Are Sugar Consumption & Obesity Correlated?

Originally Published: April 1, 2019
Last Updated: February 4, 2021

AT THE OUTSET OF HIS TALK, “Reducing Added Sugars: Will It Reverse the Trend Toward Overweight & Obesity,” John White, Ph.D., President and Founder, White Technical Research, asked how many in the audience believed that sugar consumption was correlated with obesity. About 40% said they were in agreement.

Added sugars as the root of many of contemporary American’s health problems was referred to by White as the “added sugars hypothesis” which has two key justifications: 1) Significant diseases are increasing as sugars increase in the U.S. diet and 2) high value, cause-and-effect evidence uniquely links added sugars metabolism to these diseases in humans at typical exposure levels and patterns. Neither of these hypotheses are true, asserted White. “There has been a great deal of pressure on industry to reduce added sugars,” he noted, “but is there evidence-based research to support such decisions?”

Scientific evidence is not all created equal. The evidence pyramid (see chart “Value Hierarchy in Evidence-based Medicine”) indicates that systematic reviews and meta-analyses of randomized controlled trials (RCTs), followed by randomized/non-randomized controlled trials have the least likelihood of bias. Epidemiological and animal data is often used to associate HFCS and fructose consumption with disease, although the FDA considers both to be of low evidentiary value for establishing cause and effect, noted White.

Negativity regarding fructose grew with the claim that an increase in consumption of HFCS is related to the epidemic of obesity, a temporal association that did not in any way establish cause and effect. In fact, per capita availability trends from the USDA for sucrose and HFCS show that sucrose consumption increased 40% between 1910-1921 and remained constant for >50 years. HFCS was introduced in the market in the late 1960s and rapidly gained market share at the expense of sucrose.

“What isn’t acknowledged is that HFCS use peaked in 1999,” said White, “and has been in steep decline for nearly two decades. This decline has occurred as obesity rates continued to rise,” and the data have shown no positive association between HFCS and obesity for 19 years.

White explained that U.S. per capita energy intake increased by 449 kcal/d (21%), between 1970-2010. Notably, increased energy from caloric sweeteners was minor, accounting for <8% of this energy increase. Energy from cereal grains and added fats increased disproportionately, accounting for >90% of the increase. “The most likely contributor to overweight and obesity is an imbalance between energy intake and expenditure, not increases in sugar intake,” said White.

Fructose studies don’t model the range of human intake, White explained. Using NHANES data, fructose intakes are on average 9.1% energy (E) and 14.6% E for the highest 5% of fructose consumers. White presented an overview on 57 human and animal papers reporting adverse effects of fructose. However, he stressed that these studies fed extreme fructose doses, exceeding the 95th population percentile intakes in many human studies by 1.5-3-fold, and in animals by >4-5 times.

White also emphasized that humans don’t eat fructose or glucose alone, but always in combination in the diet from fruits, vegetables and nuts, as well as added sugars. “Extreme dosing under conditions of exaggerated protocols bias biochemical out-comes,” he concluded.

In short-term studies of human subjects consuming HFCS and sucrose in randomized, controlled trials, few differences were found for clinical markers of obesity (plasma glucose and insulin; ghrelin and leptin; triglycerides and uric acid; hunger and satiety) over the range of exposure from 9%-15% E as fructose (45–75 g/d) (Rippe et al. 2013. Adv Nutr./

In longer term studies of 10 weeks and more, no significant differences between three levels of HFCS and sucrose intake (8, 18 or 30% of isocaloric energy in 342 individuals) were reported for these markers.

Recent meta-analyses—the highest evidentiary value—have assessed the relationship of sugars to chronic disease. Isocaloric (equal calorie basis) comparisons of fructose with other carbohydrates (sucrose, HFCS, lactose, starch) found no adverse effects on body weight, fasting lipids, blood pressure, uric acid concentration, glycemic control and insulin sensitivity, postprandial lipids and markers of non-alcoholic fatty liver disease (Khan et al. 2016. Eur J Nutr/ Some differences in these metabolic markers were observed with hypercaloric feeding trials, in which excess calories from fructose were added to a diet compared with the same diet without the excess calories. These variances were most likely due to confounding from extra calories, rather than fructose.

White concluded that high-level evidence from systematic reviews/ meta-analyses and randomized/non-randomized controlled studies does not support a direct causal relationship between added sugars and obesity and overall disease. He stressed that considering the disproportionate increase in consumption of added fats and cereal grains over the past 50 years, it is unlikely that reducing added sugars will reverse the trend toward overweight and obesity.

“Reducing added sugars: Will it reverse the trend toward overweight & obesity?”, John S. White, Ph.D., President and Founder, WHITE Technical Research

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