Learn more about Dr. Coy and the creation of his sugar solutions.
Dr Johannes Coy is a world-renowned scientist whose research focuses on the health benefits of sugar awareness. Dr Coy has made a number of important genetic discoveries which change our understanding of cancer and nutrition and make him the leading expert on sugars.
Book: Fit with Sugar, by Dr Johannes Coy
Dr Coy has written several books about cancer nutrition. His latest book, Fit with Sugar, is now available. In this book, you’ll discover the evolutionary role of sugar in the human body. Consuming too much conventional sugar isn’t good for our health, but with the right sugars, we can stop cell ageing, keep the brain fit, protect against diseases and switch on fat burning. Find out how you can maintain physical and mental performance using natural low- glycaemic sugars and sugar substitutes. The book includes many delicious recipes for cakes, snacks and desserts, so you can implement a sugar-conscious diet easily and intelligently, without giving up sweet treats.
Buy the book: Cancer-Fighting Diet: Diet and Nutrition Strategies to Help Weaken Cancer Cells and Improve Treatment, by Dr Johannes Coy.
Research & Resources
D-Tagatose: A Rare Sugar with Functional Properties and Antimicrobial Potential against Oral Species
D-tagatose, a low-calorie rare sugar, offers significant health benefits, particularly for oral health. With antioxidant and prebiotic properties, it has a low glycaemic impact, supports lipid profile improvement, and shows potential in managing diabetes and obesity. Studies highlight its antibacterial effects, including reducing cariogenic bacteria like S. mutans, inhibiting biofilm formation, and preventing pH decline. D-tagatose also promotes oxidative stress reduction and demonstrates effectiveness as an air-polishing powder for biofilm removal. These attributes position D-tagatose as a promising alternative sugar for preventing systemic diseases and enhancing oral health.
The genes and enzymes for the catabolism of galactitol, D-tagatose, and related carbohydrates in Klebsiella oxytoca M5a1 and other enteric bacteria display convergent evolution
Enteric bacteria (Enteriobacteriaceae) carry on their single chromosome about 4000 genes that all strains have in common (referred to here as “obligatory genes”), and up to 1300 “facultative” genes that vary from strain to strain and from species to species. In closely related species, obligatory and facultative genes are orthologous genes that are found at similar loci. We have analyzed a set of facultative genes involved in the degradation of the carbohydrates galactitol, D-tagatose, D-galactosamine and N-acetyl-galactosamine in various pathogenic and non-pathogenic strains of these bacteria. The four carbohydrates are transported into the cell by phosphotransferase (PTS) uptake systems, and are metabolized by closely related or even identical catabolic enzymes via pathways that share several intermediates. In about 60% of Escherichia coli strains the genes for galactitol degradation map to a gat operon at 46.8 min. In strains of Salmonella enterica, Klebsiella pneumoniae and K. oxytoca, the corresponding gat genes, although orthologous to their E. coli counterparts, are found at 70.7 min, clustered in a regulon together with three tag genes for the degradation of D-tagatose, an isomer of D-fructose. In contrast, in all the E. coli strains tested, this chromosomal site was found to be occupied by an aga/kba gene cluster for the degradation of D-galactosamine and N-acetyl-galactosamine. The aga/kba and the tag genes were paralogous either to the gat cluster or to the fru genes for degradation of D-fructose. Finally, in more then 90% of strains of both Klebsiella species, and in about 5% of the E. coli strains, two operons were found at 46.8 min that comprise paralogous genes for catabolism of the isomers D-arabinitol (genes atl or dal) and ribitol (genes rtl or rbt). In these strains gat genes were invariably absent from this location, and they were totally absent in S. enterica. These results strongly indicate that these various gene clusters and metabolic pathways have been subject to convergent evolution among the Enterobacteriaceae. This apparently involved recent horizontal gene transfer and recombination events, as indicated by major chromosomal rearrangements found in their immediate vicinity.
