D-Fructose
IUPAC name Fructose
Other names fruit sugar,[1] levulose,[2] D-fructofuranose, D-fructose, D-arabino-hexulose
Identifiers
CAS number	57-48-7 Y
PubChem	11769129
ChemSpider	388775 Y
UNII	6YSS42VSEV Y
EC-number	200-333-3
KEGG	C02336 Y
ChEBI	CHEBI:28645 Y
ChEMBL	CHEMBL604608 Y
Jmol-3D images	Image 1
SMILES O[C@H]1[C@H](O)[C@H](O[C@]1(O)CO)CO
InChI InChI=1S/C6H12O6/c7-1-3-4(9)5(10)6(11,2-8)12-3/h3-5,7-11H,1-2H2/t3-,4-,5+,6-/m1/s1 Y Key: RFSUNEUAIZKAJO-ARQDHWQXSA-N Y InChI=1/C6H12O6/c7-1-3-4(9)5(10)6(11,2-8)12-3/h3-5,7-11H,1-2H2/t3-,4-,5+,6-/m1/s1 Key: RFSUNEUAIZKAJO-ARQDHWQXBD
Properties
Molecular formula	C6H12O6
Molar mass	180.16 g/mol
Density	1.694 g/cm3
Melting point	103 °C
Y (verify) (what is: Y/N?) Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

Fructose, or fruit sugar, is a simple monosaccharide found in many plants. It is one of the three dietary monosaccharides, along with glucose and galactose, that are absorbed directly into the bloodstream during digestion. Fructose was discovered by French chemist Augustin-Pierre Dubrunfaut in 1847.^[3] Pure, dry fructose is a very sweet, white, odorless, crystalline solid and is the most water-soluble of all the sugars.^[4] From plant sources, fructose is found in honey, tree and vine fruits, flowers, berries and most root vegetables. In plants, fructose may be present as the monosaccharide and/or as a component of sucrose. Commercially, fructose is usually derived from sugar cane, sugar beets and corn and there are three commercially important forms. Crystalline fructose is the monosaccharide, dried and ground, and of high purity. High-fructose corn syrup (HFCS) is a mixture of glucose and fructose as monosaccharides. Sucrose is the third form. All forms of fructose, including fruits and juices, are commonly added to foods and drinks for palatability, taste enhancement and improved browning of some foods, such as baked goods.

About 240,000 tons of crystalline fructose are produced annually.^[5]

Chemical properties[link]

Figure 1: Relationship between the acyclic and the cyclic (hemiketal) isomers of fructose.

d- and l-isomers of fructose (open-chain form)

Fructose is a 6-carbon polyhydroxyketone. It is an isomer of glucose; i.e., both have the same molecular formula (C₆H₁₂O₆) but they differ structurally. Crystalline fructose adopts a cyclic six-membered structure owing to the stability of its hemiketal and internal hydrogen-bonding. This form is formally called D-fructopyranose. In solution, fructose exists as an equilibrium mixture of 70% fructopyranose and about 22% fructofuranose, as well as small amounts of three other forms, including the acyclic structure.^[6]

Reactions[link]

Fructose and fermentation[link]

Fructose may be anaerobically fermented by yeast or bacteria.^[7] Yeast enzymes convert sugar (glucose, or fructose) to ethanol and carbon dioxide. The carbon dioxide released during fermentation will remain dissolved in water, where it will reach equilibrium with carbonic acid, unless the fermentation chamber is left open to the air. The dissolved carbon dioxide and carbonic acid produce the carbonation in bottle fermented beverages.^[8]

Fructose and Maillard reaction[link]

Fructose undergoes the Maillard reaction, non-enzymatic browning, with amino acids. Because fructose exists to a greater extent in the open-chain form than does glucose, the initial stages of the Maillard reaction occurs more rapidly than with glucose. Therefore, fructose potentially may contribute to changes in food palatability, as well as other nutritional effects, such as excessive browning, volume and tenderness reduction during cake preparation, and formation of mutagenic compounds.^[9]

Dehydration[link]

