey or wine if you often drink liquors. More epidemiological studies are also necessary to clarify whether the antioxidants in liquors are related favourably to human mortality.” – (Aoshima 2004)

It does maybe provide an excuse for the purchase of an older, longer matured, fine malt whisky. Perhaps be cautious with drinking to excess, as those very same compounds may increasing any resulting hangover.


Conflicts of interest: I do rather like good whisky.

Aoshima, H., Tsunoue, H., Koda, H. & Kiso, Y. 2004, “Aging of whiskey increases 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity“, Journal of Agricultural and Food Chemistry, vol. 52, no. 16, pp. 5240-5244.
“1,1-Diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity of Japanese whiskey after various aging periods in oak barrels was measured to evaluate the antioxidative effects of whiskey. The activity of the whiskey increased with the aging period with high correlation. The activity of various types of whiskey was measured and shown to be correlated to the potentiation of the GABAA receptor response measured in a previous paper. However, the fragrant compounds in the whiskey which potentiated the GABAA receptor response had low DPPH radical scavenging activity, while phenol derivatives had high radical scavenging activity. The whiskey was extracted by pentane. The aqueous part showed the scavenging activity, whereas the pentane part did not. Thus, both the DPPH radical scavenging activity and the potentiation of the GABAA receptor response increased during whiskey aging in oak barrels, but were due to different components. The whiskey protected the H2O2-induced death of E. coli more than ethanol at the same concentration as that of the whiskey. The changes that occurred in the whiskey during aging may be the reason aged whiskies are so highly valued.
Cadahia, E., Varea, S., Munoz, L., de Simon, B. & Garcia-Vallejo, M. 2001, “Evolution of ellagitannins in Spanish, French, and American oak woods during natural seasoning and toasting“, Journal of Agricultural and Food Chemistry, vol. 49, no. 8, pp. 3677-3684.
“The evolution of tannins in Spanish oak heartwood of Quercus robur L., Quercus petraea Liebl.,Quercus pyrenaica Wild., and Quercus faginea Lam. was studied in relation to the processing of wood in barrel cooperage. Their evolution was compared with that of French oak of Q. robur (Limousin, France) and Q. petraea (Allier, France) and American oak of Quercus alba L. (Missouri), which are habitually used in cooperage. Two stages of process were researched: the seasoning of woods during 3 years in natural conditions and toasting. Total phenol and total ellagitannin contents and optical density at 420 nm of wood extracts were determined. The ellagitannins roburins A-E, grandinin, vescalagin, and castalagin were identified and quantified by HPLC, and the molecular weight distribution of ellagitannins was calculated by GPC. During the seasoning process the different ellagitannin concentrations decreased according to the duration of this process and in the same way as those in French and American woods. The toasting process also had an important influence on the ellagitannin composition of wood. Roburins A-E, grandinin, vescalagin, and castalagin decreased during this process in the Spanish wood species, in the same proportion as in the French and American ones. Also, the seasoning and toasting processes lead to qualitative variations in the structure of ellagitannins, especially in the molecular weight distribution, as was evidenced by GPC analysis of their acetylated derivatives.”
Damrau, F.,Liddy, E. 1960, “Hangovers and Whisky Congeners: Comparison of Whisky with Vodka“, Journal of the National Medical Association, vol. 52, no. 4, pp. 262–265.
“IN a field survey’ of moderate social drinkers, many of the persons interviewed reported less hangover with vodka as compared with the same amount of whisky. Further studies established an important role of the whisky congeners in causing hangover.2 Investigation of the toxicology of whisky congeners2 demonstrated that, even in as small amount as 2 ounces of whisky, the congeners increase and prolong the action of alcohol and often produce definite after-effects lasting into the following day. These after-effects were absent or minimal when the same amount of alcohol was consumed in the form of vodka.* The present report deals with mild hangovers occurring in unaccustomed or social drinkers. In this study the term “hangover” is used according to its general definition :3 namely, “headache, nausea, etc. occurring as an after-effect of drinking much alcoholic liquor.” More specifically, we have concentrated our attention on the after-effects of small quantities of whisky and vodka, respectively, so as to eliminate the overshadowing effects of large excesses of alcohol. In this way we have been able to demonstrate a definite difference between whisky and vodka with reference to the occurrence of mild hangovers in unaccustomed and social drinkers. The results can be attributed to the great difference in their congeneric content as shown in Table 1.”
Duthie, G., Pedersen, M., Gardner, P., Morrice, P., Jenkinson, A., McPhail, D. & Steele, G. 1998, “The effect of whisky and wine consumption on total phenol content and antioxidant capacity of plasma from healthy volunteers“, European Journal of Clinical Nutrition, vol. 52, no. 10, pp. 733-736.
“OBJECTIVE: To assess whether consumption of 100 ml of whisky or red wine by healthy male subjects increased plasma total phenol content and antioxidant capacity.
DESIGN: A Latin square arrangement to eliminate ordering effects whereby, after an overnight fast, nine volunteers consumed 100 ml of red wine, malt whisky or unmatured ‘new make’ spirit. Each volunteer participated on three occasions one week apart, consuming one of the beverages each time. Blood samples were obtained from the anticubital vein at intervals up to 4h after consumption of the beverages when a urine sample was also obtained.
RESULTS: Within 30 min of consumption of the wine and whisky, there was a similar and significant increase in plasma total phenol content and antioxidant capacity as determined by the ferric reducing capacity of plasma (FRAP). No changes were observed following consumption of ‘new make’ spirit.