Ecological impact of a rare sugar on grapevine phyllosphere microbial communities
Plants host a complex microbiota inside or outside their tissues, and phyllosphere microorganisms can be influenced by environmental, nutritional and agronomic factors. Rare sugars are defined as monosaccharides with limited availability in nature and they are metabolised by only few certain microbial taxa. Among rare sugars, tagatose (TAG) is a low-calories sweetener that stimulates and inhibits beneficial and pathogenic bacteria in the human gut microbiota, respectively. Based on this differential effect on human-associated microorganisms, we investigated the effect of TAG treatments on the grapevine phyllosphere microorganisms to evaluate whether it can engineer the microbiota and modify the ratio between beneficial and pathogenic plant-associated microorganisms. TAG treatments changed the structure of the leaf microbiota and they successfully reduced leaf infections of downy mildew (caused by Plasmopara viticola) and powdery mildew (caused by Erysiphe necator) under field conditions. TAG increased the relative abundance of indigenous beneficial microorganisms, such as some potential biocontrol agents, which could partially contribute to disease control. The taxonomic composition of fungal and bacterial leaf populations differed according to grapevine locations, therefore TAG effects on the microbial structure were influenced by the composition of the originally residing microbiota. TAG is a promising biopesticide that could shift the balance of pathogenic and beneficial plant-associated microorganisms, suggesting selective nutritional/anti-nutritional properties for some specific taxa. More specifically, TAG displayed possible plant prebiotic effects on the phyllosphere microbiota and this mechanism of action could represent a novel strategy that can be further developed for sustainable plant protection.
Effects of D-Tagatose on the Growth of Intestinal Microflora and the Fermentation of Yogurt
To investigate the effect of tagatose on the growth of intestinal bacteria, various species were cultivated individually on m-PYF medium containing tagatose as a carbon source. The tagatose inhibited the growth of intestinal harmful microorganisms such as Staphylococcus aureus subsp. aureus, Listeria monocytogenes, Vibrio parahaemolyticus, Salmonella Typhimurium, and Pseudomonas fluorescens. In the case of beneficial microorganisms found in the intestine, Lactobacillus casei grew effectively on m-PYF medium containing tagatose, while Lactobacillus plantarum, Lactobacillus brevis, Leuconostoc citreum, and Lactobacillus acidophilus did not. To examine the effect of tagatose on fermentation by Lactobacillus casei, yogurt was prepared with tagatose as a carbon source. The resulting acid production stimulated a remarkable growth of lactic acid bacteria in the yogurt. After fermentation for 24 hours, the viable cell count and viscosity of yogurt were above 8.49 log CFU/mL and 1,266 cps, respectively. Moreover, sensory evaluations showed that the yogurt supplemented with tagatose was as acceptable as control yogurt prepared with glucose as a carbon source. The changes in pH, titratable acidity and lactic acid bacteria in yogurt prepared with tagatose did not show any significant changes during storage for 15 days at 4°C.
Effect of L-glucose and D-tagatose on bacterial growth in media and a cooked cured ham product
Cured meats such as ham can undergo premature spoilage on account of the proliferation of lactic acid bacteria. This spoilage is generally evident from a milkiness in the purge of vacuum-packaged sliced ham. Although cured, most hams are at more risk of spoilage than other types of processed meat products because they contain considerably higher concentrations of carbohydrates, approximately 2 to 7%, usually in the form of dextrose and corn syrup solids. Unfortunately, the meat industry is restricted with respect to the choice of preservatives and bactericidal agents. An alternative approach from these chemical compounds would be to use novel carbohydrate sources that are unrecognizable to spoilage bacteria. L-Glucose and D-tagatose are two such potential sugars, and in a series of tests in vitro, the ability of bacteria to utilize each as an energy source was compared to that of D-glucose. Results showed that both L-glucose and D-tagatose are not easily catabolized by a variety of lactic bacteria and not at all by pathogenic bacteria such as Escherichia coli O157:H7, Salmonella Typhimurium, Staphylococcus aureus, Bacillus cereus, and Yersinia enterocolitica. In a separate study, D-glucose, L-glucose, and D-tagatose were added to a chopped and formed ham formulation and the rate of bacterial growth was monitored. Analysis of data by a general linear model revealed that the growth rates of total aerobic and lactic acid bacteria were significantly (P < 0.05) slower for the formulation containing D-tagatose than those containing L- or D-glucose. Levels of Enterobacteriaceae were initially low and these bacteria did not significantly (P < 0.20) change in the presence of any of the sugars used in the meat formulations. Compared to the control sample containing D-glucose, the shelf life of the chopped and formed ham containing D-tagatose at 10 degrees C was extended by 7 to 10 days. These results indicate that D-tagatose could deter the growth of microorganisms and inhibit the rate of spoilage in a meat product containing carbohydrates.
