Dr Cheney on heart function

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Preface - October 2023

In many ways, this page shows some of the thought processes that I had before reaching my "WOW!" moment about mitochondrial failure being the central cause of CFS. See CFS - The Central Cause: Mitochondrial Failure.

Remember that -

  • Chronic fatigue syndrome [‘CFS’] is characterised by poor energy delivery mechanisms.
  • Myalgic-encephalitis [‘ME’] is characterised by poor energy delivery mechanisms AND inflammation.

Poor energy delivery is caused by the wrong diet, poor sleep, mitochondrial failure, and poor adrenal and thyroid function.
Inflammation occurs when the immune system is activated. The immune system is activated in allergy, chronic infection and auto-immunity.
In both CFS and ME there may also be an emotional hole in the energy bucket.

1.The way I treat CFS and ME is now laid out in CFS/ME - my book Diagnosis and Treatment of Chronic Fatigue Syndrome and Myalgic Encephalitis and also on these pages:

2.Where there is infection, my treatment is laid out in My book The Infection Game - life is an arms race and also these pages:

3.Where there is poor thyroid [and adrenal function], my treatment is laid out in My Book - The Underactive Thyroid - Do it yourself because your doctor won't and also these pages:

4.Crucial to all is the Paleo-ketogenic diet and this is laid out in My book - Paleo-Ketogenic: The Why and The How and also these pages:


Dr Paul Cheney had been working with the CFS patients clinically and experimentally for decades and this page is based on many of his ideas. Dr Cheney's observations and ideas helped to pull together many clinical issues which I had also observed and which hitherto were inexplicable to me. Thus I was able to move my thoughts forward, as above, to reach my protocol for the treatment of CFS and ME.

Carol Sieverling and Maryann Spurgin put together this very useful document - A Cardiac Marker for Disability in Myalgic Encephalomyelitis based on Dr Cheney's work.

NOTE - Dr Cheney was a physician of Internal Medicine who was there at the centre of the CFS outbreak in Incline Village, Nevada at Lake Tahoe along with Dr. Daniel Peterson in 1984 to 1987. Later, he moved to North Carolina and shared a medical practice from 1992 to 1995 with Dr. Charles Lapp. He practised medicine in Asheville, North Carolina. Sadly, Dr. Cheney passed away on 10 June, 2021. You can read an obituary here - In Memoriam Dr Paul Cheney - American Myalgic Encephalomyelitis and Chronic Fatigue Syndrome Society based on Dr Cheney's work.

The three stages of chronic fatigue syndrome

Dr Paul Cheney recognises that there are three stages of chronic fatigue syndrome, which are characterised by different immunological and biochemical issues. Chronologically these stages are not completely distinct, each one of them may run into the others. However, if one can identify the stage that you are in, this will have implications for treatment.

  • 1. The acute alarm stage – this follows the original trigger for chronic fatigue, which may be sudden onset following viral exposure or chemical exposure, or maybe of gradual onset over some months or years. This stage is characterised by lots of symptoms which can be anything from acute fever, lymphadenopathy and malaise to headache, irritable bowel, muscle aching, anxiety, sleeplessness or whatever. This stage probably reflects immune over-activity, which might be appropriate in the case of the virus or bacterial infection, inappropriate in the case of allergy and autoimmunity and is accompanied by a heightened stress response with high levels of stress hormones to allow the body to gear up and cope with these increased energetic demands. Chronic work or emotional stress also results in such an alarm reaction.
  • 2. The second exhausted phase is characterised by biochemical and hormonal failures. Nearly always there is foggy brain, can’t think clearly, inability to multitask, inability to learn. We see more exhaustion with poor stamina and delayed fatigue, but the shopping list of symptoms starts to lessen. They may be replaced by chronic background pain and malaise. This is the stage where there are obvious biochemical failures due to exhaustion of micronutrients, toxic stress and poor healing and repair. Typically we see poor mitochondrial function, poor antioxidant status, poor quality of sleep, poor digestion of foods with hypoglycaemia, depression of the hypothalamic pituitary adrenal axis, etc.
  • 3. The third stage of maladaptation. This seems to arise after some years of the above problems. This stage is characterised by relative freedom from the above symptoms so long as one stays strictly within limits. However, this stage is characterised by a very marked push and crash. What this means is that should the sufferer go very slightly above their permitted limits (which may be bed bound), then this has the potential to make them ill for days. What Dr Cheney hypothesises here is that the normal stress response which involves cortisol, thyroid hormones, growth hormones, insulin and so on, has flipped. Normally if the body is stressed, this hormonal response allows us to move up a gear, cope with that stress and then drop back to baseline functioning. In this third maladapted stage the stress hormones seem to have the complete opposite effect. Instead of allowing the sufferer to gear up, they make him crash instead. In order to understand this third stage we need to look a little more closely at the second stage of biochemical failures.

