The dual burden of malnutrition is characterised by the coexistence of undernutrition alongside overweight/obesity and diet-related noncommunicable diseases. It is a paradox which disproportionately affects women and is applicable to those who become pregnant after weight loss surgery. Obesity before and during pregnancy is associated with increased risk of adverse perinatal outcomes in both mother and child. Overall lifestyle interventions targeting weight loss in the preconception period have not proven effective, with people, and women in particular, increasingly seeking weight loss surgery. In women with severe obesity, surgery may normalise hormonal abnormalities and improve fertility. In those who become pregnant after surgery, evidence suggests a better overall obstetric outcome compared to those with severe obesity managed conservatively; however, there is heightened risk of maternal nutritional deficiencies and infants born small for gestational age. Specifically, pregnancy soon after surgery, in the catabolic phase when rapid weight loss is occurring, has the potential for poor outcomes. Lifelong micronutrient supplementation is required, and there is considerable risk of malnutrition if nutritional aftercare guidelines are not adhered to. It is therefore recommended that pregnancy is delayed until a stable weight is achieved and is supported by individualised advice from a multidisciplinary team. Further research is required to better understand how weight loss surgery affects the chances of having a healthy pregnancy and to ultimately improve nutritional management and patient care. In this review, we aim to summarise the evidence and guidance around nutrition during pregnancy after weight loss surgery.

The huge health burden accompanying obesity is not only attributable to inadequate dietary and sedentary lifestyle habits, since a predisposing genetic make-up and other putative determinants concerning easier weight gain and fat deposition have been reported. Thus, several investigations aiming to understand energy metabolism and body composition maintenance have been performed considering the participation of perinatal nutritional programming and epigenetic processes as well as inflammation phenomena. The Developmental Origins of Health and Disease hypothesis and inheritance-oriented investigations concerning gene–nutrient interactions on energy homoeostasis and metabolic functions have suggested that inflammation could be not only a comorbidity of obesity but also a cause. There are several examples about the role of nutritional interventions in pregnancy and lactation, such as energetic deprivation, protein restriction and excess fat, which determine a cluster of disorders affecting energy efficiency in the offspring as well as different metabolic pathways, which are mediated by epigenetics encompassing the chromatin information encrypted by DNA methylation patterns, histone covalent modifications and non-coding RNA or microRNA. Epigenetic mechanisms may be boosted or impaired by dietary and environmental factors in the mother, intergenerationally or transiently transmitted, and could be involved in the obesity and inflammation susceptibility in the offspring. The aims currently pursued are the early identification of epigenetic biomarkers concerned in individual's disease susceptibility and the description of protocols for tailored dietary treatments/advice to counterbalance adverse epigenomic events. These approaches will allow diagnosis and prognosis implementation and facilitate therapeutic strategies in a personalised ‘epigenomically modelled’ manner to combat obesity and inflammation.

Despite the suggested health advantages of traditionally- over industrially-produced western 'regular' eggs and the flexibility of egg composition, studies on the effects of egg intake refer mostly to quantity and lack qualitative information. The possibility of lending differential nutritional enhancement and functional advantages, i.e. vs. cardiovascular disease (CVD) or for perinatal health, could impact the current egg intake debate. N-3 polyunsaturated fatty acid (PUFA)/long-chain PUFA (LCPUFA) fortification of regular eggs by feeding extruded linseed (5%) yielded 3.8-fold higher total n-3 PUFA and 2.4-fold higher docosahexaenoic acid (DHA), with 3.6-fold lower n-6:n-3 PUFA ratio (p≤0.0005). This resulted in human dietary contributions of 10-20% of the n-3 PUFA Dietary Reference Intake (DRI) and 40% for DHA. Together with antioxidants, they may be beneficial against CVD risks as associated with oxidative stress, endothelial dysfunction, dyslipidemia, and inflammatory processes, especially in diabetics. Eggs fortified via poultry feed supplementation could attain higher %DRI for pregnancy or lactation for key nutrients, i.e. DHA (≈120- 130%), vitamins A (9.0-15.2%) and E (51.6-65.3%), iodine (15.2-20.1%), and selenium (33.7-39.3%). For infants aged 1-3 years, the improvement in %DRI for vitamins, minerals, and n-3 PUFA needed during peak brain development could be even higher. Compared to increased low-density lipoprotein (LDL) oxidation as seen with intake of two regular high n-6 PUFA eggs/day, eggs with reduced n-6 PUFA (by 40%), increased n-9 monounsaturated FA (MUFA) (by 30%), reduced PUFA:MUFA ratio (by 50%), and increased antioxidants vitamin E and carotenoids (by >200%), were associated with a 30% drop in LDL oxidisability (p<0.01), back to levels seen with a low-egg diet (2-4 eggs/week). Because egg composition is highly feed-dependent and closely affects plasma nutrients and lipoprotein composition and physiological qualities, it has much potential for imparting both nutritional and functional benefits. Poultry feeding could be carefully tailored for egg modification to address specific risks and requirements in consumers, warranting further research regarding differential effects and corresponding quantitative recommendations for egg intake, to maximise beneficial and preventative potential.