Cytoprotection by fructose and other ketohexoses during bile salt-induced apoptosis of hepatocytes
Toxic bile salts cause hepatocyte necrosis at high concentrations and apoptosis at lower concentrations. Although fructose prevents bile salt-induced necrosis, the effect of fructose on bile salt-induced apoptosis is unclear. Our aim was to determine if fructose also protects against bile salt-induced apoptosis. Fructose inhibited glycochenodeoxycholate (GCDC)-induced apoptosis in a concentration-dependent manner with a maximum inhibition of 72% +/- 10% at 10 mmol/L. First, we determined if fructose inhibited apoptosis by decreasing adenosine triphosphate (ATP) and intracellular pH (pHi). Although fructose decreased ATP to <25% of basal values, oligomycin (an ATP synthase inhibitor) did not inhibit apoptosis despite decreasing ATP to similar values. Fructose (10 mmol/L) decreased intracellular pH (pHi) by 0.2 U. However, extracellular acidification (pH 6.8), which decreased hepatocyte pHi 0.35 U and is known to inhibit necrosis, actually potentiated apoptosis 1.6-fold. Fructose cytoprotection also could not be explained by induction of bcl-2 transcription or metal chelation. Because we could not attribute fructose cytoprotection to metabolic effects, alterations in the expression of bcl-2, or metal chelation, we next determined if the poorly metabolized ketohexoses, tagatose and sorbose, also inhibited apoptosis; unexpectedly, both ketohexoses inhibited apoptosis. Because bile salt-induced apoptosis and necrosis are inhibited by fructose, these data suggest that similar processes initiate bile salt-induced hepatocyte necrosis and apoptosis. In contrast, acidosis, which inhibits necrosis, potentiates apoptosis. Thus, ketohexose-sensitive pathways appear to initiate both bile salt-induced cell apoptosis and necrosis, whereas dissimilar, pH-sensitive, effector mechanisms execute these two different cell death processes.
Fructose and tagatose protect against oxidative cell injury by iron chelation
To further investigate the mechanism by which fructose affords protection against oxidative cell injury, cultured rat hepatocytes were exposed to cocaine (300 microM) or nitrofurantoin (400 microM). Both drugs elicited massively increased lactate dehydrogenase release. The addition of the ketohexoses D-fructose (metabolized via glycolysis) or D-tagatose (poor glycolytic substrate) significantly attenuated cocaine- and nitrofurantoin-induced cell injury, although both fructose and tagatose caused a rapid depletion of ATP and compromised the cellular energy charge. Furthermore, fructose, tagatose, and sorbose all inhibited in a concentration-dependent manner (0-16 mM) luminolenhanced chemiluminescence (CL) in cell homogenates, indicating that these compounds inhibit the iron-dependent reactive oxygen species (ROS)-mediated peroxidation of luminol. Indeed, both Fe2+ and Fe3+ further increased cocaine-stimulated CL, which was markedly quenched following addition of the ketohexoses. The iron-independent formation of superoxide anion radicals (acetylated cytochrome c reduction) induced by the prooxidant drugs remained unaffected by fructose or tagatose. The iron-chelator deferoxamine similarly protected against prooxidant-induced cell injury. In contrast, the nonchelating aldohexoses D-glucose and D-galactose did not inhibit luminol CL nor did they protect against oxidative cell injury. These data indicate that ketohexoses can effectively protect against prooxidant-induced cell injury, independent of their glycolytic metabolism, by suppressing the iron-catalyzed formation of ROS.
Antioxidant and cytoprotective properties of D-tagatose in cultured murine hepatocytes
D-Tagatose is a zero-energy producing ketohexose that is a powerful cytoprotective agent against chemically induced cell injury. To further explore the underlying mechanisms of cytoprotection, we investigated the effects of D-tagatose on both the generation of superoxide anion radicals and the consequences of oxidative stress driven by prooxidant compounds in intact cells. Primary cultures of hepatocytes derived from male C57BL/6 mice were exposed to the redox cycling drug nitrofurantoin (NFT). Lethal cell injury induced by 300 microM NFT was completely prevented by high concentrations (20 mM) of D-tagatose, whereas equimolar concentrations of glucose, mannitol, or xylose were ineffective. The extent of NFT-induced intracellular superoxide anion radical formation was not altered by D-tagatose, indicating that the ketohexose did not inhibit the reductive bioactivation of NFT. However, the NFT-induced decline of the intracellular GSH content was largely prevented by D-tagatose. The sugar also afforded complete protection against NFT toxicity in hepatocytes that had been chemically depleted of GSH. Furthermore, the ketohexose fully protected from increases in both membrane lipid peroxidation and protein carbonyl formation. In addition, D-tagatose completely prevented oxidative cell injury inflicted by toxic iron overload with ferric nitrilotriacetate (100 microM). In contrast, D-tagatose did not protect against lethal cell injury induced by tert-butyl hydroperoxide, a prooxidant which acts by hydroxyl radical-independent mechanisms and which is partitioned in the lipid bilayer. These results indicate that D-tagatose, which is a weak iron chelator, can antagonize the iron-dependent toxic consequences of intracellular oxidative stress in hepatocytes. The antioxidant properties of D-tagatose may result from sequestering the redox-active iron, thereby protecting more critical targets from the damaging potential of hydroxyl radical.
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