CONCLUSIONS: Consumption of phenolic-containing alcoholic beverages transiently raises total phenol concentration and enhances the antioxidant capacity of plasma. This is compatible with suggestions that moderate alcohol usage and increased antioxidant intake decrease the risk of coronary heart disease.”
Fujieda, M., Tanaka, T., Suwa, Y., Koshimizu, S. & Kouno, I. 2008, “Isolation and structure of whiskey polyphenols produced by oxidation of oak wood ellagitannins“, Journal of Agricultural and Food Chemistry, vol. 56, no. 16, pp. 7305-7310.
“Three new phenolic compounds named whiskey tannins A and B and carboxyl ellagic acid were isolated from commercial Japanese whiskey, along with gallic acid, ellagic acid, brevifolin carboxylic acid, three galloyl glucoses, a galloyl ester of phenolic glucoside, 2,3-(S)-hexahydroxydiphenoylglucose, and castacrenin B. Whiskey tannins A and B were oxidation products of a major oak wood ellagitannin, castalagin, in which the pyrogallol ring at the glucose C-1 position of castalagin was oxidized to a cyclopentenone moiety. These tannins originated from ellagitannins contained in the oak wood used for barrel production; however, the original oak wood ellagitannins were not detected in the whiskey. To examine whether the whiskey tannins were produced during the charring process of barrel production, pyrolysis products of castalagin were investigated. Dehydrocastalagin and a new phenolcarboxylic acid trislactone having an isocoumarin structure were isolated, along with castacrenin F and ellagic acid. However, whiskey tannins were not detected in the products.”
Iino, T., Nakahara, K., Miki, W., Kiso, Y., Ogawa, Y., Kato, S. & Takeuchi, K. 2001, “Less damaging effect of whisky in rat stomachs in comparison with pure ethanol – Role of ellagic acid, the nonalcoholic component“, Digestion, vol. 64, no. 4, pp. 214-221.
“BACKGROUND/AIM: Ellagic acid (EA), one of the polyphenols that are abundantly contained in whisky as a nonalcoholic component, has antioxidant and anti-inflammatory activities. In the present study, we compared the action of whisky and pure ethanol on the rat gastric mucosa, and examined the role of EA in the less-damaging effect of whisky in the stomach.
METHODS: Under urethane anesthesia, a rat stomach was mounted in an ex vivo chamber, perfused with saline, and the transmucosal potential difference (PD) was measured before and after exposure to whisky (Yamazaki, Suntory) and ethanol (43%). In a separate study, the animals were given whisky or ethanol (1 ml, 43%) p.o. under unanesthetized conditions, killed 1 h later, and the gastric mucosa was examined for hemorrhagic lesions.
RESULTS: Both whisky and ethanol caused a PD reduction, resulting in damage in the stomach, but these responses were less marked in the case of whisky. Although the reduced PD recovered gradually after removal of ethanol, this process was significantly expedited by co-application of EA (80 microg/ml), the recovery rate being much the same as that observed after exposure to whisky. The less-damaging effect of whisky was confirmed in unanesthetized rats after p.o. administration of these agents. In addition, EA (1-30 mg/kg), administered p.o. together with absolute ethanol (99.9%), reduced the severity of gastric lesions induced by ethanol, in a dose-dependent manner, and the effect at 30 mg/kg was equivalent to that obtained by the whisky component containing several low- and high-molecular-weight polyphenols. EA had a scavenging action against both oxygen and hydroxyl radicals in vitro, the effect being equivalent to that of catechol or alpha-tocopherol.
CONCLUSION: These results suggest that whisky is less irritating to the gastric mucosa, as compared with pure ethanol, and this property of whisky may be explained by EA, one of polyphenols contained in whisky, and its radical scavenging action.
Iino, T., Tashima, K., Umeda, M., Ogawa, Y., Takeeda, M., Takata, K. & Takeuchi, K. 2002, “Effect of ellagic acid on gastric damage induced in ischemic rat stomachs following ammonia or reperfusion“, Life Sciences, vol. 70, no. 10, pp. 1139-1150.
“We examined the effect of ellagic acid (EA), one of the polyphenols that are abundantly contained in whisky as a nonalcoholic component, on gastric lesions induced by ammonia plus ischemia or ischemia/reperfusion in rats, in relation to the antioxidative system. Under urethane anesthesia, a rat stomach was mounted in an ex vivo chamber, and the following two experiments were performed; 1) a stomach was made ischemic (1.5 ml/100 g body weight) for 20 min, followed by reperfusion for 15 min in the presence of 100 mM HCl; 2) a stomach was made ischemic by bleeding from the carotid artery (1 ml/100 g body weight), followed by intragastric application of ammonia (NH4OH: 120 mM). EA (0.1-10 mg/ml) was applied in the chamber 30 min before the onset of ischemia. Gastric potential difference (PD) and mucosal blood flow (GMBF) were measured before, during and after 20 min of ischemia. Ischemia/reperfusion caused a profound drop in GMBF followed by a return, and resulted in hemorrhagic lesions in the stomach in the presence of 100 mM HCI. These lesions were dose-dependently prevented by EA with suppression of lipid peroxidation but no effect on GMBF, and the effect at 6 mg/ml was almost equivalent to that of superoxide dismutase (SOD: 15000 unit/kg/hr) infused i.v. during a test-period. On the other hand, application of NH4OH to the ischemic stomach produced a marked reduction in PD, resulting in severe hemorrhagic lesions. These changes were prevented with both EA and SOD. In addition, EA had a potent scavenging action against monochloramine in vitro. These results suggest that EA exhibits gastric protective action against gastric lesions induced by NH4OH or reperfusion in the ischemic stomach, probably due to its anti-oxidative activity. This property of EA partly explains the less damaging effect of whisky in the stomach and may be useful as the prophylactic for Helicobacter pylori-associated gastritis.
Itoh, T., Ando, M., Tsukamasa, Y., Wakimoto, T. & Nukaya, H. 2012, “Whiskey Congeners Suppress LPS/IFN gamma-Induced NO Production in Murine Macrophage RAW 264 Cells by Inducing Heme Oxygenase-1 Expression“, Journal of Agricultural and Food Chemistry, vol. 60, no. 51, pp. 12491-12500.
