TABLE CONTENT
1.Abstract 2. Introduction 3. Sugar on the body, brain, and behavior3.1 Fructose vs. glucose3.2 Hedonic response to sugar and rewards of sugar intake3.3 Hedonic response: fructose vs glucose3.4 Sugar addiction3.5 Sugar, obesity, and cognitive functioning4. Sugar compared4.1. Sugar vs. fat4.2 Sugar vs. complex carbohydrates5. Conclusions and future directions6. Acknowledgement7. References
1. ABSTRACT
Sugar is highly palatable and rewarding, both in its taste and nutritive input. Excessive sugar consumption, however, may trigger neuroadaptations in the reward system that decouple eating behavior from caloric needs and leads to compulsive overeating. Excessive sugar intake is in turn associated with adverse health conditions, including obesity, metabolic syndrome, and inflammatory diseases. This review aims to use recent evidence to connect sugar’s impact on the body, brain, and behavior to elucidate how and why sugar consumption has been implicated in addictive behaviors and poor health outcomes.
2. INTRODUCTION
The past several years have been marked by a growing awareness of the unsavory effects of excessive sugar consumption. As of 2015, the World Health Organization recommends reducing added sugar to less than 5% of daily caloric intake to lower the risk of unhealthy weight gain and obesity (1). Last year, the American Academy of Pediatrics recommended that parents should not feed fruit juice to infants younger than one year because of its high sugar content (2). This advice reflects a growing body of research investigating added sugar as an instigator of obesity and metabolic syndrome (a combination of risk factors like high blood pressure, high triglycerides, high fasting blood glucose, etc. that increase the likelihood of cardiovascular disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease (3). Other research has examined sugar as a potentially addictive substance. However, the public is still flooded with mixed messages from advertising, health organizations, and popular press about sugar’s impact on human health. Unbiased scientific findings from the past several years have begun to help clear up this consumer confusion.
Sugar typically refers to a category of simple carbohydrates that includes monosaccharides like fructose and glucose, and disaccharides, like sucrose and lactose, which have different effects on the body and brain. The present review focuses primarily on added sugars, namely sucrose and high fructose corn syrup (HFCS), because of their negative impact on health and because they predominate in the typical western diet. Sucrose, or table sugar, is a disaccharide made up of one-part glucose And one-part fructose. In contrast, HFCS is comprised of 42% or 55% of free fructose, complemented by free glucose (4). Because most added sugar consumption comes from sucrose or HFCS, we typically consume both fructose and glucose together. However, research on the individual monosaccharides, fructose and glucose, has revealed large differences in how they affect the body.
The present review aims to explore sugar and its physiological effects on the brain and body, which may play a role in its adverse health effects. First, we discuss different types of sugar and how they are processed by the body and brain. Second, we address sugar’s hedonic effects, addictive properties, and connections with obesity, primarily focusing on imaging studies in humans with support from the animal literature. Third, we aim to compare how sugar is metabolized and processed compared to other macronutrients such as fat and fiber-rich complex carbohydrates to further emphasize any singular effects attributable to sugar.
3. SUGAR ON THE BODY, BRAIN, AND BEHAVIOR
3.1 Fructose vs. glucose
Monosaccharides differ in how they are processed by the brain and influence brain activity. Although some consumers may believe that fructose is healthier because it comes from fruit (5), this notion is misguided. The body does not respond in the same way to fructose in fruit as to added fructose. As an added sugar, fructose is particularly implicated in metabolic syndrome, hypertension, insulin resistance, lipogenesis, diabetes and associated retinopathy, kidney disease, and inflammation (4,6,7,8,9). Accordingly, reduction of fructose in the diet of at risk individuals appears to reduce these symptoms. When added fructose was replaced by glucose (in the form of starch) in the diets of obese children, liver fat, de novo lipogenesis, diastolic blood pressure, triglycerides, and LDL cholesterol decreased while insulin sensitivity improved (10,11). Furthermore, in fruit, fructose is accompanied by antioxidants, flavonols, potassium, vitamin C and high fiber, which may collectively outweigh any negative consequences of fructose content (4, 12). Importantly, the quantities of fructose in a piece of fruit and a sweetened beverage are drastically different. For example, the fructose in a peach represents approximately 1% of the fruit’s weight whereas fructose accounts for half the weight of HFCS (7).
