Sugar and Depression: Associations, Mechanisms, and Limits
Author: Ukrainian Psychological Hub · Published: September 29, 2026 · Editorial Policy
Higher sugar intake is associated with more depressive symptoms or a higher observed risk of depression in a substantial body of observational research. That is the clearest evidence-based answer to the query “sugar and depression.” It is also only the beginning of the answer. An association does not establish that sugar directly causes major depressive disorder, that every kind of sugar has the same relationship with depression, or that removing sugar is a proven treatment.
The evidence is strongest for population-level associations involving high overall sugar intake and sugar-sweetened beverages. A 2024 systematic review and meta-analysis of 40 studies involving more than 1.2 million participants reported a pooled association between higher sugar consumption and depression, but heterogeneity was extremely high, meaning the included studies differed greatly in populations, measurements, exposures, and outcomes (Xiong et al., 2024). A 2026 systematic review likewise found an overall positive association across 26 studies while concluding that causal direction and mediating mechanisms remain unresolved (Barma et al., 2026).
For readers, the practical meaning is fairly simple: high intake of added or free sugars, especially through sugar-sweetened beverages and a generally low-quality dietary pattern, is a reasonable health target to reduce. But depression is a multifactorial clinical condition. Sugar intake is one possible part of a much larger system that includes genetics, stress, sleep, physical health, social conditions, medication, activity, substance use, relationships, and other psychological and biological factors. The National Institute of Mental Health describes depression in exactly this broader way and emphasizes established treatments such as psychotherapy and medication (NIMH).
Quick answer: does sugar cause depression?
Current evidence does not justify the simple statement that sugar causes depression. It does justify a narrower statement: people with higher sugar intake, especially higher sugar-sweetened beverage intake, often show more depressive symptoms or a higher observed risk of depression in observational studies. Prospective studies strengthen the temporal case because diet is measured before later symptoms, but they still cannot remove every confounder or prove that sugar itself is the causal ingredient.
One useful umbrella review in The BMJ found that sugar-sweetened beverage consumption was associated with depression across a meta-analysis of observational studies, with a reported relative risk of 1.31 for higher versus lower consumption. The authors rated the underlying evidence as low quality, largely because it was observational and vulnerable to bias, inconsistency, and residual confounding (Huang et al., 2023). The magnitude of an association should therefore never be read as a personal prediction.
The strongest conclusion is about association and risk pattern, not diagnostic causation. Major depressive disorder cannot be diagnosed from what someone eats, and a high-sugar diet does not mean that a person has or will develop depression.
First, what does “sugar” mean in this research?
“Sugar” is not a single exposure. Studies use different definitions, and this is one of the main reasons results should not be collapsed into a single dramatic claim. Some studies estimate total dietary sugars. Others focus on added sugars, sugar-sweetened beverages, sweet foods, sucrose, or broader dietary patterns in which sugar travels together with fat, refined starch, energy density, and ultra-processed foods.
For a general explanation of the chemistry, food uses, health context, and psychological layer, see Sugar: What It Is, Types, Uses, Health, and Psychology.
Total sugar
Total sugar is a broad dietary measure that can include sugars naturally present in foods as well as sugars added during processing or preparation. A study reporting “total sugar” therefore cannot automatically tell us whether the association came from soda, candy, flavored yogurt, fruit, milk, desserts, or a mixture of many sources.
Added sugar
In U.S. food labeling, Added Sugars are a specific regulatory category. The FDA includes sugars added during food processing, sugars packaged as sweeteners, sugars from syrups and honey, and certain sugars from concentrated fruit or vegetable juices. Naturally occurring sugars in milk, fruits, and vegetables are not counted as Added Sugars on the Nutrition Facts label (FDA). For the full label-centered explanation, see Added Sugar: What It Is, Where It Hides, and How Labels Count It.
Free sugars
The World Health Organization uses the broader public-health category free sugars. It includes sugars added by manufacturers, cooks, or consumers and sugars naturally present in honey, syrups, fruit juices, and fruit juice concentrates. WHO recommends reducing free sugars to less than 10% of total energy intake and suggests that below 5% can provide additional health benefits. Those recommendations were developed principally around established outcomes such as unhealthy weight gain and dental caries, not as a depression treatment guideline (WHO guideline).
