Sugar and Memory: What Human Research Shows
Author: Ukrainian Psychological Hub · Published: September 29, 2026 · Editorial Policy
Sugar can appear to have two opposite relationships with memory in human research. In short laboratory experiments, a glucose drink sometimes improves performance on particular memory tasks. Across longer-term observational studies, higher habitual intake of added sugars or sugar-sweetened beverages is more often associated with poorer cognitive outcomes. Both statements can be true because they describe different exposures, different time scales, different study designs, and different kinds of memory.
The strongest synthesis focused specifically on free and added sugars in healthy humans found 77 studies: 65 short-term experimental trials, nine cross-sectional studies, and three cohort studies. In a meta-analysis of word-list studies, glucose produced a small improvement in immediate free recall, while delayed free recall did not show a statistically reliable benefit. The observational literature, by contrast, generally linked higher long-term added-sugar exposure with poorer cognition. The authors also emphasized major limitations in study quality, heterogeneity, and the small number of long-term studies. See the systematic review and meta-analysis by Gillespie and colleagues.
That is the central answer to the search query “sugar and memory”: human evidence does not support a simple rule that sugar either improves or destroys memory. Acute glucose facilitation is a real research finding under some conditions. Long-term high-sugar dietary patterns are a concern, but much of the human evidence is observational, often involves sugar-sweetened beverages or combined high-fat/high-sugar diets, and does not isolate one molecule or prove that sugar alone causes memory loss.
This article stays with dietary sugar and human memory research. It does not provide blood-glucose targets, continuous glucose-monitoring interpretation, A1C guidance, hypoglycemia treatment, hyperglycemia management, insulin advice, or personalized diabetes care. Those are clinical medical topics with different evidence and safety requirements.
Quick answer: does sugar affect memory?
Yes, but the effect depends on what “sugar” means and what kind of evidence is being discussed. In controlled experiments, oral glucose can transiently improve some forms of memory, especially immediate or long-term verbal recall under certain testing conditions. A 2021 systematic review and meta-analysis of glucose and sucrose interventions found mixed results across 37 trials and a significant benefit only for immediate verbal recall in a subset of parallel-design studies. Twenty-four studies were judged at high risk of bias for the selection procedure, and only three trials studied sucrose.
A newer human-only review reached a similar but more nuanced conclusion. The Gillespie et al. review found a small pooled benefit for glucose on immediate free recall, but not delayed free recall, while also finding that long-term observational studies tended to associate greater added-sugar exposure with worse cognition. The evidence therefore separates into an acute experimental question and a habitual dietary-pattern question.
The practical conclusion is straightforward: the fact that glucose can facilitate a laboratory memory task does not make candy, table sugar, or sweet drinks established memory enhancers for everyday life. Equally, an occasional dessert is not evidence of impending memory loss. Human memory is shaped by sleep, attention, stress, mood, learning strategy, age, overall diet, cardiometabolic health, medications, neurological conditions, and many other factors.
What “sugar” means in memory research
The word sugar is unusually slippery. A study can administer pure glucose, measure habitual added-sugar intake, count sugar-sweetened beverages, analyze sucrose, or examine a Western-style diet that contains both added sugar and saturated fat. Those exposures should not be collapsed into one category.
Glucose
Glucose is a monosaccharide and a major metabolic fuel. Most short-term “sugar and memory” experiments have used a measured glucose drink rather than ordinary mixed foods. That matters because a fixed dose of glucose in a controlled experiment is not equivalent to a pastry, soda, fruit, or normal meal.
Sucrose
Sucrose is table sugar: a disaccharide composed of glucose and fructose. Human intervention evidence specific to sucrose is much thinner than the glucose literature. The 2021 intervention review found only three sucrose trials, so results from glucose experiments should not automatically be rewritten as claims about all sucrose-containing foods.
Added sugar and free sugars
In U.S. labeling, added sugar refers to sugars added during processing or preparation and several closely defined sources counted under FDA rules. The WHO term free sugars is broader and includes sugars in honey, syrups, fruit juices, and fruit-juice concentrates as well as sugars added by manufacturers, cooks, or consumers. These categories overlap but are not identical.
Sugar-sweetened beverages
Many long-term studies use sugar-sweetened beverages as the exposure because beverage intake can be measured in cohorts and can contribute substantial free or added sugar. A beverage study therefore answers a question about a dietary pattern or beverage exposure; it does not prove that every gram of sucrose has the same effect regardless of food matrix, dose, or context.
