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
A Combination of Nicotinamide and D-Ribose (RiaGev) Is Safe and Effective to Increase NAD+ Metabolome in Healthy Middle-Aged Adults: A Randomized, Triple-Blind, Placebo-Controlled, Cross-Over Pilot Clinical Trial
This study evaluated the effects of RiaGev, a combination of nicotinamide and D-ribose, on NAD+ metabolome enhancement in healthy middle-aged adults. Supplementing 1520 mg twice daily for 7 days significantly increased NAD+ metabolites, reduced blood glucose without altering insulin secretion, and decreased waking cortisol levels. Participants also reported less fatigue and improved mental focus, with no adverse effects observed, demonstrating RiaGev’s safety and efficacy.
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.
Structural features of sugars that trigger or support conidial germination in the filamentous fungus Aspergillus niger
The asexual spores (conidia) of Aspergillus niger germinate to produce hyphae under appropriate conditions. Germination is initiated by conidial swelling and mobilization of internal carbon and energy stores, followed by polarization and emergence of a hyphal germ tube. The effects of different pyranose sugars, all analogues of d-glucose, on the germination of A. niger conidia were explored, and we define germination as the transition from a dormant conidium into a germling. Within germination, we distinguish two distinct stages, the initial swelling of the conidium and subsequent polarized growth. The stage of conidial swelling requires a germination trigger, which we define as a compound that is sensed by the conidium and which leads to catabolism of d-trehalose and isotropic growth. Sugars that triggered germination and outgrowth included d-glucose, d-mannose, and d-xylose. Sugars that triggered germination but did not support subsequent outgrowth included d-tagatose, d-lyxose, and 2-deoxy-d-glucose. Nontriggering sugars included d-galactose, l-glucose, and d-arabinose. Certain nontriggering sugars, including d-galactose, supported outgrowth if added in the presence of a complementary triggering sugar. This division of functions indicates that sugars are involved in two separate events in germination, triggering and subsequent outgrowth, and the structural features of sugars that support each, both, or none of these events are discussed. We also present data on the uptake of sugars during the germination process and discuss possible mechanisms of triggering in the absence of apparent sugar uptake during the initial swelling of conidia.
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.
Naturally occurring rare sugars are free radical scavengers and can ameliorate endoplasmic reticulum stress
Because of potential use of naturally occurring rare sugars as sweeteners, their effect on superoxide (SO), hydroxyl and peroxyl radicals and endoplasmic reticulum (ER) stress was examined in human coronary artery endothelial cells. SO generation was measured using the superoxide-reactive probe 2-methyl-6-(4-methoxyphenyl)-3,7-dihydroimidazo[1,2-A]pyrazin-3-one hydrochloride chemiluminescence. Phycoerythrin fluorescence based assay was used to monitor scavenging activity of sugars in the presence of hydroxyl or peroxyl radical generators [CuSO4 and azobis (2 amidinopropane) hydrochloride respectively]. Measurements were made in relative light units (RLU). ER stress was measured with an ER stress-sensitive secreted alkaline phosphatase (SAP) assay and by Western blot analysis of the expression and phosphorylation of key proteins in the unfolded protein response, namely CHOP47, eIF2α and JNK1. D-Glucose (27.5 mM) increased SO generation (5536 ± 283 vs. 2963 ± 205 RLU in controls; p < 0.0007) and decreased SAP secretion (73411 ± 3971 vs. 101749 ± 7652 RLU in controls; p < 0.005) indicating ER stress. Treatment of cells with 5.5 or 27.5 mM of D-allulose, D-allose, D-sorbose and D-tagatose reduced SO generation (all p < 0.05). This could not be attributed to inhibition of cellular uptake of dextrose by the rare sugars tested. In a cell free system, all four rare sugars had significantly more SO, hydroxyl and peroxyl radical scavenging activity compared to dextrose (all p < 0.01). Treatment of cells with rare sugars reduced ER stress. However, unlike other three rare sugars, D-sorbose did not inhibit tunicamycin-induced eIF2α phosphorylation. Naturally occurring rare sugars are free radical scavengers and can reduce ER stress.
