ABSTRACT

It is known that several mechanisms are common in the patho-physiology of diabetes, obesity, and their development towards cardiovascular disease. Inflammation, insulin resistance, atherosclerosis, metabolism of adipose tissue, etc, are under the attention of scientists. A common, and not always enough explored mechanism is the disruption of the availability, and utilization of energy: the so called metabolic fuel failure. Glucose and fatty acids represent the fuel and mitochondrion represents the bio-energetic engine of the body. Insulin secretion, adipocytes activity and metabolism, are based on the availability of glucose. Thus, the glucose level inside adipose cells is a major factor in determining whether fatty acids are released into the blood. The respiratory chain, located in the inner mitochondrial membrane, consists of multimeric protein complexes that are essential components of the mitochondrial energy generation through the oxidative and phosphorylation pathway. Those proteins are encoded in the human mitochondrial genome that consists of approximately 1500 genes, 37 encoded by the maternally inherited mitochondrial DNA (mtDNA), and the remaining ones encoded in the nuclear DNA (nDNA) (Environ Mol Mutagen. 2010;51: 440-50).

The nutrient profile of the overall (habitual) diet is an important determinant of health and the nutrient profile of a ‘balanced’ diet is defined by science based recommendations for intakes of energy and nutrients. Because diets are composed of multiple foods, overall dietary balance may be achieved through complementation of foods with different nutrient profiles so that it is not necessary for individual foods to match the nutrient profile of a ‘balanced’ diet. Nevertheless, individual foods might influence the nutrient profile of the overall diet, depending on the nutrient profile of the particular food and its intake (Proceedings of the Nutrition Society 2009, 68, 1–10 http://journals.cambridge.org/action/displayFulltext?type=1&fid=3822188&jid=PNS& volume = 68 & issued = 01&aid=3822180).
There is a quite general understanding that an individual’s health is linked to five key domains: genetics, social circumstances, environmental exposures, behavioural patterns, and health care (N Engl J Med 2007; 357: 1221-28). Changing an individual’s unhealthy behavioural pattern may yield the greatest opportunity to improve health and reduce premature mortality, particularly with respect to smoking, physical inactivity, and obesity resulting from an unhealthy diet. In all those circumstances the success in achieving the expected results depends mainly from the “head” of the individual person.
The decision on food choice is indeed an example of the “head” education of the person.

Based on models from economics, health experts and politicians often make the assumption that humans are rational decision makers, capable of maximizing their own welfare and making perfectly informed decisions when given sufficient information. In terms of dietary behavior, for example, the assumption is that, given the right information and motivation, people can successfully reduce their food intake to match their caloric expenditure over the long term. Efforts to treat and prevent obesity at a population level, therefore, depend to a large degree on educating people to regulate their food intake through publicizing general guidelines on nutrition, promoting tailored diets, and labeling foods with nutrition information. The continued growth of the obesity epidemic despite the employment of these techniques should make people question the assumptions underlying these approaches (Atherosclerosis Supp 2009; 10 (4): 29).
How long does a person need to change his/her nutrition behavior is still a big question mark.
The hypothesis of thrifty genotype (Am. J. Hum. Genet. 1962; 14: 353–62) refers to the long time requested to modify the genoma for gatherer-hunter populations, especially child-bearing women, because it would allow them to fatten more quickly during times of abundance: fatter individuals carrying the thrifty genes would thus better survive in the times of food scarcity. Whether it is a thrifty genotype or a thrifty epigenomic hypothesis (Bioessays 2008 30:156–66), in modern societies with a constant abundance of food, this genotype efficiently prepares individuals for a famine that never comes.

The early hominid diet (from about four million years ago), evolving as it did from that of primate ancestors, consisted primarily of fruits, nuts and other vegetable matter, and some meat - items that could be foraged for and eaten with little or no processing. Comparisons of primate and fossil-hominid anatomy, and of the types and distribution of plants eaten raw by modern chimpanzees, baboons and humans, as well as microscope analysis of wear patterns on fossil teeth suggest that australopithecines were mainly frugivorous omnivores with a dietary pattern similar to that of modern chimpanzees.
The diet of pre-agricultural but anatomically modern humans (from 30,000 years ago) diversified somewhat, but still consisted of meat, fruits, nuts, legumes, edible roots and tubers, with consumption of cereal seeds only increasing towards the end of the Pleistocene.
The origins of agriculture? A biological perspective and a new hypothesis (Australian Biologist 6: 96 - 105, June 1993).
A new intriguing question refers to the relation between Microbiota and obesity. In the gut are from 10 to 100 trillion bacteria, of 1.800 genera, 16.000 phylotypes. Their collective genome (microbiome) contains around 100 times the genes of the human genome. Each human possesses a metagenome (human genome + microbiome). Some functions are attributed to gut microbiota such as: protective against pathogens (barrier effect), and through the competition for available nutrients and the inhibition of pathogens growth; trophic in epithelial cell proliferation, and development and homoeostasis of immune system (maturation of gut-associated lymphoid system and stimulation of specific systemic and local immune responses); metabolic and nutritional in fermentation of non-digestible dietary residues, and salvage of energy as SCFAs and production of vitamins (Franceschi C. at the 2^nd National Congress of Gender Medicine, Padua 2010).
The absence of Toll-like receptor 5 in mice alters the gut microbiota, causing increased food intake, insulin resistance, and obesity. Is this true for humans? (Science 2010; 328:179-80 and Science 2010; 328: 228-31).