High-fat/high-sugar or Western-style diets
A large part of the hippocampal literature studies diets high in both saturated fat and added sugar. Those studies are important, but the components cannot always be separated. A 2021 systematic review and meta-analysis of human hippocampal integrity and function found a small adverse pooled effect for Western-style diet exposure, with substantial heterogeneity, but did not find significant effects for the individual macronutrients when analyzed separately. That is a critical boundary: evidence about a high-fat/high-sugar pattern is not automatically evidence about sugar alone.
What human experiments show about glucose and memory
The short-term literature is sometimes called the glucose facilitation effect. Participants typically receive a glucose drink and a placebo or equally sweet control, then complete memory tasks. Effects are often measured within minutes or hours. This design can test an acute causal effect of the administered glucose under the study conditions, which makes it stronger for short-term causality than a food-frequency questionnaire.
Immediate recall has the clearest pooled signal
In the 2023 systematic review and meta-analysis, 16 papers supplied enough comparable data for word-list meta-analysis. Glucose was associated with a small improvement in immediate free recall (standardized mean difference 0.22, 95% CI 0.08 to 0.36), while delayed free recall was not statistically significant. The effect was therefore specific rather than universal.
The earlier 2021 intervention meta-analysis also found that benefits were not spread consistently across cognitive domains. Among 37 trials, most results were mixed, and pooled evidence showed a significant advantage only for immediate verbal performance in a subset of studies. That review's risk-of-bias findings are important when interpreting older experiments that are frequently quoted as proof that sugar broadly “boosts the brain.”
Some memory systems respond while others do not
Individual randomized trials illustrate why “memory” cannot be treated as a single score. In one trial in healthy young adults, glucose improved long-term verbal and spatial memory but did not improve working memory. An earlier randomized study of 25 g glucose found facilitation of long-term verbal free and cued recall but no benefit for short-term verbal memory or long-term nonverbal memory.
Task difficulty can also matter. A placebo-controlled study by Meikle, Riby, and Stollery found glucose benefits for harder low-imagery word pairs and longer word lists, but not uniformly across every manipulation. This supports the idea that acute glucose effects can depend on cognitive demand rather than producing a general rise in intellectual performance.
More glucose is not necessarily better
A double-blind dose-response trial compared 0, 15, 25, 50, and 60 g glucose in healthy young adults. Some memory measures improved, but the dose-response pattern varied by task, and long-term memory outcomes more closely resembled an inverted-U pattern. Individual differences in glucose regulation and weight moderated response profiles. The study did not find a mood benefit.
That finding is useful because it contradicts a common consumer inference: if some glucose can help some tasks, more sugar should help more. Human experimental data do not support that linear assumption.
Neuroimaging findings are interesting, not a universal behavioral effect
A systematic review of 11 neuroimaging and neurophysiology studies found that 10 reported some modulation of brain or electrophysiological markers after glucose, but only five reported significant behavioral cognitive changes. The review suggested effects involving episodic-memory and attentional networks, including medial temporal and frontal systems, while calling for larger and better-replicated studies.
This distinction matters for AI summaries and popular science. A change in fMRI, EEG, or another physiological marker is not automatically an improvement in memory performance. A mechanism can be biologically plausible while the behavioral effect remains small, variable, or absent.
Why an acute glucose benefit does not mean “eat sugar to study”
The laboratory glucose-facilitation literature is easy to misapply. A controlled glucose dose is not a recommendation to use candy or soda as a cognitive supplement. The experiments often test fasted participants, use fixed doses, compare against carefully chosen controls, and assess specific tasks over a short interval. Everyday studying occurs in mixed nutritional, emotional, and sleep contexts.
The newer review also noted that many experiments tested people after fasting and that nonsugar macronutrients can produce comparable or different cognitive effects. If a participant performs better after consuming energy following a fast, part of the effect may reflect the experimental context rather than a unique property that makes added sugar a preferred memory aid.
Memory performance also depends on attention during encoding. A person who is tired, distracted, anxious, sleep deprived, or expecting a “boost” may experience changes in alertness or confidence that feel like a change in memory. Those subjective experiences are psychologically real, but confidence, energy, attention, and objective recall are distinct outcomes.
