Obesity-Related Metabolic Syndrome: Investigations into Novel Clinical Markers and Possible Causes

Abstract

Obesity-related metabolic syndrome (MetS) increases risks for degenerative cardiovascular disease (CVD), and has become widespread. Efforts to stem the increase of obesity are inadequate. New approaches to the problem may be required. Novel CVD Risk and Prediction Markers were investigated for use in enhancing the utility of MetS. Subsequently, a unifying hypothesis on causes of MetS was developed. MetS comprises central obesity, hypertension, dyslipidaemia and hyperglycaemia, but insufficiently reflects underlying oxidative, metabolic, inflammatory, and nutritional stresses. Novel CVD laboratory (1) Risk Markers; consisting of clinical routine screening haematology and biochemistry (CRSHaem&Biochem): Leukocytes: neutrophils; monocytes; lymphocytes; eosinophils; erythrocyte sedimentation rate (ESR); haemoglobin A1c (HbA1c); urate; ferritin; liver function tests (LFT): alkaline phosphatase (AlkPhos); alanine transferase (ALT); aspartate transferase (AST); gamma glutamyl transferase (γGT); bilirubin (2) Protective Markers; (a) serum fat cell-derived, adiponectin (Adpn) with oligomers (high, medium, low molecular weight (HMW, MMW, LMW) (b) serum fat soluble vitamins (sFSVitamins) beta carotene (sβCaro), vitamins (sVit)D, sVitA, sVitE, and VitK(INR) were investigated. Baseline, and mean over 6months (m), oxidants HbA1c and urate were strongly related to MetS marker count, a MetS index. Over 6m, on wide-ranging multivariable mixed modelling, γGT and ESR changed with MetS marker count. Adpn showed anti- and pro-inflammatory correlations. sVitA and sVitE correlated with MetS marker count, and dyslipidaemia. sβCaro and sVitD correlated with protective markers. Thus 1) HbA1c, urate, γGT, ESR, and 2) sβCaro, sVitD may be acceptable Novel CVD Risk and Protective Markers, respectively, for use with MetS. The unifying hypothesis on obesity and MetS was predicated on humans evolving proportionately large, energy demanding brains requiring co-adaptive mechanisms to: (1) increase dietary energy by developing strong neural self-reward/motivation systems for the acquisition of energy dense food and (2) economise on body energy metabolism by the co-option of many of antioxidant phytonutrients to confer long-lived cell protection. The study indicated that strong risk markers in MetS are oxidant, and associate with degenerative change, and antioxidant cytoprotection is augmented by plant food micronutrients, such as food-derived or dietary βCaro (fβCaro). The unifying hypothesis was compatible with the study results. Whole-food diets need studying for prevention and reversal of MetS.