研究表明，進化可能是人類易患心臟病的原因

研究表明，進化可能是人類易患心臟病的原因

One-third of global deaths are due to cardiovascular disease caused by atherosclerosis, when arteries are clogged with fat deposits. Although it's common for humans to experience heart attacks, the same event is rare in mammals. Now, researchers believe that they understand why.

全球三分之一的死亡是由動脈粥樣硬化導致的心血管疾病引起的，動脈因脂肪沉積而堵塞。雖然人類心臟病發(fā)作很常見，但在哺乳動物中卻很少見?，F(xiàn)在，研究人員相信他們明白了其中的原因。

Risk factors for cardiovascular disease in humans can include age, hypertension, obesity, smoking, blood cholesterol and inactivity. However, in 15% of cardiovascular events caused by atherosclerosis, none of these risk factors is at hand.

人類心血管疾病的危險因素包括年齡、高血壓、肥胖、吸煙、血液膽固醇和缺乏運動。然而，在15%由動脈粥樣硬化引起的心血管事件中，這些危險因素都不存在。

Closely related mammals like chimpanzees living in captivity share some of the same risk factors for cardiovascular disease: hypertension, inactivity and high blood lipids.

與人類關(guān)系密切的哺乳動物，比如圈養(yǎng)的黑猩猩，也有與患心血管疾病的相同風險因素:高血壓、缺乏運動和高血脂。

But these chimps rarely experience heart attacks. If they do, it's not due to atherosclerosis; the cause is scarring of the heart muscle, which has yet to be explained.

但這些黑猩猩很少患心臟病。即使有，也不是因為動脈粥樣硬化;其原因是心肌的結(jié)疤，目前還沒有得到解釋。

Researchers think that there was the loss of a single gene, CMAH, in human ancestors between 2 million and 3 million years ago, leading to a higher risk of cardiovascular disease. This gene included a sialic acid sugar molecule called Neu5Gc. Apes and chimps have maintained this gene and molecule over time.

研究人員認為，200萬至300萬年前，人類祖先的CMAH基因缺失，導致心血管疾病的風險增加。這個基因包括一種叫做Neu5Gc的唾液酸糖分子。隨著時間的推移，猿和黑猩猩一直保持著這種基因和分子。

In a new study, mice were modified to be similarly deficient in this molecule, which caused a twofold increase in atherosclerosis compared with mice who were not modified. The study was published Monday in the journal Proceedings of the National Academy of Science.

在一項新的研究中，轉(zhuǎn)基因小鼠同樣缺乏這種分子，與非轉(zhuǎn)基因小鼠相比，這導致動脈粥樣硬化增加了兩倍。這項研究周一發(fā)表在《美國國家科學院院刊》雜志上。

"The increased risk appears to be driven by multiple factors, including hyperactive white cells and a tendency to diabetes in the human-like mice," said study author Dr. Ajit Varki, Distinguished Professor of Medicine and Cellular and Molecular Medicine at the University of California San Diego School of Medicine. "This may help explain why even vegetarian humans without any other obvious cardiovascular risk factors are still very prone to heart attacks and strokes, while other evolutionary relatives are not."

“這種增加的風險似乎是由多種因素造成的，包括過度活躍的白細胞和類人小鼠患糖尿病的傾向，”研究作者阿吉特·瓦爾基博士說，他是加州大學圣地亞哥醫(yī)學院的醫(yī)學和細胞及分子醫(yī)學的杰出教授。“這可能有助于解釋，為什么沒有任何其他明顯心血管風險因素的素食者仍然很容易患心臟病和中風，而其他進化上的近親則不然。”

Even though humans lack this gene and the Neu5Gc molecule within it, those who regularly eat red meat are exposed to it. Consuming it as a byproduct of red meat causes the human body to react with an immune response as well as chronic inflammation.

即使人類缺少這種基因和Neu5Gc分子，那些經(jīng)常吃紅肉的人也會接觸到這種基因。食用紅肉的副產(chǎn)品會導致人體產(chǎn)生免疫反應和慢性炎癥。

The modified mice in the study were fed a diet similar to that of humans who eat red meat: high in fat and rich in Neu5Gc. This caused the mice to develop an additional 2.4-fold increase in atherosclerosis.

在研究中，轉(zhuǎn)基因老鼠的飲食與食用紅肉的人類相似:高脂肪，富含Neu5Gc。這導致小鼠動脈粥樣硬化增加了2.4倍。

"The human evolutionary loss of CMAH likely contributes to a predisposition to atherosclerosis by both intrinsic and extrinsic [dietary] factors and future studies could consider using this more human-like model," the study authors wrote.

該研究的作者寫道:“人類進化過程中CMAH的缺失可能會導致動脈粥樣硬化的發(fā)生，無論是內(nèi)在的還是外在的(飲食)因素，未來的研究可以考慮使用這種更像人類的模型。”

The same research team has also demonstrated that modified mice fed a Neu5Gc-rich diet were more susceptible to inflammation and cancer progression, suggesting a link between certain cancers and diets rich in red meat.

該研究小組還證明，食用富含Neu5gc的食物的轉(zhuǎn)基因老鼠更容易患炎癥和癌癥，這表明了某些癌癥與食用富含紅肉的食物之間存在聯(lián)系。