🤝 Community Munchausen's by Internet (Malingerers, Munchies, Spoonies, etc) - Feigning Illnesses for Attention

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Giving her doctors and care team benefit of the doubt, (that they’re not giving we her meropenem or whatever for fun) she’s graduated to a point where only the strongest, most side effect heavy abx work on her stupid own goal infections
That’s what confused me—the doctors and nurses are seeing this girl they just discharged two days ago as clear of any infection walk back into the ER claiming she has a fever and they just start her back on The Antibiotic From Hell again right away? Literally week after week for months on end? Maybe that’s just hospital protocol and they can’t make an exception for Aster (to start anyone complaining of sepsis symptoms on abx until proven not infected)?
 
Aces thoughts on homeschooling and a horrifying look into what she's going to teach her Child:
Wyświetl załącznik 9093713

Now enrolling for Kiwi Farms University:

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Wired has a pretty good article about long COVID out (also goes into the whole ME/CFS shitshow). I’m not so sure about the whole neuroplasticity approach that’s featured (sounds like CBT and the biopsychosocial model with a bit of trendy trauma shit thrown in), but the journo does a really good job of contextualizing LC within a culture that believes all women and where activism is allowed to curtail scientific inquiry.

NOTHING ABOUT LONG Covid adds up.
Consider prevalence rates: How could one study find it affected 3.3 percent of the population of the UK but others an alarming 51 percent of South Americans and 86 percent of Egyptians? Or treatment methods: The BMJ’s systematic review of ways to treat long Covid lists two as supported by moderate evidence, cognitive behavioral therapy and physical exercise. But if you attended the third annual Long Covid International Conference in Boston—as I did, late last year—you’d think the BMJ was encouraging medical malpractice. During two days of presentations, the world’s leading scientific authorities brought up exercise only to warn against it. Cognitive behavioral therapy received just one mention: “not recommended.”


Then there’s the scientific progress, or lack thereof. Six years since the height of the pandemic, the scientific community remains baffled by long Covid. Researchers still don’t know why some people’s symptoms persist or worsen after the acute phase of SARS-CoV-2 infection has passed. Almost $2 billion and half a decade of international effort have yielded little more than hypotheses about micro blood clots and spike proteins and mitochondrial dysfunction. There isn’t a single approved pharmaceutical treatment, not even a test to verify the presence of the illness.
Of course, the usual suspects love everything about this actual good-faith attempt at understanding the issue:

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They’re also using this absolutely anodyne & reasonable tweet of the writer to accuse him of child abuse:
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TLDR: mostly well researched article by scientifically literate journalist gets responses that prove his every point, mostly from people who like to yell BE KIND at others. Many such cases.
 
We’re the only ones that pay any attention to Ace, right? I was hoping she’d get caught up in a cancellation arc à la Judy Valentin but it’s probably for the best that no one acknowledges her stoned bullshit except us. Her poor kid…

More or less. The only people that semi-like her on Twitter are other nutjobs seeking baby masking advice. She appears to be The ExpertTM for that. Everyone else hates or fights with her over her personality or entitlement.

Her TikTok barely has 500 subscribers, with low view counts and next to no comments. She's blowing smoke into the void.

I actually feel like as far as MbP by internet specifically, she's already there. She's already using an alleged diagnosis (autism, also the ever present threat of long covid) for ass pats and sympathy from the other brain dead morons who encourage her online. And I don't know exactly how old Cloud is so maybe I'm off base, but it sounds like he's just doing fairly normal baby babbling for his age? Has anything she's posted about him actually indicated possible autism? Besides that she's obviously trying very hard with the masking. I don't think a baby shaking his head while interacting with his mother ("stimming") is exactly a smoking gun.

He’s barely 15 months old. Too young to be early screened, let alone diagnosed. Everything so far is projection on Ace's part, and her belief that autistic people will always have autistic children, no exception. Although I agree with others that while Ace is very weird, I think it's more the drugs talking than any autism. They have consumed not just her life, but her brain.

Yeah, I think it’s time for Ace to get her own thread or something - I want to laugh at retards here, not get all weepy about lil Cloud’s miserable lot in life (:_(

I can start on a containment thread. Will link it here when it’s posted in PG.
 
