Are PWME at greater risk of cardiovascular disease & diabetes? If so, what can we do about it?

At yesterday's panel following the screening of Unrest at the London School of Hygiene and Tropical Medicine, Luis Nacul (I think) said that he thought that PWME had a raised risk of cardiovascular disease and diabetes (have I got that right, @Jonathan Edwards?)

If so, is that likely to be merely due to inactivity (in which case there's not a lot we can do about it) or to other things?

I'm unclear as to the cause of these things and am not sure if that's well established.

Can we do anything about the risk?

 

Atherosclerosis perhaps, but its mitigation is easy, Vitamin A, D and K2 in sufficient (but not excessive doses). If your wisdom teeth are not removed or unerupted K2 won't be tolerable to you.
Stroke should also be decreased by the above vitamins
Other forms of heart disease i am not too sure about but genetic may be hard to mitigate by any known means.
K2 concentrates in the liver, brain, pancreas and a few other places so may reduce the risk of diabetes but there is no research testing this that i am aware of.

 

At least one paper has suggested glucose metabolism is impaired in pwME, this could, over the longer term cause issues with insulin resistance, which could lead to type 2 diabetes.

Pretty sure I've seen something else that suggests an increased risk of adult onset type 1 as well.

I have no family history of diabetes, I was not, when diagnosed with type 2, particularly overweight, a couple of stone, nowhere near enough for the extra weight to precipitate diabetes anyway. Normal first line diabetes meds do nothing, positive, to improve my BG levels. When I'm PEM'd my BG is essentially uncontrollable, when I'm not it's fairly easy to control. Keeping my BG low does not alter my baseline or affect my ME in any way ergo my BG is reacting to my ME not the other way around.

No - I can't provide links to any of the papers.

 

Just tagging @Sid.

 

I have some cardiac problems that we still need to investigate. Dr Hyde doesn’t seem too concerned about it. He said I would have problems in 10 years, but that was before we did my 2 day CPET which revealed a lot of problems.

He said not to gain weight because it would increase my cardiac risk. My BMi is within normal range.

 

I'm a skinny type 2 diabetic. My diabetes is worse since becoming inactive after the onset of ME over 6 years ago.

In the past two months I've been experiencing what might be episodes of atrial flutter which I need to get checked out. My feet are often purple due to circulatory problems which I didn't have before ME.

I have the genetic potential for diabetes type 1 and 2 and cardiac issues.

If I didn't have ME and had been able to maintain my highly active pre ME lifestyle then I don't think I would have deteriorated so much physically.

 

Diabetes can also occur due to mitochondrial disease. My fasting blood sugar is always higher when I've over-exerted recently.

 

I have always just assumed this was the case, and that I'd probably die from a cardiovascular event (like many PwMEs, dying doesn't scare me, its living that really freaks me out!!). Tachycardia and heart palpitations are common symptoms for many PwMEs, and my heart rattles away like there's no tomorrow. Inflammation and CVD seem to be really close bedfellows generally. And i have raised levels of C-reactive protein which is an inflammatory marker known to be associated with CVD risk.

My current specialist is probably more interested in my heart than anything else. So if I do get access to some decent treatments for inflammation in the future, it'll probably be thanks to that!

PS No idea about diabetes

 

Sorry to hear that so many are having these additional health problems!

But I wonder if I can steer people back to the topic of the thread... which is, are we at higher risk and if we are, what can we do about it?

 

I don't think there's any evidence of this. I think that the heart palpitations and other issues have nothing to do with the aetiology of regular-person heart disease like atherosclerosis.

 

I understand that pwme are more likely to have hypermobility issues, and that these might be linked to heart valve prolapse- this may just apply to the mitral valve. I'm not sure about that.

Dr Bansal diagnosed me with hypermobility in April this year, and I had a mitral valve prolapse diagnosed about a year ago. I need heart surgery to correct the regurgitation.

The symptoms for this were breathlessness and fatigue ( overlapping symptoms with ME). My gp did not want to refer me to a cardiologist until it could no longer be ignored. I think this is a problem for pwme. Symptoms from other illnesses may be ignored because an assumption is made that the symptoms relate to ME.

