How does ReduQur® work?
Detailed answer
ReduQur® contains a proprietary blend of 250 mg of Reducose® – scientifically proven to reduce your postprandial (after meals) blood glucose by up to 40% (Lown et al., 2017).
ReduQur® blocks a-glucosidases
For carbohydrates to be useful to humans, it must be digested to monosaccharide form. Enzymes e.g., α-amylases (salivary amylase, pancreatic amylase), and α-glucosidase (sucrase/isomaltase and maltase/glucoamylase) are needed to break down carbohydrates (starches, complex or simple sugars) to monosaccharides to be absorbed through the lining of the gut into the bloodstream. (Holesh et al., 2023), (Lebovitz, 1997)
Alpha-glucosidase (α-glucosidase) inhibitors inhibit (block) the absorption of carbohydrates from the small intestine. These competitively inhibit enzymes that convert complex nonabsorbable carbohydrates into simple absorbable carbohydrates. Alpha-glucosidases normally break down oligosaccharides (disaccharides and polysaccharides) and other complex carbohydrates into monosaccharides (glucose) for absorption in the intestine. (Holesh et al., 2023),(Lebovitz, 1997)
1-Deoxynojirimicin (1-DNJ) in Reducose® mimics sugar or carbohydrate (e.g., glucose or maltose) and binds to α-glucosidase (see image below). This prevents the breakdown of polysaccharides (many linked sugar molecules) and disaccharides (two linked sugar molecules, e.g. maltose) to monosaccharides (e.g., glucose). The bound complex travels down through the small intestine but eventually separates, allowing the Reducose® to be absorbed through the lining of the gut wall while the undigested complex sugar or carbohydrate continues their journey toward excretion. (Lown et al., 2017)
This one binding action by ReduQur® has multiple health benefits
Proposed Health Benefits of Postprandial Glucose Control
Reducose® lowers the postprandial glucose response (PPGR) and glycaemic index (GI) of carbohydrates, to regulate blood glucose. (Ahrén et al., 2021, Ding et al., 2023, Lee et al., 2024, Lown et al., 2017, Mohamed et al., 2022, Thondre et al., 2021)
Increased satiety and decreased urges to snack
Thanks to Reducose® undigested carbohydrates remain in the gut lumen and continue travelling down the small intestine. Once these reach the ileum, the last part of the small intestine, they trigger what is termed the ileal brake. The ileal brake is a nutrient-triggered inhibitory feedback mechanism to your brain that induces satiety. When macronutrients (e.g., carbohydrates) bind to receptors in the ileum, the ileal brake is triggered resulting in a slowing of upper gut motility, reduced appetite, and delayed gastric emptying. (Hester et al, 2023) These activities are mediated through the release of peptide tyrosine tyrosine (PYY), cholecystokinin (CCK), and glucagon-like polypeptide 1 (GLP-1). (Fletcher et al., 2012, Müller et al., 2019)
Weight loss and breaking the vicious cycle of obesity
One of the benefits of the second meal effect is how it may contribute to weight loss. The PPGR from the initial low GI meal, and the ‘knock-on’ lower PPGR from the second meal effect results in the body’s insulin response being moderated down. (Henry et al., 2017).
Insulin’s primary function is to stimulate cells to remove glucose from the blood to maintain glucose homeostasis. As glucose is an important energy source for the body, any excess glucose is stored initially as glycogen, and then as fat, this process is mediated by insulin.
High GI foods cause sharp spikes in postprandial blood glucose, with a resultant excess production of insulin. This excess insulin puts the body into fat storage mode. Calories that would normally be used immediately for energy as carbohydrates are instead stored as fat. To lose weight or maintain a healthy weight, it is therefore important to have a moderate insulin response. This can be achieved through eating low GI meals. Data shows that low GI meals not only reduce the glycemic response, but also improve appetite control and enhance fat oxidation (Fletcher et al, 2012, Henry et al., 2017).