Whiskey includes many nonvolatile substances (whiskey congeners; Whc) that seep from the oak cask during the maturation process. To date, many functions of Whc have reported, such as antiallergy and antimelanogenesis. This study examined the effect of Whc on LPS/IFNγ-induced nitric oxide (NO) production in murine macrophage RAW 264 cells. Whc suppressed LPS/IFNγ-induced NO production in a concentration-dependent manner. To determine the active compounds in Whc, the effect of 10 major compounds isolated from Whc on LPS/IFNγ-induced NO production was examined. Coniferylaldehyde (CA) and sinapylaldehyde (SiA) strongly suppressed LPS/IFNγ-induced NO production. Pretreatment with Whc, CA, and SiA induced heme oxygenase-1 (HO-1) expression. The expression of HO-1 by Whc, CA, and SiA pretreatment was due to activation of Nrf2/ARE signaling via the elevation of intracellular reactive oxygen species. To investigate the in vivo effects of Whc, Whc was administered to mice with antitype II collagen antibody-induced arthritis, and we the arthritis score and hind paw volume were measured. Administration of Whc remarkably suppressed the arthritis score and hind paw volume. Taken together, these findings suggest that Whc is beneficial for the treatment of inflammatory disease.
Itoh, T., Tsukane, M., Koike, M., Nakamura, C., Ohguchi, K., Ito, M., Akao, Y., Koshimizu, S., Nozawa, Y., Wakimoto, T., Nukaya, H. & Suwa, Y. 2010, “Inhibitory Effects of Whisky Congeners on IgE-Mediated Degranulation in Rat Basophilic Leukemia RBL-2H3 Cells and Passive Cutaneous Anaphylaxis Reaction in Mice“, Journal of Agricultural and Food Chemistry, vol. 58, no. 12, pp. 7149-7157.
“Whisky is matured in oak casks. Many nonvolatile substances (whisky congeners, WC) seep from the oak cask during the maturing process. In this study, three antiallergic agents (syringaldehyde, SA; lyoniresinol, Lyo; and ellagic acid, EA) were isolated from WC. Treatment with SA, Lyo, and EA reduced the elevation of intracellular free Ca(2+) concentration ([Ca(2+)]i) and intracellular ROS production caused by FcepsilonRI activation. The inhibitions of the elevation of [Ca(2+)]i and intracellular ROS production by SA and Lyo were mainly due to the suppression of the NADPH oxidase activity and scavenging of the produced radical, respectively. On the other hand, EA inactivated spleen tyrosine kinase and led to the inhibition of the elevation of [Ca(2+)]i and intracellular ROS production. Furthermore, it was found that WC strongly inhibited IgE binding to the FcepsilonRIalpha chain, whereas SA, Lyo, and EA did not indicate this inhibitory effect. These results suggest that WC inhibits allergic reactions through multiple mechanisms. To disclose the in vivo effects of WC, SA, Lyo, and EA, these compounds were administered to type I allergic model mice, and the passive cutaneous anaphylaxis (PCA) reaction was measured. These compounds remarkably suppressed the PCA reaction. Taken together, these findings suggest that WC seemed to be beneficial to ameliorate allergic reactions.
Koga, K., Taguchi, A., Koshimizu, S., Suwa, Y., Yamada, Y., Shirasaka, N. & Yoshizumi, H. 2007, “Reactive oxygen scavenging activity of matured whiskey and its active polyphenols“, Journal of Food Science, vol. 72, no. 3, pp. S212-S217.
“The quality of whiskey is known to improve remarkably by its storage over many years. This process is commonly termed “maturing.” In this process, polyphenols derived from lignin and tannin of the barrel have an important role in not only forming the matured flavor and taste but also contributing to the advance of clustering ethanol and water in whiskey. It is also likely that polyphenols generally possess reactive oxygen (RO) scavenging activity. The present study evaluated the RO scavenging activity (free-radical scavenging activity, H(2)O(2) reduction activity under peroxidase coculture, and H(2)O(2)scavenging activity) of 24 single malt whiskeys with a maturation age of 10 to 30 y produced in Japanese, Scotch (Islay), or Scotch (Speyside and Highland) regions. Single malt whiskey not only showed RO scavenging activity but there was also a positive correlation between this activity and the maturation age of whiskey exceeding the difference resulting from the manufacturing region. A nonvolatile fraction derived from the barrel was responsible for RO scavenging activity. In particular, the contents of ellagic and gallic acids and lyoniresinol, the main polyphenolic compounds in whiskey, increased with maturation age. For the free-radical scavenging activity per molecule, each compound was 1.68 to 3.14 times that of trolox (a water-soluble vitamin E). The activities of ellagic acid, gallic acid, and lyoniresinol in the whiskey (Yamazaki 18) were equivalent to that of 80.3, 31.2, and 11.1 ppm trolox, respectively. Accordingly, the total activity of these 3 compounds accounted for about 20% of the activity of the whiskey (630.7 ppm trolox).”
Lu, Y., Nakanishi, T., Fukazawa, M. & Tamai, I. 2014, “How Does Whisky Lower Serum Urate Level?”, Phytotherapy Research, vol. 28, no. 5, pp. 788-790.
“Clinical studies have shown that moderate whisky consumption increased renal excretion of urate into urine and decreased serum urate level, but the mechanism involved has not been established. Because renal reabsorption influences serum urate level, the effects of the whisky congeners on urate transporters, urate transporter 1 (URAT1), and voltage-driven urate transporter (URATv1) involved in reabsorptive transport of urate were examined. In transporter-expressing Xenopus oocytes, 12-year-old and 18-year-old whisky congeners inhibited urate uptake by URAT1 with IC50 values of 0.08 ± 0.01 and 0.04 ± 0.01 mg/mL, respectively, while urate uptake by URATv1 was inhibited only at 1 mg/mL. Decreased serum urate level after whisky consumption may be mainly due to inhibition of URAT1 by the congeners.
Nishioka, K., Sumida, T., Iwatani, M., Kusumoto, A., Ishikura, Y., Hatanaka, H., Yomo, H., Kohda, H., Ashikari, T., Shibano, Y. & Suwa, Y. 2002, “Influence of moderate drinking on purine and carbohydrate metabolism“, Alcoholism-Clinical and Experimental Research, vol. 26, no. 8, pp. 20S-25S.
BACKGROUND: We examined the influences of a moderate intake level of three types of alcoholic beverages–beer, whisky, and Shochu (Japanese distilled liquor)–on purine and carbohydrate metabolism and excretion in healthy male volunteers, concerning (1) the extent of contribution of purine bodies contained in beer to uric acid metabolism and (2) a comparison between two types of distilled spirits with (whisky) and without (Shochu) aging in oak wood barrel storage.
