Just a one hour shift in my sleep schedule can screw me up for days. 2/16
Okay, let's start this hypersomnia thread!
[note - I am not looking for unsolicited advice.]
Idiopathic hypersomnia or narcolepsy (not the same, but similar) is very hard to describe to people.
When I say "I slept 10 hours last night and I'm still tired" I'm not bragging. 1/16
Just a one hour shift in my sleep schedule can screw me up for days. 2/16
I'm going to show you ways this happens. I can usually withstand 1 day of waking up early, with some consequences, but 2 days in a row kills me. 4/16
This is when I can sleep in until 11am because I do not have an event the next day. My body is not happy because of my switch in sleep cycles. It's not great, but it's not completely terrible. 6/16
More from Health
You gotta think about this one carefully!
Imagine you go to the doctor and get tested for a rare disease (only 1 in 10,000 people get it.)
The test is 99% effective in detecting both sick and healthy people.
Your test comes back positive.
Are you really sick? Explain below 👇
The most complete answer from every reply so far is from Dr. Lena. Thanks for taking the time and going through
You can get the answer using Bayes' theorem, but let's try to come up with it in a different —maybe more intuitive— way.
👇
Here is what we know:
- Out of 10,000 people, 1 is sick
- Out of 100 sick people, 99 test positive
- Out of 100 healthy people, 99 test negative
Assuming 1 million people take the test (including you):
- 100 of them are sick
- 999,900 of them are healthy
👇
Let's now test both groups, starting with the 100 people sick:
▫️ 99 of them will be diagnosed (correctly) as sick (99%)
▫️ 1 of them is going to be diagnosed (incorrectly) as healthy (1%)
👇
Imagine you go to the doctor and get tested for a rare disease (only 1 in 10,000 people get it.)
The test is 99% effective in detecting both sick and healthy people.
Your test comes back positive.
Are you really sick? Explain below 👇
The most complete answer from every reply so far is from Dr. Lena. Thanks for taking the time and going through
Really doesn\u2019t fit well in a tweet. pic.twitter.com/xN0pAyniFS
— Dr. Lena Sugar \U0001f3f3\ufe0f\u200d\U0001f308\U0001f1ea\U0001f1fa\U0001f1ef\U0001f1f5 (@_jvs) February 18, 2021
You can get the answer using Bayes' theorem, but let's try to come up with it in a different —maybe more intuitive— way.
👇
Here is what we know:
- Out of 10,000 people, 1 is sick
- Out of 100 sick people, 99 test positive
- Out of 100 healthy people, 99 test negative
Assuming 1 million people take the test (including you):
- 100 of them are sick
- 999,900 of them are healthy
👇
Let's now test both groups, starting with the 100 people sick:
▫️ 99 of them will be diagnosed (correctly) as sick (99%)
▫️ 1 of them is going to be diagnosed (incorrectly) as healthy (1%)
👇
1/16
Why do B12 and folate deficiencies lead to HUGE red blood cells?
And, if the issue is DNA synthesis, why are red blood cells (which don't have DNA) the key cell line affected?
For answers, we'll have to go back a few billion years.
2/
RNA came first. Then, ~3-4 billion years ago, DNA emerged.
Among their differences:
🔹RNA contains uracil
🔹DNA contains thymine
But why does DNA contains thymine (T) instead of uracil (U)?
https://t.co/XlxT6cLLXg
3/
🔑Cytosine (C) can undergo spontaneous deamination to uracil (U).
In the RNA world, this meant that U could appear intensionally or unintentionally. This is clearly problematic. How can you repair RNA when you can't tell if something is an error?
https://t.co/bIZGviHBUc
4/
DNA's use of T instead of U means that spontaneous C → U deamination can be corrected without worry that an intentional U is being removed.
DNA requires greater stability than RNA so the transition to a thymine-based structure was beneficial.
https://t.co/bIZGviHBUc
5/
Let's return to megaloblastic anemia secondary to B12 or folate deficiency.
When either is severely deficient deoxythymidine monophosphate (dTMP*) production is hindered. With less dTMP, DNA synthesis is abnormal.
[*Note: thymine is the base in dTMP]
https://t.co/AnDUtKkbZh
Why do B12 and folate deficiencies lead to HUGE red blood cells?
And, if the issue is DNA synthesis, why are red blood cells (which don't have DNA) the key cell line affected?
For answers, we'll have to go back a few billion years.
2/
RNA came first. Then, ~3-4 billion years ago, DNA emerged.
Among their differences:
🔹RNA contains uracil
🔹DNA contains thymine
But why does DNA contains thymine (T) instead of uracil (U)?
https://t.co/XlxT6cLLXg
3/
🔑Cytosine (C) can undergo spontaneous deamination to uracil (U).
In the RNA world, this meant that U could appear intensionally or unintentionally. This is clearly problematic. How can you repair RNA when you can't tell if something is an error?
https://t.co/bIZGviHBUc
4/
DNA's use of T instead of U means that spontaneous C → U deamination can be corrected without worry that an intentional U is being removed.
DNA requires greater stability than RNA so the transition to a thymine-based structure was beneficial.
https://t.co/bIZGviHBUc
5/
Let's return to megaloblastic anemia secondary to B12 or folate deficiency.
When either is severely deficient deoxythymidine monophosphate (dTMP*) production is hindered. With less dTMP, DNA synthesis is abnormal.
[*Note: thymine is the base in dTMP]
https://t.co/AnDUtKkbZh