Back on the long covid thing for a quick derail, the thing I find the most frustrating about it all is when looking at research into LC, you'll find things like "Long COVID is not a single illness with a clear set of symptoms and outcomes, but rather a multisystem condition that can affect nearly every part of the body" and "more than 200 different symptoms have been described with Long COVID". source.
Okay, If the assumption is that we don't know enough yet about the pathology of exposure to SARS-CoV-2 and longterm implications then fine. But, in many other cases of viral diseases such as HIV/AIDS, there eventually was a clear pathology, in HIV/AIDS: the virus' attack on CD4 + T lymphocytes that was killing their immune system.

The fact that there's not even a guess as to why this particular virus causes longterm (200+) debilitating symptoms is now basically accepted as credible is quite funny. Boomers really missed the boat on claiming long-influenza. :lol:
 
Literally week after week for months on end?
Unfortunately nobody wants to fall victim to a "boy that cried wolf" situation. I admit I wasn't following Aster's story closely (it was too infuriating and gross) but a classic example of just starting empirical* antibiotics before waiting for any results to come back would be for a cancer patient that you know has a very low white blood cell count and can't fight infection. They're advised that if they have any fevers, even if they feel ok, to come straight to hospital and antibiotics are immediately started.

Sometimes these patients will never grow any bugs in their blood/urine/sputum and you can chalk it up to the fevers just being purely cancer related (having cancer itself can cause fevers), but you still go through the same process many, many times before someone is brave enough to say "ok let's take samples and wait until something grows before we start antibiotics".

If Aster is so colonised with horrific antibiotic-resistant bacteria + has tubes in, it would be fair for staff to just err on the side of caution and assume she's infected until proven otherwise.


*empiric antibiotics refers to the antibiotics you can safely start before you get any cultures back from the lab, and adjust if necessary. A common one would be [insert locally used antibiotic for UTIs in women of child-bearing age] - if the patient has symptoms and their urine dipstick test has white cells, it's a common UTI until proven otherwise.
 
"more than 200 different symptoms have been described with Long COVID". source.
I've been looking for an actual source on 200 symptoms, and honestly it feels like i'm chasing my tail with circular referencing and just bad bad science.

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your article cites the CDC, which then cites This study
Sixth, more than 200 symptoms of PASC have been reported, each with the potential of being life-altering and debilitating, and the symptoms highlighted herein may not reflect the severity or impact of other symptoms.
In the full cohort, 37 symptoms had frequency of 2.5% or greater and aORs were 1.5 or greater
which means the other 163 of the "200 long covid symptoms" occurred in less than 2.5% of paticipants,

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The full list of all 37 symptoms is full of so many non-symptoms like just "bladder" BLADDER WHAT??? bladder alone isn't a symptom is it a overactive bladder? Under-active bladder? Bladder pain? these are all very different symptoms you can't just classify under "bladder". this whole stuidy is like If i exposed 1000 ppl to twitter then asked them all their symptoms after using twitter to make a list of over 400 post twitter exposure syndrome symptoms, its just bad science.

the study also cites several other horrible studies with false claims like:
At least 65 million individuals around the world have long COVID, based on a conservative estimated incidence of 10% of infected people and more than 651 million documented COVID-19 cases worldwide1; the number is likely much higher due to many undocumented cases.

idk what it is abt covid but it really brought out the worst researches to make the most bold claims with little to no evidence that still get cited.

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Honestly this says literally everything, 77% women and they reported more of every symptom then men, i'd love to see more breakdowns of long covid by gender as every munchie condition has an overwhelming female over representation.

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@Flourishing Pinecone ❧ I have the dumbest question: if Aster's dip sticks are coming up positive for lymphocytes/leukocytes at presentation, is there any way to distinguish between those caused by inflammation (bc all the toobz and intentional retention) and those that will lead to infection *without* culturing? Is there any kind of cytology that could eliminate the blanket 'here, take this bactrim and I'll call you in five days if something grows.'?

PL but my 80 yr old mom has IC, and if we could close this loophole ('There are def white cells but is it an infection? Stay tuned and wreck your old lady GI tract with 5 days of unnecessary antibiotics!') my god would her care be easier. Not to sperg but it was ticking me off Aster didn't want to even try the Botox. I feel like in some ways it's given Mom her life back.
 
idk what it is abt covid but it really brought out the worst researches to make the most bold claims with little to no evidence that still get cited.
Oh yeah, I went into the trenches trying to find anything empirical data-wise and there was really nothing substantiative. Just a lot of bad science, people babbling about patient's rights/autonomy, or how long covid is just as valid as any other post-viral syndrome. Then we get into another can of worms that is EBV etc.
 
i'd love to see more breakdowns of long covid by gender
I'll admit that this thread has been very eye-opening for me on long covid. Almost everyone I've ever heard talk about it has been a woman, usually someone prone to drama.