Insulin response is therefore critical in maintaining a healthy weight and body composition. People that are overweight and are insulin resistant need to make and release more and more insulin to remove glucose from the blood. High levels of insulin drives insulin resistance and may also lead to resistance to another hormone – leptin. (Jung & Kim, 2013)
Leptin is one of our main energy regulation hormones and is a key factor in controlling how much we eat and our energy utilization. It is made by our adipose tissues (body fat) and thus, when the body fat percentage is excessive, leptin levels are high, lowering the desire to eat and increasing fat oxidation. Conversely, in situations of starvation (when leptin levels are low), the urge to eat increases, and energy utilization slows. High levels of insulin and insulin resistance are thought to cause leptin resistance, which may lead to a vicious cycle of weight gain. High insulin spikes push calories into fat storage before they can be used for energy; the fat tissue makes increasing amounts of leptin which should lower the desire to eat and increase fat utilization for energy, but due to leptin resistance the signal is not fully received. Rather, the low levels of leptin reaching the brain increases the desire to eat and slows down energy expenditure, making it more difficult to lose weight and in many cases, potentially leading to further weight gain. (Jung & Kim, 2013)
Reducose® has been shown in several clinical trials to significantly lower the insulin response after consuming carbohydrates as well as lowering the glycemic index of food. This helps to put the body into fat burning mode and decreases glucose calories stored as fat. Reducose® has also been shown to increase insulin sensitivity (Liu et al., 2016), and published literature reports that the active compound in Reducose®, 1-DNJ, increases leptin sensitivity (Kim et al., 2017).
This combination of activities may help break the vicious cycle of weight gain, and for people trying to lose weight, Reducose® may have additional weight loss benefits. Reducose® blocks a portion of carbohydrate calories from getting into the body, which can stimulate the ileal brake further increasing satiety (important for people restricting calories). It may help trigger the second meal effect (a lower PPGR of the second meal) and increase fat utilization for energy.
Benefits for the gut microbiome
An additional benefit of Reducose® is the effect it has on the microbiome. After passing through the ileum, the carbohydrates that were not digested due to Reducose® enter the large intestine where they are fermented to short-chain fatty acids by the gut microbiome. (Schillinger et al., 2023)
There are numerous health benefits associated with providing carbohydrates, especially slowly digestible starch (SDS) and resistant starch (RS), to the microbiome. These carbohydrates feed and nourish the bacteria in the microbiome that have a saccharolytic (carbohydrate) metabolism. Lactobacilli and bifidobacteria are important beneficial bacteria and are almost exclusively saccharolytic. Having healthy colonic and mucosal microflora helps prevent pathogenic bacteria from invading the GI tract. The beneficial effects these bacteria have in humans is attributed to how they consume the carbohydrates that were not digested in the upper GI. The bacteria ferment these carbohydrates and convert them into short-chain fatty acids (SCFA) such as acetate, propionate, and butyrate. SCFA have several potential beneficial health effects. For example, colonic epithelial cells preferentially use butyrate as an energy source and its presence in the colon aides the growth of colonocytes, which are reported to have a protective function against colonic disorders. (Slavin, 2013)
SCFA production also inhibits the growth of pathogenic organisms in the colon by reducing luminal and faecal pH. This low pH reduces peptide degradation and the consequent formation of toxic compounds such as ammonia, amines, and phenolic compounds (Slavin, 2013). SCFAs are readily absorbed back into the body. Circulating SCFA can improve immune functions by increasing the number of T-helper cells, macrophages, and neutrophils. They also lower the hepatic production of cholesterol through interfering with its synthesis. (Slavin, 2013)
The colonic bacteria use a range of carbohydrate hydrolyzing enzymes to produce these beneficial SCFAs and it is here that the difference between Reducose® and other ‘carb blockers’ becomes apparent. The enzymes that the microbiome use are analogous to human glycosidase enzymes. If inhibitors of these hydrolyzing enzymes are present in the large intestine, then the microbiome’s fermentation ability is reduced, which can result in unwanted gastrointestinal symptom. For example, if sugars are left unfermented in the colon, they have an osmotic effect and draw water out of the body into the colon, which could result in diarrhoea. Clinical studies have shown that Reducose® does not cause any increase in gastrointestinal symptoms (Lown et al., 2017).