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.
The impact of sugar consumption on stress driven, emotional and addictive behaviors
High rates of overweight and obesity are a global concern, with overconsumption of high fat/sugar foods playing a significant role. Long-term sugar consumption can lead to neural plasticity, reducing impulse control and increasing susceptibility to high fat/sugar foods. The neural pathways involved in emotions and survival responses overlap, suggesting a link between stress, emotions, and obesity. Sucrose consumption activates the mesocorticolimbic system similarly to addictive substances, resulting in neuronal changes, altered emotional processing, and modified behavior in both animals and humans. This comprehensive review examines over 300 studies on the interaction between sugar consumption, stress, and emotions, emphasizing the neurochemical changes and neural adaptations that influence emotion and behavior after sugar consumption. Understanding these mechanisms can aid in the development of novel therapeutic strategies for obesity.
D-Tagatose Feeding Reduces the Risk of Sugar-Induced Exacerbation of Myocardial I/R Injury When Compared to Its Isomer Fructose
In a study comparing the effects of fructose and D-tagatose on heart health, rats fed a diet high in fructose experienced weight gain, negative changes in glucose, insulin, and lipid levels, and increased heart damage from ischemia/reperfusion injury. In contrast, rats consuming a diet high in D-tagatose, a low-calorie fructose isomer, showed less oxidative stress, lower inflammation, and improved heart protection. D-tagatose also reduced inflammation markers and improved heart enzyme levels compared to fructose. This suggests that D-tagatose may be a healthier alternative to fructose, with less impact on metabolic health and heart disease vulnerability.
Daily limited access to sweetened drink attenuates hypothalamic-pituitary-adrenocortical axis stress responses
A rat model was developed to explore the relationship between preferred food consumption and stress responses. Rats were given access to sweetened drinks (sucrose or saccharin) or water in addition to their regular water intake. Half of the rats were subjected to chronic variable stress (CVS) while the others served as nonhandled controls. The results showed that sucrose consumption reduced the stress hormone corticosterone response to restraint stress in both CVS rats and nonhandled controls. Saccharin had a similar but less pronounced effect. Sucrose consumption also affected gene expression in brain regions associated with stress regulation. These findings suggest that limited consumption of sweetened drinks can attenuate stress responses, indicating that the intake of palatable substances may serve as a natural mechanism to dampen physiological stress responses.
Expression and nuclear translocation of glucocorticoid receptors in type 2 taste receptor cells
The secretion of glucocorticoids (GCs) in response to stress affects ingestive behavior and taste preferences. This study investigated the presence of glucocorticoid receptors (GRs) in taste tissue and their potential role in modulating the response of the taste system to stress. The researchers found mRNA expression of GRα in taste papillae and non-taste tissue, with higher levels in taste tissue. GR protein was detected in various taste bud populations. In transgenic mice, the majority of sweet-/umami-sensitive taste cells expressed GR. When mice were subjected to restraint stress, GR protein in sweet-sensitive taste cells relocated to the nucleus. These findings suggest that GR activation in taste receptor cells may influence taste qualities such as sweet, umami, and bitter, potentially shaping the response of the taste system to stress.
Cross-lagged associations between children’s stress and adiposity: the Children’s Body Composition and Stress study
This longitudinal study found that adiposity (body fat) in children is associated with increased stress levels over time. However, stress does not directly cause increases in adiposity. The relationship between stress and adiposity is influenced by cortisol levels and lifestyle factors. These findings highlight the importance of considering multiple factors in obesity prevention programs and the negative impact of unhealthy body composition on children’s well-being.
Get in touch with Intelligent Sugar
Got a question about Dr Coy’s sugars? Contact info@intelligentsugar.info
If you have a question about a specific health condition, please speak to your doctor.