Cheney believes that all these stages result from how the body deals with free radical stress. He calls this the “redox” state. In the first stage to cope with increased demands we greatly increase our output of energy, but this brings free radical stress. It is our ability to deal with this which determines who recovers and who goes on to develop chronic fatigue syndrome.

Implications for Treatment

  • ALARM STAGE - the first stage of chronic fatigue syndrome

This is most often triggered by viral infection so all the recommendations for Viral infections - avoid them and treat them aggressively which should be applied. Any causes (such as chemical poisoning, psychological stress) should be avoided – the problem is that they are often not recognised at the time. Indeed this is a major problem. Good quality sleep is essential since this is when healing and repair takes place daily – many of the above problems are accompanied by insomnia.

  • EXHAUSTED PHASE - the second stage of chronic fatigue syndrome

This is the stage of biochemical and hormonal failures characterised by poor mitochondrial function. Poor mitochondrial function has been clearly demonstrated in the scientific papers I wrote together with Dr John McLaren Howard and Dr Norman Booth, which clearly demonstrates that the degree of disability is directly proportionate to mitochondrial function, which is the energy available to cells. I also see considerable success treating this by addressing all the issues that can result in poor energy supply and this is all detailed in my CFS book with respect to diet, sleep, supplements support, mitochondria, correcting antioxidant status and so on. See CFS/ME - my book Diagnosis and Treatment of Chronic Fatigue Syndrome and Myalgic Encephalitis See also my scientific papers:

Mitochondrial function is closely linked with free radical stress. Mitochondria are a major source of free radicals, and if not handled efficiently, are easily damaged by them. This is why antioxidant status is so important. The balance between producing free radicals and our ability to deal with them is called our “redox” state. This is important because redox state determines how well we deal with acute and chronic infections.

Dr Paul Cheney has also developed a biochemical tool for looking at the energy available to cells. The cellular free energy can be measured in the heart using echocardiography. The heart is the most energetic organ in the body and indeed more than 50% of the heart is made up by mitochondria. Mitochondria make energy in the form of ATP and this ATP is used to pump calcium into the sarcoplasmic reticulum where the muscle fibres are. This it does rather slowly, but when the concentration becomes critical, calcium rushes back and the energy generated by this allows the muscle fibres to contract. If mitochondria go rather slowly it takes longer for this charging up to take place. So the time between the start of atrial charging and mitral valve closing (which is called the isometric volume relaxation time) is a direct reflection of mitochondrial function. The more efficient the mitochondria, the more available cellular free energy and the shorter the IVRT. A normal result could be 75 milliseconds. Heart failure occurs at 150 milliseconds. This test is highly accurate and reproducible within 2%. It allows Dr Cheney to assess within minutes the effect of various stressors on the availability of energy to cells in the heart. It is an instant measure of mitochondrial function.

We already know that people with chronic fatigue syndrome are in a low output cardiac state secondary to poor mitochondrial function and Dr Cheney has demonstrated this elegantly with his echocardiogram studies. In the process of doing these studies, he has identified two further problems which worsen the low cardiac output and can lead to a downward spiral in symptoms – one is a patent foramen ovale, the other is the problem of oxygen stress and free radical activity. Indeed he believes that how we deal with free radicals (our redox state) is what defines and controls CFS.

See also Patent foramen ovale as a cause of fatigue

  • MALADAPTED STAGE - the third stage of chronic fatigue syndrome

Cheney believes that this third and maladapted stage of chronic fatigue syndrome arises because of abnormal control mechanisms. Normally in a stress situation there is a release of stress hormones from the thyroid gland, the adrenal gland, the pituitary gland in the brain and so on. Dr Cheney has been looking at the heart response when these hormones are applied to controls and to patients with fatigue syndromes. He has developed extracts of these tissues and applies them transdermally. He sees a response in the heart within 30 seconds. This alone is quite astonishing! What he finds is that when he applies these extracts to normal people, the heart improves its function. However, when he applies these extracts to patients with chronic fatigue syndrome the heart response invariably gets worse.