I have a vague recollection that at one time, the Nice guidelines even advised that GPs should not refer pwme for more tests because it would reinforce illness beliefs. So our heart issues may be being ignored. I don't know about other heart issues.

 

General health advice encourages engaging in activity to manage or avoid the development of diabetes type 2 and cardio problems.

What I was trying to highlight in my post is that I have the genetic potential for both, already had diabetes and that since ME and the inactivity that comes with it my diabetes is worse and cardio issues have emerged.

In my case I think the inactivity associated with ME put me at higher risk of development/deterioration of these conditions.

Are we at higher risk? I think we are, particularly those of us with genetic potential for these conditions and rendered inactive by ME.

What can we do about it? Well I can't increase my activity level. I can only look to diet and drugs.

 

@AndyPandy

You are right on about this.

My best friend who suffered from M.E passed away last year after an 18 year battle. He predicted he would die soon.

He developed t2 diabetes and autonomic/heart related symptoms. He was just 5 days shy of seeing a cardiologist rec'd by Dr.Chia, but it was too late. He had a genetic predisposition for heart issues. He was 53.

 

So sorry to hear that, @Mij.

 

@AndyPandy
As I understand it, ME brings with it higher risk of hypermobility and heart valve problems. Perhaps pwme should talk to their gp re this. An echo will show up valve problems.
I also remember from the past one of the US ME doctors writing about the extreme amount of rest we need serves the function of protecting us from heart disease. I cannot remember who it was - was it Lerner? Perhaps someone else can remember. I haven't read this point of view recently.

http://www.treatmentcenterforcfs.com/personal_statement/index.html

It was Lerner who wrote about ME and the heart. Have just posted a link. Need to read it myself now.

EDIT: so sorry about your friend @Mij

EDIT 2: Cheney also wrote in this vein.

 

I just tested positive for echovirus 30 from ARUP Labs and have been reading up a bit (as we do with any lead...). It seems that enteroviruses have been implicated in diabetes: http://news.bbc.co.uk/2/hi/health/7926026.stm

There is also a link to myocarditis and pericarditis according to Wikipedia:

 

Autopsy Evidence of Chronic EV Infection in ME Patient Presented by Dr. John Chia at IACFSME Conference October 2016

Poster 13
Chronic enterovirus (EV) infection in a patient with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) – Clinical, Virologic and Pathological Analysis

John Chia, David Wang, Andrew Chia, Rabiha El-Habbal. EV Med Research. Lomita, CA
Objectives: A 23 y/o Caucasian male developed prolonged, recurrent gastrointestinal symptoms, followed by onset of severe ME/CFS (CDC criteria, ICC).

At initial evaluation, Echovirus 11 antibody titer was >1:640 (normal <1:10); IgG and IgM antibody for EBV and HHV6 were negative, CMV IgG was positive. He failed to respond to combination of alpha and gamma interferon; and debilitating symptoms of the stomach and central nervous system were minimally alleviated by SSRI, benzodiazepine and acid-suppressant.

Repeated MRI scans of brain and spinal cords showed normal results. The patient committed suicide 6 years after the onset of symptoms. Brain was harvested and frozen within 24 hours of death for evaluation of chronic viral infection.

Method: Using EV- and dsRNA-specific monoclonal antibody (5D8/1 and J2 mAb), stomach and colon biopsies obtained 5 months after onset of illness were stained for viral capsid protein (VP1) and dsRNA by immunoperoxidase technique. Blood drawn in Paxgene tube 3 years after illness was screened for enterovirus RNA by RT-PCR. ~1 cm3 sample was taken from the ponto-medullary junction (PM), medial temporal lobe (MT), frontal lobe (FL), occipital lobe (OL), cerebellum (CL) and midbrain / hypothalamus area (MB) of brain.
The brain samples were homogenized in 10 ml of serum-free medium. Aliquots were processed for viral cultures. Trizol-LS reagent was used for RNA and protein extraction, as well as other lysis agents.
'
Tris-Glycine and MES gels, wet and semi-dry transfer, then western blot was performed with Ibind (Life technology) using EV-, CMV- and HHV6-specific mAbs, patient’s own serum and control serum samples. Viral culture was performed in WI-38 and BGMK-DAF cell lines. RT-PCR for conserved highly-conserved sequences of 5’ end and 3D polymerase sequence were performed on extracted RNA.