Differences in health effects between glucose and fructose may be caused by the different metabolic pathways they follow. Digestion and absorption of sugars takes place in the top half of the digestive tract (13). Most of the glucose in the blood stream is not stored in the liver but rather, through the action of insulin, quickly passes through to muscle, adipose, and other peripheral tissues where it can immediately be used as energy (13). Fructose, on the other hand, is a less direct source of energy. Independent of insulin, the liver converts fructose to glucose, lactate, and/or fatty acids before passing it to the blood stream where it can be oxidized in other tissues for energy (14,15,8). Compared to glucose, fructose produces smaller increases in plasma glucose and circulating satiety hormones such as glucagon-like peptide-1 (GLP-1) and insulin (16). Fructose also attenuates suppression of ghrelin, an appetitive hormone, while glucose does not (17). Therefore, fructose allows overconsumption of calories by failing to activate the body’s signals to stop eating.
Beyond weight gain and obesity, other diseases are linked to fructose’s metabolic pathway. High dietary fructose can increase de novo lipogenesis in the liver (18) in a way that is reminiscent of ethanol (19). This is because fructose bypasses the main rate limiting step of glycolysis to act as a precursor for fatty acid synthesis (20,21,8). This bypass may also explain the increased rates of non-alcoholic fatty liver disease and resulting insulin resistance associated with fructose ingestion (20). Fructose also seems to contribute to inflammation in the body. When in excess in the intestinal lumen, fructose generates advanced glycation end products (AGE’s), which are related to neurodegenerative diseases, atherosclerosis, and chronic inflammatory diseases such as asthma, diabetes, and associated cognitive decline (22,9,23,24,25).
Glucose and fructose have differing impacts on the brain. Compared to other organs, the brain has vastly disproportionate energy requirements relative to its weight. Neurons have an especially high energy demand for generating postsynaptic potentials and action potentials, necessitating large amounts of energy (26). Glucose from the bloodstream is the main source of energy for the brain (26,27). Glucose transporters in astrocytes and the epithelial cells of the blood brain barrier (BBB) are responsible for transporting glucose into the brain (16,26). Neurons then absorb glucose from astrocytes using glucose transporters. In contrast, fructose cannot directly supply the brain with energy as it crosses the blood brain barrier to a much lesser degree than glucose (16,26). However, fructose administered intraperitoneally in rodents crossed the BBB to some degree and triggered neuronal activation. This fructose was metabolized into lactate, an alternate energy source, in the hypothalamus (16). Fructose’s ability to cross the BBB has not yet been studied in humans, so more research is needed on the direct effects of fructose in the brain. Nonetheless, the differential effects of the two monosaccharides may be attributed in part to glucose’s more immediate and direct availability to the brain as an energy source as compared to fructose.
3.2 Hedonic response to sugar and rewards of sugar intake
While the hypothalamus regulates food intake in terms of energetic needs, the dopamine reward/motivation circuitry involving striatal, limbic and cortical areas also drives eating behavior (28). Other neurotransmitters including serotonin, endogenous opioids, and endocannabinoids confer the rewarding effects of food in part by modulating its hedonic properties (29). Ingestion of palatable food releases dopamine (DA) in the ventral and dorsal striatum and dorsal striatal DA release is proportional to the self-reported level of pleasure gained by eating the food (30). Highly palatable foods, namely those rich in sugar or fat, can strongly trigger these reward/motivation and hedonic systems, encouraging food intake beyond the necessary energy requirements (31). While this may have been evolutionarily advantageous by encouraging fat storage when food was scarce, overeating becomes a liability in our current environment, which has no shortage of highly caloric and processed foods.
There are two principal rewarding aspects of sugar consumption: nutrition and taste.
No comments:
Post a Comment