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Frontiers in Bioscience (Landmark... Jun 2018Sugar is highly palatable and rewarding, both in its taste and nutritive input. Excessive sugar consumption, however, may trigger neuroadaptations in the reward system... (Review)
Review
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.
Topics: Brain; Feeding Behavior; Humans; Inflammation; Metabolic Syndrome; Obesity; Reward; Sugars; Sweetening Agents; Taste
PubMed: 29772560
DOI: 10.2741/4704 -
BMJ (Clinical Research Ed.) Apr 2023To evaluate the quality of evidence, potential biases, and validity of all available studies on dietary sugar consumption and health outcomes.
OBJECTIVE
To evaluate the quality of evidence, potential biases, and validity of all available studies on dietary sugar consumption and health outcomes.
DESIGN
Umbrella review of existing meta-analyses.
DATA SOURCES
PubMed, Embase, Web of Science, Cochrane Database of Systematic Reviews, and hand searching of reference lists.
INCLUSION CRITERIA
Systematic reviews and meta-analyses of randomised controlled trials, cohort studies, case-control studies, or cross sectional studies that evaluated the effect of dietary sugar consumption on any health outcomes in humans free from acute or chronic diseases.
RESULTS
The search identified 73 meta-analyses and 83 health outcomes from 8601 unique articles, including 74 unique outcomes in meta-analyses of observational studies and nine unique outcomes in meta-analyses of randomised controlled trials. Significant harmful associations between dietary sugar consumption and 18 endocrine/metabolic outcomes, 10 cardiovascular outcomes, seven cancer outcomes, and 10 other outcomes (neuropsychiatric, dental, hepatic, osteal, and allergic) were detected. Moderate quality evidence suggested that the highest versus lowest dietary sugar consumption was associated with increased body weight (sugar sweetened beverages) (class IV evidence) and ectopic fatty accumulation (added sugars) (class IV evidence). Low quality evidence indicated that each serving/week increment of sugar sweetened beverage consumption was associated with a 4% higher risk of gout (class III evidence) and each 250 mL/day increment of sugar sweetened beverage consumption was associated with a 17% and 4% higher risk of coronary heart disease (class II evidence) and all cause mortality (class III evidence), respectively. In addition, low quality evidence suggested that every 25 g/day increment of fructose consumption was associated with a 22% higher risk of pancreatic cancer (class III evidence).
CONCLUSIONS
High dietary sugar consumption is generally more harmful than beneficial for health, especially in cardiometabolic disease. Reducing the consumption of free sugars or added sugars to below 25 g/day (approximately 6 teaspoons/day) and limiting the consumption of sugar sweetened beverages to less than one serving/week (approximately 200-355 mL/week) are recommended to reduce the adverse effect of sugars on health.
SYSTEMATIC REVIEW REGISTRATION
PROSPERO CRD42022300982.
Topics: Humans; Dietary Sugars; Cross-Sectional Studies; Systematic Reviews as Topic; Weight Gain; Sugars; Beverages
PubMed: 37019448
DOI: 10.1136/bmj-2022-071609 -
Journal of Hepatology May 2018Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome; its rising prevalence parallels the rise in obesity and diabetes.... (Review)
Review
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome; its rising prevalence parallels the rise in obesity and diabetes. Historically thought to result from overnutrition and a sedentary lifestyle, recent evidence suggests that diets high in sugar (from sucrose and/or high-fructose corn syrup [HFCS]) not only increase the risk of NAFLD, but also non-alcoholic steatohepatitis (NASH). Herein, we review the experimental and clinical evidence that fructose precipitates fat accumulation in the liver, due to both increased lipogenesis and impaired fat oxidation. Recent evidence suggests that the predisposition to fatty liver is linked to the metabolism of fructose by fructokinase C, which results in ATP consumption, nucleotide turnover and uric acid generation that mediate fat accumulation. Alterations to gut permeability, the microbiome, and associated endotoxemia contribute to the risk of NAFLD and NASH. Early clinical studies suggest that reducing sugary beverages and total fructose intake, especially from added sugars, may have a significant benefit on reducing hepatic fat accumulation. We suggest larger, more definitive trials to determine if lowering sugar/HFCS intake, and/or blocking uric acid generation, may help reduce NAFLD and its downstream complications of cirrhosis and chronic liver disease.
