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当我阅读美国生理学学会的生理学手册时，该部门有一个开始，研究人员应该具有不同的目标而不是医生。1967年，我被指控在佛罗伦萨大学治疗营养不良和腹泻。我读了手册，了解粘性消化和吸收。当时，必须诊断这些点治疗营养不良的儿童。在开始任何研究之前，我打算将摄入摄入肠道生理学。我读到了人体的50-60％或更多的免疫细胞位于小肠的粘膜[1-3]。细菌在没有氧气的情况下通过慢的能量产生而在小而大肠中生长。所有纤维和少量糖，碳水化合物，蛋白质，脂肪逃逸肠道消化，为每天一种细菌复制提供能量[4]。食物避免吸收由于过度摄入或无法消化的能力。纤维如纤维素和果胶逃逸消化，促进免疫原性细菌种类差的缓慢生长，并防止有害的微生物组发育。 Bacterial growth becomes immunogenic and harmful when energy dense food is largely available. In the mammal intestine, bacterial indiscriminate, harmful growth is proportionate to a positive energy balance in blood and in body. Thus, I studied bacteria number on intestinal mucosa in time after last meal. A longer interval from the meal produced a decrease in bacteria number. An increase in mucosal and overall immune stimulation is associated with bacteria growth on intestinal mucosa, with preprandial blood glucose (BG) and with a slowdown of meal absorption [5,6]. Energy balance directly affects these correlated variables either increasing or lowering the conflict between bacteria activity and mucosal immune response. The initial hunger meal pattern (IHMP) was devised to reduce bacterial growth and reduce the mucosal immune response at nutrient absorption. This conflictual state between bacteria and mucosa has been confirmed [7,8]. The many successful cures of gastrointestinal pathologies suggest that the conflictual theory that was used for recovery was objective, i.e. reproduced the events in small and large intestine. In this view, the question: “what food provokes cancer?” is absurd. Malignancy needs to be surveilled and prevented through an increase in efficiency of immune system [9]. Lower intestinal stimulation may be the way to achieve higher immune efficiency also in the body [2,3,5,10,11]. Thus health (general immune efficiency) follows the relation between energy intake and expenditure. Hundreds or thousands of bacterial species live and multiply in the intestine, 5-15% of the species elicit IgG production, the intestinal mucosa responds with an immune reaction and, lastly, the immune stimulation by bacterial antigens spreads to all body tissues (Overall Subclinical Inflammation). Thus, many observations sustain the conflictual view for the absorption of every energy dense food. Now, hundreds of scientific Journals ask me for submitting articles. I am alone and cannot produce hundred articles that are new and different each other to repeat the statements about the conflictual absorption and the IHMP solution for health maintenance and recovery. Yet, the upsurge of malignant and vascular risks, not to mention malnutrition that affects one billion of malnourished people, impose to spread the awareness on this issue [12-15].

承认

该综述已列于：“修改饮食行为：降低体重，减轻体重恢复和减少慢性疾病风险”ASN的年会和科学会议2014年4月26日至30日的新方法。

参考

1. Mowat Am（1987）胃肠道免疫的细胞基础。在：小肠的沼泽Mn（Ed。）免疫病理学。John Wiley＆Sons，Chichester PP：44。
2. Brandtzaeg P, Halstensen TS, Kett K, Krajci P, Kvale D, et al.(1989)人类肠道黏膜的免疫生物学和免疫病理学:体液免疫和上皮内淋巴细胞。胃肠病学97: 1562 - 1584。[crossref]
3. 微生物对黏膜结构和功能的影响。我是J clininnutr吗30: 1980 - 86。
4. Humgate Re（1967）瘤胃发酵。in：heidel w，code cf，生理手册，sect 6，消化运河。华盛顿特区：AM Physiol SoC，PP：2725-2746。
5. (1)儿童十二指肠-空肠平坦或正常黏膜的菌群持久性。physiol才能60：1551-1556。[crossref]
6. 陈志强，陈志强，陈志强(2000)代谢饥饿及其对幽门螺杆菌感染的影响。physiol才能70：287-296。[crossref]
7. Cooper IF, Siadaty MS (2014)“细菌”与“血糖水平检测”有关。生物医学文献综述2014/6/26705207661。
8. Mccoy KD, Köller Y(2015)为微生物群对过敏性疾病影响的机制提供了新进展。中国免疫学05：007·[crossref]
9. Kristensen VN（2017）肿瘤细胞的抗原性。n Engl J Med376：491-493。[crossref]
10. (1)肝脏无菌性炎症。胃肠道143：1158-1172。[crossref]
11. Lynch SV, Pedersen O(2016)人体肠道微生物群在健康和疾病中的作用。n Engl J Med375: 2369 - 2379。[crossref]
12. Ciampolini M, Bianchi R(2006)评估血糖和与初始饥饿形成关联的培训。Nutr Metab（Lond）3: 42。[crossref]
13. Ciampolini M，Sifone M（2011）维持平均血糖（BG）的差异及其与“识别饥饿”的反应。国际医学杂志4：403-412。[crossref]
14. (1)能量摄入的持续自我调节。体重减轻。体重正常的受试者保持体重。Nutr Metab（Lond）7：1-4。[crossref]
15. Van der Waaij LA, Limburg PC, Mesander G, Van der Waaij D(1996)人体粪便中厌氧细菌的体内IgA包被。肠道38：348-354。[crossref]