This short journey into the relations between human development and nutrition is highlighting many further questions. What we learn from the comparison with more simple life species (sea anemone e.g.), from the bio-chemical, bio-social, bio-cultural development, is posing many criticisms on the interventional policies of authorities that are trying to regulate food choice.
Nutrition is a very complex process that is impacting on, among others, digestive system (gut, liver, pancreas, etc), brain, heart, muscles. The endocannabinoid system (ECS) affects a number of physiologic functions. Among those, recent evidence points to a role for this system in the modulation of food intake and body weight. Some of the processes in which the ECS plays a role are those involving the stimulus to consume nutrients, the digestion and transport of ingested nutrients, and the storage or metabolism of substrates.

Further critical issues deserve to be focused on, such as:

- the countries’ specific food education and culture

- the local policy programs and guidelines

- the individual food choice motivations and the rewarding aspect of food

- the local food distribution and price realities

ABSTRACT

Nutrition is able to alter the health status of the general population. The World Health Organization, in fact, strongly emphasized the role of unhealthy eating habits, along with sedentary lifestyle and cigarette smoking as a risk factor for the onset of chronic diseases such as cardiovascular disease, cancer, respiratory and metabolic disorders (WHO Study Group, 2003).
In industrialized countries such as Italy the most important association between diet and health is certainly the relationship with cardiovascular disease, the leading cause of death and disability. The ability to identify with certainty, therefore, the relationship between diet and cardiovascular disease appears to be a key element in the implementation of specific primary prevention strategies.
The first evidence of association between diet and physical well-being was found in the 60s’ following the first results of a study named the Seven Countries’ Study. The first results of this study were surprising because they clearly showed that the countries of the Mediterranean basin (Italy and Greece) had the lowest incidence of death from cardiovascular disease and cancer than all other countries. From here the Mediterranean diet concept came out (Keys et al., 1986).
But what are the cornerstones of this diet?
The main characteristics of this diet, summarized today in the iconography of the famous food pyramid are: daily consumption of carbohydrates and plant foods (fruits, vegetables, grains, nuts and legumes), olive oil as the main source of fat, low consumption of red meat, moderate consumption of wine, normally with meals.
In recent years, several studies have shown that strict adherence to a healthy dietary pattern, such as that characteristic of the Mediterranean diet is associated with a lower incidence of mortality.
In 2003, in the New England Journal of Medicine, Trichopoulou et al. have documented, in a population of 22.043 individuals followed for 44 months, that the mortality risk is inversely correlated with the grade of adherence to Mediterranean diet assessed by a score. It was observed that an increase of 2 points in this score was significantly associated with a reduction of 25% of global mortality. These results were confirmed in two meta-analyses performed by our group, which showed a population of over 2,000,000 people that an increase of 2 points of adherence to the Mediterranean diet led to a substantial reduction of overall mortality, of mortality and / or incidence of cardiovascular diseases, neoplastic diseases, as well as of neurodegenerative diseases like Parkinson's and Alzheimer’s diseases (Sofi et al., 2008; Sofi et al., 2010).
In recent years, however, despite the pressing claims of adherence to a nutritional profile similar to that of the classic Mediterranean diet, the Mediterranean populations and in particular Italy have gradually lost their grade of adherence to Mediterranean diet in favour of a more Westernized diet.

References

Keys A, Menotti A, Karvonen MJ, Aravanis C, Blackburn H, Buzina R, Djordevic BS, Dontas AS, Fidanza F, Keys MH, Kromhout D, Nedelijkovic S, Punsar S, Seccareccia F, Toshima H. The diet and 15-year death rate in the seven countries study. Am J Epidemiol 1986; 124: 903-15.

Trichopoulou A, Costacou T, Bamia C, Tricopoulou D. Adherence to a Mediterranean diet and survival in a Greek population. N Engl J Med 2003; 348: 2599-608.

World Health Organization Study Group. Diet, Nutrition, and the Prevention of Chronic Diseases. Geneva, Switzerland: World Health Organization; Technical Report Series, 916, 2003.

Sofi F, Cesari F, Abbate R, Gensini GF, Casini A. Adherence to Mediterranean diet and health status. A meta-analysis. BMJ 2008; 337: a1344.

Sofi F, Abbate R, Gensini GF, Casini A. Accruing evidence about benefits of adherence to Mediterranean diet on health: an updated systematic review with meta-analysis. Am J Clin Nutr 2010; doi: 10.3945/ajcn.2010.29673.