But, I do have a friend who had "long covid" before it was really known as a thing. He got covid March 2020 in that first bad wave of NYC cases and was sick for a month. After that he said he couldn't exercise without pain in his lungs for maybe 9-12 months. But then he got over it, and only started calling it long covid retroactively.
I do wonder if especially those early strains were causing some sort of lasting lung damage, which led researchers to say "hey maybe we should study this!" And that led to where we are now. Everyone who is prone to munching or melodrama or wants to be able to claim disability as an intersectional identity can claim long covid. But because of my friend's case, before it even had a name, I always assumed there was something more legitimate about it. But wow, turns out there really is not! Just another excuse to claim POTS.

Edit: pressed send too early yet again
 
Ostatnio edytowane:
PL but my 80 yr old mom has IC, and if we could close this loophole ('There are def white cells but is it an infection?
So prefacing this that I'm not a Urologist or Infectious Diseases specialist, but it seems reasonable that if you have someone with established IC (that doesn't have a urinary catheter etc) you could hold off on antibiotics until the cultures come back. But this can differ depending on where you live due to what common bacteria are in the environment (eg. someone in metropolitan Sweden will have different risks for bacteria/infections compared to someone in rural Morocco).
 
I'll admit that this thread has been very eye-opening for me on long covid. Almost everyone I've ever heard talk about it has been a woman, usually someone prone to drama.

But, I do have a friend who had "long covid" before it was really known as a thing. He got covid March 2020 in that first bad wave of NYC cases and was sick for a month. After that he said he couldn't exercise without pain in his lungs for maybe 9-12 months. But then he got over it, and only started calling it long covid retroactively.
I do wonder if especially those early strains were causing some sort of lasting lung damage, which led researchers to say "hey maybe we should study this!" And that led to where we are now. Everyone who is prone to munching or melodrama or wants to be able to claim disability as an intersectional identity can claim long covid. But because of my friend's case, before it even had a name, I always assumed there was something more legitimate about it. But wow, turns out there really is not! Just another excuse to claim POTS.

Edit: pressed send too early yet again
It seems that the early COVID strains did give people permanent or semi-permanent lung and heart problems (anecdotally I know an otherwise healthy male who got heart damage from COVID) but it really doesn’t seem like that’s what any of this “long COVID” stuff is about. It seems more similar to the equally fake “chronic Lyme” where there’s no evidence of infection and the symptoms are just “I don’t feel good most of the time,” which could be something psychosomatic (or an ED which is what I suspect a lot of these munchie girls are covering for).
 
The full list of all 37 symptoms is full of so many non-symptoms like just "bladder" BLADDER WHAT??? bladder alone isn't a symptom
Nearly spit out my coffee. Not sure why I find this so hilarious.

“Teeth” is also a symptom. Teeth.

Ah, fuck, I got both of those

:lossmanjack::lossmanjack::lossmanjack:

I'll admit that this thread has been very eye-opening for me on long covid. Almost everyone I've ever heard talk about it has been a woman, usually someone prone to drama.

But, I do have a friend who had "long covid" before it was really known as a thing. He got covid March 2020 in that first bad wave of NYC cases and was sick for a month. After that he said he couldn't exercise without pain in his lungs for maybe 9-12 months. But then he got over it, and only started calling it long covid retroactively.
I do wonder if especially those early strains were causing some sort of lasting lung damage, which led researchers to say "hey maybe we should study this!" And that led to where we are now. Everyone who is prone to munching or melodrama or wants to be able to claim disability as an intersectional identity can claim long covid. But because of my friend's case, before it even had a name, I always assumed there was something more legitimate about it. But wow, turns out there really is not! Just another excuse to claim POTS.

Edit: pressed send too early yet again

It seems that the early COVID strains did give people permanent or semi-permanent lung and heart problems (anecdotally I know an otherwise healthy male who got heart damage from COVID) but it really doesn’t seem like that’s what any of this “long COVID” stuff is about. It seems more similar to the equally fake “chronic Lyme” where there’s no evidence of infection and the symptoms are just “I don’t feel good most of the time,” which could be something psychosomatic (or an ED which is what I suspect a lot of these munchie girls are covering for).
Post-viral infection is common with diseases in general. The OG strains of Covid-19 were also going to be more intense than later strains since they were that different to what the immune system usually experienced.