Fructose readily dehydrates to give hydroxymethylfurfural ("HMF"). This process may in the future be part of a low-cost, carbon-neutral system to produce replacements for petrol and diesel from plantations.^[10]

Physical and functional properties[link]

Relative sweetness[link]

The primary reason that fructose is used commercially in foods and beverages, besides its low cost, is its high relative sweetness. It is the sweetest of all naturally occurring carbohydrates. Fructose is generally regarded as being 1.73 times as sweet as sucrose.^[11][12] However, it is the 5-ring form of fructose that is sweeter; the 6-ring form tastes about the same as usual table sugar. Warming fructose leads to formation of the 6-ring form.^[13]

Figure 2: Relative sweetness of sugars and sweeteners.

The sweetness of fructose is perceived earlier than that of sucrose or dextrose, and the taste sensation reaches a peak (higher than that of sucrose) and diminishes more quickly than that of sucrose. Fructose can also enhance other flavors in the system.^[11]

Sweetness synergy[link]

Fructose exhibits a sweetness synergy effect when used in combination with other sweeteners. The relative sweetness of fructose blended with sucrose, aspartame, or saccharin is perceived to be greater than the sweetness calculated from individual components.^[14]

Fructose solubility and crystallization[link]

Fructose has higher solubility than other sugars as well as other sugar alcohols. Fructose is, therefore, difficult to crystallize from an aqueous solution.^[11] Sugar mixes containing fructose, such as candies, are softer than those containing other sugars because of the greater solubility of fructose.^[15]

Fructose hygroscopicity and humectancy[link]

Fructose is quicker to absorb moisture and slower to release it to the environment than sucrose, dextrose, or other nutritive sweeteners.^[14] Fructose is an excellent humectant and retains moisture for a long period of time even at low relative humidity (RH). Therefore, fructose can contribute to improved quality, better texture, and longer shelf life to the food products in which it is used.^[11]

Freezing point[link]

Fructose has a greater effect on freezing point depression than disaccharides or oligosaccharides, which may protect the integrity of cell walls of fruit by reducing ice crystal formation. However, this characteristic may be undesirable in soft-serve or hard-frozen dairy desserts.^[11]

Fructose and starch functionality in food systems[link]

Fructose increases starch viscosity more rapidly and achieves a higher final viscosity than sucrose because fructose lowers the temperature required during gelatinizing of starch, causing a greater final viscosity.^[16]

Many artificial sweeteners are not suitable for home-baking, but, with a little adjustment, many traditional recipes can be prepared using fructose.^[17]

Food sources[link]

Crystalline fructose

Natural sources of fructose include fruits, vegetables (including sugar cane), and honey.^[18] Fructose is often further concentrated from these sources. The highest dietary sources of fructose, besides pure crystalline fructose, are foods containing table sugar (sucrose), high-fructose corn syrup, agave nectar, honey, molasses, maple syrup, and fruit juices, as these have the highest percentages of fructose (including fructose in sucrose) per serving compared to other common foods and ingredients. Fructose exists in foods either as a free monosaccharide or bound to glucose as sucrose, a disaccharide. Fructose, glucose, and sucrose may all be present in a food; however, different foods will have varying levels of each of these three sugars.

The sugar contents of common fruits and vegetables are presented in Table 1. In general, in foods that contain free fructose, the ratio of fructose to glucose is approximately 1:1; that is, foods with fructose usually contain about an equal amount of free glucose. A value that is above 1 indicates a higher proportion of fructose to glucose, and below 1 a lower proportion. Some fruits have larger proportions of fructose to glucose compared to others. For example, apples and pears contain more than twice as much free fructose as glucose, while for apricots the proportion is less than half as much fructose as glucose.

Apple and pear juices are of particular interest to pediatricians because the high concentrations of free fructose in these juices can cause diarrhea in children. The cells (enterocytes) that line children's small intestines have less affinity for fructose absorption than for glucose and sucrose.^[19] Unabsorbed fructose creates higher osmolarity in the small intestine, which draws water into the gastrointestinal tract, resulting in osmotic diarrhea. This phenomenon is discussed in greater detail in the Health Effects section.

