杰拉德·C·许
简介:本文中,作者提出了大脑在葡萄糖生成中的作用的假说,特别是空腹血糖(FPG)生成的模拟模型,以及体重作为大脑的刺激器的功能。
方法:作者患 2 型糖尿病 (T2D) 已有 25 年多。在最初的 20 年里,他严重依赖药物来控制疾病症状,直到 2010 年病情恶化,当时他出现了大多数严重并发症,包括五次心脏病发作、肾脏并发症、膀胱感染、足部溃疡、甲状腺和视网膜问题。到那时,药物似乎不再起作用。因此,他专注于生活方式问题,尤其是饮食和运动,以控制餐后血糖 (PPG),因为它占 HbA1C 形成的 75% 至 85%。2016 年 11 月,他飞往檀香山并在夏威夷呆了一段时间。他突然注意到早上他的 FPG 值持续升高。在接下来的四个月里,他用尽了所有基于他所知道的方法来检查他的身体出了什么问题。 2017年3月17日凌晨3点,他做了一个梦,想深入研究输出因素之间的关系,而不是输入类别和输出类别之间的关系,因为他受过40年的工程师教育和培训。在运行了四个小时的计算机软件来检查血糖、血脂、血压和体重之间的关系后,他发现体重增加是导致空腹血糖升高的原因!此后,在过去的两年半里,他一直在研究这个课题,并为这种惊人的关系提供了更多的证据。
Results: Among all of the human internal organs, only the brain has the power of cognition, decision-making, and issuing order capabilities. The brain instructs the liver to produce glucose and the pancreatic alpha cells to produce glucagon to raise glucose level if it is too low and beta cells to produce insulin to reduce glucose level if it is too high. In other words, the liver and pancreas are merely working machines for the master, the brain. In the scope of FPG, what is the stimulator for the brain to instruct liver producing glucose and at what appropriate level of glucose? During our sleep time (other than the continuous operations of the internal organs and somewhat natural sweating, vaporization, nighttime urination), our body lacks the heavy physical activities such as eating, drinking, and exercising. It is the author’s hypothesis that our brain knows our body weight level and situation continuously and then used this vital information as the yardstick to decide how much glucose level our body needs. Based on this hypothesis, the author tried to prove these available physical characteristics of our biomedical phenomenon via some mathematical and computational tools.
As the first evidence, Figure 1 shows that the 77% high correlation coefficient exists between weight and FPG from a time-series analysis using data from 1/1/2014 through 10/18/2019 (a total of 2,116 days in ~5.5 years). Furthermore, a spatial analysis diagram in the lower part of Figure 1 also depicts a skewed cucumber shape of these data sets between weight and FPG without time factor. It indicates that when body weight increases or decreases, the FPG changes upward or downward accordingly. Based on this finding, the author developed a prediction model for FPG by using weight as its major input (~80%) and a cold weather temperature (FPG drops 0.3 mg/dL for every degree of weather temperature drop when it is below 67 degrees Fahrenheit) as its secondary factor due to “hibernation” (~10%).
图2显示,使用2018年5月5日至2019年10月18日(共532天)的数据,预测FPG和测量FPG之间存在99.97%的极高相关性。他之所以选择这个时间段,是因为他使用了“使用连续血糖监测传感器设备和用试纸刺破手指进行的双重并行测量”。虽然手指FPG和传感器FPG之间的模式相似性较低,但它们的平均FPG值偏差在0.9%到1.2%以内(传感器FPG为113 mg/dL,手指FPG为112 mg/dL)。图3显示了他2012年至2019年的年平均体重和年平均FPG。值得注意的是,它们都在随着时间的推移而下降。换句话说,他的体重从189磅减了下来。体重增加到 173 磅后,他的 FPG 也从 135 mg/dL 下降到 113 mg/dL。FPG 的下降确实使他整体 A1C 下降了约 20%,从 2010 年体重 198 磅时的 10% 下降到 2019 年体重 172 磅时的 ~6.5%。总之,基于体重的 FPG 水平的发现和证据非常准确,足以让他基于这一假设开发 FPG 模拟或预测模型。
结论:体重是大脑决定清晨空腹血糖生成及其适宜量的刺激因素,空腹血糖预测模型只是一个数学模拟模型,用来解释大脑与肝脏和胰腺等器官沟通后产生的空腹血糖的复杂运作。