Journal of Endocrinology and Diabetes

ICI Journals Master ICV(Index Copernicus Value) 2022 = 104.00

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.
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, and the study of genetics. A confrontationinside 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 pieceis intended to be published in many Journals that requested writing from mine. The piece is sufficient to show a valid although intolerable situation.

This review has been shown in: “Modifying Eating Behavior: Novel Approaches for Reducing Body Weight, Preventing Weight Regain and Reducing Chronic Disease Risk” ASN’s Annual Meeting & Scientific Sessionsat Experimental Biology 2014, April 26- 30.

1. Abrams  GD.  Microbial  effects   on  mucosal  structure  and function. Am J ClinNutr. 1977;30: 1980-1986.
2. Brandtzaeg P, Halstensen TS, Kett K, Krajci P, Kvale D, et al. Immunobiology and Immunopathology ofHuman Gut Mucosa: Humoral Immunity and Intreaepithelial Lymphocytes. Gastroenterology. 1989;97(6):1562-1584.
3. Ciampolini M, Bini S. Orsi A. Microflora persistence on duodeno-jejunal flat or normal mucosa in time after a meal in children. PhysiolBehav 1996;60()6:1551-1556.             
4. Ciampolini, M., Borselli, L. and Giannellini, V. Attention to Metabolic Hunger and Its Effects on Helicobacter pylori Infection. Physiology &Behavior. 200;70(3-4):287-296.    Doi:10.1016/s0031-9384(00)00273-0
5. Ciampolini M, Bianchi R. Training to estimate blood glucose and to form associations with initial hunger. NutrMetab (Lond). 2006;3:42.  Doi:10.1186/1743-7075-3-42
6. Ciampolini M, Sifone M. Differences in maintenance of mean Blood glucose (BG) and their association with response to “Recognizing Hunger”. Int J Gen Med. 2011;4:403-412.
7. Ciampolini M, Lovell-Smith D, Sifone M. Sustained self-regulation of energy intake.  Loss of weight in overweight subjects.  Maintenance of weight in normal-weight subjects. NutrMetab (Lond). 2010;7:1-4.  Doi: 10.1186/1743-7075-7-4.
8. Cooper IF, Siadaty MS: 'Bacteriums' associated with 'Blood Glucose Level Finding': BioMed Lib Review. 2014.
9. Alimentary canal. In: Hungate RE. Handbook of physiology. VIth ed. Washington DC : Ruminal fermentation;1967. 
10. Mccoy K, KöllerY. New developments providing mechanistic insight into the impact of the microbiota on allergic disease. Clin Immunology. 2015;159(2):170-176.  Doi: 10.1016/j.clim.2015.05.007
11. Mowat A McI. Chapter3, The cellular basis of Gastrointestinal Immunity. In: Marsh MN Ed, Immunopathology of the Small Intestine. Wiley J and Sons, Chichester UK, Page 44.
12. Van der Waaij LA, Limburg PC, Mesander G, van der Waaij D. In vivo IgA coating of anaerobic bacteria in human faeces. Gut.   1996;38(3):348-354.