Table 1 also shows the amount of sucrose found in common fruits and vegetables. Sugarcane and sugar beet have a high concentration of sucrose, and are used for commercial preparation of pure sucrose. Extracted cane or beet juice is clarified, removing impurities; and concentrated by removing excess water. The end product is 99.9% pure sucrose. Sucrose-containing sugars include common table white granulated sugar and powdered sugar, as well as brown sugar.^[20]

All data with a unit of g (gram) are based on 100 g of a food item. The fructose / glucose ratio is calculated by dividing the sum of free fructose plus half sucrose by the sum of free glucose plus half sucrose.

Fructose is also found in the synthetically manufactured sweetener, high-fructose corn syrup (HFCS). Hydrolyzed corn starch is used as the raw material for production of HFCS. Through the enzymatic treatment, glucose molecules are converted into fructose.^[20] There are three types of HFCS, each with a different proportion of fructose: HFCS-42, HFCS-55, and HFCS-90. The number for each HFCS corresponds to the percentage of synthesized fructose present in the syrup. HFCS-90 has the highest concentration of fructose, and is typically used to manufacture HFCS-55; HFCS-55 is used as sweetener in soft drinks, whereas HFCS-42 is used in many processed foods and baked goods.

Carbohydrate content of commercial sweeteners (percent)[link]

Data obtained from Kretchmer, N. & Hollenbeck, CB (1991). Sugars and Sweeteners, Boca Raton, FL: CRC Press, Inc.^[20] for HFCS, and USDA for fruits and vegetables and the other refined sugars.^[21]

Cane and beet sugars have been used as the major sweetener in food manufacturing for centuries. However, with the development of HFCS, a significant shift occurred in the type of sweetener consumption. As seen in Figure 3, this change happened in the 1970s. Contrary to the popular belief, however, with the increase of HFCS consumption, the total fructose intake has not dramatically changed. Granulated sugar is 99.9% pure sucrose, which means that it has equal ratio of fructose to glucose. The most commonly used forms of HFCS, HFCS-42 and HFCS-55, have a roughly equal ratio of fructose to glucose, with minor differences. HFCS has simply replaced sucrose as a sweetener. Therefore, despite the changes in the sweetener consumption, the ratio of glucose to fructose intake has remained relatively constant.^[22]

Figure 3: Adjusted consumption of refined sugar per capita in the U.S.

Fructose digestion and absorption in humans[link]

Fructose exists in foods either as a monosaccharide (free fructose) or as a unit of a disaccharide (sucrose). Free fructose is absorbed directly by the intestine. When fructose is consumed in the form of sucrose, it is digested (broken down) and then absorbed as free fructose. As sucrose comes into contact with the membrane of the small intestine, the enzyme sucrase catalyzes the cleavage of sucrose to yield one glucose unit and one fructose unit, which are then each absorbed. After absorption it enters the hepatic portal vein and is directed toward the liver.

Figure 4: Hydrolysis of sucrose to glucose and fructose by sucrase.

The mechanism of fructose absorption in the small intestine is not completely understood. Some evidence suggests active transport, because fructose uptake has been shown to occur against a concentration gradient.^[23] However, the majority of research supports the claim that fructose absorption occurs on the mucosal membrane via facilitated transport involving GLUT5 transport proteins. Since the concentration of fructose is higher in the lumen, fructose is able to flow down a concentration gradient into the enterocytes, assisted by transport proteins. Fructose may be transported out of the enterocyte across the basolateral membrane by either GLUT2 or GLUT5, although the GLUT2 transporter has a greater capacity for transporting fructose, and, therefore, the majority of fructose is transported out of the enterocyte through GLUT2.

Figure 5: Intestinal sugar transport proteins.