Sugar-sweetened beverages
Sugar-sweetened beverages are studied frequently because they provide a large, relatively measurable source of added or free sugar and are consumed repeatedly by many people. They also differ from solid foods in satiety, eating context, portion size, and the other nutrients they provide. Evidence about soda or other sugar-sweetened beverages should not be silently transferred to whole fruit or every food containing carbohydrate.
What does “depression” mean in these studies?
The word depression also covers several different research outcomes. Some studies use validated symptom questionnaires such as the PHQ-9, CES-D, or HADS. Some identify probable depression using a score threshold. Some use physician diagnoses, medication use, or health records. Others combine depression with broader categories such as common mental disorder.
A symptom score is not identical to a clinical diagnosis. NIMH describes major depression as a disorder involving persistent symptoms that affect mood, thinking, sleep, appetite, concentration, motivation, and daily functioning; diagnosis depends on symptom pattern, duration, impairment, and clinical assessment (NIMH). That distinction matters because nutrition studies often measure depressive symptoms rather than formally diagnosed major depressive disorder.
Depression and anxiety can appear together in nutrition datasets and can co-occur clinically, but they are distinct outcomes. For the anxiety-specific evidence and its separate causal limits, see Sugar and Anxiety: What the Evidence Can and Cannot Show.
Evidence status at a glance
Established evidence
There is a reproducible observational association between higher sugar intake—particularly sugar-sweetened beverage intake—and depressive symptoms or depression risk across multiple populations. The association appears in systematic reviews, meta-analyses, cross-sectional datasets, and some prospective cohorts. Public-health guidance also independently supports limiting free or added sugars for broader health reasons.
Supported but still uncertain
Several pathways could help explain the association: overall diet quality, excess energy intake and adiposity, metabolic and inflammatory processes, stress-related eating, sleep disruption, reward learning, and socioeconomic or behavioral factors that influence both diet and mental health. These pathways are biologically and psychologically plausible, and some are supported by human data, but they do not establish one universal mechanism by which sugar produces depression.
Not established
It is not established that ordinary sugar intake directly causes major depressive disorder in an individual, that a specific number of grams of sugar triggers depression, that a “sugar crash” is the same thing as depression, that craving sugar proves addiction, or that eliminating sugar is an antidepressant treatment. A medically meaningful distinction must also be maintained between dietary sugar and blood-glucose disorders; fasting glucose, A1C, hypoglycemia, hyperglycemia, continuous glucose monitoring, and diabetes treatment belong to clinical glucose management rather than this dietary-psychology article.
What the major studies actually show
2024 meta-analysis: a pooled association, with extreme heterogeneity
The 2024 Frontiers in Nutrition systematic review and meta-analysis included 40 studies and 1,212,107 participants. The pooled analysis reported that higher sugar intake was associated with a 21% higher odds of depression. The headline is striking, but the heterogeneity statistic was I² = 99.7%, an extraordinary level of between-study variation. That means the studies were not all estimating the same clean exposure-outcome relationship, and the pooled number should be interpreted cautiously rather than treated as a universal biological effect size (Xiong et al., 2024).
2026 systematic review: broad consistency, unresolved causality
A newer 2026 systematic review included 26 studies: 14 cross-sectional, 10 cohort, and two case-control studies. Nineteen were rated high quality by the review’s chosen risk-of-bias method and seven moderate quality. The authors observed an overall positive association between higher sugar intake and anxiety or depressive outcomes, yet they did not pool the studies because age groups, outcome tools, and other features were too heterogeneous. They specifically called for better evidence on causal direction and mechanisms (Barma et al., 2026).
Sugar-sweetened beverages: prospective dose-response evidence
A 2022 systematic review and meta-analysis of prospective studies found that higher sugar-sweetened beverage consumption was associated with a higher risk of depression. Comparing higher with lower intake produced a relative risk of 1.25, and the dose-response model estimated an 8% higher relative risk per additional 250 mL per day. Because these were prospective studies, the temporal evidence is stronger than in a one-time survey, but prospective observation still does not equal random assignment (Wang et al., 2022).
