What a dread disease dementia is. At its worst dementia can result in the total loss of one’s personality: loved ones don’t register, reasoning is gone, even simple matters such as dressing and bathing require assistance. Even in its more moderate forms dementia can be all-encompassing causing memory loss, problems doing ordinary tasks, mood swings and more.
Could fibro-fog be a prelude to dementia?
Dementia is a broad term used to refer to several conditions that cause a severe enough reduction in the ability to think so as to impact one’s daily living. If you live long enough, you have a very good chance of developing dementia. While just 1-2% of people aged 65 have dementia, the risk of developing it after that doubles roughly every five years. If you make it to 85 your risk of developing dementia is somewhere between 30-50%. For those of us with aging parents, the costs that dementia imposes can become painfully clear.
Fibromyalgia, of course poses its own unique costs. Those costs were made clear in the 2017 study on FM and dementia.
“Fibromyalgia is a widespread musculoskeletal pain disorder associated with chronic fatigue, emotional distresses, and sleep disturbance. Previous studies revealed that fibromyalgia is associated with the increased risk of irritable bowel syndrome, dry eye syndromes, depression, suicide rates, stroke, and coronary artery diseases.”
They left out migraine (55% of FM patients met the criteria in one study), and chronic fatigue syndrome, but never mind; fibromyalgia is “widespread” and is associated with a boatload of other conditions.
The pain, fatigue and sleep issues, of course, can be terrible but the problems don’t stop there. There’s also the “fibro-fog”; the short-term concentration and word-finding problems, the problems with multi-tasking, and the general fogginess where clarity used to reign. FM, then, is a kind of all-inclusive disease; it causes pain, fatigue, sleep issues, throws people off emotionally, and causes problems with cognition.
Diseases don’t ordinarily cause cognitive issues. Look up diseases that cause cognitive problems and you’ll find mostly brain disorders like autism, stroke, Parkinson’s disease, Huntington’s disease, brain injuries, multiple sclerosis (brain-fog), cancer (chemo-brain), chronic fatigue syndrome (brain-fog) and, of course, Alzheimer’s. The cognitive issues in FM are pretty mild compared with the issues found in some of these diseases, but they obviously raise a concern: could fibro-fog be a prelude to something worse? Do people with FM have to be concerned with early-onset dementia as well?
Distraction or Dementia?
A 94-person 2016 study suggested not. The study suggested that the cognitive issues in FM are different in kind from those found in Alzheimer’s. It found that the “encoding mechanisms” needed to transfer personal events into memory that are broken in Alzheimer’s were, for the most part, functioning in fibromyalgia. FM patients may have cognitive problems but they didn’t experience the “episodic memory losses” or progressive cognitive decline seen in Alzheimer’s.
The major cognitive problem in FM, the authors said, comes from their brains’ inability to correctly filter out irrelevant data. Several studies suggests that fibromyalgia patients brains keep focusing on innocuous stimuli that healthy controls are able to quickly assess and then stop paying attention to. A correlation between reduced pain inhibition and cognitive issues also suggests that being in pain causes cognitive issues. The cognitive findings suggest that even ordinary tasks such as dressing and personal hygiene take longer, are more difficult, and require more mental thought for people with fibromyalgia.
But what about dementia? The 2016 study suggested that when faced with distractions, FM patients actually do have the problems “encoding” personal memories. When placed in quiet, distraction-free environments, however, they do just fine. The authors concluded that the cognitive problems in FM relate to problems with cognitive distraction, rather than an Alzheimer’s-like process. They hoped that their findings “allay the worries of many with fibromyalgia who fear that fibro-fog is the start of a dementing process.”
Distraction and Possibly Dementia
Not so fast, though. This year, an 165,000 person Taiwanese study, the Fibromyalgia and Risk of Dementia -A Nationwide, Population-based, Cohort study, concluded differently. The study followed 41,000 FM patients and 124,000 healthy controls over 50 years old for ten years.