Capacity and rate of absorption[link]

The absorption capacity for fructose in monosaccharide form ranges from less than 5 g to 50 g and adapts with changes in dietary fructose intake. Studies show the greatest absorption rate occurs when glucose and fructose are administered in equal quantities.^[24] When fructose is ingested as part of the disaccharide sucrose, absorption capacity is much higher because fructose exists in a 1:1 ratio with glucose. It appears that the GLUT5 transfer rate may be saturated at low levels, and absorption is increased through joint absorption with glucose.^[25] One proposed mechanism for this phenomenon is a glucose-dependent cotransport of fructose. In addition, fructose transfer activity increases with dietary fructose intake. The presence of fructose in the lumen causes increased mRNA transcription of GLUT5, leading to increased transport proteins. High-fructose diets^[vague] have been shown to increase abundance of transport proteins within 3 days of intake.^[26]

Malabsorption[link]

Several studies have measured the intestinal absorption of fructose using hydrogen breath test.^{[27][28][29][30]} These studies indicate that fructose is not completely absorbed in the small intestine. When fructose is not absorbed in the small intestine, it is transported into the large intestine, where it is fermented by the colonic flora. Hydrogen is produced during the fermentation process and dissolves into the blood of the portal vein. This hydrogen is transported to the lungs, where it is exchanged across the lungs and is measurable by the hydrogen breath test. The colonic flora also produces carbon dioxide, short-chain fatty acids, organic acids, and trace gases in the presence of unabsorbed fructose.^[31] The presence of gases and organic acids in the large intestine causes gastrointestinal symptoms such as bloating, diarrhea, flatulence, and gastrointestial pain^[27] Exercise immediately after consumption can exacerbate these symptoms by decreasing transit time in the small intestine, resulting in a greater amount of fructose emptied into the large intestine.^[32]

Fructose metabolism[link]

All three dietary monosaccharides are transported into the liver by the GLUT2 transporter.^[33] Fructose and galactose are phosphorylated in the liver by fructokinase (K_m= 0.5 mM) and galactokinase (K_m = 0.8 mM). By contrast, glucose tends to pass through the liver (K_m of hepatic glucokinase = 10 mM) and can be metabolised anywhere in the body. Uptake of fructose by the liver is not regulated by insulin. However, insulin is capable of increasing the abundance and functional activity of GLUT5 in skeletal muscle cells.^[34]

Fructolysis[link]

The initial catabolism of fructose is sometimes referred to as fructolysis, in analogy with glycolysis, the catabolism of glucose. In fructolysis, the enzyme fructokinase initially produces fructose 1-phosphate, which is split by aldolase B to produce the trioses dihydroxyacetone phosphate and glyceraldehyde [2]. Unlike glycolysis, in fructolysis the triose glyceraldehyde lacks a phosphate group. A third enzyme, triokinase, is therefore required to phosphorylate glyceraldehyde, producing glyceraldehyde-3-phosphate. The resulting trioses are identical to those obtained in glycolysis and can enter the gluconeogenic pathway for glucose or glycogen synthesis, or be further catabolized through the lower glycolytic pathway to pyruvate.

Metabolism of fructose to DHAP and glyceraldehyde[link]

The first step in the metabolism of fructose is the phosphorylation of fructose to fructose 1-phosphate by fructokinase, thus trapping fructose for metabolism in the liver. Fructose 1-phosphate then undergoes hydrolysis by aldolase B to form DHAP and glyceraldehydes; DHAP can either be isomerized to glyceraldehyde 3-phosphate by triosephosphate isomerase or undergo reduction to glycerol 3-phosphate by glycerol 3-phosphate dehydrogenase. The glyceraldehyde produced may also be converted to glyceraldehyde 3-phosphate by glyceraldehyde kinase or converted to glycerol 3-phosphate by glyceraldehyde 3-phosphate dehydrogenase. The metabolism of fructose at this point yields intermediates in the gluconeogenic and fructolytic pathways leading to glycogen synthesis as well as fatty acid and triglyceride synthesis.

Synthesis of glycogen from DHAP and glyceraldehyde 3 phosphate[link]

The resultant glyceraldehyde formed by aldolase B then undergoes phosphorylation to glyceraldehyde 3-phosphate. Increased concentrations of DHAP and glyceraldehyde 3-phosphate in the liver drive the gluconeogenic pathway toward glucose and subsequent glycogen synthesis.^[35] It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes precedence over triglyceride formation.^{[citation needed]} Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.^{[citation needed]}

Figure 6: Metabolic conversion of fructose to glycogen in the liver.