U.S. NHANES: a large cross-sectional association
A 2024 analysis of 18,439 U.S. adults in NHANES 2011–2018 reported that each 100 g/day increase in dietary sugar intake was associated with 28% higher odds of depression after statistical adjustment for demographic, socioeconomic, health, behavioral, and energy-intake covariates. This is useful population evidence, but the design is cross-sectional: diet and depressive symptoms were measured in the same general period, so it cannot determine which came first (Zhang et al., 2024).
Whitehall II: prospective findings and a careful look at reverse causation
In the Whitehall II cohort, researchers examined repeated dietary and mental-health measurements. Men in the highest tertile of sugar intake from sweet foods and beverages had higher odds of incident common mental disorder five years later. The study also tested whether prior mood problems predicted later changes in sweet-food intake and did not find evidence for that specific reverse pathway. Yet some depression-specific estimates weakened after adjustment, illustrating why individual study conclusions must remain narrower than popular headlines (Knüppel et al., 2017).
TwinsUK 2026: association persists after accounting for fat subtypes
A 2026 TwinsUK study found that higher total sugar intake was associated with greater odds of HADS-defined depression in cross-sectional analyses, and increasing sugar intake was associated with higher HADS depression scores longitudinally. The authors explicitly noted that sugar intake may reflect a broader pattern that includes ultra-processed foods and called for randomized trials to test whether reducing sugar improves depressive symptoms (Mughal et al., 2026).
Not every study points in the same direction
A prospective Whitehall II analysis published in 2018 found no association between high-sugar or high-sugar/high-saturated-fat dietary patterns and incident or recurrent depressive symptoms over five years (Vermeulen et al., 2018). A 2024 Mendelian-randomization study even found that genetically predicted relative sugar intake was associated with lower major-depression risk, a result that runs in the opposite direction from most conventional observational findings. The authors emphasized important limitations in the genetic instruments and exposure measures and called for more research (Buczkowska & Iob, 2024).
These discordant findings are not an inconvenience to hide. They are part of the evidence. They show why “sugar causes depression” is stronger than the current science allows.
Why association does not prove causation
Nutrition and depression are both difficult to study causally. People are not randomly assigned for years to high-sugar and low-sugar lifestyles under controlled conditions. Most long-term evidence therefore comes from observation, where many variables travel together.
Confounding by the rest of the diet
A person who consumes a large amount of sugar-sweetened beverages may also differ in fiber intake, fruit and vegetable intake, meal regularity, total calories, alcohol use, caffeine intake, ultra-processed food consumption, or other dietary features. A sweet pastry contains more than sugar. A cola habit is more than sucrose or high-fructose corn syrup. Statistical adjustment helps but cannot perfectly reconstruct a randomized experiment.
Confounding by lifestyle and social conditions
Sleep, physical activity, smoking, income, education, work conditions, chronic stress, access to food, loneliness, illness, and medication can influence both depression and what people eat. Researchers adjust for many of these factors, but measurement error and unmeasured variables remain.
Measurement error
Diet is often estimated with food-frequency questionnaires or short dietary recalls. Depressive symptoms are often estimated with self-report scales. Both are useful research tools, but neither provides perfect measurement. When studies define “sugar,” “high intake,” and “depression” differently, combining them becomes harder.
Reverse causation
Depression can itself alter appetite, energy, reward sensitivity, sleep, shopping, cooking, social eating, and interest in food. Some people eat more sweet or convenient foods during depressed periods; others lose appetite and eat less. This means the causal arrow can plausibly run from diet toward mood, from mood toward diet, or in both directions depending on the person and context.
Possible mechanisms: what could connect high sugar intake and depression?
Mechanisms are best understood as candidate pathways rather than a single chain. Most human evidence does not identify one decisive route. Multiple pathways may overlap, and some may reflect the dietary pattern around sugar rather than sugar molecules alone.
Overall diet quality and nutrient displacement
When a large share of dietary energy comes from sweet drinks, desserts, and other low-nutrient foods, those foods can displace foods that provide fiber, protein, vitamins, minerals, and diverse plant compounds. Prospective research on diet quality generally finds that healthier dietary patterns are associated with a lower risk of depressive symptoms, although causality and treatment effects remain more uncertain than the association itself (Molendijk et al., 2025). This supports looking at the whole diet rather than treating sugar as an isolated psychiatric toxin.