After adjusting for confounding factors (gender, age, monthly income, urbanization level, geographic region, comorbidities) the study concluded that FM is indeed associated with a significantly increased risk (hazard ratio- 2.7 x’s) of dementia, and not just one type of dementia, either. All types of dementia were increased in FM patients as they aged with Alzheimer’s (3.35-fold increase) and non-vascular dementia (3.14-fold increase) showing the highest increases. FM patients suffering with depression, epilepsy, Parkinson’s disease, stroke, TBI, or liver issues had a further increased risk of dementia. Interestingly, the rate of depression in the FM patients in this study was quite low.
(Hazard ratio is associated with an increased hazard of an event occurring. The 2.77 HR of FM means that FM patients over 50 were 2.77 times more likely to be diagnosed with dementia than the healthy controls).
It should be noted that this study does not suggest that dementia is imminent or even common in people over 60 who have fibromyalgia; the rate of dementia is simply increased. Just over 4% of the FM patients developed dementia in the study – as opposed to the 1.2% of the healthy controls.
It’s not clear why dementia is increased in FM, but citing the role that inflammation may play in other dementia-prone diseases, the authors suggested that systemic and/or brain inflammation might be the culprit.
Neuroinflammation is certainly present in dementia but whether it’s causing it is unclear. A 2013 review study, which reported that anti-inflammatory drug trials have not been effective in Alzheimer’s, discounted the idea that inflammation is a key player in the disease.
A more recent review, however, suggested that the very idea of what constitutes inflammation in Alzheimer’s needs to be re-assessed and that targeting different parts of the immune system may be helpful. (A similar re-assessment regarding inflammation may be occurring in FM and chronic fatigue syndrome (ME/CFS)).
Stopping Dementia?
That more recent review suggests that if you’re worried about developing dementia, finding ways to reduce inflammation could help. A UCLA study employing a multidimensional approach called metabolic enhancement for neurodegeneration (MEND) which involved reducing inflammation was able to reverse Alzheimer’s symptoms in all of the participants.
The idea was to “target multiple pathways simultaneously in order to effect an improvement in symptoms and pathophysiology.” The protocol involved low glycemic/carbohydrate/grain diets, short fasts, stress reduction (yoga), exercise, brain stimulation, and supplements to reduce inflammation, enhance cognition, improve mitochondrial functioning, improve sleep, etc.
The study was very small (n=10) and bigger studies will be needed to validate the results, but they were astonishing for such a treatment resistant disease. One man’s cognitive test score increased from 3rd percentile to 84th percentile (3 standard deviations). Other participants scores increased from the 1st to the 50th percentile, from the 13th percentile to the 79th percentile, and from the 24th to the 74th percentile. One person went from considerably below average to considerably above average in many of his cognitive tests. An expanded study is reportedly underway.
Cognitive Resources
- Science Daily has a section devoted to the latest in Alzheimer’s/dementia findings
- Sign up for updates from the Alzheimer’s organization
- Take short home cognitive tests for dementia – the Mini-cog test, the General Practitioner Assessment of Cognition, Differentiating Aging from Dementia, Questionnaire on Cognitive Decline in the Elderly
Yes, I could have told them that…..I watched both parents die with forms of dementia. Both had FMS labels. I have fears of “getting” this too. I also have the FMS label.
Having had a Neuro Quant MRI and knowing I have brain swelling and compression due to that – in the memory area – I’m certain inflammation is playing a part. Docs addressing CIRS and trying to treat mold and biotoxins – with a genetic inability to detox, properly. Hoping this will help. I’m already seeing improvement in my brain fog.
Issie
You and your parents having FMS and dementia is exactly like mine! My father died from Alzheimer’s and my mother is still alive but has other major issues. MS and Lupus are also problems in my immediate family. I take Lyrica but I noticed the brain fog two years. Makes me mad because I used to multi-task and was a very quick thinker with no memory problems.
http://aperiomics.com/ I just noticed this new testing company and didn’t know if anyone had seen this or had an opinion on it. Seems this may be of help to many.
I’ve been interested in Dale Bredesen’s work on Alzheimer’s for a while, especially since he has such a strong interest in toxic mold. But I wasn’t sure exactly what treatments he was using, since in his previous talks he had suggested that what he was doing was really complex and could vary from person to person.
