Does anyone else experience most of their fatigue in the afternoon?

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I am currently in a continuing PEM episode that started almost a month ago. I feel ok and need to put the bulk of activity between 9 am (if I am able to get up at 7) and 3 pm. I always need 2 hours in the morning to get over the high fatigue and fibro pain I wake up with. I have noticed that at about 3 pm I start tanking, but unlike many of you, the fatigue just builds and builds till it forces me into bed. If I wait till 9 to do my bedtime routine, I can hardly get through it. I have to do it in pieces starting 7:30 ish.
 
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I always need 2 hours in the morning to get over the high fatigue and fibro pain I wake up with. I have noticed that at about 3 pm I start tanking
This is pretty much what happens to me each day. A long long time to wake up, from the unrefreshing, a few hours of being sort of OK, then the symptoms creep in (or sweep in). Then they seem to win.

Sickness Behavior very strong here. The whole suite of symptoms- EATING is hard, for instance. I can hardly chew.
 

gbells

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One obvious reason symptoms are worse in the afternoon has to do with the circadian rhythm of the cortisol hormone. In the morning it is higher so inflammatory symptoms are lowered/suppressed. As it drops they increase. It indicates high inflammation is present.

 

Wishful

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One obvious reason symptoms are worse in the afternoon has to do with the circadian rhythm of the cortisol hormone.
That may be an obvious hypothesis, but it doesn't seem to fit my observations. My symptoms increase abruptly around 2:30PM and then taper off over the next hour or two. Your graph doesn't show any sort of abrupt change in the afternoon.

If it was because the immune system abruptly switched state when cortisol reached a certain low level, I'd expect to see a much wider variability of trigger time. Instead, at times in the past, I've felt abruptly worse, looked at the clock, and seen that it was 2:30 +/- maybe 15 minutes. I'm not sure what system in the body is involved in such precise timing, but cortisol level doesn't seem to fit.
 
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My symptoms increase abruptly around 2:30PM and then taper off over the next hour or two.
I can set my watch to 2:30 most days. The neck aching, the throat hoarse and painful., particularly if I spoke or chatted.... My symptoms don;t taper off, they continue to worsen.

Some of these timing issues are why I find the Yin Deficiency...to serve to explain the increased HEAT and INFLAMMATION which is generated later in the day. Yin is built up at nite, so our "unrefreshning sleep symptom" makes some sense as many body repairs occur in the nite. this Yin Deficiency here is likely my genetic predispostions, not the CAUSE of the ME.
 

Sidny

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Oh and his colleagues have a different theory. Rather than stemming from a lack of sleep from the night before, they suggest that excessive daytime sleepiness is caused by direct degeneration of wake-promoting neurons.

Looking at brain tissue, the team found a significant tau buildup in three wakefulness-promoting brain centres, including the locus coeruleus (LC), the lateral hypothalamic area (LHA), and the tuberomammillary nucleus (TMN). Remarkably, this complex system had lost as many as 75 percent of its neurons.
Among the many fatalities was a type of neuron in the LHA that produces a neuropeptide called orexin. This neuron plays a crucial role in wakefulness; when it is deleted in mouse models, the animals show similar patterns to human narcolepsy - a chronic sleep disorder characterised by daytime drowsiness.

In the brains of patients with AD, UCSF researchers found orexin practically annihilated. In fact, the abundance of these orexin-producing neurons had decreased by more than 71 percent.

"To put this into another perspective, patients with narcolepsy .. have been reported to show 85-95 [percent] reduction in the number of orexinergic neurons, almost comparable to what we see in patients with AD," the authors write.
https://www.sciencealert.com/alzhei...he-neurons-that-keep-us-awake-study-shows/amp
Something similar might be happening to CFS sufferers who need naps during the day.

If indeed orexin is reduced in those patients and this can be proven clinically, then this is also quite a good argument for disability and proof that something is physically wrong.

I've also heard of several people who were diagnosed with narcolepsy. Maybe the narcolepsy was caused by CFS?
Dying neurons? Sounds like a logical explanation to me. Since the onset of my illness after a viral brain infection, I’ve suffered from a significant diminishment in overall arousal and the Locus coeruleus plays a big role in that.

I’m not quite at the point of needing many naps or narcolepsy though. Obviously like with any neurodegenerative disease the damage doesn’t happen overnight but is long term and cumulative.

It’s amazing how the pathologies of so many differently labeled diseases all seem to overlap. The question is what can we do now to stop tau and b amyloid accumulation and prevent these neurons from dying?

Is the protein build up and subsequent neuron death due to pathogens and the immune response to them? Maybe an anti infective could help slow neurodegenerative progression, like how antivirals lowered the incidence of Alzheimer’s in the group who took them long term vs the group that didn’t.

As far as proving any of this clinically it seems like time and time again we find the “proof” in corpses but don’t have the technology to observe the physical change in living people besides obvious symptoms. (Ie enteroviruses in ME patients brains, herpes virus lesions in Sophia Mizras spine etc.)
 
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It’s amazing how the pathologies of so many differently labeled diseases all seem to overlap
I don't think thats particularly amazing...I see so many inter-connections between various versions of ME and other odd diseases....perhaps bodies have a repetoire of responses to a whole slew of things, which are in fact all variations of some theme. Just depends on what part of the brain is swollen up at any particular time..

So I have 10 Provigil I bought, a nooptropic which: is supposed to wake up the narcoleptic. I' ve yet to take one as apparently, I'm nervous about it, plus never feel good enough to care to: be MORE AWAKE. So if there is a permanent damage to key neurons, wonder how the nootropics like Provigil: work.
 
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Modafinil has helped a lot of people in this forum, but I dont balme you for being hesitant. It is a drug, and everyone reacts differently.
Its just pretty funny: my doctor gave me the scrip, to get thru the airport and I don't even try it.

the Notion of being: like fully AWAKE...seems to me to be counter-intuitive and therefore scary.

What I was GOING to do was figure out if I could actually get it here, for less money.

So I flunked that assignment. Instead I tried to get LDN, can't, and not only can't: I cannot even ask a friend to Fed Ex my own pills to me: they will stop it apparently. G-F.

I did ask in a thread: about experiences with Modafinil and received few responses. Later i seem to recall reading it might help strengthen veins...in which case maybe thats a GOOD THING.
 

Sidny

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So if there is a permanent damage to key neurons, wonder how the nootropics like Provigil: work.
I don’t think Provigil working excludes that key neurons haven’t been damaged it just may improve the functioning of ones that haven’t been compromised.

https://en.m.wikipedia.org/w/index.php?title=Modafinil&action=edit§ion=11
As of 2017, the therapeutic mechanism of action of modafinil for narcolepsy and sleep-wake disorders remains unknown.[34][35] Modafinil acts as an atypical, selective, and weak dopamine reuptake inhibitor which indirectly activates the release of orexin neuropeptides and histamine from the lateral hypothalamus and tuberomammillary nucleus, respectively all of which may contribute to heightened arousal.[34][35][36]
https://en.m.wikipedia.org/wiki/Modafinil#cite_note-pmid22640618-36