Why do you get a fever when you're sick? - Christian Moro

譯者: Jennifer Yan 審譯者: Helen Chang

In 1917, doctors proposed an outlandish treatment for syphilis,

1917 年，醫生提出了一個 異乎尋常的方法治療梅毒，

the incurable bacterial infection that had ravaged Europe for centuries.

肆虐了歐洲幾百年的 無法治癒的細菌感染。

Step 1: Infect patients suffering from the later stages of syphilis

第一步：讓梅毒晚期患者

with the parasite that causes malaria,

感染上導致瘧疾的寄生蟲——

the deadly but curable mosquito-borne disease.

瘧疾是一種蚊子傳播的疾病， 雖會致命但可療癒。

Step 2: Hope that malarial fevers clear the syphilis.

第二步：希望瘧疾引起的 發燒清除梅毒。

And step 3: Administer quinine to curb the malaria.

第三步：用奎寧抑制瘧疾。

If all went according to plan,

如果一切順利，

their patient would be left alive and free of both diseases.

不但能保住患者的性命， 而且能清除梅毒和瘧疾。

This killed some 15% of patients, but for those who survived,

15% 的患者因此而死， 但對於活下來的人，

it seemed to work.

它看來是見效的。

It actually became the standard treatment for syphilis

這變成了梅毒的標準治療方法，

until penicillin was widely used decades later.

幾十年後，青黴素才被廣泛使用。

And its driving force was fever.

而這種治療的主力是發燒。

There are many mysteries around fever,

圍繞發燒這個話題有許多謎團，

but what we do know is that all mammals,

但我們知道所有的哺乳動物、

some birds and even a few invertebrate and plant species feel fever’s heat.

某些鳥類，甚至一些無脊椎動物和植物 能感受到發燒引起的熱。

It has persisted for over 600 million years of evolution.

這種發燒感受隨著進化 已經持續發展 6 億多年。

But it has a significant cost.

但代價巨大。

For every 1 degree Celsius of temperature increase in the human body,

人的體溫每升高一攝氏度，

there’s a 12.5 percent increase in energy required,

所需能量就會增加 12.5％，

the equivalent of about 20 minutes of jogging for some.

對於某些人相當於 跑 20 分鐘消耗的能量。

So, why and how does your body produce a fever?

那我們的身體為什麼 又是怎樣發燒的呢？

Your core temperature is maintained via thermoregulation,

經由溫度的調節，

a set of processes that usually keep you around 37 degrees Celsius.

一系列的過程把你的體溫通常 保持在 37 攝氏度左右。

These mechanisms are controlled by the brain’s hypothalamus,

經由探測微小的溫度變化，

which detects minute temperature shifts

下丘腦發送信號給身體各個部位，

and sends signals throughout the body accordingly.

控制溫度調節的機理。

If you’re too hot, the hypothalamus produces signals

如果你的體溫太高， 下丘腦將產生信號

that activate your sweat glands or make your blood vessels dilate,

啟動你的汗腺或讓你的血管擴張，

moving blood closer to the skin’s surface—

讓血液更靠近皮膚的表層——

all of which releases heat and cools you off.

釋放熱量，讓體溫下降。

And if you’re too cold,

如果你太冷了，

your blood vessels will constrict and you may start to shiver,

你的血管會收縮， 你可能會打哆嗦

which generates heat.

而打哆嗦產生熱量。

Your body will disrupt its usual temperature equilibrium to induce a fever,

要發燒，你的身體得 打破它平常的溫度平衡，

which sets in above 38 degrees Celsius.

達到 38 攝氏度以上。

Meanwhile, it has mechanisms in place to prevent it

同時，為了防止器官功能損傷， 身體利用它的機理

from exceeding 41 degrees Celsius, when organ damage could occur.

避免體溫超過 41 攝氏度。

Immune cells that are fighting an infection can induce a fever

抵抗感染的免疫細胞 經由激發連串的生化反應

by triggering a biochemical cascade that ultimately instructs

指示下丘腦提高基礎體溫，

your hypothalamus to increase your baseline temperature.

導致發燒。

Your body then gets to work to meet its new “set point” using the mechanisms

你的身體用那些在體溫 太低的時候產生熱量的機理

it would to generate heat when cold.

努力達到新的 「平衡點」。

Until it reaches this new temperature, you’ll feel comparatively cool,

在達到這個新的平衡體溫前， 你會覺得比較冷，

which is why you might experience chills.

也是為什麼你有可能打寒顫。

But why does your body do this?

但你的身體為什麼會做這些？

While the jury's still out on how higher temperatures directly affect pathogens,

雖然對升高的體溫是怎麼 直接影響病原體的還尚不清楚，

it seems that fever's main effect

但發燒的主要作用看上去是

is in rapidly inducing a whole-body immune response.

迅速地調動整個身體的免疫反應。

Upon exposure to raised internal temperatures,

當體內溫度升高時，

some of your cells release heat shock proteins, or HSPs,

一些細胞會釋放出 熱體克蛋白（HSPs），

a family of molecules produced in response to stressful conditions.

一種應對壓力情形時產生的分子家族。

These proteins aid lymphocytes, one of several kinds of white blood cells

這些蛋白會幫助淋巴球—— 一種抵抗病原體的白血球——

that fight pathogens, to travel more rapidly to infection sites.

更快地運輸到被感染的部位。

HSPs do this by enhancing the “stickiness” of lymphocytes,

熱體克蛋白經由 提升淋巴球的 「粘度」，

enabling them to adhere to and squeeze through blood vessel walls

使它們附著和擠過血管壁，

so they can reach the areas where infection is raging.

最終到達感染嚴重的部位。

In the case of viral infections,

在病毒感染的情况下，

HSPs help tell nearby cells to dampen their protein production,

熱體克蛋白要鄰近細胞 減少蛋白質的生產，

which limits their ability to replicate.

限制它們複製的能力。

This stunts the virus’s spread because they depend on

這會阻礙病毒的擴散，

因為病毒依靠宿主的機制來複製。

their host’s replicative machinery to reproduce.

It also protects surrounding cells from damage since some viruses spread

這也防止周圍細胞受損，

因為某些病毒 經由爆破宿主細胞而擴散，

by rupturing their host cells, which can lead to large-scale destruction,

其大規模的碎屑聚積

the build-up of detritus, and potentially even organ damage.

甚至造成器官衰竭。

The ability of HSPs to protect host cells and enhance immune activity

熱體克蛋白保護宿主細胞 和提高免疫活性的能力

can limit the pathogen’s path of destruction inside of the body.

能夠限制病原體在人體內致傷的途徑。

But for all we know about fever’s role in immune activation,

雖然我們都知道 發燒激活免疫系統的作用，

some clinical trials have shown that fever suppressor drugs

有些臨床試驗表明

退燒藥不會惡化病狀 或減緩恢復的速度。

don’t worsen symptoms or recovery rates.

This is why there’s no definitive rule on whether to suppress a fever

因此是要抑制發燒還是順其自然

or let it ride.

並沒有一定之規。

Doctors decide on a case-by-case basis.

醫生按個體的情況做決定。

The fever’s duration and intensity, as well as their patient’s immune status,

發燒持續多久、嚴重性、 患者的免疫力、

comfort level, and age will all play a role in their choice of treatments.

舒適度、和年齡 都會影響醫生的治療方案。

And if they do let a fever ride,

如果他們讓發燒順其自然，

they’ll likely prescribe rest and plenty of fluids to prevent dehydration

醫生很有可能叮囑休息和補充液體，

以防止患者的身體在激戰時脫水。

while the body wages its heated battle.