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Bariatric surgery: how does it shift cellular aging?

Obesity increases the risk of a number of serious conditions, not least, diabetes and cardiovascular problems. Being clinically obese also hastens the aging process, a fact which, over the last few years, has been pinned down to certain molecular processes. Earlier research has shown that obesity increases levels of reactive oxygen species (ROS; free radicals) in fat cells, leading to a shortening of the telomeres – a marker of aging. Telomeres are structures positioned at the ends of each chromosome, providing protection to the DNA. Each time a cell divides, a small portion of the telomere is lost. Once the telomere reaches a critical limit, the cell goes through a process of senescence (cells age and stop dividing permanently) or apoptosis (cells commit suicide to avoid cancer committment). Various lifestyle choices can increase the rate at which the telomeres are degraded; these include smoking, a nutritionally poor diet, lack of exercise and obesity. Obese people are known to have shorter telomeres, but they also show other hallmarks of premature cellular aging; they display higher levels of inflammation and increased volumes of inflammatory cytokines – cellular messengers which often act to make disease worse.

A recent study examined whether bariatric surgery could reverse these cellular signs of aging. Bariatric surgery is a procedure that significantly reduces the size of the stomach. Weight loss can be dramatic; the surgery can reduce body weight by 30-40% over the course of just 1 year. A team of researchers from the University of Vienna, Austria, set out to discover whether the cellular processes of aging were also reversed. The team, led by Dr. Philipp Hohensinner, in 2016 ago already studied 76 patients with an average age of 40 and an average body mass index (BMI) of 44.5 kg/m2. All participants had struggled to lose weight through lifestyle changes alone and had been referred for bariatric surgery. Blood samples were taken before the surgery, then at the 12-month and 24-month mark. Across the group, on average, BMI had a 38% reduction. As far as cellular changes were concerned, they were also clear cut. There were significant reductions in cytokines that promote inflammation, such as PAI-1 and IL-6; they also charted a rise in a cytokine that reduces inflammation, known as IL-10. Two years after the surgery, the patients’ telomeres were an impressive 80% longer in both cells and blood samples.

In addition to measuring the telomeres, the team also evaluated telomere oxidation, one of the causes of telomere shortening. After 2 years, oxidative damage to the telomeres had been reduced three-fold. Major weaknesses for this study include the relatively small sample size and the lack of a control group. For this study, those with shorter baseline telomere lengths significantly increased after surgery and those with long baseline telomere lengths had a non-significant decrease in telomere length. Results were confermed in 2018 with two papers: The first showing that markers of premature aging including IL-6, CRP, PAI-1 and seven miRNAs, as well as telomere length and telomere oxidation in mononuclear cells, changed hugely in all those patients undergone to bariatric surgery. MicroRNA pattern of gene expression changed significantly; since miRNAs are involved in several aspects of cellular biologiy, included inflammation, response to oxidative stress and abnormal proliferation (e.g. for cancer), the results prove that bariatric surgery sharply changes cell viability parameters. The subsequent also proved that endothelial markers for inflammation (E-selectin, soluble trombomodulin and protein C) dropped as well, reflecting an improved vascular health. Therefore, surgical weight loss drastically improves some parameters for cellular aging.

  • Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry

Scientific references

Hohensinner PJ et al. Obes Surg. 2018; 28(9):2804-2810.

Rega-Kaun G et al. J Thromb Thrombolysis. 2018 Sep 26.

Dershem R et al. Int J Obes (Lond). 2017; 41(11):1718-20.

Laimer M et al. Int J Obes (Lond). 2016 May; 40(5):773-78.

Formichi C et al. Obesity Surg. 2014 Dec; 24(12):2089-93.

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Dott. Gianfrancesco Cormaci
Dott. Gianfrancesco Cormaci
Laurea in Medicina e Chirurgia nel 1998, specialista in Biochimica Clinica dal 2002, ha conseguito dottorato in Neurobiologia nel 2006. Ex-ricercatore, ha trascorso 5 anni negli USA alle dipendenze dell' NIH/NIDA e poi della Johns Hopkins University. Guardia medica presso la casa di Cura Sant'Agata a Catania. In libera professione, si occupa di Medicina Preventiva personalizzata e intolleranze alimentari. Detentore di un brevetto per la fabbricazione di sfarinati gluten-free a partire da regolare farina di grano. Responsabile della sezione R&D della CoFood s.r.l. per la ricerca e sviluppo di nuovi prodotti alimentari, inclusi quelli a fini medici speciali.

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