The anti-insulin effects of pregnancy are a well-known history. At the end of the day, a few weeks with high glycaemic values do not represent a health problem for the adult woman and a large baby can be safely delivered by caesarean section, and its possible neonatal metabolic disturbances might be safely treated in any hospital setting. So what? This first player in the unbalanced “metabolism” frequently covers in the clinical practice the more complex picture that is associated with maternal gestational diabetes and promotes a critical intrauterine environment.

The role of lipids has been frequently overlooked by obstetricians in gestational diabetes. Indeed, dyslipidaemia is a constitutional part of metabolic syndrome in adults and, more specifically, in type 2 diabetes in a way that resemble normal gestation: dense LDL and triglyceride increases versus low level of HDL. Elevated levels of free fatty acids (FFA) cause insulin resistance in muscle and liver cells. Saturated fatty acids are among the most detrimental of FFA, being the main culprit of insulin resistance and inflammation. On the other hand, FFAs act on the beta cell of the pancreas to stimulate insulin secretion, both directly improving the glucose-stimulated insulin secretion and potentiating glucose-stimulated insulin secretion. To some extent, this counterbalances peripheral insulin resistance.

A third player comes on stage to promote an accelerated metabolic syndrome in pregnancy. The pregnant state modify the intestinal microbiome [6] in a way that faeces of third-trimester mothers showed increased signs of inflammation and energy loss. In a germ free mice, transplant of faeces of third trimester human pregnant women, but not first trimester pregnant women, increased adiposity, insulin resistance and inflammation were determined (Fig. 10.3).

The higher prevalence of firmicutes over bacteroides observed by Koren et al. [6] in human pregnancy matches similar findings in obese adults [7].

The final fourth player of this picture introduces us to the substantial impact of lifestyle in nutrition in Western societies of lipid metabolism. The original balance of n-6 (linoleic acid metabolised to arachidonic acid) and n-3 (alfa linolenic metabolised to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) essential fatty acid that at the best of our knowledge as qualified human diets for at least 160 thousand years in a 2:1 and 1:1 ratio has been dramatically changed in Western diets up to a ratio of 10:1 and 25:1. n-3 essential fatty acids are indeed essential in an array of positive human metabolic pathways [8]. Beyond this, it might be of relevant interest the recent association of n-3 essential fatty acid with the biosynthesis of a specialised family of pro-resolving mediators of inflammation [9] (resolvins, protectins and maresins). This is probably what is needed to soothe the strained insulin receptors and the endothelium.

These two latter elements, microbiota and nutrition interact to lessen or increase the risk of the accelerated metabolic syndrome of pregnancy. What is not widely and properly acknowledged in nutritional counselling is the importance of the phenotype of different macro-ethnicities in which this interaction takes place. Asian, mestizos and AmerInds (sometimes defined as Hispanics in North American literature) and Native American women, as compared with white women of Caucasian ancestry, have an increased risk of GDM [10]. The large human migrations from Asia and South America [11] into Europe and the USA and the spread of Western-style diet (Fig. 10.4) have proved that the metabolic syndrome, originally a rare phenomenon in these macro-ethnicities, has become a major health problem both in Western countries and in these original countries [12, 13].

A special mention is deserved to slave trade from Western Africa and the fate of these macro-ethnicities in North America and the Caribbean. Agriculture and farming entered East Africa eight thousands years ago. We can trace its slowly spreading south in millennia, thanks to archaeological findings, and the prevalence of lactose persistence in micro-ethnicities of Eastern Africa [14]. When slave trade was started by “colonial powers”, in the sixteenth century, farming products as we know them (protein-rich grains such as wheat, cow milk and dairy products; fat-rich meat from cattle raising) had not yet entered the nutritional profile of black ethnicities of West Africa. The descendants of the forced migration exposed to Western-style diet are even more prone to obesity and abdominal obesity than populations of Caucasian ancestry in whom such a prevalence occurs only in areas of very low income (http://​www.​cdc.​gov/​obesity/​data/​prevalence see maps 2011–2013 of white adults – and maps of Black Adults).

Metabolic syndrome in these macro-ethnicities is not just eating too much but is an accelerated consequence of the mismatch between their genome and their nutritional profile that is even more alien to them than to population of Caucasian ancestry.

All these “players” conjure to make pregnancy a possible pray of an accelerated metabolic syndrome both igniting a trans-generational legacy of diabetes-causing diabetes [15] and signalling the future risk to develop a full-blown type 2 diabetes in the fifth decade [16] up to 11 times the risk of women who did not suffer of GDM.

Troubles begin when one has to enter the field of defining what a healthy diet is. For decades this has been defined just by relative amounts of protein, fats and carbohydrates. Such useless profile avoids to meet the real-world problems where governmental regulatory bodies live under tremendous pressure of the agro-industrial system. A huge amount of literature on dietary prevention and treatment of gestational diabetes came to almost no conclusions until a few years ago [18]. However some pillars can be deducted by good-quality pre-pregnancy studies [10] and by the few more recent studies [19, 20].

According to these studies, the culprit of an increased incidence of gestational diabetes in pre-pregnancy studies are (a) insufficient consumption of vegetables and fruit; (b) refined cereal that deprives the organism of the natural fibre content of these nutrients; (c) sugar-sweetened beverages, sugary snacks and fruit juices; (d) products rich in cholesterol and other animal fats; and (e) overconsumption of red meat and processed meats. The latter item comes to a surprise and requires some explanatory notes. First of all, red meat from farm-raised cattle is rich in cholesterol that was pretty scarce in the game meat of our ancestors; nitrites used in processed meat might be transformed into nitrosamine that might damage the pancreatic beta cell; heating cholesterol-rich meat produced glycated compounds, excess of haem iron in women without iron deficiency, and eventually the pro-inflammatory role of the sialic acid of cell walls of mammalians (N-glycolylneuraminic acid) that differ from human sialic acid by one acetyl compound (N-acetylneuraminic acid) [21]. This latter unwanted interaction of mammalian red meat with our immune system is caused by a single gene mutation that sets human cell membrane apart from anthropoid monkeys and all other mammalians including cattle. This mutation makes the human red cell membrane free from the aggression of the lethal malaria agent, the Plasmodium reichenowi that infects monkeys [22]. However, the continued supplementation of this molecule through diet stimulates a low-grade immune reaction and eventually this alien immunogenic sialic acid might be incorporated in high turnover tissues, such as the endothelium [23].

One single aspect has been sorted out by many studies and requires a proper focus. We know that pregnancy in patients fed on a Western diet induces diabetogenic changes in the intestinal microbiota [6]. The intestinal microbiota modulates the immune system and this might balance the low-grade inflammation of visceral obesity and of term pregnancy. Obviously, negligible supplementation with one billion single-strain bacteria for a negligible number of weeks does not achieve any results in reducing risk factors [24]. Positive results were observed by single trials adopting proper dosage and length of administration [25–27]. In addition to this, preliminary data show how probiotic yogurt can reduce the inflammatory profile in pregnancy [20] as well as it has been proved in non-pregnant adults [28].

The nutritional prevention of gestational diabetes should then be tailored on each woman who requires the assistance of health-care providers.

Macro-ethnicity, cultural values, nutritional traditions and family habits, individual intolerance to food, lactose non-persistence and gastrointestinal signs and symptoms – all these elements should be investigated and become the background for nutritional advice. The healthy plate should accommodate all nutritional balances based on vegetable and fruit carbohydrate oligo elements and fibres, a variety of whole grains, healthy vegetable fats and healthy proteins including a prudent weekly share of fermented dairy products and red meat.