You will be presented with a collection of medical randomized controlled trial (RCT) reports addressing a shared clinical question -- for instance, the efficacy of a medical intervention on a disease or condition. Given the titles and abstracts of these reports, your task is to generate the conclusion of the systematic review article synthesizing the key findings. Your conclusion should be a few sentences long. In your response, include only the conclusion and no other text. The RCT reports are below.



Title 1:
Low fructose and low salt diets increase mitochondrial DNA in white blood cells of overweight subjects.
Abstract 1:
OBJECTIVE To evaluate the effect of sodium and fructose restriction on mitochondrial DNA ( mtDNA ) content and systemic oxidative stress in a sample of overweight and pre hypertensive subjects . MATERIAL / METHODS Data and blood sample s were collected from 36 overweight and pre hypertensive patients r and omly assigned to either an isocaloric ( with respect to baseline ) low sodium-fructose diet or an isocaloric low sodium diet . Patients were followed for 8 weeks . We measured mitochondrial DNA ( mtDNA ) content from peripheral blood white cells by Real-time PCR and plasma malondialdehyde ( MDA ) and 2,4-dinitrophenylhydrazine ( DNPH ) as markers of reactive oxygen species ( ROS ) . RESULTS Compared to baseline , at week 8 there was a continued and significant increase in mtDNA in both the low sodium diet group [ 2.4 vs. 13.1 ( relative copy number ) , p<0.05 ] and the low sodium diet-fructose group ( 1.9 vs. 147.2 , p<0.05 ) . By week 8 there was a continued decrease in plasma DNPH levels in the low sodium diet group ( 4.6 vs. 2.6 , p<0.05 ) and in the low sodium diet-fructose group ( 5.8 vs. 2.2 , p<0.05 ) . No significant differences were found with MDA . CONCLUSION Our studies suggest that simple dietary measures such as reducing salt with or without restricting fructose can increase mtDNA and improve markers of oxidative stress
The combination of low sodium and low fructose did increase mtDNA but it did not increase it more than the low sodium diet alone without fructose restriction .
This suggests that the eff ect appears dependent on sodium but not fructose .
Conversely , in isocaloric comparisons where energy intake is matched , these eff ects are not observed .
That is , fructose behaves no worse than any other carbohydrate [ 4 – 8 ] , although there may be a dosethreshold for some fasting lipid eff ects [ 4 , 10 – 12 ] .
This lack of eff ect remains true even under conditions of fructose overfeeding ( positive energy balance ) , as long as the comparison is matched for the excess calories .
Taken together , the main driver mediating any harm attributable to fructose appears to be excess energy .
In conclusion , there is insuffi cient evidence to conclude that fructose restriction has a signifi ca nt eff ect on mtDNA and oxidative stress when holding energy equal .
Energy imbalance appears to be a prerequisite for eliciting an eff ect .