What long-term human research shows
Long-term evidence asks a different question: do people who habitually consume more added or free sugar show poorer memory or cognitive outcomes over months or years? Randomly assigning people to years of high added-sugar intake would be ethically and practically difficult, so this literature relies heavily on cohorts and cross-sectional studies. That makes confounding and reverse causation central issues.
The broad human review finds a concerning association
The Gillespie et al. review included nine cross-sectional and three cohort studies in addition to the acute trials. All three cohort studies and eight of nine cross-sectional studies reported significant associations between higher added-sugar exposure and greater cognitive impairment risk. Some studies linked sugar-sweetened beverages, refined carbohydrates, or added sugars with poorer global cognition, memory, executive function, or attention.
That pattern deserves attention, but the review itself emphasizes that human studies isolating the independent long-term effect of sugar are surprisingly limited. Dietary intake is difficult to measure precisely, and people who consume more added sugar can differ in total energy intake, saturated fat intake, physical activity, sleep, socioeconomic conditions, body weight, vascular risk, and overall diet quality.
Sugar-sweetened beverage meta-analyses do not all give the same answer
A 2022 meta-analysis of 13 studies involving 242,014 participants reported that sugar-sweetened beverage intake was associated with a higher prevalence of cognitive disorders (pooled OR 1.17, 95% CI 1.05 to 1.29). Heterogeneity was very high (I² 90.1%), which means the studies varied substantially.
Another 2022 meta-analysis focused on middle-aged and older adults included 10 studies and concluded that evidence was insufficient to state conclusively that sugar-sweetened beverage intake causes cognitive dysfunction. Its pooled estimate for cognitive impairment was not statistically significant, although some dementia subgroup estimates were elevated. The disagreement is a reminder that pooled observational results depend on study selection, definitions, populations, and outcomes.
Newer Alzheimer’s-disease evidence remains observational
A 2025 systematic review and dose-response meta-analysis of prospective cohorts reported an association between higher sugar-sweetened beverage intake and Alzheimer’s disease risk (pooled RR 1.49, 95% CI 1.03 to 2.15; I² 79%). The same review also found an association for artificially sweetened beverages, which makes simplistic “sugar molecule causes Alzheimer’s” interpretations especially inappropriate. Prospective cohorts improve temporal ordering, but they remain observational and cannot eliminate residual confounding or establish a single causal pathway.
The wording should therefore stay precise: higher intake of sugar-sweetened beverages has been associated with cognitive impairment and Alzheimer’s-disease outcomes in several observational syntheses. That is different from saying that sugar has been proven to cause dementia.
Sugar, the hippocampus, and memory
The hippocampus is central to several forms of learning and episodic memory, which is why it appears frequently in diet-and-memory research. It is also the region most often invoked in animal high-sugar studies. Human evidence is more restrained.
The Taylor et al. systematic review and meta-analysis identified 20 human studies of Western-style diet exposure and hippocampal structure or function. Western-style diet was associated with poorer hippocampal integrity and functioning with a small pooled effect, but most studies were correlational, heterogeneity was high, and significant effects were not found for saturated fat or added sugar analyzed as individual macronutrients.
A 2023 study of 349 young adults found that higher self-reported high-fat/high-sugar intake was associated with worse pattern-separation performance and poorer executive-function measures. Pattern separation is a hippocampus-dependent process that helps distinguish similar memories or representations. The study controlled for several confounders, but it was still correlational and measured a combined high-fat/high-sugar dietary pattern rather than isolated sugar exposure.
The hippocampal evidence therefore supports a plausible human link between Western-style eating patterns and memory-related function. It does not justify claiming that one sugary food acutely damages the hippocampus or that a specific dose of added sugar has been shown to shrink human memory structures.
Different kinds of memory give different answers
Immediate verbal recall
This is the outcome with the most reproducible short-term glucose-facilitation signal in meta-analysis. Participants learn a word list and recall it shortly afterward. A small improvement here is a specific laboratory effect, not a universal memory enhancement.
Delayed recall and long-term retention
Delayed recall results are less consistent at the meta-analytic level. Individual trials have reported benefits for longer-term verbal recall, but the pooled evidence does not show the same clarity as immediate free recall. Timing of glucose administration, task difficulty, participant age, fasting, and baseline metabolic regulation can all matter.
Working memory
Working memory is the short-term maintenance and manipulation of information needed for ongoing tasks. Several glucose studies have failed to show the same benefit seen in verbal recall. That difference is one reason this article does not use “memory improved” as shorthand for every memory system.