Synthesis of triglyceride from DHAP and glyceraldehyde 3 phosphate[link]

Carbons from dietary fructose are found in both the free fatty acid and glycerol moieties of plasma triglycerides. High fructose consumption can lead to excess pyruvate production, causing a buildup of Krebs cycle intermediates.^[36] Accumulated citrate can be transported from the mitochondria into the cytosol of hepatocytes, converted to acetyl CoA by citrate lyase and directed toward fatty acid synthesis.^[36][37] Additionally, DHAP can be converted to glycerol 3-phosphate as previously mentioned, providing the glycerol backbone for the triglyceride molecule.^[37] Triglycerides are incorporated into very low density lipoproteins (VLDL), which are released from the liver destined toward peripheral tissues for storage in both fat and muscle cells.

Figure 7: Metabolic conversion of fructose to triglyceride in the liver.

Potential health effects[link]

Digestion[link]

Fructose absorption occurs in the small intestine via the GLUT-5^[38] (fructose only) transporter, and the GLUT2 transporter, for which it competes with glucose and galactose. Over-consumption of fructose, inhibition of GLUT2 by other phytochemicals, such as flavonoids,^[39] or other issues, may result in unabsorbed fructose being carried into the large intestine, where, like any sugar, it may provide nutrients for the existing gut flora.

Metabolism[link]

In a 2012 meta-analysis of controlled feeding clinical trials, fructose was not an independent factor for weight gain. Fructose consumption did cause weight gain in a diet with excessive calories, which could be due to the extra calories rather than fructose per se.^[40]

Excess fructose consumption has been hypothesized to be a cause of insulin resistance, obesity,^[41] elevated LDL cholesterol and triglycerides, leading to metabolic syndrome.^[42] In preliminary research, fructose consumption was correlated with obesity.^[43][44] A study in mice showed that a high fructose intake may increase adiposity.^[45]

Although all simple sugars have nearly identical chemical formulae, each has distinct chemical properties. This can be illustrated with pure fructose. A journal article reports that, "...fructose given alone increased the blood glucose almost as much as a similar amount of glucose (78% of the glucose-alone area)".^{[46][47][48][48][49]}

One study concluded that fructose "produced significantly higher fasting plasma triacylglycerol values than did the glucose diet in men" and "...if plasma triacylglycerols are a risk factor for cardiovascular disease, then diets high in fructose may be undesirable".^[50]

Fructose is a reducing sugar, as are all monosaccharides. The spontaneous chemical reaction of simple sugar molecules binding to proteins is known as glycation. Showing potential cause of skin and bone damage in a rat model of diabetes, investigators suggested "that long-term fructose consumption negatively affects the aging process."^[51] Another study using human proteins showed that the glycation caused by fructose appears to be equivalent to glucose and so does not seem to be a better answer for diabetes for this reason alone, save for the smaller quantities required to achieve equivalent sweetness in some foods. It also found evidence for glycation of human lens proteins caused by fructose.^[52]

Compared to sucrose[link]

Studies that have compared high-fructose corn syrup (an ingredient in nearly all soft drinks sold in the US) to sucrose (common table sugar) find that most measured short term physiological effects are equivalent.^{[dubious – discuss]}; however, studies that compare the long term effects between sucrose and fructose have yet to be conducted. For instance, Melanson et al. (2006), studied the short term effects of HFCS and sucrose-sweetened drinks on blood glucose, insulin, leptin, and ghrelin levels. They found no significant differences in any of these parameters.^[53] This is not surprising since sucrose is a disaccharide that digests to 50% fructose and 50% glucose, whereas the high-fructose corn syrup most commonly used on soft drinks is 55% fructose and 45% glucose. The difference between the two lies in the fact that HFCS contains little sucrose, the fructose and glucose being independent moieties. Even so, Melanson et al. found that "Longer-term studies on connections between HFCS, potential mechanisms, and body weight have not been conducted".

