Macrophages just want to watch the whole body burn.
From what I’ve read, anything over about 101F is doing more harm than good.
Pretty sure it’s anything at 42°C or above that is a vital emergency, as it starts to destroy neurons
39°C is basically a normal fever
This does not appear to match the evidence anymore: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7717216/
The body is generally unable to raise the core temperature to the point where it can cause permanent damage, unless the ambient temperature is high. That is, unless there is a pre-existing heart or other vital organ condition.
In fact, fevers >=39C (102.2F) showed better outcomes in covid patients.
To me Macrophages are the single most interesting creatures(symbiotes?) in the human body. I’ve read so much about them yet know so little.
I’ve had this Excel workbook open for an hour now and my boss is asking why I’m just staring at it. But thank you?
I only know ibuprofen as a pain killer, but good to know it can also reduce fever!
It was the key drug being deployed during the covid war. I survived tks to it. Saw god a few times.
Having a fever I can deal with, but I will immediately take some meds to not have a headache. Unfortunately, usually a fever comes with a headache.:(
Ibuprofen does not reduce a fever, it reduces inflammation. Tylenol would have made this meme work
Edit: I was wrong
The first sentence on ibuprofens wikipedia page under “Medical uses”:
Ibuprofen is used primarily to treat fever
Anti-inflammatories reduce fevers, are there even anti-inflammatories that don’t have that effect to some extent?
So I was about to correct you that Tylenol is actually acetaminophen; turns out paracetamol is just another name for the same chemical. TIL
Paracetamol is not anti-inflammatory in any serious context, which is to say taking paracetamol to reduce actual inflammation (think gout or rheumatoid arthritis) is more or less useless. From the wikipedia article on paracetamol:
Paracetamol inhibits prostaglandin synthesis by reducing the active form of COX-1 and COX-2 enzymes. This occurs only when the concentration of arachidonic acid and peroxides is low. Under these conditions, COX-2 is the predominant form of cyclooxygenase, which explains the apparent COX-2 selectivity of paracetamol. Under the conditions of inflammation, the concentration of peroxides is high, which counteracts the reducing effect of paracetamol. Accordingly, the anti-inflammatory action of paracetamol is slight.
It is, however, an analgesic.
I’ll be damned, I was almost certain it wasn’t an antipyretic, but it looks like I was wrong. Thanks for correcting me.
You didn’t need to use such condescending language though, there was no need to be rude.
Apologies. I do think making it sting a little when correcting someone on something they should have double checked, is warranted, if for no other reason than to make it clear to others reading which take to go home with.
But in response to your edit I’ve softened my correction as well.
When you post wrong information online you’re responsible for perpetuating idiocy. Someone who had better things to do had to go out of their way, waste their time, to correct you.
Think before you post.
Take both at the same time. They’re synergistic and will reduce pain, inflammation, and fever better than a higher dose of each by themselves
Nevermind that Tylenol’s effective ingredient is paracetamol, which is also “just” an anti-inflammatory.
Aspirin is bad for your liver as well, especially for kids. It disrupts the electron transport chain in the Krebs cycle which leads to fatty acids not being converted and since they don’t belong into the mitochondria, they are expunged into small deposits in the liver. It’s called microvesicular steatosis, or more commonly called fat liver.
