A recent study published in the Science journal showed that limiting sugar up to 1000 days from conception can reduce the risk and delay the onset of type 2 diabetes (T2D) and hypertension later in life, in their 60s.
Study cohort
This study was based on a UK cohort of 60,183 participants born between October 1951 and March 1956, aged 51 to 66 years when surveyed. After World War II, sugar rationing ended in September 1953. During the rationing, adult sugar consumption was limited to 40 g per day, which is the current recommendation from WHO (World Health Organization) and AHA (American Heart Association). However, once the rationing ended in 1953, sugar consumption almost doubled immediately. The cohort was divided into two groups – individuals born from July 1954 to March 1956 were considered “never rationed” and used as a reference group. Individuals conceived 1000 days before September 1953 i.e. born from October 1951 to June 1954 were considered as “rationed”, further sub-grouped into – rationed in-utero only, rationed up to 6/12/18/24 months + in-utero. No significant difference in other nutrients- fats, produce, or proteins- was found between the two groups. Thus, making them a good case-control cohort.
Results
- The risk of T2D and hypertension diagnosis increased with age but faster in adults with no exposure to rationing. With increasing rationing, the risk of T2D and hypertension decreased by 35% and 20% respectively compared to the never rationed group (Table 1).
- 92.2% and 65.4% of rationed adults had a higher chance of living without T2D and hypertension at age 60, respectively, compared to 89.1% and 61.4% of never rationed.
- Rationing also delayed the onset of T2D and hypertension by 4 and 2 years respectively (Table 1).
- Lastly,a 30% decrease in obesity risk was also observed in the rationed group.
Table 1 – Disease hazard ratio and delay in age onset for T2D and hypertension.
| Rationing exposure | Type 2 diabetes (T2D) | Hypertension |
| Disease hazard ratio (SE) compared to never rationed group | ||
| In utero | 0.87*** (0.03) | 0.92**(0.02) |
| In utero + up to 1 year | 0.75*** (0.04) | 0.85*** (0.02) |
| In utero + up to 2 years | 0.64*** (0.02) | 0.81*** (0.02) |
| Delay in age onset in years (SE) compared to never rationed group | ||
| In utero | 1.46**(0.52) | 0.53*(0.24) |
| In utero + up to 1 year | 2.8**(0.61) | 1.47***(0.28) |
| In utero + up to 2 years | 4.17***(0.55) | 2.12**(0.24) |
Asterisks indicate significance, *P<0.05, **P<0.01, ***P<0.001.
Hazard ratio measures the rate at which the disease develops in one group vs another. A hazard ratio of greater than 1 indicates high risk and less than 1, is low risk.
Strengths of the study
- Large sample size.
- Sugar was the only different nutrient, excluding the effect of any other nutrient.
- Many rodent studies have shown the adverse effects of excessive dietary sugar early in life, but human studies were limited. This study supported the findings of the rodent studies and had cohorts with varying levels of sugar consumption.
Limitations of the study
- UK Biobank is not nationally representative and skews toward wealthier, healthier individuals. However, the study is exposure outcome-based and the biobank provides a large sample.
- This study did not consider any mortality information but previous reports have observed similar low mortality rates between rationed and never rationed adults.
Vinny Negi, Ph.D.
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