Energy balance, adiposity, and cardiometabolic pathways
High intakes of free sugars, especially in beverages, can contribute to excess energy intake and unhealthy weight gain. Cardiometabolic disease and depression also interact in complex, bidirectional ways. These pathways are relevant to long-term health, but they should not be converted into a claim that every episode of sweet eating produces a depressive biological state.
Inflammatory and oxidative-stress hypotheses
Inflammation and oxidative stress are active areas of depression research, and high-sugar dietary patterns can influence metabolic and inflammatory physiology. Reviews have proposed these systems as possible mediators of the sugar–depression association. Human causal evidence specific to dietary sugar and clinical depression, however, remains incomplete. Mechanistic plausibility strengthens a hypothesis; it does not by itself prove the hypothesis.
Stress, coping, reward, and learned associations
Sweet foods can acquire psychological meaning through repetition. A dessert after conflict, sweet coffee during exhausting work, or candy during studying can become linked with relief, reward, breaks, comfort, social rituals, or predictable pleasure. Stress can also alter food choice and craving. A 2024 prospective community study found that baseline sugar-sweetened beverage intake predicted later depressive symptoms after adjustment for stress, while total added sugar did not remain significant after that adjustment, illustrating how stress and diet can overlap statistically (Fish-Williamson & Hahn-Holbrook, 2024).
For the dedicated behavioral mechanism, see Stress and Sugar Cravings: Why Stress Can Shift Food Choice and Sugar Cravings: Why They Happen and What Psychology Can Explain.
Sleep and fatigue
Depression often involves insomnia, fragmented sleep, early waking, hypersomnia, fatigue, or altered daily rhythms. Sleep loss can also change appetite, reward sensitivity, and food choice. That creates another route by which depression and sweet-food intake can become correlated without sugar being the sole initiating cause. The behavioral side of this link is covered in Sleep and Sugar Cravings: How Sleep Loss Can Change Appetite and Reward.
Brain energy and reward: important, but easy to oversimplify
Glucose is an essential energy substrate, and eating carbohydrates engages normal metabolic and reward systems. Popular explanations often jump from that fact to claims that sugar “hijacks dopamine” and thereby causes depression. The evidence is much more complex. Dopamine is involved in learning, motivation, salience, movement, and reward prediction; it is not a simple pleasure meter, and a transient reward response is not a diagnosis or an explanation of major depressive disorder. For the broader neuroscience boundary, see Sugar and the Brain: Glucose, Energy, Reward, and Common Myths.
Sugar rush, sugar crash, and depression are different questions
For the dedicated evidence on acute energy, expectation, mood, and the familiar “sugar rush” claim, see Sugar Rush: Is It Real? Energy, Expectation, and the Evidence.
The idea that sugar produces an immediate emotional high followed by a depressive crash is culturally familiar, but acute carbohydrate studies do not support a reliable positive “sugar rush.” A systematic review and meta-analysis of 31 studies found no positive effect of carbohydrate ingestion on mood at any measured time point; within the first hour, carbohydrate administration was associated with greater fatigue and lower alertness than placebo in some analyses (Mantantzis et al., 2019).
Even when a person experiences transient tiredness, irritability, hunger, or low energy after eating, that experience should not be equated with clinical depression. Acute subjective fluctuations occur on a different time scale and have different diagnostic meaning from a depressive episode.
Does the source of sugar matter?
Sugar-sweetened beverages
This is the exposure with some of the clearest observational depression signal. That may reflect dose, frequency, liquid calories, dietary context, or correlated behaviors. It does not prove that the sugar molecule is the only relevant feature of the beverage.
Desserts and sweet foods
Desserts often combine sugar with fat, refined flour or starch, flavorings, chocolate, dairy, salt, and strong sensory cues. Studies of “sweet food” therefore measure a complex food category rather than an isolated nutrient.
Whole fruit
The sugar in intact fruit comes within a food matrix containing water, fiber, micronutrients, and plant compounds. WHO’s free-sugar definition does not include intrinsic sugars in whole fresh fruits and vegetables. Evidence linking sugar-sweetened beverages with depression is not a scientific reason to avoid whole fruit.
