CoChat
Sign Up
Cited by 739Diet, Metabolism, and DiseaseNutritional Studies and DietBiochemical Analysis and Sensing Techniques

Sugar consumption, metabolic disease and obesity: The state of the controversy

Open access
Stanhope, Kimber L.·2016·Critical Reviews in Clinical Laboratory Sciences
DOI 10.3109/10408363.2015.1084990PMC PMC4822166
Open this paper in CoChat — free account

Abstract

The impact of sugar consumption on health continues to be a controversial topic. The objective of this review is to discuss the evidence and lack of evidence that allows the controversy to continue, and why resolution of the controversy is important. There are plausible mechanisms and research evidence that supports the suggestion that consumption of excess sugar promotes the development of cardiovascular disease (CVD) and type 2 diabetes (T2DM) both directly and indirectly. The direct pathway involves the unregulated hepatic uptake and metabolism of fructose, leading to liver lipid accumulation, dyslipidemia, decreased insulin sensitivity and increased uric acid levels. The epidemiological data suggest that these direct effects of fructose are pertinent to the consumption of the fructose-containing sugars, sucrose and high fructose corn syrup (HFCS), which are the predominant added sugars. Consumption of added sugar is associated with development and/or prevalence of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, CVD and T2DM, often independent of body weight gain or total energy intake. There are diet intervention studies in which human subjects exhibited increased circulating lipids and decreased insulin sensitivity when consuming high sugar compared with control diets. Most recently, our group has reported that supplementing the ad libitum diets of young adults with beverages containing 0%, 10%, 17.5% or 25% of daily energy requirement (Ereq) as HFCS increased lipid/lipoprotein risk factors for CVD and uric acid in a dose-response manner. However, un-confounded studies conducted in healthy humans under a controlled, energy-balanced diet protocol that enables determination of the effects of sugar with diets that do not allow for body weight gain are lacking. Furthermore, recent reports conclude that there are no adverse effects of consuming beverages containing up to 30% Ereq sucrose or HFCS, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate. Consumption of excess sugar may also promote the development of CVD and T2DM indirectly by causing increased body weight and fat gain, but this is also a topic of controversy. Mechanistically, it is plausible that fructose consumption causes increased energy intake and reduced energy expenditure due to its failure to stimulate leptin production. Functional magnetic resonance imaging (fMRI) of the brain demonstrates that the brain responds differently to fructose or fructose-containing sugars compared with glucose or aspartame. Some epidemiological studies show that sugar consumption is associated with body weight gain, and there are intervention studies in which consumption of ad libitum high-sugar diets promoted increased body weight gain compared with consumption of ad libitum low- sugar diets. However, there are no studies in which energy intake and weight gain were compared in subjects consuming high or low sugar, blinded, ad libitum diets formulated to ensure both groups consumed a comparable macronutrient distribution and the same amounts of fiber. There is also little data to determine whether the form in which added sugar is consumed, as beverage or as solid food, affects its potential to promote weight gain. It will be very challenging to obtain the funding to conduct the clinical diet studies needed to address these evidence gaps, especially at the levels of added sugar that are commonly consumed. Yet, filling these evidence gaps may be necessary for supporting the policy changes that will help to turn the food environment into one that does not promote the development of obesity and metabolic disease.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3109/10408363.2015.1084990

Cites

157 of 157 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Excessive sugar intake directly correlates with hyperglycemia and its complications.

    “Excessive sugar intake directly correlates with hyperglycemia and its complications [8].”

    From Impact of Dietary Patterns on Metabolic Syndrome in Young Adults: A Cross-Sectional Study (2024) · cites this paper as [8]

    The Abstract links excess added sugar to insulin resistance, type 2 diabetes and cardiovascular disease. The Introduction’s “Direct experimental data from diet intervention studies” also reports higher fasting glucose after a high-sucrose diet. The paper does not establish the claimed direct correlation with hyperglycemia and its complications as a whole; its broader conclusions are framed as associations or suggested mechanisms. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • This rapid digestion may induce multiple adverse effects, potentially stimulating reward/craving areas in the brain, activating hepatic de novo lipogenesis, increasing uric acid production, and promoting visceral adiposity.

    “This rapid digestion may induce multiple adverse effects, potentially stimulating reward/craving areas in the brain, activating hepatic de novo lipogenesis, increasing uric acid production, and promoting visceral adiposity.49, 162-166”

    From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [165]

  • Poor quality carbohydrates are associated with long-term weight gain, diabetes, and CVD.

    “Consistent with this constellation of adverse effects, poor quality carbohydrates are associated with long-term weight gain, diabetes, and CVD.29, 89, 158, 167”

    From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [165]

  • There are important metabolic differences between glucose and fructose.

    “In contrast, there are important metabolic differences between glucose and fructose – each equally present in both high-fructose corn syrup and natural sugar (sucrose).”

    From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [165]

  • High doses of rapidly digested glucose induce postprandial hyperglycemia, hyperinsulinemia, and related metabolic disturbances.

    “High doses of rapidly digested glucose induce postprandial hyperglycemia, hyperinsulinemia, and related metabolic disturbances.”

    From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [165]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Stanhope, K. L.
Affiliations
University of California, Davis (US)
Corresponding author
Stanhope, Kimber L.
ORCID
Stanhope, Kimber L.
Venue
Critical Reviews in Clinical Laboratory Sciences
Publisher
Informa UK Limited
Published
2015-09-17
Volume
53
Issue
1
Pages
52-67
ISSN
  • 1040-8363 (ISSN-L)
  • 1549-781X
DOI
10.3109/10408363.2015.1084990
PMC
PMC4822166
OpenAlex
W2193179560
Cited by
739
References
157
Citations by year
2026: 51 · 2025: 72 · 2024: 79 · 2023: 90 · 2022: 84 · 2021: 94 · 2020: 68 · 2019: 64 · 2018: 60 · 2017: 53 · 2016: 24
FWCI
6.90
Type
journal article
Language
en
Open access
Locations
  • Critical Reviews in Clinical Laboratory Sciences (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (5r01hl075675-05, 5r01hl091333-02)
  • National Heart, Lung, and Blood Institute (R01 HL-075675, R01 HL-091333, R01HL121324, R01HL107256, 1R01 HL091333)
  • National Center for Research Resources (UL1RR024131, UL1RR024146)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (K12HD051958)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Nutritional Studies and Diet
  • Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
Keywords
sugar consumption, fructose, high fructose corn syrup, sucrose, added sugars, obesity, type 2 diabetes, cardiovascular disease, insulin resistance, hyperuricemia, dyslipidemia, hepatic lipid accumulation, hepatic steatosis, leptin, energy balance, weight gain, energy expenditure, dose-response relationship
MeSH terms
Humans, Metabolic Diseases, Models, Biological, Obesity, Risk Assessment, Evidence-Based Medicine, Dietary Sucrose

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review