Pattern separation and hippocampal memory
Pattern separation is a more specialized hippocampal-dependent process. Human high-fat/high-sugar studies have reported associations with poorer performance, but these findings come from dietary-pattern research rather than randomized long-term sugar exposure.
Global cognition and dementia outcomes
Global cognitive screening, mild cognitive impairment, dementia, and Alzheimer’s disease are broader clinical or epidemiological outcomes. They are not equivalent to forgetting a word list or feeling mentally foggy after lunch. Studies that use these outcomes should be discussed as cognitive-disorder or aging evidence, not quietly converted into claims about everyday memory lapses.
Does sugar cause memory loss?
Human research does not establish a direct one-to-one causal rule in which dietary sugar by itself causes ordinary memory loss. Acute glucose experiments can improve some memory tasks. Long-term observational studies more often point in the opposite direction, linking higher added-sugar or sugar-sweetened beverage exposure with poorer cognition. The causal contribution of sugar itself remains difficult to separate from the rest of the diet, metabolic health, lifestyle, and social factors.
For an individual person, new or progressive memory difficulty should not be self-diagnosed as “too much sugar.” Memory symptoms can reflect sleep deprivation, depression, anxiety, medication effects, substance use, endocrine or nutritional problems, neurological disease, normal aging, acute illness, and many other causes. Persistent or worsening changes that interfere with daily functioning warrant clinical evaluation.
Does sugar cause dementia or Alzheimer’s disease?
The best answer is that several prospective and pooled observational studies report associations between higher sugar-sweetened beverage consumption and later cognitive impairment or Alzheimer’s disease, but this is not the same as proving that sugar causes dementia. Dementia develops through multiple biological and social pathways over long periods, and beverage intake can be a marker for broader dietary and lifestyle patterns.
The 2025 prospective-cohort meta-analysis is important because it is newer and restricted to longitudinal evidence, yet it still cannot randomize exposure or fully remove residual confounding. Its high heterogeneity for sugar-sweetened beverages also argues against treating the pooled number as a universal personal risk estimate.
A useful way to phrase the evidence is: frequent sugar-sweetened beverage intake may be one component of a dietary pattern associated with poorer long-term cognitive health. It is not an established diagnostic explanation for a person's memory symptoms, and no human evidence supports using a single sugar cutoff as a dementia threshold.
What about fruit sugar?
Naturally occurring sugars in whole fruit should not be treated as interchangeable with added sugar or sugar-sweetened beverages. Foods differ in fiber, water, micronutrients, polyphenols, energy density, chewing, satiety, and the rate at which nutrients are delivered. The Gillespie et al. review noted that several studies associated natural fructose-containing foods with better rather than worse cognitive outcomes.
That does not prove that fructose itself improves memory. It illustrates the food-matrix problem: an observational association with fruit is an association with a whole food, not an experiment isolating fructose. Likewise, evidence about high-fructose corn syrup or sugar-sweetened beverages should not be transferred to intact fruit.
Sugar rush, sugar crash, brain fog, and subjective memory
People often describe a sequence of feeling energized after something sweet and then tired, foggy, or forgetful later. Those subjective experiences can involve hunger, meal size, sleep, caffeine, expectation, stress, hydration, gastrointestinal sensations, and learned associations. They should not be assumed to represent a discrete neurological injury or a proven “memory crash.”
For the separate acute energy-and-expectation question, see Sugar Rush: Is It Real? Energy, Expectation, and the Evidence.
A perceived drop in mental clarity can also affect memory indirectly. If attention is poorer during encoding, less information is stored well enough to be recalled later. A person may then experience the result as forgetfulness even when the primary change was alertness or attention. This is one reason the cluster separates memory, focus, broader cognition, and “brain fog” into different search intents.
For the distinct attention and concentration intent, see Sugar and Focus: Attention, Energy, and Expectation.
The psychology of expectation is relevant here. Many glucose experiments use sweet-matched placebo drinks so that participants cannot easily infer condition from taste. That design helps separate a nutrient effect from the expectation that sweetness should provide energy. In everyday life, labels, routines, context, and prior beliefs are less controlled, so subjective “boost” and “crash” reports can include both physiological and expectancy components.
Possible mechanisms: what is plausible and what is established?