Don't have studies on hand, but if anyone remembers the 2003 SARS pandemic, there were cases of people from the first waves that experienced lung problems for years afterwards. It was often referred to as Post Sars Syndrome. Even then, most of them recovered (often completely) within five years post-infection.

So I can believe there were people that got fucked up by Covid and still struggle with complications to this day. I can also believe that many of the people with those symptoms will eventually recover. The amount of people suffering from it and the causes/effects, however, have been grossly exaggerated. Especially once you get to blaming Long Covid on your self-diagnosed dementia and tooth decay.
 
Ostatnio edytowane:
We should have a long covid thread. While some are munchies, many are true believers and the community is more like a cult than anything. Sending death threats to doctors for recommending light exercise is insane.

In 2018, two parents in southern Sweden killed their daughters and themselves after the girls were diagnosed with chronic fatigue. They felt there was no way out, that ME had robbed their daughters (and them) of any quality of life and there was no hope of recovery. It’s an isolated case but just knowing about it always makes me nervous when I hear the long covid crowd talk about how no treatments work, they just have to be allowed to bedrot in perpetuity until someone invents a magic pill that fixes everything. I wonder if the parents of those girls spent time in these types of pessimistic long covid/ME groups.
 
We should have a long covid thread. While some are munchies, many are true believers and the community is more like a cult than anything. Sending death threats to doctors for recommending light exercise is insane.
Absolutely, ME/CFS is such a bullshit lazy condition i am just absolutely tired of dealing with it, genuinely nothing makes me instantly hate someone more then hearing "they have ME/CFS or FND" their all lazy shits with partners and poor family members that are struggling to deal with their constant antics but also enable their lazy behaviour, my heart truly goes out to anyone who has to deal with them 24/7, i can barely stand a shift with such lazy shits that expect me to be their mummy.

I'll believe ME/CFS or FND are real conditions when i see any study showing it actually exists outside of the most luxurious first world nations that can afford to keep these malingers alive on endless welfare.

Baseline (CPET-1) aerobic capacity was similar and low in these groups of ME/CFS and inactive controls, although it was only ME/CFS that experienced a notable reduction in peak O2 on CPET-2. However, it is the relevance of a lower baseline gas exchange threshold (VAT) that underscores the challenge of those with ME/CFS to accomplish daily activities without exceeding the VAT level of energy production and exacerbating illness symptoms. In addition to an array of illness symptoms that comprise the post-exertional response in ME/CFS, the reduction in VAT effectively shrinks the ‘energy envelope’ further reducing tolerance of energy-demanding activities. These results implicate oxygen consumption at VAT, or a shift in energy production increasingly to anaerobic processes, to be central in the metabolic dysfunction of ME/CFS [180]. Similarly, these same findings in ME/CFS extended to the case–control pairs matched for sex, age, and peak O2 indicating that a low aerobic capacity does not explain the deleterious impact of exertion intolerance in ME/CFS. Ventilatory dysfunction was another prominent feature of ME/CFS in both the total group and matched-pairs cohort, with ventilatory inefficiency emerging particularly at the VAT level of exertion. Applying measures of peak O2, O2@VAT, and /CO2 to established impairment standards revealed that for ME/CFS; 1) severity of impairment was worse based on results from CPET-2 compared to CPET-1, 2) severity of impairment was worse in ME/CFS compared to controls, even in ME/CFS matched for sex, age, and peak O2, and 3) an alarming proportion of inactive control subjects met impairment standards based on these physiological indices. Because post-exertional malaise is a hallmark symptom of ME/CFS, assessing severity of impairment must account for the diminished energy producing capacity due to PEM.

Note that the "notable reduction in peak O2 on CPET-2" was only a median change for the ME/CFS group of -5.1% compared to -2% in controls, so once again literally nothing, Post excursion malaise is evidently bullshit as you can see below.

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Source of chart

For any of you who love to read research papers, i can't more highly recommend the pubpeer plugin which is a great way to highlight when an article is full of shit but sadly pubpeer is also full of a bunch of losers who still think ME/CFS is actually real. If ur interested there still coping over the PACE trial from 2011, which definitively proved that yes, graduated exercise is safe and effective for treating ME/CFS big shock i know, the cure isn't actually being a lazy shit all day 😲. The full Pubpeer PACE cope is here | Archive

Controversies surrounding myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS) diagnosis and management (Geraghty, 2017; Geraghty and Esmail, 2016) have affected clinical practice and public perceptions and have led to disagreements between doctors and patients (Campion, 2016). There is still a lack of understanding and recognition of ME/CFS among many general practitioners (GPs) (Horton et al., 2010).