METHODS: Three sets of studies were conducted in which 10 to 13 healthy adult men were instructed to drink three types of alcoholic beverages at a slightly higher level (0.8 ml of ethanol equivalent/kg body weight) than moderate drinking (approximately 30.4 ml or less for men). A low purine beer was test-manufactured by treating nucleosides that were contained in wort and remained in beer with purine nucleoside phosphorylase derived from Ochrobacterium anthropi, thereby converting them into corresponding purine bases that were easily assimilated by beer yeast.
RESULTS: Although beer intake enhanced the level of serum uric acid by 13.6%, blood glucose by 26.7%, and insulin level by 5.1-fold, drinking a moderate level of distilled liquor (whisky, Shochu) did not increase the serum uric acid level or the other two parameters. The serum uric acid level observed after drinking beer with a purine body concentration reduced by 28% (68% in nucleosides and purine bases) was almost identical to the level observed after drinking regular beer. Whisky has been found to have a property that decreases the serum uric acid level. Excretion of uric acid from blood is increased by 27% after drinking whisky.
CONCLUSIONS: Moderate drinking of distilled liquors did not enhance serum uric acid level, blood glucose, or insulin level in healthy male subjects. Increased serum uric acid after beer intake could not be explained mostly with their purine body congeners. Whisky showed the eliminative property in serum uric acid through excretion of it from blood to urine. At a moderate drinking level, beer and whisky have different effects on purine metabolism or excretion.”
Suzuki, K., Nemoto, A., Tanaka, I., Koshimizu, S., Suwa, Y. & Ishihara, H. 2010, “Induction of Heme Oxygenase-1 by Whisky Congeners in Human Endothelial Cells“, Journal of Food Science, vol. 75, no. 6, pp. H163-H166.
“It is expected that the production of the cytoprotective heme oxygenase-1 (HO-1) protein in endothelial cells would reduce severity of vascular injuries, while phenolic compounds are known to induce HO-1 mRNA and protein in various cells. We investigated the activation of HO-1 by whisky, which contains various phenolic substances. The congeners of whisky stored from 4 to 18 y in oak barrels were shown to induce an increase of HO-1 protein in human umbilical vein endothelial cells, while those of freshly distilled whisky spirit exhibited no activity. To determine the compounds with potent HO-1-inducing activity among the whisky congeners, several chemicals that had been reported to exist in whisky or oak barrels were screened, and coniferyl aldehyde and sinapyl aldehyde showed the activity. Thus, compounds that emerged in whisky during barrel storage induced cytoprotective protein, HO-1, in human endothelial cells.”
Tanaka, T., Matsuo, Y. & Kouno, I. 2010, “Chemistry of Secondary Polyphenols Produced during Processing of Tea and Selected Foods“, International Journal of Molecular Sciences, vol. 11, no. 1, pp. 14-40.
“This review will discuss recent progress in the chemistry of secondary polyphenols produced during food processing. The production mechanism of the secondary polyphenols in black tea, whisky, cinnamon, and persimmon fruits will be introduced. In the process of black tea production, tea leaf catechins are enzymatically oxidized to yield a complex mixture of oxidation products, including theaflavins and thearubigins. Despite the importance of the beverage, most of the chemical constituents have not yet been confirmed due to the complexity of the mixture. However, the reaction mechanisms at the initial stages of catechin oxidation are explained by simple quinone–phenol coupling reactions. In vitro model experiments indicated the presence of interesting regio- and stereoselective reactions. Recent results on the reaction mechanisms will be introduced. During the aging of whisky in oak wood barrels, ellagitannins originating from oak wood are oxidized and react with ethanol to give characteristic secondary ellagitannins. The major part of the cinnamon procyanidins is polymerized by copolymerization with cinnamaldehyde. In addition, anthocyanidin structural units are generated in the polymer molecules by oxidation which accounts for the reddish coloration of the cinnamon extract. This reaction is related to the insolubilization of proanthocyanidins in persimmon fruits by condensation with acetaldehyde. In addition to oxidation, the reaction of polyphenols with aldehydes may be important in food processing.”
Yao, R., Yasuoka, A., Kamei, A., Ushiama, S., Kitagawa, Y., Rogi, T., Shibata, H., Abe, K. & Misaka, T. 2014, “Nuclear Receptor-Mediated Alleviation of Alcoholic Fatty Liver by Polyphenols Contained in Alcoholic Beverages“, Plos One, vol. 9, no. 2, pp. e87142.
“To elucidate the effect of the polyphenols contained in alcoholic beverages on the metabolic stress induced by ethanol consumption, four groups of mice were fed for five weeks on Lieber’s diet with or without ethanol, with ethanol plus ellagic acid, and with ethanol plus trans-resveratrol. Alcoholic fatty liver was observed in the group fed the ethanol diet but not in those fed the ethanol plus polyphenol diets. Liver transcriptome analysis revealed that the addition of the polyphenols suppressed the expression of the genes related to cell stress that were up-regulated by ethanol alone. Conversely, the polyphenols up-regulated the genes involved in bile acid synthesis, unsaturated fatty acid elongation, and tetrahydrofolate synthesis that were down-regulated by ethanol alone. Because parts of these genes were known to be regulated by the constitutive androstane receptor (CAR), we performed the same experiment in the CAR-deficient mice. As a result, fatty liver was observed not only in the ethanol group but also with the ethanol plus polyphenol groups. In addition, there was no segregation of the gene expression profiles among these groups. These results provide a molecular basis for the prevention of alcohol-induced stress by the polyphenols in alcoholic beverages.”
Posted in Articles, Drink, Nutrition, Scottish | 6 Comments

