The World Health Organization (WHO 2000) described metabolic nutrition disturbances, which lead to MORBID OBESITY (MO), as one of the most obvious public health problems, affecting both developed and developing countries. However, obesity and MO were universally acknowledged as a public health problem only in the past 10 ten years, while malnutrition and infectious diseases have always been acknowledged as such. MO has assumed epidemic proportions, as more than 1 million adults have higher than normal weight. MO and excess weight are known risk factors for a wide variety of diseases, such as gout, hypertension, hyperlipidaemia, type II diabetes, cardiovascular disease, stroke, gallstones, kidney stones, osteoarthritis, sleep apnoea, breathing problems, gastro-oesophageal and intestinal problems, infertility, complications during pregnancy and psychological disorders, as well as some types of cancer. Furthermore, the effects of MO extend to psychosocial parameters. MO affects the individual’s self-esteem, with adverse consequences for their mental and social situation. In addition, adults who were obese during their teenage life are more likely to have lower incomes and often face exclusion from their social milieu.

Complications of MORBID OBESITY: The aetiology of MO is multifactorial. It is the result of the effect of genetic and environmental factors on the energy balance. Children of obese parents are more likely to become obese in relation to the children of non-obese parents. Studies in twins and their families have shown that more than 80% of the variance in body mass index (BMI) is attributable to genetic factors. Genes influence many parameters associated with both energy intake and energy expenditure. The imbalance of energy (increased energy intake relative to energy expenditure) causes an increase in stored fat, and obesity. There is a synergistic relationship between genes and the environment. Of those exposed to an environment that promotes obesity, those with an increased genetic predisposition to obesity will have the greatest increase in weight, while those are resistant to obesity are less likely to increase their weight or increase it more slowly. This susceptibility to specific environmental stimuli due to genes is referred to as gene-nutrient interaction.

Nutrigenomics – Dietogenomics.

Two sides of the same coin (The FASEB journal, 2005)

A well-known example of precisely this relationship is that of the American “Pima” Red Indians, who have a population-level predisposition to type II diabetes and obesity. The Red Indians of this tribe living in their mountains of origin have a much lower rate of obesity and type II diabetes than those living in the high-risk environment of the State of Arizona.

Some dozens of genes have so far been linked with obesity markers, but most of them have little effect on weight. The development of technology has made possible the analysis of many hereditary markers simultaneously and the conclusions drawn can give us reliable information on whether we have a predisposition to obesity and/or major complications thereof, such as diabetes mellitus, hypertension, etc. Furthermore, they provide information on the epigenetic effect of possible doping.

These polymorphisms are activated or inactivated through protective or non-protective adipocytes, cytokines, which are associated with supply and nutrition (Leptin, Adiponectin, Interleukin-6, TNF-a etc.).

These substances are triggered in response to cellular oxidative stress, i.e. the imbalance between the production of free radicals and antioxidant mechanisms in favour of the first that potentially lead to cell damage (Azzi et al., 2004).

Free radicals (ROS) are chemicals that contain one or more unpaired electrons, are produced in all living cells and are capable of independent existence.

ROS are involved in some useful physiological functions, such as the reaction of the body’s immune system, the regulation of gene transcription and the activation of intracellular signalling pathways (Vollaard et al., 2005). However, an excessive and/or prolonged increase in ROS production has been implicated in the pathogenesis of cancer, diabetes, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischaemic lesions, renal failure, etc.

Finally, aerobic active recovery (walking) activates the metabolic pathways that promote cell oxygenation and the burning of fatty tissue, the production of endogenous antioxidants and the removal of inflammatory cytokines.

Latest research shows that moderate continuous aerobic exercise for 30 minutes may contribute to diminishing the expression of gene polymorphisms associated with MO and the activation of protective cellular factors.


The latest review and research data demonstrate the great significance and affect of the psychic and brain function as to the onset and development of the metabolic syndrome, as well as metabolic disorders in general. We know that the state and reactions of stress derive from a complex of ways of psychological function and organization, characterized by an intense fragility, inability to cope with and give meaning to subjective emotions and emotional situations. These vary from personality disorders, acute emotional and traumatic reactions to alexithymia. The often observed predisposition for stress and psychosomatic diseases, in patients with metabolic syndrome, is also correlated with types of nervous system and peripheral nervous system dysfunctions. From a psychopathological as well as a neuroscientific point of view, we can distinguish two channels through which is the predisposition, the onset and the course of the metabolic syndrome is formed: a top- down and a top- up function, in the axis of the functions of the cortex- sub cortex structures-autonomic nervous system, digestive system and metabolic organs.

In this axis also integrate the reactions of the connections between the hypothalamic- pituitary-adrenal (HPA), as well as between ventral prefrontal cortex, NAcc, limbic system and cores of the brain stem (periaqueductal gray, PAG). the function of these structures is connected with the function of the emotional command systems, with the appearance of binging behaviors, addiction behaviors and disorders of the affective function. In the same frame is situated the action of the class of neuromodulators of the peptides (neuropeptides), whose highly specific mode of action is closely linked to the emotional systems.


