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Sweet Tooth Gene Tied to Less Body Fat

A study of more than 450,000 people finds a certain genetic variant associated with eating more carbs is linked to a thicker waist and higher blood pressure, but less fat.  

By Kerry Grens | April 11, 2018

ISTOCK, CHAMPJAA variant in the gene for a certain hormone is tied to people eating more carbs. Yet a new study of 451,000 people finds that the allele doesn’t universally mean poorer health. Researchers reported yesterday (April 10) in Cell Reports that those with the sweet-tooth variant actually have lower body fat than others, and no higher risk for type 2 diabetes. They did, however, find a link between the allele and high blood pressure and a thicker waistline.

“This goes against the current perception that eating sugar is bad for health. It may reduce body fat because the same allele also results in a lower consumption of protein and fat in the diet,” study coauthor Timothy Frayling, a molecular geneticist at the University of Exeter Medical School in the U.K., says in a press release. “But whilst this version of the gene lowers body fat, it also redistributes fat to the upper body, where it’s more likely to cause harm, including higher blood pressure.”

The gene of interest here is FGF21, which encodes fibroblast growth factor 21, a hormone involved in alcohol and sugar consumption and insulin sensitization. The authors note that it’s a target of weight loss interventions.

People with a particular allele of FGF21—20 percent of Europeans are homozygous for the varianttend to consume relatively more sugar and alcohol than those without the allele. To see what consequences this might have on people’s health, Frayling and his colleagues collected data on 451,000 people whose genetic and health information is part of the UK Biobank.

Although those with the sweet-tooth allele had less body fat than others, they had a higher waist-to-hip ratio. They also had higher blood pressure, but no greater risk for heart disease or type 2 diabetes. “These results suggest that FGF21 has pleiotropic effects, with separate effects on macronutrient intake to those on body shape and blood pressure,” the authors write in their report.

Stephen Simpson, a nutrition scientist at Sydney University, tells Cosmos that the results may warrant a rethink of the idea that “no matter what, sugar consumption is bad. This villainisation needs proper exploration.”

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Comments

Avatar of: Rajeevdsamuel

Rajeevdsamuel

Posts: 1

April 11, 2018

Fake Science.  Carbohydrates cause cancer, obesity, heart disease, liver disease, diabetes, PCOS, IBS, acid reflux, dementia, parkinsons, autism and eventual death.

Avatar of: skinny

skinny

Posts: 6

Replied to a comment from Rajeevdsamuel made on April 11, 2018

April 11, 2018

Eventual death? Are you serious? Since everyone eventually dies, that could cover about anything. Piano playing, chasing tornados, driving to Toledo, running on the beach, eating squid, etc. Every person who has done these things has eventually died. In fact every person who has eaten fats, proteins, and carbohydrates has eventually died; as have all those people who ate none of those.

Avatar of: James V. Kohl

James V. Kohl

Posts: 515

April 11, 2018

See All About that Base (Meghan Trainor Parody) 12/10/14 from the Zechiedrich lab and their 2015 published work: Structural diversity of supercoiled DNA

A Common Allele in FGF21 Associated with Sugar Intake Is Associated with Body Shape, Lower Total Body-Fat Percentage, and Higher Blood Pressure is an open access publication.

The authors link one food energy-dependent change in a base pair from rs838133, which is an A/G/T single-nucleotide variation on human chromosome 19, to biophysically constrained viral latency and healthy longevity in the mouse-primate-human model of pheromone-controlled reproduction.

In that model, and in all model organisms feedback loops link what organisms eat to all morphological and behavioral diversity. See: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

The atoms to ecosystems model of sympatric speciation refutes neo-Darwinian pseudoscentific nonsense by linking rs3827760, also known as 1540T/C, 370A, V370A, or Val370Ala, from a SNP in the ectodysplasin A receptor EDAR gene on chromosome 2 to conserved morphological and behavioral phenotypes in mice and humans.

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