Experimental mead making: Wild fermentations


I have wanted to try brewing something for sometime, and as both mead and honey are particular interests of mine, mead seemed the obvious thing to try for myself. However, the usual methods employed to brew mead at home require at a minimum certain brewing equipment that I currently lack. Standard methods include sterilizing the honey and water used, adding a specific brewing yeast, and carrying out the fermentation in a specialised brewing vessel fitted with an air lock.

Lacking any of these, and inspired by The Art of Fermentation by Sandor Katz, I decided to try a different approach using the wild yeasts naturally found in honey. I am also rather curious as to how people in ancient times produced their mead, after all it was mostly likely one of the first alcoholic beverages, and they surely had a certain lack of specialised brewing equipment.

While honey itself is remarkably resistant to microbial action, this property is dependent on the water content remaining low, and as soon as the honey is diluted with water the dormant wilds present in the honey reawaken and soon get to work converting the honey sugar into alcohol. This of course depends on the honey still being in a raw state and not heat treated during its processing. The random selection of wild yeast strains and other assorted bacteria present in unheated honey naturally make this rather a shot in the dark in terms of how the resulting mead may turn out. But as I only wish to make a small amount there seems little loss for me to give it a try.

In his book Sandor recommends a ratio of four parts water to one part honey as a good starting point. Looking for a good honey to use I decided on the Organic Forest Honey from Zambia as this should not have been heat treated and also happens to be the cheapest raw honey available to me for an initial experiment. Dissolving a 250 ml jars worth of honey into 1 L of water took some time and a quite a lot of stirring. When eventually dissolved I put it into a couple of glass Acqua Panna mineral water bottles for the brewing. As I bought bottles for the purpose the mineral water was using to make the mead. A party balloon with a pinprick hole in the top makes a very simple airlock, allowing any pressure inside to escape while keeping air out.

It took a few days of shaking the honey and water up each day before the yeast seemed to become active but now liquid has been bubbling away well for about a week with the balloons on top inflated with carbon dioxide from the fermentation. I have read that this initial fermentation will continue for a a couple of weeks during which time all the glucose in the honey is rapidly fermented. When that slows down the mead can then be bottled where it continues to slowing ferment the remaining fructose becoming drier and less sweet with increased aging.

While the outcome cannot be predicted, I await the results with hopeful expectations. It will be interesting to see the results of those yeasts so recently inhabiting the wild Zambian forests.

Posted in Drink, Honey, Uncategorized | 3 Comments

Himalayan Rock Salt


Photo credit: julajp.

A relatively recent addition to our British shops, and once restricted to health food shops, it now seems that pink Himalayan salt can be found almost everywhere even appearing in major supermarkets. A quick browse of the topic of Himalayan salt online quickly reveals a plethora of wild health claims related to these rather attractive pink salt crystals. Curious as to where this product had so suddenly appeared from in recent years I started to look into the subject online but was dissatisfied to find the information available disappointingly repetitive without any reputable sources provided.

For a start this salt does not come from the Himalayas mountains but instead from a few hundred miles south in the mountains of Pakistan. While the Khewra salt mine from which the pink salt originates is an interesting subject in itself, the term Himalayan Salt was clearly a stroke of marketing genius.

The story of the appearance of Himalayan salt as a health food in Europe seems to have begun in Germany with a man name Peter Ferreira, whose real name seems to be Peter Druf according to this sceptic website and has it seems been called by some the “König der Scharlatane” or king of charlatans. Apparently still selling Himalayan salt, as his biography on this site suggests, he claims to be a Biophysicist although no proof of this is forthcoming. His rise to prominence began it seems in late 1990’s Germany with public lectures and tape recordings claiming this Himalayan salt to be a panacea for all ills. Although I cannot speak German, recordings of some of these have been posed on youtube including this audience exhausting five hour monologue. Further prominence in Europe was achieved with the release of the book Water and Salt: The Essence of Life – The Healing Power of Nature that details “the powerful healing qualities of Himalayan Crystal Salt” co-authored with a Dr Barbara Hendel who is apparently still working as some sort of holistic medicine doctor in Germany.