Glucose as brain fuel
The brain relies heavily on glucose under ordinary physiological conditions. That fact is established. It is explained in more detail in our Sugar and the Brain and Glucose articles. It does not follow that the brain requires added sugar. Glucose can come from many digestible carbohydrates and can also be produced endogenously.
Acute modulation of memory circuits
The short-term facilitation literature supports the possibility that glucose availability can modulate memory processing under particular conditions. The neuroimaging review found glucose-related changes in medial temporal and frontal markers more consistently than it found behavioral improvements. This is mechanistically suggestive, while the exact neural pathway and the conditions required for reliable behavioral benefit remain incompletely resolved.
Cardiometabolic and vascular pathways
Long-term high added-sugar intake can contribute to overall dietary patterns associated with excess energy intake and cardiometabolic risk. Cardiovascular and metabolic health are themselves related to brain aging and cognition. These pathways are biologically plausible mediators, but an observational association between sugar intake and memory does not tell us how much of the relationship is mediated by weight, insulin sensitivity, blood pressure, vascular health, or other factors.
Inflammation and hippocampal signaling
Inflammatory, neurotrophic, gut-brain, and hippocampal signaling mechanisms are frequently proposed from animal models. They are useful for generating hypotheses, but the human evidence is less direct. A strong article should not import rodent molecular findings into people as if those mechanisms had already been demonstrated as the cause of ordinary sugar-related memory changes.
Reward learning and dietary behavior
Sweet foods can become strongly learned rewards, and cues can shape wanting, habits, and food choice. That behavioral pathway can influence how often high-sugar foods are consumed, which in turn affects long-term dietary exposure. Reward learning is therefore relevant to the behavior that produces the exposure; it is not evidence that every memory effect of sugar is caused by dopamine.
Why observational sugar-and-memory studies are hard to interpret
Diet is a correlated system. People do not randomly consume one nutrient while holding everything else constant for decades. Added-sugar intake can travel with saturated fat, ultra-processed food intake, lower fiber intake, different sleep patterns, activity levels, socioeconomic factors, smoking, alcohol use, stress, obesity, and chronic disease. Statistical adjustment helps but cannot guarantee that every relevant difference has been measured correctly.
Dietary exposure is also often self-reported. Food-frequency questionnaires can misclassify intake, serving sizes, and ingredients. Cognitive outcomes vary too: one study may use a word list, another a global screening test, another pattern separation, and another a dementia diagnosis. Combining them can reveal a general signal while also producing heterogeneity.
Reverse causation is another concern in aging studies. Early cognitive change can alter shopping, cooking, appetite, and beverage habits before a formal diagnosis. Prospective cohorts reduce this problem by establishing temporal order, but long preclinical periods make it difficult to eliminate completely.
Evidence status: what can we say with confidence?
Established
Glucose is a major brain fuel in ordinary physiology. Acute oral glucose can improve performance on some memory tasks under controlled conditions. The most consistent pooled acute signal is in immediate verbal/free recall, and effects vary by task and participant characteristics.
Supported but limited
Higher habitual added-sugar or sugar-sweetened beverage intake is associated with poorer cognitive outcomes in many human observational studies. Western-style high-fat/high-sugar dietary patterns are associated with poorer hippocampal function in human syntheses. These findings support concern about long-term dietary patterns while leaving uncertainty about sugar-specific causality.
Preliminary or context-dependent
Specific dose-response curves, individual susceptibility, neuroimaging mechanisms, and claims that particular people benefit cognitively from a fixed glucose dose remain context-dependent. Older small trials and heterogeneous methods limit precision.
Contested or overstated
Claims that sugar universally damages memory, that one dessert causes hippocampal injury, that a specific “sugar crash” directly erases memories, or that sugar has been proven to cause Alzheimer’s disease exceed the human evidence. The same is true of using rodent high-sugar mechanisms as direct proof of what happens in an individual human.
Practical meaning for everyday eating and memory
There is no evidence-based reason to use added sugar as a routine memory supplement. If a person is eating normally, the brain's need for glucose does not create a nutritional requirement for table sugar, candy, or soda. For studying and cognitive performance, sleep, regular meals, hydration, physical activity, and effective learning strategies have broader relevance than trying to engineer an acute glucose boost.