Honey, syrups, and “natural” sugars
Calling a sweetener natural does not move it outside sugar physiology or public-health definitions. WHO counts sugars in honey and syrups as free sugars, while U.S. labeling counts relevant sugars from honey and syrups within Added Sugars. A naturalness label may change consumer expectation, but it does not create a special antidepressant category.
Can sugar make existing depression worse?
For an individual with depression, it is plausible that a high-sugar dietary pattern could interact with energy regulation, sleep, appetite, weight, cardiometabolic health, meal regularity, or emotional eating in ways that make overall functioning harder. Population evidence also links higher sugar intake with depressive symptoms. Yet there is no clinical rule stating that a particular amount of sugar will worsen symptoms in every person with depression.
The more useful question is often behavioral and contextual: Is a person relying heavily on sugar-sweetened drinks? Are sweet foods replacing meals? Is eating becoming chaotic because of low energy or poor sleep? Is a craving pattern tied to stress, isolation, or medication-related appetite changes? Those patterns can be addressed without treating sugar as the sole cause of the disorder.
Can cutting sugar improve depression?
There is no strong sugar-specific randomized-trial evidence showing that cutting added sugar by itself treats major depressive disorder. This is one of the most important limits in the literature. Observational associations can identify a possible modifiable risk factor; they cannot tell us that a sugar-reduction intervention will produce the reverse effect.
Randomized trials of broader dietary improvement have found small average reductions in depressive symptoms in meta-analysis, but those interventions alter many things simultaneously—food quality, meal structure, fruit and vegetable intake, fiber, fat quality, and sometimes weight or social support. Their results cannot be assigned specifically to sugar reduction (Firth et al., 2019).
Reducing added or free sugars can still be a sensible health choice, particularly when intake is high, because established dietary guidelines already recommend moderation. It should be framed as one part of overall nutrition rather than as a substitute for depression treatment.
Depression can also change sugar intake
Depression can reduce motivation to shop, cook, or prepare balanced meals. Fatigue can increase reliance on convenient foods. Anhedonia can change how rewarding food feels. Sleep disruption can alter hunger and cue reactivity. Some medications can affect appetite or weight. Stress may increase or decrease eating. Social withdrawal can remove shared meals. All of these can change sugar intake without requiring a direct biochemical craving for sucrose.
If the personal question is “why am I craving sugar?”, the broader decision tree is covered in Why Am I Craving Sugar? Hunger, Habit, Stress, Sleep, and Reward.
Sugar cravings are not the same as sugar addiction
A craving is a strong desire for a particular food or sensory experience. It can be shaped by hunger, cues, habit, stress, sleep, learned reward, availability, and restriction. Craving alone does not establish addiction.
“Sugar addiction” is a popular and contested construct rather than an established clinical diagnosis. Human eating behavior usually involves foods that combine sugar with fat, starch, flavor, texture, and learned meaning, making it difficult to infer a substance-addiction mechanism from craving or overconsumption alone. Depression can coexist with compulsive or dysregulated eating, but one diagnosis should not be inferred from the other.
Does quitting sugar cause depression or withdrawal?
People sometimes report headaches, irritability, fatigue, low mood, or cravings after abruptly changing a highly sweetened diet. Those experiences can be real, but there is no established clinical “sugar withdrawal” syndrome equivalent to withdrawal syndromes defined for substances such as alcohol or opioids. Sudden changes may also alter caffeine intake, total calories, meal timing, hydration, expectations, routines, and reward cues at the same time.
A temporary low mood after changing a diet should therefore not be automatically labeled depression or proof of dependence. Persistent depressive symptoms deserve their own assessment.
Practical meaning: how to reduce sugar without turning food into a mental-health test
A practical approach starts with the highest-impact sources rather than moralizing every sweet taste. For many people, sugar-sweetened beverages are the easiest place to notice repeated intake. The Nutrition Facts label can help identify Added Sugars in packaged foods, and the WHO free-sugars framework is useful for understanding the broader public-health category.
Changes tend to be easier to sustain when they preserve regular eating and adequate nutrition: replace rather than merely remove; keep satisfying meals; include fiber-rich carbohydrate sources; maintain protein and dietary variety; and choose sweet foods deliberately rather than through rigid prohibition. If cravings are strongest during stress, poor sleep, or long gaps between meals, addressing those conditions may be more useful than declaring war on sweetness.