Topics: Animals; Beverages; Carbonated Beverages; Eating; Fructokinases; Fructose; Gastrointestinal Microbiome; Glucose; High Fructose Corn Syrup; Humans; Lipid Metabolism; Lipogenesis; Non-alcoholic Fatty Liver Disease; Oxidation-Reduction; Risk Factors; Sugars; Uric Acid
PubMed: 29408694
DOI: 10.1016/j.jhep.2018.01.019 -
Frontiers in Immunology 2022High sugar intake has long been recognized as a potential environmental risk factor for increased incidence of many non-communicable diseases, including obesity,... (Review)
Review
High sugar intake has long been recognized as a potential environmental risk factor for increased incidence of many non-communicable diseases, including obesity, cardiovascular disease, metabolic syndrome, and type 2 diabetes (T2D). Dietary sugars are mainly hexoses, including glucose, fructose, sucrose and High Fructose Corn Syrup (HFCS). These sugars are primarily absorbed in the gut as fructose and glucose. The consumption of high sugar beverages and processed foods has increased significantly over the past 30 years. Here, we summarize the effects of consuming high levels of dietary hexose on rheumatoid arthritis (RA), multiple sclerosis (MS), psoriasis, inflammatory bowel disease (IBD) and low-grade chronic inflammation. Based on these reported findings, we emphasize that dietary sugars and mixed processed foods may be a key factor leading to the occurrence and aggravation of inflammation. We concluded that by revealing the roles that excessive intake of hexose has on the regulation of human inflammatory diseases are fundamental questions that need to be solved urgently. Moreover, close attention should also be paid to the combination of high glucose-mediated immune imbalance and tumor development, and strive to make substantial contributions to reverse tumor immune escape.
Topics: Diabetes Mellitus, Type 2; Fructose; Glucose; High Fructose Corn Syrup; Humans; Inflammation; Sucrose; Sugars
PubMed: 36119103
DOI: 10.3389/fimmu.2022.988481 -
Nature Reviews. Neuroscience Oct 2022When it comes to food, one tempting substance is sugar. Although sweetness is detected by the tongue, the desire to consume sugar arises from the gut. Even when sweet... (Review)
Review
When it comes to food, one tempting substance is sugar. Although sweetness is detected by the tongue, the desire to consume sugar arises from the gut. Even when sweet taste is impaired, animals can distinguish sugars from non-nutritive sweeteners guided by sensory cues arising from the gut epithelium. Here, we review the molecular receptors, cells, circuits and behavioural consequences associated with sugar sensing in the gut. Recent work demonstrates that some duodenal cells, termed neuropod cells, can detect glucose using sodium-glucose co-transporter 1 and release glutamate onto vagal afferent neurons. Based on these and other data, we propose a model in which specific populations of vagal neurons relay these sensory cues to distinct sets of neurons in the brain, including neurons in the caudal nucleus of the solitary tract, dopaminergic reward circuits in the basal ganglia and homeostatic feeding circuits in the hypothalamus, that alter current and future sugar consumption. This emerging model highlights the critical role of the gut in sensing the chemical properties of ingested nutrients to guide appetitive decisions.
Topics: Animals; Dietary Sugars; Glucose; Glutamates; Non-Nutritive Sweeteners; Sodium; Sugars; Symporters; Taste
PubMed: 35879409
DOI: 10.1038/s41583-022-00613-5 -
Nature Apr 2020The taste of sugar is one of the most basic sensory percepts for humans and other animals. Animals can develop a strong preference for sugar even if they lack sweet...
The taste of sugar is one of the most basic sensory percepts for humans and other animals. Animals can develop a strong preference for sugar even if they lack sweet taste receptors, indicating a mechanism independent of taste. Here we examined the neural basis for sugar preference and demonstrate that a population of neurons in the vagal ganglia and brainstem are activated via the gut-brain axis to create preference for sugar. These neurons are stimulated in response to sugar but not artificial sweeteners, and are activated by direct delivery of sugar to the gut. Using functional imaging we monitored activity of the gut-brain axis, and identified the vagal neurons activated by intestinal delivery of glucose. Next, we engineered mice in which synaptic activity in this gut-to-brain circuit was genetically silenced, and prevented the development of behavioural preference for sugar. Moreover, we show that co-opting this circuit by chemogenetic activation can create preferences to otherwise less-preferred stimuli. Together, these findings reveal a gut-to-brain post-ingestive sugar-sensing pathway critical for the development of sugar preference. In addition, they explain the neural basis for differences in the behavioural effects of sweeteners versus sugar, and uncover an essential circuit underlying the highly appetitive effects of sugar.
Topics: Animals; Brain; Choice Behavior; Dietary Sugars; Food Preferences; Glucose; Intestines; Male; Methylglucosides; Mice; Mice, Inbred C57BL; Neurons; Taste; Thiazines; Water
PubMed: 32322067
DOI: 10.1038/s41586-020-2199-7 -
Caries Research 2019The World Health Organization guideline to use less sugar may be an opportunity and support for dentistry in its goal to get the message of using less sugar across to... (Review)
Review
The World Health Organization guideline to use less sugar may be an opportunity and support for dentistry in its goal to get the message of using less sugar across to the public. Two ways (with all the combinations of these) to achieve a reduction of sugar consumption are the reduction of the amount of sugar in products or the reduction of the frequency of consumption of sugar-containing products. Which sugar-reducing strategy is best for caries prevention? To answer this question, this manuscript discusses the shape of the dose-response association between sugar intake and caries, the influence of fluoridated toothpaste on the association of sugar intake and caries and the relative contribution of frequency and amount of sugar intake to caries levels. The results suggest that when fluoride is appropriately used, the relation between sugar consumption and caries is very low or absent. The high correlation between amount and frequency hampers the decision related to which of both is of more importance, but frequency (and stickiness) fits better in our understanding of the caries process. Reducing the amount without reducing the frequency does not seem to be an effective caries preventive approach in contrast to the reciprocity. Goals set in terms of frequency may also be more tangible for patients to follow than goals set in amount. Yet, in sessions of dietary counselling to prevent dental caries, the counsellor should not forget the importance of quality tooth brushing with fluoride toothpaste.
