Adiposano® Case Studies
Data from 32 patients treated with Adiposano® was gathered and analyzed. The results were very consistent with the RCT data published in the original trial and with the clinical experiences of the science team in Spain. The case study was performed in the Dallas, Texas area in order that American diets and genetics could be used to confirm the RCT findings. The overall results show that Adiposano® administration over the course of six months had an impact on: body fat mass and an associated reduction in plasma leptin concentration. The other metabolic markers were also affected in the same way as observed in the RCT.
ADIPOSANO® OBSERVATIONAL STUDY
© 2017 as Data On File by Bioiberca S.A.U. All rights reserved and no distribution may occur without expressed written permission.
NEW VIEW OF excess WHITE ADIPOSE TISSUE (eWATS)
“White adipose tissue (WAT) is a metabolically active organ that secretes several cytokine signaling molecules, known as adipokines, into systemic circulation.”
90 Days to Change
The clinical studies for Adiposano® have shown some remarkable impact by inhibiting adipogenesis, regulating adipokines and cytokines to thereby reduce systemic inflammation. In a sense, obesity can be viewed as the loss of homeostasis for cytokines such as leptin. Adiposano® works over time to restore that metabolic balance.
In the 3-month case study with Adiposano®, patients experienced a decrease in BMI due to a change in their body fat composition. In particular, their leptin/adiponectin ratio decreased significantly (7.19 to 5.23 or x%). NOTE: More accurate approaches than BMI (such as DEXA scans) are recommended for more accurate body fat assessment.]
How does Adiposano® work?
The mechanism of action of Adiposano® has not been completely elucidated. Research suggests Adiposano® can inhibit adipogenesis (the creation of new fat cells), decrease pro-inflammatory cytokines, and decrease inflammation both systemically and in the synovial fluid. We believe that Adiposano® works block or restrict an upstream mechanism (perhaps CD44) which prevents a broad cascade of inflammatory response.