Blood Type Diets (BTD) and Aging: An Overview

M. Menapace
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Abstract

It has recently been proposed that glycans, being the third alphabet of life, interact intricately with endogenous biomolecules to modulate tolerance, immune and inflammatory responses. Specifically, food glycans could impact health and be a source of inflammation and age-related diseases. These special carbohydrates are present as glycoconjugates (glycoproteins or glycolipids) in and on the surface of all the cells (glycocalyx) of all organisms or are found in free form in biological fluids. Recent advances in glycobiology and glycochemistry have shown how glycans bind with naturally present human proteins (lectins), through protein-carbohydrate interactions (or PCI), but also how oligosaccharides can interact with other glycans, present throughout the human body (through carbohydrate-carbohydrate interactions, or CCI). Oligosaccharides present in food sources, which go beyond the definition of normal fibers, once ingested are then either absorbed in the bloodstream, where they are recognized by the immune system, or interact with the surface of GI epithelial cells, thus generating appropriate biochemical cascades that induce a tolerance or immune/inflammatory response. Because the ABO epitopes have been encountered on all human cells, not just erythrocytes and based on the different biotypology (A, AB, B, and O) impose morphic changes in the distribution of the glycans on the glycocalyx (lipid rafts and clustered saccharide patches), their CCI with food and microbe glycans will be different, thus, eliciting contrasting responses. This can explain the epidemiological data for blood type diets (BTD). Through continuous consumption of the wrong types of glycans, processes of chronic inflammation could be initiated and progress to accelerated aging. Four basic modes of action have been identified showing how glycans can trigger inflamm-aging. Since glycobiology is a young science, further studies with newer technologies are warranted for advancement in this field.
血型饮食(BTD)与衰老:综述
最近有人提出,甘聚糖作为生命的第三字母表,与内源性生物分子相互作用,调节耐受性、免疫和炎症反应。具体来说,食物聚糖可能会影响健康,成为炎症和与年龄有关的疾病的来源。这些特殊的碳水化合物以糖缀合物(糖蛋白或糖脂)的形式存在于所有生物体的所有细胞(糖萼)内和表面,或以自由形式存在于生物液体中。糖生物学和糖化学的最新进展表明,聚糖如何通过蛋白质-碳水化合物相互作用(PCI)与天然存在的人类蛋白质(凝集素)结合,以及低聚糖如何与存在于人体各处的其他聚糖相互作用(通过碳水化合物-碳水化合物相互作用,CCI)。存在于食物中的低聚糖超出了正常纤维的定义,一旦被摄入,要么被血液吸收,在那里它们被免疫系统识别,要么与胃肠道上皮细胞表面相互作用,从而产生适当的生化级联反应,诱导耐受性或免疫/炎症反应。由于ABO表位存在于所有人类细胞中,而不仅仅是红细胞,而且基于不同的生物类型(A、AB、B和O),糖萼(脂筏和簇状糖块)上的聚糖分布会发生形态变化,因此它们与食物和微生物聚糖的CCI将会不同,从而引发不同的反应。这可以解释血型饮食(BTD)的流行病学数据。通过持续消耗错误类型的聚糖,慢性炎症的过程可能被启动,并进展到加速衰老。已经确定了四种基本的作用模式,表明聚糖如何引发炎症老化。由于糖生物学是一门年轻的科学,因此有必要采用更新的技术进行进一步的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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