Strict “sugar detox” rules can also create all-or-nothing thinking around food. The scientific goal is not zero exposure at any cost. It is an eating pattern that supports health and functioning while respecting individual needs, culture, access, and preferences.
When depression needs clinical care
Depression is treatable. If low mood, loss of interest, hopelessness, sleep or appetite change, fatigue, concentration problems, guilt, or other symptoms persist and interfere with daily life, a qualified health professional can assess what is happening and discuss evidence-based options. NIMH lists psychotherapy, medication, and—in selected cases—brain-stimulation treatments among established approaches (NIMH). Dietary changes can sit alongside clinical care; they are not a replacement for it.
If you are in immediate danger or thinking about suicide, contact local emergency services or a crisis service in your country. In the United States and its territories, call or text 988.
Frequently asked questions
Can sugar cause depression?
Research consistently finds an association between higher sugar intake—especially sugar-sweetened beverage intake—and depressive symptoms or depression risk. Direct causation has not been established, and depression has many interacting causes and risk factors.
Does sugar make depression worse?
It may contribute to an overall dietary or behavioral pattern associated with worse mental and physical health, but there is no universal dose at which sugar predictably worsens depression in every person. Individual context, overall diet, sleep, stress, health, and treatment matter.
Will quitting sugar cure depression?
No evidence supports treating sugar elimination as a cure for major depressive disorder. Reducing excessive added or free sugar can be part of a healthy dietary pattern, while depression treatment should follow appropriate clinical care.
Why do I crave sugar when I feel depressed?
Possible contributors include learned comfort associations, reward seeking, stress, poor sleep, irregular meals, hunger, fatigue, convenience, environmental cues, and changes in appetite. A craving does not identify one mechanism by itself and does not prove addiction.
Is a sugar crash the same as depression?
No. Short-term changes in fatigue, alertness, hunger, or mood after eating occur on a different time scale from clinical depression. Acute carbohydrate research does not support a reliable positive sugar rush, and transient low energy should not be treated as a depression diagnosis.
Does fruit sugar cause depression?
Evidence about sugar-sweetened beverages or high total sugar intake should not be transferred to intact fruit. Whole fruit contains fiber, water, micronutrients, and a distinct food matrix, and intrinsic sugars in whole fresh fruit are not classified as free sugars by WHO.
Should someone with depression avoid all added sugar?
There is no depression-specific rule requiring complete avoidance. Public-health guidance supports limiting added or free sugars within an overall healthy diet. Personal medical or nutritional needs can be discussed with an appropriate clinician or dietitian.
Bottom line
The most defensible conclusion is that higher sugar consumption is associated with depression at the population level, with particularly consistent signals for sugar-sweetened beverages. The association survives many statistical adjustments and appears in prospective data, so it deserves attention. At the same time, the evidence does not establish a simple one-way causal law, a universal mechanism, or a sugar-free treatment for major depressive disorder.
Sugar is best treated as one modifiable component of a larger dietary and behavioral system. Depression is best treated as a clinical and psychological condition with multiple determinants. Keeping those two levels distinct produces a more accurate and more useful answer than either “sugar has nothing to do with mood” or “sugar causes depression.”
Related Articles
Sugar and the Brain: Glucose, Energy, Reward, and Common Myths — how glucose, reward, dopamine, energy, and common brain myths fit together.
Sugar Cravings: Why They Happen and What Psychology Can Explain — a broader framework for hunger, cues, reward learning, habit, and craving.
Stress and Sugar Cravings: Why Stress Can Shift Food Choice — evidence on stress-related eating, coping, and individual differences.
Sleep and Sugar Cravings: How Sleep Loss Can Change Appetite and Reward — how sleep loss can change appetite, reward sensitivity, and food choice.
Added Sugar: What It Is, Where It Hides, and How Labels Count It — the U.S. labeling definition and the difference between added and total sugars.
Sugar Rush: Is It Real? Energy, Expectation, and the Evidence — the acute sugar-rush question, expectation effects, and controlled evidence.
Sugar and Anxiety: What the Evidence Can and Cannot Show — adjacent mental-health evidence with its own observational and causal limits.