Public-health guidance on sugar is based mainly on overall health outcomes rather than a memory-specific threshold. The World Health Organization guideline recommends reducing free sugars to less than 10% of total energy intake and suggests a further reduction below 5% for additional health benefits. Those recommendations were developed primarily around unhealthy weight gain and dental caries, not because a specific percentage has been proven to optimize memory.
In the United States, the FDA explains that Added Sugars on the Nutrition Facts label include sugars added during processing as well as several defined sweetener sources, while Total Sugars also include naturally occurring sugars in foods such as fruit and milk. The Daily Value for added sugars is 50 g on a 2,000-calorie diet. Again, that labeling reference is not a memory cutoff.
For someone who wants to reduce added sugar without turning eating into a fear-based cognitive experiment, the useful target is the dietary pattern: compare labels, notice sugar-sweetened beverages, choose foods that support overall nutritional quality, and avoid interpreting every ordinary lapse in concentration as evidence of “sugar damage.”
When memory problems deserve medical attention
Memory complaints that are persistent, progressive, new, or disruptive to work, relationships, medication management, finances, navigation, or other daily functions deserve professional assessment. Sudden confusion or an abrupt major cognitive change can require urgent medical evaluation. Dietary sugar is only one possible contextual factor and should not delay evaluation of neurological, psychiatric, sleep-related, endocrine, medication-related, or other medical causes.
People with diabetes, recurrent hypoglycemia, hyperglycemia, or other disorders of glucose regulation have additional clinical considerations that are outside this article's scope. The findings from healthy-participant glucose experiments should not be used to change diabetes treatment, glucose targets, medication, or monitoring.
Frequently asked questions
Does sugar improve memory?
Sometimes, in controlled experiments. Oral glucose has improved certain memory tasks, especially immediate verbal recall, but the effect is not universal across memory systems, doses, or people. That evidence does not establish added sugar as a practical memory supplement.
Can too much sugar make memory worse?
Higher habitual added-sugar and sugar-sweetened beverage intake is associated with poorer cognitive outcomes in many observational studies. Human evidence is more convincing for an association with long-term dietary patterns than for a simple direct causal effect of sugar alone.
Does sugar cause memory loss?
Human evidence does not establish that dietary sugar by itself directly causes ordinary memory loss in an individual. Persistent or worsening memory problems have many possible causes and should be evaluated on their own merits.
Does sugar cause Alzheimer’s disease?
Prospective meta-analyses report associations between higher sugar-sweetened beverage intake and Alzheimer’s disease risk, but observational association is not proof of causation. Dementia is multifactorial, and the underlying studies cannot fully isolate sugar from correlated dietary and health factors.
Is glucose good for studying?
A glucose drink can improve some laboratory memory tasks under certain conditions, but there is no strong basis for recommending added sugar as a study aid. Adequate sleep, attention, learning strategy, normal nutrition, and breaks are more broadly applicable.
Why can sugar seem to help when I am tired?
Sweetness, expectation, hunger, energy intake, caffeine consumed with sugar, and the relief of fasting can all change subjective alertness. Feeling more awake is not identical to showing better objective memory performance.
Can a sugar crash cause forgetfulness?
People can feel tired or mentally foggy after eating, but ordinary subjective “crash” experiences should not be assumed to represent memory damage. Attention and alertness can influence encoding, which can later feel like forgetfulness.
Is fruit sugar bad for memory?
Whole fruit should not be equated with added sugar or sugar-sweetened beverages. Human observational studies cited in the major review sometimes associated natural fructose-containing foods with better cognitive outcomes. That reflects whole-food exposure and does not establish a beneficial effect of isolated fructose.
Is there a daily sugar limit specifically for memory?
No validated daily sugar threshold has been established specifically to prevent memory problems. Public-health limits on added or free sugars are based on broader health outcomes, not a proven memory cutoff.
Do children get memory problems from sugar?
Human studies in children are limited and mixed, and food behavior should not be used to infer ADHD or another clinical condition. Claims that a sweet food reliably causes a child's memory impairment exceed the available evidence.
Does the brain need added sugar because it uses glucose?
No. The brain uses glucose, but dietary glucose can arise from many carbohydrates and the body can produce glucose. A physiological need for glucose is not a dietary requirement for sucrose or added sugar. See Sugar and the Brain for the full distinction.
For the broader cognition evidence synthesis that places memory alongside attention, executive function, processing speed, and subjective mental performance, see Sugar and Cognition: Attention, Memory, and Mental Performance.
Related Articles
References
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