So I was interested to read the details in his new book, “The End of Alzheimer’s.”
As it turns out, everything that he brings up are things that I already was familiar with – because they all are things that people seem to be successful with in terms of treating ME/CFS, fibro, toxic mold illness, chronic Lyme, etc.
Which of course does make some sense since he is suggesting that Alzheimer’s is a disease of inflammation, but still is very interesting to read.
This is actually the first document that I have read that I feel that I can hand to someone with ME/CFS and say, just read this and you will understand what the most successful approach to addressing this disease seems to be at this point.
https://www.amazon.com/End-Alzheimers-Program-Prevent-Cognitive-ebook/dp/B01M28ROCU/
Dr. Bredesen does suggest that the type of Alzheimer’s that he believes is caused directly by toxic exposures (including toxic mold exposures) is especially difficult to treat. But I suspect that is because he has not been successful in getting those patients away from mold exposures.
At best, he is suggesting Dr. Ritchie Shoemaker’s avoidance approach, which is not rigorous enough to help most ME/CFS patients very much. And he is not even being very insistent on their following Shoemaker’s approach. (Like most physicians who start out looking at mold, he seems to think that most people just are plain not going to be willing to put a lot of effort and money into avoiding mold – apparently they just don’t understand how bad these inflammatory diseases can be and how desperate people are to be able to regain or retain their health with regard to them.)
So I don’t see what he is suggesting as a substitute for mold avoidance. As an adjunct treatment though, I think that what he is doing is really useful and important.
He might be an interesting person to interview for this blog, actually, Cort.
Best,
Lisa Petrison, Ph.D.
Executive Director
Paradigm Change
It may be that there is an overlap in the cohort of the populations who are vulnerable to FM and dementia, without there necessarily being a connection “from” FM “to” dementia.
Yes, correlation is not causation. I’ve had severe FM for 30 years and, at 69, no cognitive problems. Have never had fibro fog, just pain. If you want to help research, take Dr. Bruce Gillis’ FM/a test, get your whole genome sequenced by him, and into his planned 250k FM patient database, and hopefully be cured by the vaccine being approved by FDA, hopefully soon. His hypothesis of brain inflammation causing cytokines release is a hypothesis but has some background and he is sincere, smart, and committed. I do al I can (unpaid) to further this company.
hi,
where can I find the FM/test? I have had the fibro fog.
Nancy
This is Scary
Other studies tell us that loneliness puts us at greater risk for developing dementia. And who with serious or even moderately serious ME/CFS isn’t lonely?
Boy is that ever true. Isolation has real costs. More like cheese and stuff like that don’t you think
I might as well move to the North Pole. I’m about as isolated as someone who lives there! I know loneliness all too well!
I very much dislike the idea of having increased chances for having dementia as a plus-disease too. So the study does not make me feel all to happy.
On the bright side, controlling the rising cost of aging is one of the few longterm projects most countries have in common. The cost of age related dementia and Alzheimer takes quite a chunk out of those projected costs.
If this studies results would to be confirmed this could create a sense of urgency to finally fund FM and ME research in a big way. It would become even more urgent if dementia prevalence at ages 65, 70, 75 would be remarkably increased too. That is where the real costs are.
In countries with public health insurance, cost benefits to the government are plain clear. In countries with private health insurance those companies might recalculate their numbers and no longer conclude that the fake CBT/GET therapy for both diseases is the cheapest “solution” to these companies. While very few companies think long term, most insurance companies do re-insure themselves with another bigger company. And those will most likely see costs/risks if they are there as it allows them to charge higher rates.
Could this bad news be turned into a new funding angle?
Nice idea. I hope we see more studies although I kind of dread what the findings are as we get older and older.
I think the same applies for pain; pain is such a problem for so many that hopefully some advance elsewhere will work for FM.
Hi Cort,
You have treated this subject very well.
I want to remind you of the role of acetylcholine in most or all of the main processes difficult for Fibro and cfs patients.
As I mentioned before, one particular cholinergic receptor type seems to me to link the main fm/cfs dysfunctions: Nicotinic a7 receptors.