Cheney ran a trial whereby he took patients with CFS and for six months gave them transdermal liver extracts. Liver is rich in SODase and catalase. Although they improved with the heart tests, clinically they were no better. It was only when he added a heart extract, rich in glutathione peroxidase, that he saw clinical improvements. What Cheney was doing here I believe was to improve antioxidant status. Cheney thinks he was using these as “cell signalling factors” and believes this may be a way of reversing this “flip” in the HPA axis.

What Cheney is hypothesising from this is that the control mechanisms for chronic fatigue syndrome have flipped. Instead of hormones improving efficiency and function of the heart, when you have a chronic fatigue syndrome they do the opposite. This has to be a protective mechanism.

The brain is constantly monitoring energy available to the body. Endurance athletes do this brilliantly well! There is a lovely story which illustrates this point reported in New Scientist. A runner who was also a sport’s psychologist, was competing in a marathon and had been told that the entire race was on the flat. At 18 miles he was running comfortably. He came round a corner and suddenly realised he had a mountain to climb. Within a millisecond of appreciating this, he felt the most over-whelming fatigue so he could barely walk and really struggled to complete the course! This cannot be explained by physical mechanisms – the brain suddenly realised there was much more to be done than had been previously appreciated and shut down the system to a level where completion was possible but at a much slower rate. The brain was switched into "protective" mode. See also

I believe it is reasonable to imagine very sick mitochondria as being stuck in a dysfunctional mode similar to a heart muscle that is “fibrillating”. In ventricular fibrillation, if all you do is inject supportive drugs (i.e. lidocaine), nothing happens. It is only upon “kick starting” the heart with a jolt of energy that a normal heart rhythm once again occurs.

This also fits with the ideas of Robert K. Naviaux, MD, PhD who hypothesises a a human dauer syndrome that is maintained by persistent activation of the cell danger response (CDR) through purinergic signalling. See Naviaux Lab Webpage on CFS Research

The brain is wired to learn – it does so by association and experience. Interestingly the NMDA receptor is central to the learning process and we know this is activated in inflammation and pro-oxidant stress.

It is important to realise that CFS is a protective adaptive state. If one did not switch into a CFS, then the uncontrolled free radical stress would most likely kill you! Just complete lack of sleep for 2 weeks is sufficient! If we force the system against its will, we risk creating more free radicals and making things much worse!

All the therapies we are using have an excellent logical basis: Vis:

  • Reduce generation of free radicals
  • Rest and pacing
  • Low toxin diet - ie PK diet.
  • Get rid of toxins such as pesticides, heavy metals, VOCs and drug medication all of which are excellent at generating free radicals
  • Improve ability to mop up free radicals
  • Improve micronutrient status
  • Improve length and quality of sleep

Feedback from Dr John McLaren Howard

Redox state is greatly affected by pH (massive change in oxidation/reduction balance for small change in pH). This is particularly true when major components of the redox system are heavily protein-buffered. In CFS patients, the degree to which they switch to anaerobic metabolism is one of the major factors. Those who 'struggle on regardless' soon begin to depend on anerobic mechanisms and build tolerance to increased lactate (acidosis). This has to be a major stress factor on general and cell-specific redox balance.

In the leucocyte respiration studies, we also see another major factor is electron transport/oxidative phosphorylation is uncoupled.

Catalase – this is a very interesting area and I have been trying to sort out a way of assessing it that throws light on the sort of mechanisms 'we' explore. There is so much of it that it is not difficult to measure just difficult to interpret any findings. One thing to keep in mind is that catalase 'reduces' organic forms of metals (including some detoxification conjugates) back to simple organic forms of the metals. This is a real problem in some cases because the inorganic - non fat soluble form cannot then escape the cell.

There is so much catalase in cells that this process is inevitable - at least for some toxic metals. As with increases in intracellular calcium, if it promotes apoptosis then at least the normal cell replacement cycle can continue. However, in some CFS patients we now know that calcium-binding proteins are induced as Ca-Actin binding increases. If that happens with heavy metals then even more damage is possible and normal cell-replacement is not promoted because apoptosis is inhibited (not triggered is a better way of putting it).

The high affinity cation binding site of actin that I have investigated extensively re the i/c calcium problem, is capable of binding a wide range of metals - it has been investigated in terms of cadmium toxicity for example. One you have my write up on this (its almost ready and gives full referenced details of the whole process of exploring the i/c Ca issue and Ca-Actin binding) you will see how significant this may be. Not in terms of calcium but for the toxic metals, catalase may be worsening the situation to a very great degree.

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