本篇文章共分 6 段，針對科學界尋找衰老基因的主要研究方向以及限制熱量攝取與延長壽命間的關係做有系統的整理與說明。

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Research into Aging and Extending Life Span 衰老和延長壽命之研究

1. 衰老基因仍未有定論

   The mounting evidence for age genes that influence the aging process is by no means conclusive, but it is quite impressive, coming from a variety of independent research from aging in worms and fruit flies to antioxidants and gene repair mechanisms, and human mutations. Still, the connections are circumstantial.

   影響衰老過程的衰老基因日益增加的證據絕不代表一切已經底定，但卻令人讚嘆，這些證據來自各種獨立的研究，從蠕蟲和果蠅的衰老到抗氧化劑和基因修復機制，以及人類的突變。儘管如此，這些聯繫仍然是間接的。

2. 動物研究尋找衰老基因

   Christopher Wills, professor of biology at the University of California in San Diego, thinks that by 2025 science will likely isolate the mammalian age genes in mice. We share roughly 75 percent of our genes with mice and have much the same body chemistry; this is a strong reason to believe that an age gene found in mice could also be at work in humans. If such genes are located, the next step would be to find out if these age genes have their counterparts in humans. Wills believes that if they are found in humans, they may extend the human life span perhaps to 150 years.

   加州大學聖地牙哥分校生物學教授克里斯多福．威爾斯認為，到 2025 年，科學將可能在小鼠身上分離出哺乳動物的衰老基因。我們與小鼠共享大約 75% 的基因，並且具有大致相同的身體化學特性；這是一個強有力的理由，可以相信在小鼠身上發現的衰老基因也可能在人類身上發揮作用。如果找到了這樣的基因，下一步將是找出這些衰老基因在人類身上是否有對應的基因。威爾斯認為，如果它們在人類中被發現，它們可能會將人類的壽命延長到 150 年。

3. 分析DNA尋找衰老基因

   But by 2020, when personalized DNA sequencing becomes widespread, a second tactic may prove fruitful as well. By analyzing populations of healthy individuals in their nineties and beyond, scientists will find it possible to use computers to compare their genetic backgrounds and cross-check for similarities in key genes that are suspected of influencing aging. A combination of studies on the DNA of long-lived animals and on the personalized DNA sequences of elderly individuals may considerably narrow down the search for the age gene.

   但到 2020 年時，當個性化的 DNA 測序變得普遍時，第二種策略也可能被證明是成效卓著的。透過分析 90 歲以上的健康人群，科學家將發現有可能使用電腦來比較他們的遺傳背景，並交叉檢查那些被懷疑影響衰老的關鍵基因的相似性。對長壽動物的 DNA 和老年人的個性化 DNA 序列的研究相結合，可能會大大縮小對衰老基因的搜索範圍。

4. 熱量限制理論

   As yet, none of these methods can prove that we can increase the human life span. Indeed, the only theory with a proven track record of extending the life span of animals is the caloric restriction theory, which states that animals which consume calories just above starvation levels live significantly longer than the average. Although this theory flies in the face of common sense (a well-fed animal is well nourished and healthy, and should have greater resistance to disease and aging), it has held up under repeated testing among a wide range of animals. Scientists have consistently increased the life span of rats and mice in the laboratory by 50 to 100 percent. It is the only laboratory-tested theory of age extension for animals that has held up under decades of careful scrutiny. Why?

   到目前為止，這些方法都無法證明我們可以延長人類的壽命。事實上，唯一有延長動物壽命記錄的理論是熱量限制理論，該理論指出，消耗的熱量剛剛超過飢餓程度的動物的壽命明顯長於一般平均。儘管這一理論與常識相悖（吃得好的動物營養豐富，身體健康，對疾病和衰老的抵抗力應該更強），但它在各種動物中的反覆測試中還是得到了證實。科學家們在實驗室中不斷地將大鼠和小鼠的壽命延長了 50% 至 100%。這是唯一經過實驗測試的動物年齡延長理論，歷經幾十年的詳細檢核依然成立。為何如此？

5. 新陳代謝與長壽

   Across the animal kingdom, the life span of animals is roughly inversely correlated to the metabolism rate. The slower their normal metabolism rate, the longer their normal life span. In 1996, in a study that reduced the calorie intake of 200 monkeys by 30 percent, the monkeys were shown to have a slower metabolism rate, a longer life span, and reduced rates of cancer, heart disease, and diabetes. “We have known for 70 years that if you feed laboratory mice less food, they age slower, they live longer, and they get diseases less frequently. We find that monkeys respond in the same way as rodents and that the same biological changes may be in play here,” says George Roth of the National Institute of Aging.

   在整個動物界，動物的壽命與新陳代謝率大致成反比。它們的正常新陳代謝率越慢，其正常壽命就越長。1996 年，在一項將 200 隻猴子的卡路里攝入量減少 30% 的研究中，顯示猴子的新陳代謝率更慢，壽命更長，癌症、心臟病和糖尿病的發病率也有所下降。「我們已經知道 70 年了，如果你給實驗室的小鼠餵食較少的食物，它們就會衰老得更慢，壽命更長，而且得病的頻率更低。我們發現猴子的反應與齧齒類動物相同，同樣的生物變化可能在這裡發揮作用。」國家老化研究所的喬治．羅斯說。

6. 體溫與壽命

   There is still room for scientific debate on the question “why?” Ron Hart, a scientist at the National Center for Toxicological Research, believes that the answer may lie in the high body temperature of mammals, and humans in particular. “Heat causes pieces of the DNA molecule to split off randomly, and it must be repaired,” Hart says “Under calorie restriction, though, the engine runs cooler and there's less damage. Merely reducing caloric intake by 40 percent reduced this form of spontaneous DNA damage almost 24 percent!” Furthermore, at a higher internal body temperature, oxygen is being burned at a greater rate, creating more free radicals, which also speed up the aging process. Cooling the body, on the other hand, increases the amount of antioxidants in the body. Hart found a fourfold increase in the enzyme catalase and a threefold increase in superoxide dismutase in animals on a restricted diet. “What's fascinating,” Hart concludes, “is that reduced food intake is the only experimental paradigm ever found that enhances DNA repair.” Hart is so convinced of the importance of this work that in 1993 he began the first systematic studies of caloric restrictions in humans.

   關於「為什麼？」這個問題仍有科學辯論的餘地。國家毒理學研究中心的科學家羅恩．哈特認為，答案可能在於哺乳動物的高體溫，尤其是人類。「熱量導致 DNA 分子的碎片隨機分裂，它必須被修復。」哈特說。「不過，在限制熱量的情況下，發動機運行的溫度更低，損害也更小。僅僅減少 40% 的熱量攝入就使這種形式的自發性 DNA 損傷減少了近24%！」 此外，在較高的內部體溫下，氧氣被更快地燃燒，產生更多的自由基，這也加速了衰老過程。另一方面，冷卻身體會增加體內的抗氧化劑數量。哈特發現在限制飲食的動物中，過氧化氫酶增加了四倍，超氧化物歧化酶增加了三倍。「令人著迷的是，」哈特總結說，「減少食物攝入量是迄今為止發現的唯一能增強 DNA 修復的實驗範式。」 哈特對這項工作的重要性深信不疑，因此在 1993 年，他開始對人類的熱量限制進行首次系統研究。