At first all I had heard of was that our bodies’ acetylcholine production starts a downward trend after 40 years old. So the news said if we can boost production then we can retain a sharper mind and better memory formation and recall.
So thats why when I learned that acetylcholine not only creates a long-term electrical potentiation of memory cells but also creates a potential in skeletal muscle which must be maintained through rapid release and reuptake of acetylcholine for, say, carrying one end of a couch, I sought further commonalities.
And it turns out that a7 nicotinic receptors are present on the eyeball outer surface, as well as on the retina. I am convinced that my friend who has fibro and cfs and cant tolerate bright light nor drive in the dark, and who has dry eyes as well, has retinopathy related to blood vessels. And while dry eyes feel dry, I believe they are not. The surface is irritated– i would guess from sfn. The rest of the eye uses muscarinic receptors, so its seems more than a coincidence that the “dry” outside and the oversensitive retina both rely on a7 nicotinic.
Add that to skeletal muscle flexion, executive function, triggering pain relief in the analgesic system (descendending), and a7 nicotinics being crucial in at least 7 areas of the brain involved in the limbic system — which we credit with emotions— and we seem to have a uniquely a7 nAChR problem.
As an aside: we consider this (cfs) Systemic Exertion Intolerance Disease to be crosslinked. Body fatigue brings brain fatigue often. Brain fatigue can lead to tears. The one uniting factor is nicotinic cholinergic function.
If I didnt say it before, all the main systems highlighted in fm/cfs are nicotinic receptor dependent, including endothelial cells, and dont forget microvessels in the kidneys, lungs and liver. None of them are muscarinic. By the same token, there arent any other uses of nAChR except the ones dysfunctioning. No a7s are spared, and no muscarinic receptor is implicated. However the nerves on the coating of the eye heavily influence the muscarinic action of the iris, and tear production.
That realzation
was a eureka moment because it tells us what huge system is NOT at issue: muscarinic receptors. Eliminating possibilities is good.
Its a chicken and egg scenario, though — i cant be sure without scientific blood analysis whether there is too little acetylcholine, or too few remaining receptors for it.
There certainly is an autoantibody against cholinergic receptors in Myasthenia Gravis, which is like SEID, except with a quick recovery, not PEM. This antibody can be found in blood tests.
Im mostly repeating this because you brought in dry eyes and retinopathy. No other part of the eye except those two parts use a7 nAChRs.
Finally, there is the issue of non-restorative sleep. You did say the wakeful mind is distracted by extraneous activity, interfering with learning . Did yiu know what all happens during REM sleep? One thing is that your brain compares what it already knew to what you encountered today. It will revise knowledge if you got a new piece of the puzzle, but it much about erasing irrelevant data. “Need to know basis !!” If someone said something patently false today, then my brain will either erase the disinformation or add the knowledge that the speaker is not reliable.
But if you cant sleep soundly, can you even do proper memory management? Tomorrow, do you have intellectual baggage still?
Lastly, part of restorative sleep is that the melatonin release damps signals from the body to free up the brain. As you know, the thalamus has a threshhold and a balancing act of “deciding” what your body should act on and what is unimportant . So chronic pain or incorrect temperature can easily keep your brain somewhat more awake. It has been shown that if you stay up 4 hours past bedtime or miss out on 4 hours of sleep, your brain activity (agitation) increases, the fatigue does not decrease it.
Also, the melatonin blocking feature gives your central receptors a holiday. This allows them to reset to normal. But if the stimulation never ends, you are not only half-asleep, not fully, but also your receptors will maintain pain and other noxious nociceptive things. So sleep is central, and part of the cure.
It is acceptable and recoverable to have one poor sleep during flu-induced fever/chills. But it is not sustainable nor recoverable to be constantly under autoimmune attack. And YES you can end up with low cortisol– when you reach adrenal fatigue. My friend did. She got medication to raise it.
You know that cute saying “shop til you drop?” Well stress management by cortisol is *rise til it drops* You need an intervention
Chris
This is a fascinating read, I would love to receive regular e-mails on health from you if that is possible, many thanks, Andrea Taylor
Hi Andrea – checkout the subscribe button on the right hand side of the page.