While there are plenty of rather wacky language used in relation to this salt many of the claims rest on its mineral content, as it is reputed to contain 84 minerals. The details of its mineral composition that are widely quoted are shown here, although the site itself is not making any wild claims, the table is reproduced from the Peter Ferreira’s book Water and Salt. Some investigation uncovered that the source of this detailed analysis is an Institute of Biophysical Research, Las Vegas USA, which it seems Peter Ferreira is the director of and appears to exist in name only. As Ferreira was also the owner of the main company selling this salt at the time it makes me wonder who carried out the analysis or whether is was just made up from Ferreira’s imagination. According to wikipedia a German TV show tested some Himalayan salt available for sale in that country and only found 10 minerals other than sodium chloride were detectable, although sadly this information does not seem to be available online anywhere.

Looking more closely at the reputed 84 minerals it is clear that the table is laid out in a way that can easily mislead the unwary, as it clearly has done. For example this site which states “The Easy Way To Sneak 84 Minerals Into Your Diet Daily“, with a copy of the pages from the book helpfully included at the bottom of the page. In fact when the table lists the salt as containing <0.001 ppm of boron this means that the test used could not detect any boron within the limits of the test. As scientific tests usually have a lower limit of detection when nothing is measured the results are presented as “less than” the detection limit, as such a test cannot prove that none is present. So 53 of the elements in the table were not detected in the salt. Many of those elements that were detected were present in such absolutely tiny amounts as could be found as contamination in almost anything you might test.

After searching for some independent testing I found a recent study published in the Journal of The Chemical Society of Pakistan that investigated the mineral and trace element content of a range of different coloured salt samples from the Khewra salt mine. The main constituents are shown in Table 1 below and this clearly shows that sodium and chloride were the main mineral in all the samples, whatever the colour, making up between 97.55% and 98.3% of the salt. Small amounts of calcium, magnesium, sulphate, and potassium were also detected although as these each formed less than 1% of the Khewra salt they are probably of no nutritional significance.

salt table 1

Source: (Sharif 2007).

The same paper analysed the trace element content of the salt for iron (Fe), zinc (Zn), copper (Cu), manganese (Mn), chromium (Cr), lead (Pb), and cadmium (Cd).

salt table 2

Source: (Sharif 2007).

Reassuringly the levels of toxic metals like lead and cadmium were very low or undetectable. Iron was found which is to be expected as it is iron oxide that gives the salt its distinctive pink colour. However at less than 1 mg/kg of salt the quantities of iron in the salt are exceedingly small and of no relevance to our human health. To put it into perspective according to this study a 6 gram teaspoonful of this salt would contain at most 6 mcg or iron, compared to 150 mcg or iron is a small raw carrot.  The other trace elements measured were also found in extremely small amounts. These results would agree with the reported ten minerals that were detected in samples of salt tested in Germany. Another study I came across published in the Journal of Sensory Studies looked at many different salts from around the world also included Himalayan salt in their analysis. Their analysis of Himalayan salt found similar levels of calcium, potassium and sodium and slightly higher levels of zinc. This analysis found higher levels of iron in the salt, reported to be 39 mcg/g, which is a lot more than the previous study and so perhaps there is quite a lot of variety between different batches of salt. However, this would still only equate to  235 mcg in a teaspoon of salt.

In summary “Himalayan” rock salt contains mostly sodium chloride with a small amount of magnesium and calcium as found in most unrefined salt. Any other trace elements it contains are in really tiny amounts, which is a good thing as many of those like lead would not be desirable in any larger quantities. I don’t see anything wrong with using some of this salt as its colour is quite attractive though it may not really be worth the prices that are often charged for it. However, the origin of its rise to prominence in Europe is really rather dubious and any health claims surrounding it are deeply suspect. I think it unlikely to have any effect on my health beyond any other type of unrefined salt.

What interested me more after looking into the origin of this salt is the mines in Khewra salt mine from which it originates. Apparently in use for more than two thousand years the workers of the mine have used blocks of the many hued salt to construct beautiful underground constructions including the tiny mosque in the photo below.


Photo credit: Fakhir Shaheen.


Posted in Articles, Food, Nutrition, Research, Uncategorized | Tagged , , , , , , , , , | 8 Comments

Eating DNA: Dietary Nucleotides in Nutrition

Nucleotides are biological molecules that are essential to almost all biological processes in the human body. Probably best known as the components that make up DNA and RNA they are also involved in many other cellular functions. With such essential roles, it is no surprise that our body is capable of producing these molecules itself, as well as salvaging and recycling used nucleotides in the body. There is an additional less well-known source as nucleotides are normal components of our diets and our bodies have ways of absorbing and making use of these. How much these three sources contribute to our nucleotide needs is unclear though regular healthy people seem to be capable of making and recycling enough to satisfy their regular needs. However, when the demand for nucleotides is increased, such as in the case of gut injury, rapid growth, decreased protein intakes, or when the immune system is activated, we may no longer be able to make quite enough . Under these conditions is has been proposed that dietary nucleotides may be termed conditionally essential and some extra in the diet may provide some benefits to systems like the gut and the immune system (Van Buren 1997).


 Structural elements of common nucleic acid constituents. Because they contain at least one phosphate group, the compounds marked nucleoside monophosphatenucleoside diphosphate and nucleoside triphosphate are all nucleotides (Wikipedia).