Topics: Dental Caries; Dietary Sugars; Fluorides; Humans; Sugars; Toothbrushing; Toothpastes
PubMed: 30089285
DOI: 10.1159/000489571 -
Nutrients Feb 2023The importance of nutrition in human health has been understood for over a century. However, debate is ongoing regarding the role of added and free sugars in... (Review)
Review
The importance of nutrition in human health has been understood for over a century. However, debate is ongoing regarding the role of added and free sugars in physiological and neurological health. In this narrative review, we have addressed several key issues around this debate and the major health conditions previously associated with sugar. We aim to determine the current evidence regarding the role of free sugars in human health, specifically obesity, diabetes, cardiovascular diseases, cognition, and mood. We also present some predominant theories on mechanisms of action. The findings suggest a negative effect of excessive added sugar consumption on human health and wellbeing. Specific class and source of carbohydrate appears to greatly influence the impact of these macronutrients on health. Further research into individual effects of carbohydrate forms in diverse populations is needed to understand the complex relationship between sugar and health.
Topics: Humans; Sugars; Dietary Sucrose; Beverages; Obesity; Diabetes Mellitus; Fructose
PubMed: 36839247
DOI: 10.3390/nu15040889 -
Advances in Nutrition (Bethesda, Md.) May 2017Fructose-containing added sugars, such as sucrose and high-fructose corn syrup, have been experimentally, epidemiologically, and clinically shown to be involved in the... (Review)
Review
Fructose-containing added sugars, such as sucrose and high-fructose corn syrup, have been experimentally, epidemiologically, and clinically shown to be involved in the current epidemics of obesity and diabetes. Here we track this history of intake of sugar as it relates to these epidemics. Key experimental studies that have identified mechanisms by which fructose causes obesity and diabetes are reviewed, as well as the evidence that the uricase mutation that occurred in the mid-Miocene in ancestral humans acted as a "thrifty gene" that increases our susceptibility for fructose-associated obesity today. We briefly review recent evidence that obesity can also be induced by nondietary sources of fructose, such as from the metabolism of glucose (from high-glycemic carbohydrates) through the polyol pathway. These studies suggest that fructose-induced obesity is driven by engagement of a "fat switch" and provide novel insights into new approaches for the prevention and treatment of these important diseases.
Topics: Diabetes Mellitus; Diet; Dietary Sugars; Feeding Behavior; Flavoring Agents; Fructose; Glucose; Humans; Obesity; Sucrose; Urate Oxidase
PubMed: 28507007
DOI: 10.3945/an.116.014654 -
Journal of Affective Disorders Jan 2019Attention-deficit/hyperactivity disorder (ADHD) is characterized by persistent symptoms of lack of attention, impulsivity and hyperactivity. The association between...
BACKGROUND
Attention-deficit/hyperactivity disorder (ADHD) is characterized by persistent symptoms of lack of attention, impulsivity and hyperactivity. The association between nutritional exposures and ADHD has been investigated and some studies have identified adverse effects from higher intake of sugar. The objective of the present study was to evaluate the association between change in sugar consumption between 6 and 11 years of age and incidence of attention-deficit/hyperactivity disorder (ADHD).
METHODS
Pelotas 2004 Birth Cohort Study in Brazil. A food frequency questionnaire (FFQ) was used to estimate sugar consumption and the Development and Well-Being Assessment (DAWBA) was applied to mothers to assess the presence of ADHD.
RESULTS
Only children without ADHD at 6 years and with complete information from FFQ and DAWBA at 6 and 11 years were included in the analyses (n = 2924). Odds ratios with 95% confidence intervals were calculated. Incidence of ADHD between 6 and 11 years was 4.6% (3.6-5.6%) among boys and 1.8% (1.2-2.5%) among girls. Adjusted analyses showed no association between always high sucrose consumption between 6 and 11 years and incidence of ADHD, compared with individuals who always presented low consumption, both among boys (OR = 0.66; 0.21-2.04) and girls (OR = 2.71; 0.24-30.35).
LIMITATIONS
Reflect those that are inherent to use of FFQs, such as memory bias and lack of precision in quantifying the diet.
CONCLUSIONS
The results suggest that there is no association between sucrose consumption between 6 and 11 years of age and incidence of ADHD.
Topics: Attention Deficit Disorder with Hyperactivity; Brazil; Child; Cohort Studies; Female; Humans; Male; Nutrition Surveys; Sex Distribution; Socioeconomic Factors; Sugars
PubMed: 30257225
DOI: 10.1016/j.jad.2018.09.051