Fructose is often recommended for diabetics because it does not trigger the production of insulin by pancreatic β cells, probably because β cells have low levels of GLUT5.^[54][55][56] Fructose has a very low glycemic index of 19 ± 2, compared with 100 for glucose and 68 ± 5 for sucrose.^[57] Fructose is also seventy-three percent sweeter than sucrose (see relative sweetness) at room temperature, so diabetics can use less of it. Studies show that fructose consumed before a meal may even lessen the glycemic response of the meal.^[58]

Liver function[link]

While a few other tissues (e.g., sperm cells^[59] and some intestinal cells) do use fructose directly, fructose is metabolized primarily in the liver.^[60]

Compared with consumption of high glucose beverages, drinking high fructose beverages with meals results in lower circulating insulin and leptin levels, and higher ghrelin levels after the meal.^[61] Since leptin and insulin decrease appetite and ghrelin increases appetite, some researchers suspect that eating large amounts of fructose increases the likelihood of weight gain.^[62]

Excessive fructose consumption may contribute to the development of non-alcoholic fatty liver disease.^[63]

Gout[link]

A 2008 study found a substantial risk of incident gout associated with the consumption of fructose or fructose rich foods.^[64] Cases of gout have risen in recent years, despite commonly being thought of as a Victorian disease, and it is suspected that the fructose found in soft drinks (e.g., carbonated beverages) and other sweetened drinks is the reason for this.^[65][66]

Glycemic index[link]

Because fructose is metabolized in the liver to glucose, fructose has the lowest glycemic index (GI = 19) of all the natural sugars and may be recommended for use by diabetics. In comparison, ordinary table sugar (sucrose, which is half fructose) has a GI of 65 and honey (usually about 50% fructose content) has a GI of 55. Due to the potential that excessive consumption of fructose may be a factor in some diseases, including metabolic syndrome and insulin resistance,^[67] products containing high contents of fructose may be discouraged.

See also[link]

• Tagatose
• Inverted sugar
• DMF (potential fructose-based biofuel)
• Fructose intolerance
• Fructose malabsorption
• Fructan (fructose polymer)
• Galactose
• Glucose
• Glycation
• High fructose corn syrup
• Hyperuricemia
• Seliwanoff's test
• Sucrose
• Sugars in wine
• Agave nectar

References[link]

External links[link]

• [3] Hereditary Fructose Intolerance
• [4]
• How Fructose Impairs the Memory
• Cancer cells metabolize fructose to increase proliferation

Robert H. Lustig, MD is Professor of Clinical Pediatrics, at the University of California, San Francisco (UCSF).^[1] He is nationally recognized in the field of neuroendocrinology, with an emphasis on the regulation of energy balance by the central nervous system.^[2] He has a special interest in childhood obesity.^[2] He has become publicly notable through his efforts to draw attention to the effects that the natural sugar fructose can have on human and especially children's health if consumed in large amounts.^[3] On May 26, 2009, Lustig gave a lecture called “Sugar: The Bitter Truth” which was posted on YouTube the following July and has become a viral success with over nearly 2.5 million viewings (as of Jun 2, 2012).^[3] In this lecture, Lustig notably calls fructose a "poison" and compares its metabolic effects with those of ethanol. Lustig is particularly critical of the widespread use of high-fructose corn syrup in the United States.

Career[link]

Lustig grew up in Brooklyn, New York, and attended Stuyvesant High School in Manhattan.^[4] He obtained his bachelors degree from MIT in 1976, and received his M.D. from Cornell University Medical College in 1980.^[5] From there, he spent six years as a research associate in neuroendocrinology at The Rockefeller University.^[5] He performed his pediatric residency at St. Louis Children's Hospital, and his clinical fellowship at UCSF which he joined in 1984.^[1][2]

He has authored over 85 research articles and 45 chapters. He is the former Chairman of the Obesity Task Force of the Pediatric Endocrine Society, a member of the Obesity Task force of The Endocrine Society, and on the Steering Committee of the International Endocrine Alliance to Combat Obesity.^[1][5]

See also[link]

Sugar Blues - book with a similar theme and Low Blood Sugar and You by Carlton Fredericks 1969

References[link]

External links[link]

