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SAN ANTONIO -- Limiting exposure to sugar starting in utero reduced risk and delayed onset of type 2 diabetes and hypertension in adulthood, a study showed.

Adults exposed to early-life sugar rationing in the U.K. for at least 19 months (including in utero) had a 38% reduced risk of type 2 diabetes (HR 0.62, 95% CI 0.55-0.69) and a 21% reduced risk of hypertension (HR 0.79, 95% CI 0.74-0.85) compared to those never exposed to rationing, reported Tadeja Gracner, PhD, of the University of Southern California in Los Angeles, at the ObesityWeek annual meeting. The findings were also published in .

"In-utero exposure alone explained about a third of the total reduction in type 2 diabetes and hypertension risk compared to exposure in utero and beyond age 1," the researchers reported. Further, adults exposed to sugar rationing prenatally through their first birthday had about a 4-year delay in type 2 diabetes diagnosis and a 2-year delay in hypertension diagnosis.

John Clark, MD, PhD, the chief population health officer with Sharp Rees-Stealy Medical Group in San Diego, told MedPage Today he was not necessarily surprised by the findings, but he was impressed with the researchers' ability to get longitudinal data with such a clear cutoff of sugar exposure.

"It is a very unique analysis and just adds to the evidence that suggests that there really, truly is an association or causation between" sugar consumption and development of type 2 diabetes and hypertension, Clark said. While the study cannot "definitively determine" causation, "it's one piece of the puzzle and hypothesis-generating," he said.

Dietary guidelines recommend that sugar should be limited to less than 10% of adults' total energy intake and that children under age 2 should consume no added sugars. , however, that 70% of pregnant people consume more than the recommended 10% limit during pregnancy, taking in an average of 20 teaspoons of sugar a day, or about 15% of total energy intake. Similarly, about 61% of infants and 98% of toddlers eat sugars daily, some of which comes from baby foods since about have at least 20% of their calories from sugars.

"There's a broad literature showing that the first 1,000 days of life are a critical window for optimal growth and development," Gracner told attendees, and research has also shown that excessive sugar intake is associated with increased risk for type 2 diabetes and hypertension and for adults' increased preference for sweetness.

While animal studies have shown that early-life exposure to sugar causally contributes to development of chronic disease, human studies attempting to make this connection are only correlational and often short in duration or from extreme events, such as famine, that aren't generalizable, Gracner said. It's particularly difficult to isolate sugar exposure from other confounding factors that can increase disease risk later.

However, the researchers were able to use historical data that did separate sugar consumption from many other confounders. Post-World War II sugar rationing in the U.K. ended in September 1953, and adults who were conceived or born before the end of sugar rationing have similar disease trajectories and other environmental exposures as those born after the end of rationing except in their exposure to sugar and sweets.

From 1942-1953, estimated daily consumption of sugar from 1950-1953 was 6.5% of total energy intake. U.K. residents' intake of fats, produce, and protein did not change in the 3 years before 1953 compared with the 3 years after, but sugar intake nearly doubled soon after sugar rationing ended, Gracner reported. Overall calorie intake also increased substantially after 1953, but an average 77% of that intake came from sugar.

Using the National Health Service's U.K. Biobank Resource, the researchers compared type 2 diabetes and hypertension risk in adults born before and after sugar rationing from October 1951-March 1956. Adults born in the earlier period were progressively exposed to more sugar. Those born later were only rationed in utero whereas those born earliest in the cohort had minimal sugar exposure through age 2.

Among the 60,183 participants, the 38,155 conceived in the 1,000 days prior to September 1953 -- born from October 1951-June 1954 -- were categorized as rationed while the other 22,028, born from July 1954-March 1956, were non-rationed. Race, sex, family history of diabetes, and genetic risk for obesity were similar between the two cohorts, and the only significant difference was that rationed adults were slightly more likely to be born in England (85.8%) than outside England (85.1%, P<0.05).

Data from surveys of these adults at ages 51-66 revealed that 3,936 had been diagnosed with diabetes and 19,644 had hypertension. Although disease risk increased with age in both cohorts, it increased faster in those with little or no rationing exposure, with that divergence starting when participants were in their mid-50s and particularly increasing after age 60. Further, participants' risk of type 2 diabetes or hypertension decreased in inverse proportion to their exposure to rationing.

Adults exposed only prenatally to early-life sugar rationing had a 16% lower risk of type 2 diabetes (HR 0.84, 95% CI 0.75-0.95) and a 6% lower risk of hypertension (HR 0.94, 95% CI 0.88-1.00) compared to those never exposed to sugar rationing. Prenatal exposure to sugar rationing also delayed diagnosis by 1.46 years for type 2 diabetes (95% CI 0.45-2.48) and 0.53 years for hypertension (95% CI 0.07-1.00).

Those exposed to sugar rationing prenatally and through their first birthday had a 31% reduced risk of obesity compared to those never exposed to rationing (HR 0.69, 95% CI 0.60-0.80).

"We all want our children to have a good start in life, and reducing and restricting added sugar early is a powerful step in that direction," Gracner said.

For adults born after December 1954, the risk for type 2 diabetes and hypertension remained constant, which the researchers wrote "supported our assumption of a similar disease risk trajectory between rationed and non-rationed cohorts independent of rationing" and "mitigated concerns about improvements in diagnostics or other events such as improved access to medical care over time influencing the age of initial diagnosis."

Although other food went off rationing after sugar, such as butter in May 1954, adults' relative intake of fats and later risk of disease did not significantly change before and after then.

"If fat rather than sugar alone affected these adults' health, we would expect that adults conceived after butter de-rationing (post-May 1954) would fare differently than adults conceived prior (October 1953-April 1954), and that disease risk would increase for younger cohorts," the researchers wrote, but no such patterns emerged.

Further, other conditions unlikely to be affected by sugar intake -- such as type 1 diabetes, depression, menarche, and myopia or hyperopia -- were not significantly different between the pre- versus post-1953 cohorts.

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