The Ghost Aim in Medical Research - Preventing Fattening/ Insulin Resistance

In the world, physicians more and more appreciate findings on preprandial hunger arousal and less and less deny their validity in my country (Tuscany).People taking food after perceiving signals of hunger (Initial Hunger Meal Pattern, IHMP) prevent fattening/insulin resistance that causes an overall inflammation, diseases, vascular and malignancy risks. I wonder why scientists denied value to my endeavor. The division had a start when I read the Handbook of Physiology of the American Society for Physiology, in 1967. I was charged with the treatment of malnutrition and diarrhea. I read the handbook to become aware about mucosal digestion and absorption. At that time, these points had to be diagnosed to treat malnourished children. Before beginning any research, a dynamic, reversible condition seemed instead to operate in chronic diarrhea children and had to be found.I read that 50% 60% or more immune cells of the human body reside in the mucosa of small intestine(Mowat, 1987, 44; Brandtzaeg et al., 1989; Abrams, 1977).Bacteria grow in the small and large intestine in dependence on nutrients, mainly those nutrients that produce energy availability (sugars, carbohydrates, amino-acids, fats (Hungate, 1967).I studied bacteria number on the intestinal mucosa in time after last meal. A longer interval from the meal produced a decrease in bacteria number. Thus I concluded that meal absorption develops in a competition between mucosa cells and bacteria (Ciampolini et al. 1996, 2000). The conflictual nature of mucosal absorption has been confirmed (Cooper, Siadaty, 2014; Mccoy, Köller, 2015).I personally provided many demonstrations that current meal pattern provides a lot of illnesses. I add here another proof: The many successful cures of gastrointestinal pathologies by IHMP suggest that the theory used for recovery was objective. In this view, the question:”what food provokes cancer?” Is absurd. Health is a relation.Both the existence of hundreds or thousands of bacterial species in intestine and the existence of a local huge immune reaction in intestinal mucosa sustained the conflictual view. Reading the Handbook isolated me in a Medical World that was unaware of microbiology. Physicians saw improvements in the children I treated, but did not understand the intestinal mechanisms that were far away from their observation. They repeated: Ciampolini is alone in his statements. Now, hundreds of printing houses, and hundreds ofscientific Journals ask me for submitting articles. I am alone and cannot produce hundred articles that are new and different each other. The growing number of electronic Journals created a “Babel” condition that may be useful for commercial exploitation (or for maintenance of power in editors) but not for the “ghost aim” of understanding the human and the personal condition. The general confusion is unable to meet the expectation of one billion of malnourished people.

I n the world, physicians more and more appreciate findings on preprandial hunger arousal and less and less deny their validity in my country (Tuscany). People taking food after perceiving signals of hunger (Initial Hunger Meal Pattern, IHMP) prevent fattening/insulin resistance that causes an overall inflammation, diseases like asthma, vascular and malignancy risks. I wonder why scientists denied value to my endeavor. The division had a start when I read the Handbook of Physiology of the American Society for Physiology, in 1967. I was charged with the treatment of malnutrition and diarrhea. I read the handbook to become aware about mucosal digestion and absorption. At that time, these points had to be diagnosed to treat malnourished children. Before beginning any research, a dynamic, reversible condition seemed instead to operate in chronic diarrhea children and had to be found. I read that 50% -60% or more immune cells of the human body reside in the mucosa of small intestine (Mowat, 1987, 44;Brandtzaeg et al., 1989;Abrams, 1977). Bacteria grow in the small and large intestine in dependence on nutrients, mainly those nutrients that produce energy availability (sugars, carbohydrates, amino-acids, fats (Hungate, 1967). Thus bacterial growth is proportionate to positive energy balance. I studied bacteria number on the intestinal mucosa in time after last meal. A longer interval from the meal produced a decrease in bacteria number. Thus I concluded that meal absorption develops in a competition between mucosa cells and bacteria (Ciampolini et al. 1996(Ciampolini et al. , 2000. The conflictual nature of mucosal absorption has been confirmed (Cooper, Siadaty, 2014;Mccoy, Köller, 2015). I personally provided many demonstrations that current meal pattern provides a lot of illnesses. I add here another proof: The many successful cures of gastrointestinal pathologies by IHMP suggest that the theory used for recovery was objective. In this view, the question: "what food provokes cancer?" is absurd. Tumor heterogeneity is a problem for cancer therapeutics. I am pleased by this information. Malignancy needs to be prevented through a better maintenance of immune system. Health follows the relation between energy intake and expenditure. Both the existence of hundreds or thousands of bacterial species in intestine and the existence of a local huge immune reaction in intestinal mucosa sustained the conflictual view. Reading the Handbook isolated myself in a Medical World that was unaware of microbiology. Physicians saw improvements in the children I treated, but did not understand the intestinal mechanisms that were far away from their observation. They repeated: Ciampolini is alone in his statements. Now, hundreds of printing houses, and hundreds of scientific Journals ask me for submitting articles. I am alone and cannot produce hundred articles that are new and different each other. The growing number of electronic Journals created a "Babel" condition that may be useful for commercial exploitation (or for maintenance of power in some editors) but not for the "ghost aim" of improving awareness about the upsurge of malignant and vascular risks, not to meet the expectation of one billion of malnourished people.
Do we have to go on in the illusion of promoting knowledge by printing ten similar articles instead of one? I would prefer a grouping of Journals on basic assumptions: the study of contagion, the study of energy balance, the study of essential nutrients, the study of genetics. A confrontation inside groups is necessary to decide either the opening of new research fields or the fusion of similar Journals.
Publishing on Health requires an absence of conflicts of interest. This becomes more and more difficult. I was stopped in my institute just because I was unable at constructing a profit from my findings. Individuals devoid of conflicts of interest are precious and rare in a complex world founded on the commerce of innovation and research. Heads of Journals might join together in an endeavor for the construction of a new order. Having forwarded this claim for a shared action, I expect that somebody will respond to my address to discuss chances.
The first step within the ghost aim should be the creation of a consensus among scientists on the pathogenic principal mechanism(s). The second step would be much easier: teaching the consented mechanism to the population. Other mechanisms might better function.
This small piece is intended to be published in many Journals that requested a writing from mine. The piece is sufficient to show a valid although intolerable situation.