• Sugar: The Bitter Truth UCSF Mini Medical School for the Public 7/2009 given by Dr. Lustig , Health and Medicine, Show ID: 16717. Accessed April 2011 (1 hour 30 mins)

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Chris Berens
Chris Berens in his studio in Amsterdam
Born	June 19, 1976 Oss, the Netherlands
Nationality	Dutch
Field	Painter
Training	The Academy of Art and Design in 's-Hertogenbosch
Works	Circle of Friends On a Midnight Voyage The Departure Utopiary

Chris Berens (born June 19, 1976) is a Dutch painter. While he takes inspiration from the quality of light in the paintings of Vermeer and Rembrandt, his themes lie more within the realms of surrealism and visionary art than traditional painting.^[1] Although his work is completely hand-painted, his paintings are often assumed to be digital photographic manipulation.^[2] He lives in Amsterdam with his wife Esther and their daughter Emma Leeuwenhart.

Life[link]

Chris Berens was born in 1976 in Oss, the Netherlands, near the historic town of 's-Hertogenbosch (a.k.a. Den Bosch), the birthplace of Hieronymous Bosch.^[1] When he was a boy, his father brought him to many exhibitions of the Dutch Golden Age painters, including Frans Hals, Rembrandt and Vermeer, and those images became infused into the internal world he began imagining as a child.^[2] He studied illustration at the Academy of Art and Design in Den Bosch, graduating in 1999. While working as a freelance illustrator, Berens began to teach himself to paint in several dilapidated buildings in the rural area near his childhood home.^[3] Attempting to emulate the painting methods of the Old Masters and 19th-century academic artists like Ingres and Bouguereau, he learned by copying their work, and eventually came upon a technique which allowed him to achieve an otherwordly dreamlike impression of the qualities he admired in his predecessors.^[1] More recently, Berens relocated to Amsterdam, where he began exhibiting his work in 2004.^[4] After four sold-out shows at Amsterdam's Jaski Gallery, Berens made the move to infiltrate the American art market in 2008, at Seattle's well-known pop surrealism gallery, Roq la Rue. That sold-out show was his first exposure to American collectors, and the sudden appearance of an artist exhibiting his technical sophistication and evocative dreamlike motifs caused a sensation in pop surrealism circles.^[5] In 2009, he had his first museum retrospective, in which 13 of his paintings were exhibited at the Noordbrabants Museum in Den Bosch.^[1] In 2010, Berens was commissioned to create the cover for Blondie's album Panic of Girls.^[6] He also supplied the artwork for German singer Xavier Naidoo's 2009 album Alles kann besser werden,^[7] which features a painting called "The Big Blue."

Work[link]

In his work, Berens represents an imaginary world he has been seeing since he was a child. "As a boy, I was pretty much what I am now – a dreamer... I always had this really special feeling over me... It's a feeling of another place, a warm place, deep inside me, and I fill that place with all that I see and hear."^[1] This internal universe is painted as if it is being viewed through a distorted lens, which gives the viewer a sense of peering into a secret world, inhabited by mysterious human figures from another age and a menagerie of real and fanciful animals.^[4] He told an interviewer, "I simply try to paint the world inside my head. This world has been with me since I was a child. It is populated by people and animals and is filled with landscapes, villages, cities and scenes. All kinds of things happen in this world and various stories unfold. But it's not the ‘normal’ world, and they are not the things that happen in the regular world."^[3]

Although his 2009 exhibition, "The Only Living Boy In New York," was inspired by the impending birth of his first child,^[8] his most frequently revisited theme is death. In paintings like "In Paradisum," "Circle of Friends," "On a Midnight Voyage" and "First Snow, Guide Me Home," he had explored various facets of the experience of dying,^[1] as he believes that there is "a great deal of beauty present in the moment of death. After witnessing the pain and struggle of dying, you also experience the lightness of acceptance and letting go."^[3] While he feels he is not yet capable of depicting what he envisions to its full potential, he says he strives to improve his skills rapidly, because he is driven to bring these visions into reality. "The reason I paint, is because for me, for now, this is the way to get closest to what I actually see. I suppose you could call it my soul, or the center of me, or my essence."^[1]