One of the main issues has been the absence of established diagnostic biomarkers and the reliance on diagnostic criteria (with over 20 proposed to date) largely based on clinical symptoms for diagnosis and research purposes. This has been problematic, especially when such criteria have been broad (Jason et al., 2014; Morris and Maes, 2013) and have not stratified cases into sub-groups. The challenge presented by diagnosis misclassification, which results in ‘false positives’ (or ‘spurious’ cases) is evident when prevalence rates of ME/CFS using different criteria are compared. A systematic review showed a greater than 100-fold variation in disease prevalence across studies (Brurberg et al., 2014), ranging from 0.1 per cent (Nacul et al., 2011) using the Canadian Consensus Criteria (Carruthers et al., 2003), a relatively specific classification which is considered by many to most closely represent ‘genuine’ ME/CFS cases, to 3.7 and 7.6 per cent in a study using the Oxford and Australian definitions, respectively (Lindal et al., 2002).

Even if we assume differences in methodology and geographical variations in prevalence, it is clear that rates are influenced markedly by the diagnostic criteria used. Brurberg et al. (2014) also showed that the Oxford criteria (Sharpe et al., 2015) yielded the highest median prevalence across studies, 1.5 per cent, 15 times greater than that obtained using the Canadian criteria, albeit in different populations. If it is assumed that the Oxford criteria always capture Canadian-positive cases, then, based on the above figures, we expect that of a sample of 15 cases selected using the Oxford criteria, 14 will not meet the Canadian criteria. Therefore, if Oxford-positive cases are used to test a hypothesis related to a specific pathophysiological process observed in Canadian-positive cases, this could lead to the selection of 14 non-cases (false positives) for every 15 recruited; an unacceptable level of misclassification.

Of every ME/CFS article i've ever read this by far has been the most grounded that highlights many of the major issues with ME/CFS research, principally the diagnostic criteria which unsurprisingly is the most lax in Australia and the UK. "A systematic review showed a greater than 100-fold variation in disease prevalence across studies" genuinely what other condition is even similar to this???

(I'm sorry for the formatting it got all messed up copying and sadly this isn't a publicly available article but i have attached a PDF of it you can read if this is too illegible)

Method Procedure

Eight research assistants from Enugu were recruited. All assistants were proficient in Englishand the Igbo language. Training of research assis-tants occurred in several phases. First, the assistantscompleted the ‘Human Participant Training’ offeredby the US National Institute of Health. During thesecond phase, all research assistants were familiar-ized with the questionnaire and procedures. Thisensured that the assistants understood the technicalterms and medical concepts in the survey so theywere able to explain the terms and concepts to theparticipants. Regular meetings were held with theassistants during data collection where progress andissues were discussed and resolved.All adults above 18 years of age within the sam-pled area were eligible to participate in the survey,while those that were under 18 years of age wereexcluded from the study. Each research assistantbegan sampling on one street, which was randomlyselected, and then proceeded to each house on thestreet where a resident answered the door. Once theentire block of houses was sampled, the researchassistant began the same process at a second street.The survey was translated into Igbo and English,the two major languages spoken by Enugu resi-dents. Respondents were told that their answers tothe questions would be kept confidential. Mostefforts to contact the respondents occurred in theevenings when more respondents were available intheir homes. In 98 percent of households, theresearch assistant provided directions for complet-ing the questionnaire and then left the questionnairewith the respondent and returned at a scheduledtime to pick up the questionnaire. Only 2 percent ofrespondents requested to fill out the survey whilethe interviewer was in the home.