References
Barma, M. D., Purohit, B. M., Priya, H., Malhotra, S., Bhadauria, U. S., & Duggal, R. (2026). Sweet Misery: Association of Sugar Consumption With Anxiety and Depression—A Systematic Review. Obesity Reviews, 27(1), 1–19. PubMed. DOI: 10.1111/obr.70003.
Buczkowska, M., & Iob, E. (2024). Testing the causal relationship of fat and sugar intake with depression and cortisol: a Mendelian Randomisation study. Translational Psychiatry, 14, 368. PubMed. DOI: 10.1038/s41398-024-03089-2.
Fish-Williamson, A., & Hahn-Holbrook, J. (2024). The Interrelationship between Stress, Sugar Consumption and Depression. Nutrients, 16(19), 3389. PubMed. DOI: 10.3390/nu16193389.
Firth, J., et al. (2019). The Effects of Dietary Improvement on Symptoms of Depression and Anxiety: A Meta-Analysis of Randomized Controlled Trials. Psychosomatic Medicine, 81(3), 265–280. PubMed. DOI: 10.1097/PSY.0000000000000673.
Huang, Y., et al. (2023). Dietary sugar consumption and health: umbrella review. BMJ, 381, e071609. BMJ. DOI: 10.1136/bmj-2022-071609.
Knüppel, A., Shipley, M. J., Llewellyn, C. H., & Brunner, E. J. (2017). Sugar intake from sweet food and beverages, common mental disorder and depression: prospective findings from the Whitehall II study. Scientific Reports, 7, 6287. PubMed. DOI: 10.1038/s41598-017-05649-7.
Mantantzis, K., Schlaghecken, F., Sünram-Lea, S. I., & Maylor, E. A. (2019). Sugar rush or sugar crash? A meta-analysis of carbohydrate effects on mood. Neuroscience & Biobehavioral Reviews, 101, 45–67. PubMed. DOI: 10.1016/j.neubiorev.2019.03.016.
Molendijk, M. L., et al. (2025). Diet quality and depression risk: A systematic review and meta-analysis of prospective studies. Journal of Affective Disorders. PubMed. DOI: 10.1016/j.jad.2025.03.162.
Mughal, I., Mughal, Z., Mistry, K., Dhakal, N., & Mughal, F. (2026). Dietary sugar intake and risk of depression: findings from the TwinsUK cohort. Nutritional Psychiatry, 3, 100025. PubMed. DOI: 10.1016/j.nupsyc.2026.100025.
National Institute of Mental Health. Depression. NIMH.
U.S. Food and Drug Administration. Added Sugars on the Nutrition Facts Label. FDA.
Vermeulen, E., Knüppel, A., Shipley, M. J., Brouwer, I. A., Visser, M., Akbaraly, T., Brunner, E. J., & Nicolaou, M. (2018). High-Sugar, High-Saturated-Fat Dietary Patterns Are Not Associated with Depressive Symptoms in Middle-Aged Adults in a Prospective Study. The Journal of Nutrition, 148(10), 1598–1604. PubMed. DOI: 10.1093/jn/nxy154.
Wang, Y., Zhao, R., Wang, B., Zhao, C., Zhu, B., & Tian, X. (2022). The Dose-Response Associations of Sugar-Sweetened Beverage Intake with the Risk of Stroke, Depression, Cancer, and Cause-Specific Mortality: A Systematic Review and Meta-Analysis of Prospective Studies. Nutrients, 14(4), 777. PubMed. DOI: 10.3390/nu14040777.
World Health Organization. (2015). Guideline: sugars intake for adults and children. WHO.
Xiong, J., Wang, L., Huang, H., Xiong, S., Zhang, S., Fu, Q., Tang, R., & Zhang, Q. (2024). Association of sugar consumption with risk of depression and anxiety: a systematic review and meta-analysis. Frontiers in Nutrition, 11, 1472612. PubMed. DOI: 10.3389/fnut.2024.1472612.
Zhang, L., Sun, H., Liu, Z., Yang, J., & Liu, Y. (2024). Association between dietary sugar intake and depression in US adults: a cross-sectional study using data from the National Health and Nutrition Examination Survey 2011–2018. BMC Psychiatry, 24, 110. PubMed. DOI: 10.1186/s12888-024-05531-7.