In reference to his most recent exhibition, his Seattle gallerist stated, "This new series of works, entitled "Leeuwenhart" ("Lion Heart") takes a turn from his last body of work, which depicted icicle-like skyscrapers and New York cityscapes that sparkled like diamonds, to more of a lush, fairytale world of forests, rolling green hills, and ancient looking villages. And while the usual assortment of magical animal spirits show up in all the works, another character makes an appearance, Chris' newborn daughter Emma Leeuwenhart Berens."^[9]

On occasion, Berens openly references the work of past masters like Ingres, Bouguereau, and Delaroche, because his youthful immersion in their work introduced their subjects, environments and atmosphere into his visionary universe. While these homage paintings often borrow specific elements such as costume and composition, they invariably lift their subjects into a surreal narrative that could never have been conceived by their original creators. Berens explained, "Bouguereau, Ingres, Vermeer and others, I've known by heart ever since I was a little boy... I know them. I'm safe with them. Sometimes I miss them as you can suddenly miss your childhood. So I recreate them, for comfort."^[1]

Technique[link]

Berens is notable for his unique and startlingly photorealistic painting methods, which he developed after teaching himself to paint with oils, in an attempt to emulate Old Master techniques. Although he was dissatisfied with the results he was getting with oil, he discovered that drawing inks, which remain fluid and mutable for up to two days, had a similar flexibility to oil paint.^[3] He explained, "When painting in oil, there are a lot of 'presents' you get from the medium. The way colors mix. The way the paint behaves, from your brush onto your canvas, how fast it dries, what happens if you force-dry it, etc. And oil is the medium that is closest to what I use. The amount of possible interference is at a maximum."^[1] When combined with a recent invention, plastic-coated inkjet printing paper, these fluid inks offered a new opportunity that had not been available to earlier generations of painters – an utterly smooth, semi-transparent surface designed specifically for the absorption of ink.^[1] He said, "I use plastic because it has no texture. I use the plastic on printing paper because it is extremely thin, and clever people have scratched their heads over how to keep the ink put."^[1]

Beginning with pencil sketches and then moving into inks, Berens paints many multiple versions of a figure on inkjet paper. Because the ink remains wet, he is able to work with it for some time – for example, dragging though it with a knife to create fur effects, or using a blow dryer to blur areas into soft focus.^[2] After a large number of small drawings have been completed, he chooses the portions of the figures he is satisfied with and cuts the paper into pieces, retaining the successful sections of the drawings. Peeling the paper backing off the inkjet paper, he is left with fragments of clear plastic bearing semi-transparent ink paintings. These fragments are then collaged onto board with bookbinder's glue, often six or seven layers deep, which creates an illusion of depth.^[4] He says, "I use the transparent layers because some things – such as skin, fur and light – can not be done in one layer (by me, that is). It's the same as real skin – the color and texture you see comes from all those semi-transparent layers of tones, and bumps and holes, that your mind blends into 'skin.'"^[1] Once he is satisfied with the composition, he marries the disparate elements together with ink and varnish, creating a layered assemblage which often includes hundreds of different elements.^[4] In 2011, to demonstrate this unusual technique, the artist recorded a time lapse video of the creation of his painting "Zadok the Deer."

Major Exhibitions[link]

• 2010 "Leeuwenhart," Roq La Rue, Seattle, WA
• 2009 "The Only Living Boy In New York," Sloan Fine Art, New York, NY
• 2009 "Chris Berens: Paintings," Noordbrabants Museum, 's-Hertogenbosch, the Netherlands
• 2009 "White Ones," Jaski Gallery, Amsterdam, the Netherlands
• 2008 "Go West," Roq La Rue, Seattle, WA
• 2008 "Delicate," Jaski Gallery, Amsterdam, the Netherlands
• 2007 "The Heaven Show," Jaski Gallery, Amsterdam, the Netherlands
• 2006 "Zilver," Jaski Gallery, Amsterdam, the Netherlands

Publications[link]

• "Mapping Infinity" (2011)
• "Ninety-Nine" (2008)
• "2239" (2008)
• "Zilver" (2006)

References[link]

External links[link]

• Chris Berens' official website