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:
Common Genetic Variations in CCK, Leptin, and Leptin Receptor Genes Are Associated With Specific Human Eating Patterns
Abstract 1:
Obesity has a heritable component ; however , the heterogeneity of obesity complicates dissection of its genetic background . In this study , we therefore focused on eating patterns as specific traits within obesity . These traits have a heritable component ; genes associated with a specific eating pattern have not yet been reported at the population level . In this study , we determined whether genetic variations in cholecystokinin ( CCK ) and leptin genes underlie specific eating patterns . We selected obese individuals showing extreme snacking behavior or use of excessive portion sizes from a large population -based sample ( n = 17,357 ) from the Prospect -EPIC ( European Prospect i ve Study into Cancer and Nutrition ) study . Using allele-specific PCRs , we tested several single nucleotide polymorphisms in the c and i date genes and performed haplotype analysis . Obese carriers of common allelic variations in leptin or the leptin receptor gene had an increased risk to display extreme snacking behavior . In contrast , obese carriers of common allelic variations in CCK had an increased risk to eating increased meal sizes . In conclusion , we identified common allelic variants specifically associated with distinctly different eating patterns , namely extreme snacking behavior or excessive portion size


Title 2:
Hypertension in obesity and the leptin receptor gene locus.
Abstract 2:
Recent animal studies indicate that leptin is involved in the regulation of blood pressure through the leptin receptor . Therefore , 51-yr-old men ( N = 284 ) were selected ; and anthropometric , endocrine , metabolic , and hemodynamic variables were examined in relation to polymorphisms of the leptin receptor gene ( LEPR ) , by restriction fragment length polymorphism technique . Three polymorphisms were examined : Lys109Arg in exon 4 , Gln223Arg in exon 6 , and Lys656Asn in exon 14 . In comparison with Lys109 homozygotes , Arg109 homozygotes ( 9 % ) showed lower body mass index ( BMI ) and abdominal sagittal diameter , as well as lower systolic ( 10.0 mm Hg ) and diastolic ( 7.8 mm Hg ) blood pressure . Additionally , Arg223 homozygotes ( 26.8 % ) showed lower blood pressure ( 7.6/5.7 mm Hg ) than Gln223 homozygotes . These lower blood pressure levels were independent of other variables . No differences were found with the Lys656Asn polymorphism . Measurements of body fat mass correlated with leptin concentration in Lys109 homozygotes and in Lys109 heterozygotes but not in Arg109 homozygotes . Blood pressure correlated with leptin only in men carrying the wild-type allele Lys109 . With both elevated BMI and leptin , Lys109 homozygotes had higher blood pressure than the Arg109 homozygous men ( 12.4/6.9 mm Hg ) . Men with blood pressure  > or = 140/90 mm Hg had , in comparison with normotensive men , increased BMI and leptin levels , and Lys109 homozygotes were significantly more prevalent . These results suggest that leptin is associated with blood pressure regulation in men through the leptin receptor . When BMI and leptin are elevated , increased blood pressure is found only with the most prevalent LEPR genotype at codons 109 and 223 , whereas variants of this receptor seem to protect from hypertension . This might explain why not all obese men are hypertensive


Title 3:
The effect of the Neolithic expansion on European molecular diversity
Abstract 3:
We performed extensive and realistic simulations of the colonization process of Europe by Neolithic farmers , as well as their potential admixture and competition with local Palaeolithic hunter – gatherers . We find that minute amounts of gene flow between Palaeolithic and Neolithic population s should lead to a massive Palaeolithic contribution to the current gene pool of Europeans . This large Palaeolithic contribution is not expected under the demic diffusion ( DD ) model , which postulates that agriculture diffused over Europe by a massive migration of individuals from the Near East . However , genetic evidence in favour of this model mainly consisted in the observation of allele frequency clines over Europe , which are shown here to be equally probable under a pure DD or a pure acculturation model . The examination of the consequence of range expansions on single nucleotide polymorphism ( SNP ) diversity reveals that an ascertainment bias consisting of selecting SNPs with high frequencies will promote the observation of genetic clines ( which are not expected for r and om SNPs ) and will lead to multimodal mismatch distributions . We conclude that the different patterns of molecular diversity observed for Y chromosome and mitochondrial DNA can be at least partly owing to an ascertainment bias when selecting Y chromosome SNPs for study ing European population
The meta- analysis of published data did not show an overall association between any of the tested LEPR variants and overweight .
However , the choice of a BMI cut-off value to distinguish cases from controls was crucial to explain heterogeneity in Q223R .
Differences in allele frequencies across ethnic groups are compatible with natural selection of derived alleles in Q223R and K109R and of the ancient allele in K656N in Asians .
In CoLaus , the rs10128072 , rs3790438 and rs3790437 variants showed interaction with sex for their association with overweight , waist circumference and fat mass in linear regressions .
Conclusions Our systematic review and analysis of primary data from the CoLaus study did not show an overall association between LEPR SNPs and overweight .