May 18, 2016

Please enjoy these reviews of three recent high quality research studies on topics we think you may find relevant and useful.

A meta-analysis of the relationship between brain dopamine receptors and obesity: a matter of changes in behavior rather than food addiction?

Benton D, Young HA. Int J Obes (Lond). 2016 Mar;40 Suppl 1:S12-21.

Background - The drug addiction theory: Many drugs of abuse stimulate the reward mechanism so intensely that, in order to compensate, dopamine D2 receptors (DD2R) declines. The result is a higher drug intake necessary to experience the same degree of reward. People with an A1 allele in the Taq1A polymorphism naturally have 30-40% lower DD2R, which is considered a risk factor for drug addiction.

Hypothesis: If obesity reflects an addiction, people with decreased levels of DD2R would have increased food intake and subsequently increased risk of obesity (higher BMI).

Results: Meta-analysis of 33 observational studies comparing children and adults with A1 allele or without showed no difference in BMI between those with and without the A1 allele. Among those already obese, there was also no difference observed in the presence of the A1 allele. Overall, the results did not support the hypothesis.

Conclusions:

  • There is no association between reduced dopamine D2 receptors and the occurrence of obesity.
  • The findings do not support the assumption that food addiction resembles drug abuse.
  • The DD2R polymorphism may be associated with eating behavior, not food itself and “food addiction” may be more accurately described as “eating addiction”.
  • Instead of taking the “addiction” approach of decreasing particular foods/nutrients, the aim should be to encourage intake of nutrient-dense, satiating and palatable foods and incorporating coordinated behavioral changes that acknowledge the complexity and multifaceted nature of the problem.

 

Orange  juice  consumption  and  its  effect  on  blood lipid profile and indices of the metabolic syndrome; a randomized, controlled trial in an at-risk population.

Simpson EJ, Mendis B, Macdonald IA. Food Funct. 2016 Apr 20;7(4):1884-91.

Background: Reports in the media claim drinking 100% orange juice can have detrimental health consequences, including weight-gain and adverse effects on insulin sensitivity and blood lipid profile. In the World Health Organization sugars guidelines, fruit juices are grouped into sources of free sugars.

Study design: A parallel randomized controlled trial (RCT) was conducted among overweight but otherwise healthy men with elevated total cholesterol levels (n=36, 40-60 years). They consumed 250 mL/day orange juice (OJ) or an energy and sugars-matched orange flavoured drink (control) for 12 weeks with an ad-libitum background diet.

Results: No change in BMI, lipid parameters, insulin sensitivity, uric acid or inflammatory markers between groups. The OJ group had higher energy, and total carbohydrate (CHO) intake as compared to the control group at baseline, but there was no change in these intakes between groups, except for CHO in the control group, which increased to similar levels as the OJ group. Interestingly, the total sugars intake did not change with the intake of OJ or the control beverage and the total Calories remained stable. Those in the OJ group with the highest initial triglyceride (TG) levels showed more reduction in TG as compared to the control group.

Conclusion: Daily consumption of 250 mL orange juice for 3 months did not result in an increase in total sugars intake but reduced blood TG levels among those with high TG levels at baseline. No effect was observed on body weight, insulin resistance or fasting blood lipids.  

 

Fructose  containing  sugars  at  normal  levels  of  consumption  do not effect adversely components of the Metabolic Syndrome and risk factors for Cardiovascular Disease.

Angelopoulos TJ, Lowndes J, Sinnett S, Rippe JM. Nutrients. 2016 Mar 23;8(4). pii: E179. 

Background: Most clinical trials of fructose have used a dose of 25% Calories or greater, which is hardly achieved in the human diet. The objective of the study was to explore the hypothesis that consumption of fructose and fructose containing sugars at normal doses would not increase risk factors for cardiovascular disease (CVD) and the metabolic syndrome (MetS).

Study design: A double blinded, parallel RCT (n=267) during which normal-weight to obese individuals consumed either 18%E of calories from high fructose corn syrup (HFCS), 18%E sucrose, 9%E fructose or 9%E glucose (in the form of sweetened  low fat milk) for 10 weeks on a weight maintenance diet. The 9%E dose of fructose was chosen at 50th percentile of population consumption of fructose, and the 18%E sucrose/HFCS provides an equivalent of 9%E fructose.

Results: There was an overall increase in total Caloric intake and %Calories from CHO, and a decrease in %Calories from fat in all groups. Very small increase were seen in waist circumference (by 0.6cm), BMI (by 0.3 kg/m2), TG (by 0.9 mmol/L), and total cholesterol (by 0.1 mmol/L) in all groups. Systolic blood pressure and diastolic blood pressure were lower, and there was no change in HDL or fasting glucose. No other components of MetS were influenced by the types or doses of sugars. None of the changes were considered clinically significant (still well within the normal range). The increase in BMI, waist circumference etc. may be contributed by increased overall Caloric consumption since no difference was observed between groups.

Conclusion: When consumed as a part of a normal diet at typical levels, the effects of these sugars on components of the MetS and CVD risk factors are minimal, mixed and not clinically significant.