Results: Stomach and colon biopsies stained positive for EV VP1 soon after initial infection documenting the initial viral infection; dsRNA was detected in the stomach biopsies. EV RNA was not detected in blood 3 years after illness.
Initial culture of brain samples did not grow virus; 5’ EV RNA sequence was not detected by RT-PCR. Using 5 D8/1 mAb, western blot revealed 37-42K and 46K protein bands in the brain samples, which corresponded to viral protein and creatine kinase b extracted from infected stomach biopsies, but not in brain biopsy samples taking from patients with brain tuberculoma and lymphoma. 3D pol gene was amplified from the DNase-treated RNA extracted from PM, MT and FL. 5’ RNA sequence was in one of the FL specimens.
'
Conclusion: The analysis of the second brain specimen taken from ME/CFS patient replicated the British findings published in 1994 (Ann. IM). The finding of viral protein and RNA in the brain specimens 6 years after documented acute enterovirus infection of the gastrointestinal tract is consistent with a chronic, persistent infection of the brain causing debilitating symptoms.

'EV is clearly one of the causes of ME/CFS, and antiviral therapy should be developed for chronic EV infection.

John Chia MD, 25332 Narbonne Ave. # 170, Lomita, CA 90717. evmed@sbcglobal.net

 

So very sorry about your friend @Mij

I anticipate that my health will decline at a faster rate due to diabetes and cardio issues exacerbated by the inactivity associated with ME.

 

@AndyPandy

Unsure if you have tried antivirals, but in the link I posted above, Lerner does claim that antivirals improve both cardiac and CFS symptoms. He also claims that rest is essential. I try to keep my heart rate as low as I can helped by a wheelchair. OI stresses the heart when I am upright.

I have just completed 6 months on acyclovir. I have both ME and heart problems diagnosed such that it is difficult to know which causes what symptom. I Incline to thinking that there is beginning to be some improvement so long as I work to avoid PEM.

In the article posted by @Mij , there is a recommendation that antivirals be developed.
Not sure if this is an appropriate treatment for you to think about.

 

I think there is a problem, though I have approached it from the other side, as it were--after 70 very active and healthy years, I developed a "severely stenotic" aortic valve, and had to have surgery. There followed 2 good years, and then at 74 I developed ME. One of my first reads was Paul Cheney's essay "The heart of the matter," which argued that diastolic dysfunction was at the heart of our problems, and the essay was followed up by a couple of his amazing DVDs, based on very detailed echocardiogram work, showing just how we could develop even angina without any stenosis of heart arteries.

Key to his argument was that it takes more metabolic energy to fill the heart than to empty it--calcium channel stuff--and he argued that in effect we all had some degree of heart failure, though not of a kind that cardiologist would recognize. I think this ties in with the recent work on mitochondrial energy defects and metabolic defects.

This understanding ties in with Leonard Jason's paper on the ways in which we most frequently die--heart failure, cancer, and suicide. So I think we all do have some degree of cardiac impairment, and since the heart muscle is densely packed with mitochondria--is almost one giant mitochondrion--we should expect any mito dysfunction to show up in its performance. Whether this will manifest as atherosclerosis or valve impairment are other questions.

I totally sympathize with Binkie4's dilemma--I had trouble trying to distinguish whether difficulties I was having last year were due to heart or ME; this February my 13 year old bioprosthetic aortic valve failed dramatically, and I had emergency surgery-with 2 litres of fluid in my lungs and acute heart failure--but the replacement bioprosthetic valve seem to be functioning well.

This leads to some difficulties, of course--Beta Blockers and statins are both mito disrupters, but the first is necessary protection for a while after heart surgery, and the second is still beloved by most cardiologists, though increasingly under serious criticism. Makes life more difficult...