Seven of the 17 (41%) individuals who screenedpositive for CFS-like illness and five of five (100%)individuals randomly selected from 1057 screenednegative participants at phase one agreed to com-plete phase two. These participants in the CFS-likegroup and a non CFS-like control group completeda psychiatric and medical evaluation. After fillingout a Human Subjects Consent Form, the SCID wasadministered by a trained master’s level clinician.This was followed by a complete medical examina-tion. The examining physician conducted a detailedmedical evaluation at Annunciation Hospital Enugu,Nigeria to rule out exclusionary medical conditionscausing the fatigue. A tender point examination wasused to examine for fibromyalgia. Non-medicallyexplained chronic fatigue was defined as a chronicfatigue for which no medical explanation could befound. None of the participants had fibromyalgia.The participants completed the laboratory examina-tion, which included a chemistry screen (glucose,calcium, electrolytes, uric acid and liver and renalfunction tests), complete blood cell counts, thyrox-ine, thyrotropin, erythrocyte sedimentation rate,arthritic profile, hepatitis B surface antigen, humanimmunodeficiency virus screen, malaria parasites,typhoid screen and urinalysis. Three physiciansreviewed the data on these 12 persons, and thosewho met the Fukuda et al. (1994) CFS definitionwere classified as having CFS. Three of the sevenCFS-like group received a final diagnosis of CFSJOURNAL OF HEALTH PSYCHOLOGY 12(3)466while none of the five screened negative met the CFS criteria.

Pediatric prevalence rates
The prevalence of chronic fatigue was determinedfrom parents’ reports of their children or teenagershaving constantly or repeatedly during the past sixmonths a lack of energy or missing activities due tobeing too tired or sick. Thirty-seven cases out of atotal of 249 reports completed by parents indicatedchronic fatigue, yielding a chronic fatigue prevalencerate of 15,000 cases per 100,000 (15%). Of these 37cases, three individuals had at least four additionalcriteria symptoms (out of eight Fukuda et al. symp-toms and four additional symptoms mentioned in themethods section). Defining CFS-like illness as atleast six months of lack of energy or missing activitybecause of tiredness or sickness, and the presence offour or more criteria symptoms, the prevalence of CFS-like illness is 2400 cases per 100,000 (2.4%)

Discussion

The present study reports for the first time rates ofCFS in a community-based sample in a developingcountry. Whereas a 0.68 percent CFS adult prevalencerate was noted in this study, two community-basedCFS epidemiologic studies in the USA found preva-lence rates of 0.42 percent (Jason et al., 1999) and0.24 percent (Reyes et al., 2003). The slightly higherCFS rates in Nigeria might be due to the fact thatpoverty and malnourishment, which occur more fre-quently in developing countries, increase a person’srisk of having health problems (Singer & Clair, 2003;Whiteside & Friberg, 1998). Other factors that mighthave contributed to slightly higher rates of CFSinclude lack of access to healthcare resources, lack ofadequate nutrition and higher prevalence of a varietyof other medical illnesses (Patel et al., 2005). In termsof participants’ attributions, dominant causes ofNJOKU ET AL.: THE PREVALENCE OF CFS IN NIGERIA469Table 3. Percentage of symptomsSymptom Chronic fatigue CFS-like CFS Sig.Fatigue 100.00 100.00 100.0Headaches+ 25.2a 92.9a 66.7 **Muscle pain+ 18.4a 57.1a 66.7 **Unrefreshing sleep+ 24.3a 78.6a 66.7 **Post-exertional malaise+ 19.4a 85.7a 66.7 **Impaired memory & 17.5a 71.4a 66.7 **concentration+Fever & chills 17.5 a 85.7a 66.7 **Multiple joint pain+ 10.0a 64.3a 66.7 **Muscle weakness 19.4 a 58.8a 66.7 **Sore throat+ 11.7a 42.9a 33.3 **Sensitivity to alcohol 8.7 a 42.9a 0 **Nausea 14.6 a 64.3a 0 *Tender/sore lymph nodes+ 7.8a 28.6a 0 *+ Fukuda et al. (1994) symptomsComparisons were between CF and CFS-like groups. CFS group was too small to be includeda Indicate groups that are significantly different for each symptom** = significant at 0.01 level; * = significant at 0.05 levelfatigue were ‘overwork, not having enough money tocare for family, stress, sickness, malaria/typhoid, lackof money and lack of job, family problem, lack ofhealthcare, and health condition’.Adult rates of chronic fatigue were also higher inthis study than in the two US community-based stud-ies (Jason et al., 1999; Reyes et al., 2003). In thisNigerian sample, the rate of chronic fatigue was 9.5percent, whereas the rates in the US studies were 4.2percent (Jason et al., 1999) and 4.9 percent (Reyeset al., 2003). The higher rate of chronic fatigue foundin this Nigerian sample may be due to the higherprevalence of fatiguing illnesses such as malaria andtyphoid. This pattern is consistent with a multi-national study conducted by Skapinakis et al. (2003),which found that individuals from less developedcountries such as Nigeria, in contrast to more devel-oped countries, reported higher rates of fatigue tophysicians. Poverty, lack of proper nutrition (Jasonet al., 1999; Patel et al., 2005), and other environ-mental conditions (e.g. lack of jobs, and inflation)might make inhabitants of developing countries morevulnerable to persistent fatiguing illnesses.In the present study, the Igbos reported greaterfatigue severity than other ethnic groups. It is possi-ble that socio-political factors such as unequal dis-tribution of basic amenities may play a significantrole in the Igbos’ experience of fatigue. Since 1967when the Nigerian civil war began, the Igbos havehad a strained relationship with the Yorubas andHausas. The stress of needing to fight for theirrights, and lack of access to basic amenities, mayhave contributed to more severe fatigue experiencedby the Igbos. However, participants of the Igbo eth-nic group attributed their chronic fatigue to factorssuch as ‘stress, hard work, lack of healthcare, lackof funds and family problems’.In the current Nigerian study, women did not sig-nificantly differ from men in any of the fatiguegroups examined. While the three individuals iden-tified with CFS were all women, and this does cor-roborate findings in developed countries (Jason et al.,1999; Reyes et al., 2003), the small sample size lim-its any firm conclusions regarding gender. In addition,women and men did not differ on fatigue severity.This is in contrast to studies in other countries thathave found that women experienced greater fatigueseverity than men (Jason et al., 1999; Reyes et al.,2003; Taylor et al., 2003).