The oxidative metabolism of glucose and fat- the main substrates for exercise- depends on O2 availability and produces CO2 and water. The rate of O2 and CO2 exchange in the lungs normally equals the rate of usage and release by the body tissues. With this knowledge, we can measure caloric expenditure by measuring respiratory gases. Respiratory gas exchange is determinate through the measurement of the volume O2 and CO2 that enters and leaves the lungs during a given period of time .To estimate the amount of energy used by the body, it is necessary to know the type of food substrate (combination of carbohydrate, fat, protein) being oxidized. The carbon and oxygen contents of glucose, free fatty acids, and amino acids differ dramatically. As a result, the amount of oxygen used during metabolism depends on the type of fuel being oxidized. Indirect calorimetry measures the amount of CO2 released (VCO2) and oxygen consumed (VO2). The ratio between these two values is termed the respiratory exchange ratio (RER). The RER value at rest is usually 0.78 to 0.80. The RER value for the oxidation of fat is 0.70 and is 1.00 for carbohydrates. With the techniques described above, exercise scientist can measure the amount of energy a person expends at rest as well as during and following exercise. They can measure metabolic rate, under resting conditions, during sub maximal and maximal exercise intensities, and during the period of recovery following an exercise bout.

Willmore J.H., Costill D.L., Kenney W.L. Physiology of Sport and Exercise. 4th edition, Human Kinetics.


Up until today many nutritional models have been created to treat obesity. The most important ones are the Mediterranean Diet, Tone Diet and Atkins Diet. Benefits and drawbacks of these models have been recorded in research and clinical practice. Recently the Mediterranean Diet failed to regulate metabolically tis geographical sample, due to increased percentile of severe obesity. Furthermore there has not been any record of a correlation sample of Mediterranean populations between adiposides, gut hormones and biochemical indicators before and after the treatment with the nutritional approaches.

The iso-glucaemic model offers a sound proposition as to the regulation of the metabolic disorder, but cannot be used intensively because of the limited information we have about the glucaemic loads and the glucaemic indicators of the different foods.

Analysing  all this parametrs , in over 12.000 Med. citizens , We creating an individual nutritional algorythm that will not cause further disorder in the Brain-gut axis ,changing holistic the  nutritional habits , regulating the BBB ( blood brain barier) via specify  portional andioxidant funcional  food in a dailly remedy of 6-7 meals!


Results of research concerning fascia and its manipulation

The following scientific theories and study results may show the importance of the fascial treatment. An excerpt from: Schleip R 2002 Fascial plasticity – a new neurobiological exlanation. Journal of bodywork and movement therapies, January 2003:
The stimulation of nerve receptors in deep tissue sheets – e.g. the periosteum – (which usually happens only in extreme survival situations in nature) tends to trigger a high release of endorphins similar to an extreme survival situation. If this is true it would explain how deep tissue manipulation could trigger deeper changes in neural brain connections than superficial manipulations. That stimulation of deep tissue nerve receptors triggers a high amount of endorphins, which then leads to an increased “plasticity” of habitual programs in our nervous system. Stimulation of fascial mechanoreceptors can trigger viscosity changes in the ground substance. The discovery and implications of the existence of fascial smooth muscle cells are of special interest in relation to fibromyalgia. Practitioner’s intervention are seen as stimulation for self regulatory processes within the client’s organism.

Mechanoreceptors have been found abundantly in visceral ligaments as well as in the Dura mater of the spinal cord and cranium. It seems quite plausible that most of the effects of visceral or craniosacral osteopathy could be sufficiently explained by a simulation of mechanoreceptors with resulting profound autonomic changes.

In the myofascial manipulation an immediate tissue release is often felt under the working hand. This feature is attributed to mechanical properties of the connective tissue. Fascia is densely innervated by mechanoreceptors which are responsive to manual pressure. Stimulation of these sensory receptors has been shown to lead to an altered proprioceptive input to the central nervous system which then results in a changed tonus regulation of motor units associated with this tissue.

At least some of these responses are primarily regulated by a change in gamma motor tone, rather than in the more volitional alpha motor system. Of particular interest are the Ruffini organs (with their high responsiveness to tangential pressure) and the very rich network of interstitial receptors, since stimulation of both of these receptors can trigger profound changes in the autonomic nervous system. Fascia and the autonomic nervous system appear to be intimately connected. It is the large group of interstitial receptors that make up the majority of sensory input from myofascial tissue.

The interstitial mechanoreceptors can trigger an increase in vagal tone which leads towards more trophotropic tuning of the hypothalamus. Based on Gellhorn (1967) this results in global neuromuscular, emotional, cortical and endocrinal changes that are associated with deep and healthy relaxation. 1996, a German anatomy professor, Staubesand published an exciting new paper. He and his Chinese co-worker Li studied the fascia cruris in humans with electron photomicroscopy for several years and found smooth muscle cells embedded within the collagen fibers (Staubesand & Li 1996).

Interestingly, this article also reported – similar to Yahia’s innervation study – the widespread existence of intrafascial nerves. Staubesand describes a rich intrafascial supply of capillaries, autonomic nerves and sensory nerve endings.  The discovery of fascial muscle cells therefore opens a doorway for exciting speculations about a direct link between fascial behaviour and the pH of the body, which is directly linked to breathing function and CO2 levels. As Chaitow, Bradley and Gilbert showed (Chaitow et al. 2002) there is already a clear link between smooth muscle contraction and depleted levels of CO2 such as occurs in relative respiratory alkalinity.
When there is a shift toward increased alkalinity due to – for example – hyperventilation – Vasoconstriction is automatic and dramatic. Possibly, at this same time fascial smooth muscle cells contract and increase overall fascial tension. The implications for such changes in conditions such as fibromyalgia and chronic fatigue are enormous, since a common clinical finding is that most people with FMS and CFS are frank or borderline hyperventilators.