Promote fat burning through the second meal effect
Linked to the ileal brake is the second meal effect. The second meal effect is a phenomenon where the glycaemic index (GI) of one meal can influence the glycemic response to a subsequent meal. Having a low GI intake in one meal lowers the postprandial glycemic response (PPGR) in a subsequent meal. This effect is thought to be mediated through several interacting mechanisms, including through the actions of incretin hormones, e.g., Glucagon-like polypeptide 1 and Gastric inhibitory polypeptide (GLP-1 and GIP) and by the fermentation of undigested carbohydrates to short-chain fatty acids by the microbiome and their subsequent absorption. (Fletcher et al., 2012)
The benefits of the second meal effect, while observable as a lower postprandial glucose response, extends to weight management. The second meal effect increases the rate of fat oxidation and favours the use of fat (lipids) to meet the body’s energy requirements, while people who eat high GI meals favour fat storage and the use of carbohydrates for energy. (Henry et al., 2017)
Promotes Longevity
Elevated glucose levels are associated with many age-related conditions, and restricting calories, especially glucose calories, has been shown to significantly increase lifespan. Our bodies have natural repair mechanisms to limit and repair damage, however, many of these pathways are inactivated by constant glucose flux. Examples of these repair pathways are the sirtuin and PARP (poly-ADP-ribose polymerase) pathways, which when activated, repair damaged proteins and DNA respectively. To activate these pathways, our bodies require a co-factor called nicotinamide adenine dinucleotide (NAD), which is consumed by the sirtuins and PARP during protein and DNA repair. NAD is involved in many processes apart from sirtuin-mediated repair, one of which is acting as a redox enzyme during energy metabolism. (Cantó et al., 2013, Brewer et al., 2016)
Our bodies generate energy via different pathways and when there are high levels of glucose available, our bodies convert the glucose into energy through glycolysis in the cytoplasm, which involves the conversion of NAD to NADH. As this is an efficient energy production mechanism, it is favoured whenever glucose is available. This pathway depletes the NAD pool, resulting in an inability to activate sirtuins or PARP. When calories are restricted, especially glucose calories, our bodies generate energy in the mitochondria, and the reverse redox reaction takes place: NAD is produced from NADH, shifting the balance to excess NAD, allowing our repair processes to be activated. Decreasing glucose calorie intake directly favours energy production through secondary pathways, and preserves the NAD pool of the body, allowing it to maintain its efficient DNA-repair and protection mechanisms. (Cantó et al., 2013; Brewer et al., 2016)
The US National Institute of Aging has run a research programme for the past 18 years that evaluates the effects of various compounds on life extension. To date, only seven compounds have significantly increased lifespan, two of which are diabetic drugs that lower postprandial glucose levels. When looking at the effects of these compounds in mice, while there were increases in glucose tolerance and lowered fasting glucose levels, there was no change in the HbA1c (a three-month average indicator of blood glucose levels), suggesting that the benefit is due to lowering postprandial glucose spikes rather than lowering average glucose levels (glucose spikes are the only difference between the blood glucose profiles between test and control groups). The causes of death between test and control groups were equivalent, showing that lowering the glucose spikes led to a delay in morbidities of ageing and, not only were the animals living longer but the extra time they had was spent in a healthy state. (Miller et al., 2017; Strong et al., 2016; Harrison et al., 2014)
Reducose® acts in a similar manner through its ability to blunt postprandial glucose rises. By lowering the amount of glucose that enters the bloodstream, it is anticipated that there would also be a shift of the NAD:NADH ratio, making available NAD for activation of the sirtuin and PARP repair pathways. This enables the body to maintain healthy and efficient repair mechanisms, potentially increasing our chances to live longer in good health. Reducose® is an ideal cornerstone ingredient for longevity and healthy ageing products delivering its health benefits in a serving size of only 250 mg.
Healthy Ageing - Improvement in cognitive function
An often-overlooked benefit of eating low GI foods is the effect it has on supporting healthy cognitive performance. Younger brains are relatively bigger, more active, and use more glucose per unit weight compared with adults, which makes them more responsive to (and susceptible to changes in) glucose provision. Studies have shown that low GI meals resulted in better cognitive performance in the postprandial period, better-sustained attention, better memory, and better learning. The brain is sensitive to changes in nutrient supply, and it has been suggested that it is not the amount of glucose but rather the fluctuations in glucose levels that may negatively affect cognitive performance. (Philippou and Constantinou, 2014)
The constant postprandial concentration that is delivered by low GI foods results in better cognitive performance compared with the rapid increase and subsequent disposal of glucose (often below the fasted level) seen with high GI foods. This is supported by studies that have shown that the low GI benefits are more predominant in the late postprandial phase due to the more stable glucose and insulin profiles. The brain is also an insulin-sensitive organ and individuals that are insulin resistant and have poor glucose regulation have a higher risk of cognitive dysfunction. Low GI diets benefit whole-body insulin sensitivity, and therefore a low GI diet can potentially influence cognitive function in both the short term through better control of glucose release, and in the long term through its effects linking glucose regulation and cognition. (Philippou and Constantinou, 2014)