Fatigue severity was highest among individualsin the 40 to 49 years age range and lowest in the 18to 29 years age range. In the Nigerian context,younger individuals have less pressure to providefor family needs. By age 40 to 49, Nigerians areexpected to contribute to the financial well-being oftheir immediate and extended family. With thisadditional obligation, the older individuals may bemore vulnerable to fatigue. This finding is consis-tent with other studies that have found that olderindividuals are at more risk for fatigue (Jason et al.,1999; Reyes et al., 2003).Educational level did not impact rates of fatigueand its severity among this Nigerian sample. This isin contrast to other research that has found that lesseducation is associated with higher levels of fatigue(Bierl et al., 2004; Jason et al., 2000; Patel et al.,2005). It is possible that in a country such asNigeria, where many individuals encounter unem-ployment, inadequate amenities and access tohealthcare, education may not play a significant rolein the experience of fatigue.Regarding occupation, unskilled workersreported higher rates of chronic fatigue than skilledworkers. Other researchers have also found thatindividuals working in unskilled jobs are at greaterrisk for having fatiguing illnesses (Jason et al.,1999; Lloyd et al., 1990). These findings might bedue to unskilled workers being required to workmore hours, being compensated less, experiencingmore economic difficulties and ultimately havingfewer resources to buffer the effect of stress.Psychological distress increased progressivelyamong the four fatigue groups. Psychological dis-tress was also a significant predictor of fatigue sever-ity. Other studies have found an association betweenfatigue syndromes and psychological distress(Pawlikowska et al., 1994; Wessely, Chalder, Hirsch,Wallace, & Wright, 1996). Some researchers havesuggested that psychological distress may be a reac-tion to this chronic illness and, therefore, a secondarydiagnosis. Others consider that the overlapping cri-teria for chronic fatigue and psychological disordersmay contribute to the association between fatigueseverity and psychological distress (Cope, Mann,Pelosi, & David, 1996; Skapinakis, Lewis, & Meltzer,2000).PediatricThe prevalence of CFS-like illness for the pediatricsample in Nigeria was slightly higher than the ratesfound in other pediatric studies. Whereas a 2.4 per-cent CFS-like prevalence rate was noted in thisNigerian sample, two community-based CFS-likepediatric studies in the USA found prevalence ratesJOURNAL OF HEALTH PSYCHOLOGY 12(3)470of 0.3 percent (Jones, Nisenbaum, Solomon, Reyes,& Reeves, 2004) and 2.05 percent (Jordan et al.,2000). This pediatric Nigerian CFS-like rate ishigher than the CFS-like rate found among theNigerian adult sample (1.3%). It is to be noted thatboth the Nigerian pediatric and Jordan et al. (2000)CFS-like rates are based on a symptom checklistthat included four symptoms in addition to the eightFukuda et al. (1994) minor CFS symptoms.Rate of chronic fatigue was higher among thisNigerian pediatric sample (12.4%) than in the twoUS community-based studies (1.3%, Jones et al.,2004; 4.4%, Jordan et al., 2000). The pediatricchronic fatigue rate (12.4%) was higher than the ratefound among the adult sample (9.5%). It is possiblethat the higher chronic fatigue rates in Nigerian chil-dren were due to malnourishment, which might leadto greater risks for health problems. Studies indicatethat 30.7 percent of children in Nigeria are malnour-ished and more than 50 percent of all childhooddeaths have malnutrition as the underlying cause(World Bank Group, 2005; US Agency forInternational Development (USAID), 2002).