At their base nucleotides do in fact contain a base, small nitrogen containing compounds classified as either purines or pyrimidines, these nucleobases are adenine, guanine, cytosine, uracil, and thymine. When these bases have a pentose sugar attached, either ribose or deoxyribose, they become nucleosides and if this sugar has one to three phosphate groups attached they are collectively known as nucleotides.

Best known for being the building blocks of DNA and RNA, forming our genetic code, and carrying the messages that are translated into proteins these nucleotides are involved in many other processes. Nucleotides as adenosine triphosphates (ATP) transport the chemical energy for the physiological processes within our cells while others play an essential role in metabolism. Nucleotides also participate in cell signaling, as cGMP and cAMP, and form a part of vital cofactors of enzymatic reactions like coenzyme A, NAD, and NADP+).

When we eat food that contains nucleotides, as any unrefined food containing whole cells will contain a little of, our body has ways to digest and absorb them. Nucleotides are mostly eaten along with protein in the diet bound up in nucleoproteins. Digestion takes place in the small intestine as protease and nuclease enzymes break the nucleoproteins and then nucleotides down into smaller parts, most of them being absorbed into the cells of the gut as nucleosides with over 90% of them being absorbed (Hess 2012).

nucleotide digestion

The digestions and absorption of dietary nucleotides (Hes 2012).

The first tissue to absorb dietary nucleotides and the first to make use of them is the gut. The cells of the gut are unusual in relying on a supply of nucleotides from the liver as generating these molecules from scratch is metabolically expensive and the rapidly dividing cells struggle to generate enough to fulfil their own needs (Grimble 1994). While only about 5% of the absorbed nucleotides are eventually retained for synthesis of DNA or RNA between 25-50% of those that are remain the gut cells (Hes 2012).

Compared to those on nucleotide free diets the intestines of weanling rats supplemented with nucleotides matured faster, had more mucosal protein, taller villi and more sugar digesting enzymes (Uauy 1990). Research on infant intestinal tissues suggests that adenosine monophosphate in particular plays a role in maintaining the balance of cell growth in the developing human intestine (Tanaka 1996). Another time when rapid cell growth occurs in the gut is during recovery from injury. In rats, the presence of nucleotides in their diet improved their recovery from intestinal surgery (Ogita 2002) and speeded up the recovery of the gut after five days of food deprivation in older rats (Ortega 1995). The presence of nucloetides in the diet also resulted in a faster recovery from diarrhea (Bueno 1994). After being absorbed in the gut the liver can also make use of dietary nucleotides with a range of effects on growth and repair (Carver 1994).

The cells of immune system can also struggle to fulfil their own nucleotide needs during periods rapid proliferation during immune responses and prefer to use salvage pathways and dietary sources (Gif 2002). Studies of the effects of nucleotides on human immunity have been limited to healthy individuals and the effects of exercise. High intensity and endurance exercise have been studied. In those receiving extra nucleotides, their level of salivary IgA was higher and their cortisol was lower than those taking the placebo (Mc Naughton 2006; Mc Naughton 2007). This suggests a long-term increased intake of nucleotides in the diet can enhance the immune response and blunt the hormones responses associated with the physiological stress of exercise.

Even if these nucleotides are not used and eventually excreted, they could have transient effects such as increasing blood circulation to the gut. Infants fed nucleotide-supplemented formula showed an increased blood flow to the small intestine after feeding compared to those without nucleotides (Carver 2004). This may be due to the adenosine as this triggers increased blood flow to the small intestine in dogs (Sawmiller 1992). Adenosine may have other anti-inflammatory roles as it is absorbed into the lining of the gut through interactions with the A2a receptor on T cells (Ye 2009).

No mention of health influences of food is complete now without mention of the gut microbiota and nucleotides are no exception. Infants fed formula with added nucleotides may have reduced cases of diarrhea (Yau 2003), possibly through enhancing the growth of Bifidobacterium, which is thought to help protect infants from gut infections. The addition of nucleotides has been shown to improve the composition of the microbiota of formula fed babies (Singhal 2008). What effect that dietary nucleotide might have on adult microbiota is currently unknown. It should come as no surprise that breast milk is a good source of nucleotides for the growing baby providing a number of beneficial effect on the health and development of the infant (Thorell 1996). As a curious aside the levels of different nucleotides in breast milk change during the day and night and may help babies get to sleep in the evening (Sánchez 2009). Many infant formulas now seem to have added nucleotides.

Purines in foods

The purine content of selected foods from Clifford and Story (1979).

Given the wide range of potential effect of these molecules, it is worth a look at where you might find them in your food. Sadly, there is very little good published evidence for the nucleotide contents of different foods. What is known is that any food made up of living cells will contain them. However, the highest concentrations are in foods that have a high cell density and are from metabolically active tissues. This means that animal foods generally contain much more than plant foods, with the exception of beans and other legumes that have a relatively high amount in their seeds. Milk products may also contain significant amounts of nucleotides (Gil 1981). The table above published in 1978 shows the purine and RNA content of a few different foods, while not measured the pyrimidines tend to occur in roughly similar amounts to the purines. It is clear that offal like liver and heart, small fish, shell fish and beans are all good sources. All of these are measured as milligrams per 100 grams of food.



The nucleotide content of typical portion sizes (Verkerk 2012).

Another source is the graph above originating from a recently published article on nucleotides and health. This is the result of testing by a private company and shows the total nucleotide content in a typical portion size, unfortunately the details of what those portion sizes are is not provided. It is clear to see that offal and animal products are a rich source of these compounds with bean products, mushrooms and vegetables also contributing some. What it seems certain does not contain nucleotides is the refined food ingredients that are now commonly found in our diets such as, sugar, flour and vegetable oils. It happens to be the case that these ingredients are what is used to make nucleotide free diets for animal studies. Based on current evidence there can be no recommendation as to what quantity of nucleotides may be beneficial in our diet other than to suggest that some is better than none and perhaps more than most of us eat now.

The foods that are most abundant in nucleotides are now the ones that have become most scarce in our diets. The offal like liver, tripe and heart that were once popular are now largely avoided, while foods like beef are officially discouraged. This was likely to be even more true of our more distant hunting ancestors before the advent of farming who would have prized the parts of the animal we now squeamishly avoid. Even in more recent history those for whom animal products were out of reach often had diets relying on beans and other minimally processed plant foods or seafoods such as oysters.

It may be proposed that until recently a relatively higher intake of dietary nucleotides than now was a normal feature of human diets. While they may not be essential to survival, their absence does not result in any classic form of deficiency disease, it seems plausible to me that a regular intake may provide small but meaningful benefits to the health our gut and immune system and perhaps other systems of the body. While some may use this suggestion as a reason to promote nucleotides as yet another dietary supplement to sell to me it makes more sense to see this as yet another reason to include in our diets the nutritious foods our ancestors have always eaten.

Bueno J, Torres M, Almendros A, Carmona R, Nuñez MC, Rios A, Gil A. (1994 ) Effect of dietary nucleotides on small intestinal repair after diarrhoea. Histological and ultrastructural changes. Gut. 35(7):926-33.
Carver JD. (1994) Dietary nucleotides: cellular immune, intestinal and hepatic system effects. The Journal of Nutrition. 124(1 Suppl):144S-148S.
Carver JD, Sosa R, Saste M, Kuchan M. (2004) Dietary nucleotides and intestinal blood flow velocity in term infants. Journal of Pediatric Gastroenterology and Nutrition. 39(1):38-42.
Clifford AJ and Story DL. (1976) Levels of purines in foods and their metabolic effects in rats. The Journal of Nutrition. 106:435-42.
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Caboc and Crowdie: Traditional cheeses of Scotland


Originating in the Western highlands Caboc is one of Scotlands oldest cheeses. Dating back to the 15th Century it was known as a chieftain’s cheese, due to its rich double cream ingredients and high fat content. Reputedly the recipe originates from the daughter of the chieftain MacDonald of the Isles, Mariota de Ile. At the age of 12 she was in danger from the Clan Campbell who had plans to steal her away to forcefully marry one of their and seize her lands. Escaping to Ireland and finding refuge in a nunnery she there learnt the arts of cheese making from her Irish hosts. Later returning to a more suitable marriage Mariota passed on her recipe, which still a family secret, has been past down from mother to daughter to the present day. The current descendant of the clan and owner of the recipe Susannah Stone who working from her farm in Tain makes and sells the cheese under the seal of Highland Fine Cheeses.

The caboc is make using double cream from local cows and soured using a bacterial culture without rennet the cheese is shaped into small logs rolled in toasted pinhead oatmeal. The high fat content at 67% gives the cheese a primrose yellow color and a rich smooth, buttery taste with a slight acid tang while the oatmeal adds a nutty flavour. Usually eaten within a few days of being made it will keep for up to three weeks in the fridge. It adds a rich buttery addition to Scottish oatcakes.


In contrast to caboc, crowdie was the universal cheese of the Scottish crofter and most likely Scotlands most ancient cheese, its origin perhaps stretching back into the mists of time to Viking invaders or perhaps even further to the ancient Picts. At one time made across the Highlands by crofters it formed a staple part of their diet. The cheese was commonly made after most of the cream had been skimmed off the milk, to use or make into butter, resulting in a low-fat resulting cheese that is very different from the rich creamy Caboc. The term crowdie was originally used by the Scots to describe the dishes of oatmeal and water that were such a staple of the old Scottish diet. Being so ubiquitous the name crowdie eventually became transferred to the meal itself and all kinds of commonly eaten dishes ended up with the word Crowdie added to them, an indication of how often this cheese was on the menu for ordinary crofters.

This particular variation known as Black Crowdie, or Gruth Dhu in Gaelic, is rolled in toasted oatmeal mixed with cracked black pepper giving the cheese quite a hot kick to it.

An unusual feature of Crowdie is that it is semi-cooked. The fresh unpasteurized milk was left to naturally sour beside the stove resulting in a lovely sharp, citric flavour in the cheese. The cream was skimmed off and the soured milk was then scrambled over the heat of the fire and hung up in a muslin cloth to allow the whey to separate out. Once the whey had been strained off salt and sometimes a little cream was added to the curds, making a soft, crumbly white cheese. In the traditional manner this crowdie from Highland Fine Cheeses is soured with lactic acid cultures and without the use of rennet resulting in a traditional sharp flavour.

As in the case of Caboc the survival of Crowdie is largely thanks to Susannah Stone, who has been producing these traditional Scottish cheeses since 1963. Crowdie making had declined after the Second World War with the passing of crofting traditions but Susannah Stone continued to make it at her home in the Ross-shire village of Tain. Apparently one day in 1962, after making too much and offering the surplus to a local grocer her cheese became popular enough that her crowdie became the first artisan cheese produced by family business Highland Fine Cheeses, still produced now 50 years later with the company managed by her son Rory Stone. This ancient cheese is unique to the Highland and Islands of Scotland and is apparently not made anywhere else in Europe.

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