Gender was not a significant factor among thepediatric sample. Some studies have found that girlsreport chronic fatigue more often than boys(Farmer, Fowler, Scourfield, & Thapar, 2004; Viner& Hotopf, 2004), while others such as Jones et al.(2004) and Jordan et al. (2000) found that girls didnot differ from boys in rates of chronic fatigue. It ispossible that factors such as malnutrition and otherillnesses experienced by both genders in Nigeriamake them equally susceptible to chronic fatigue.The present study found that children zero to sixyears of age were reported by parents as experienc-ing more chronic fatigue than those of seven to12and 13 to18 age ranges. Other studies have foundthat older children and adolescents are at higher riskfor chronic fatigue (Chalder, Goodman, Wessely,Hotopf, & Meltzer, 2003; Dobbins et al., 1997). Thedifferences in findings may be explained by theimpact of malnourishment and childhood diseasessuch as malaria, diarrhea, acute respiratory infec-tion and vaccine-preventable diseases in Nigeriaand children aged zero to five years are more at riskfor these illnesses, which are associated with severefatigue (USAID, 2002).Overall, this study shows that fatigue and CFS arenot solely illnesses that affect individuals in devel-oped countries but rather are illnesses that occur inboth developed and developing countries. As thisis the first community-based CFS prevalence studyin a developing country, the findings need to bereplicated in other countries before any firm conclu-sions can be made about the rates of CFS in devel-oping countries. Also, the small sample size limitsthe generalizations that can be made. For example,the CFS group was not included in all demographicanalyses because of small sample size. In addition,the Igbos were overrepresented in this sample andtherefore the ethnic differences found should beinterpreted with caution. Future research with largersamples is needed to prospectively follow-up theparticipants over time to estimate the natural historyof CFS, and determine the incidence of CFS.Community-based studies are needed to betterunderstand the onset, prognosis, risk factors andsymptom types among samples in both developedand developing countries (Jason et al., 2005–2006).​
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I find this study quite interesting, however the study is full of several severe confounding variables, firstly this study was nothing more then a survey with only 7 individuals who screened positive for CFS actually selected to undergo medical testing to confirm a diagnosis, with only 3 of that 7 receiving a confirmed diagnosis of CFS. But by far the biggest confounding variable is the inability to separate ME/CFS from malaria, malnutrition and other conditions endemic to Nigeria that cause fatigue.

Overall this study was done with more academic integrity then most modern ME/CFS studies which grasp at the most asinine straws for proof.

Chronic Fatigue Syndrome (CFS) is characterized by unexplained fatigue that lasts for at least 6 months alongside a constellation of other symptoms. CFS was historically thought to be most common among White women of higher socio-economic status.

Results
Meta-analysis showed that compared with the White American majority, African Americans and Native Americans have a higher risk of CFS [Odds Ratio (OR) 2.95, 95% confidence interval (CI): 0.69–10.4; OR = 11.5, CI: 1.1–56.4, respectively] and CF (OR = 1.56, CI: 1.03–2.24; OR = 3.28, CI: 1.63–5.88, respectively). Minority ethnic groups with CF and CFS experience more severe symptoms and may be more likely to use religion, denial and behavioural disengagement to cope with their condition compared with the White majority.
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Everything so far is projection on Ace's part, and her belief that autistic people will always have autistic children, no exception. Although I agree with others that while Ace is very
Yeah I know a diagnosed autist who married a normal woman and none of their kids have the tism or any kind of neurological problems. He's great with babies as he said their needs are more like a checklist he can go through and it makes sense. Toddlers make no sense and he always struggled with those years. Even if Ace was a proper autist, it wouldn't excuse the shit she's done to her son since conception.

Does Ace's baby daddy have any SM presence? I know he works and is the primary caregiver of a malicious retard and baby but that's about it.
 
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