As many CFS sufferers will be able to verify, CFS affects not just the hormonal patterns, energy levels, the digestive tract, and general biochemical function of the body, but also seems to affect the heart and blood flow. In some patients, the heart feels like it feels overstrained (beats fast) with gentle exercise, prolonged periods of mental concentration or even when deprived of sleep for a short time; sometimes even generally sensitive or uncomfortable and perhaps prone to frequent palpitations. Patients may often feel short of breath. Low blood pressure affects some but not all patients, or at least a propensity for blood pressure to drop more readily. Some CFS patients may also feel better when lying down than when standing up, on account of postural hypotension, whilst others may feel better when sitting up than when lying down (on account of poor O2 diffusion in the supine position). Some patients may feel better after gentle stretching (that does not involve too much exertion) as more blood circulates and also seems to reach the brain. So what is actually going on here?
Cardiomyopathy literally means 'heart muscle disease' and is the deterioration of the function of the heart muscle, or myocardium, itself for a variety of reasons. With respect to CFS, we are concerned with specific types of cardiomyopathy, meaning specific causes or routes to cardiomyopathy.
The focus of much of Dr. Paul Cheney's current work on Cardiac Insufficiency hypothesis and its connection to CFS, which is considered on this page in conjunction with the work of other specialists, is based on the groundwork laid out by the following publication:
'Abnormal Impedance Cardiography Predicts Symptom Severity in Chronic Fatigue Syndrome.' Peckerman, et al; The American Journal of the Medical Sciences. 2003; 326(2):55-60.
A (recent) related paper by Dr Vegard Bruun Wyller is listed below:
'Usefulness of an Abnormal Cardiovascular Response During Low-Grade Head-Up Tilt-Test for Discriminating Adolescents With Chronic Fatigue from Healthy Controls.' Vergard Bruun Wyller MD, Reidar Due MD, J. Philip Saul MD, Jan P. Amlie MD PhD and Erik Thaulow MD PhD; American Journal of Cardiology 2007;99:997-1001.
In his studies, Dr Cheney has linked significantly decreased values of Cardiac Output in Litres per Minute (a.k.a. 'Q') to CFS cases and post-malaise fatigue (up to 30%), more closely than any other high level determinand. Dr Cheney hypothesises that Compensated Idiopathic Cardiomyopathy (a.k.a. Idiopathic Dilated Cardiomyopathy or IDCM, pictured below) is a heart condition or heart failure that goes undetected by cardiologists. Idiopathic cardiomyopathy literally means heart condition of unknown cause or origin. According to Cheney, Compensated Idiopathic Cardiomyopathy in CFS is the body's response to protect the heart from complete failure on account of its low levels of available energy. This lack of energy is a result of poor mitochondrial function. The heart, having less energy available and being less capable of fulfilling its normal output requirements, and the body in general requiring less oxygen because of reduced mitochondrial function, reduces its output in order to prevent total heart failure. The body defends the blood pressure, which should not be allowed to drop below a certain level or life cannot be sustained. It does this by restricting the blood flow to some of the organs by closing valves within the circulatory system (this combined with the slightly lowered blood pressure having a corresponding negative effect on the lymphatic system and circulation). The body initially tries to mask this deficit according to Cheney by increased adrenaline and stress hormone outputs, which puts a strain on the endocrine system, but eventually these will become overburdened and deficient, resulting in further decreases in cardiac function and metabolic rate. The systematic sacrifice or shutting down of the body's organs results in the progression of the condition of CFS according to Cheney, and simply aiming to boost blood circulation to these organs and their oxygen requirements puts more strain on the heart and potentially makes the whole condition worse. Cheney's hypothesis works on the basis of boosting mitochondrial function and the factors that are holding back mitochondrial function, in order to bring the heart and other organs functions back to normal in the right sequence.
What other symptoms are there of cardiomyopathy in CFS patients besides lower cardiac output and a decreased propensity for heavy exercise? Other symptoms can include elevated pulse rate (during rest, standing up from a reclining posture - known as Postural Orthostatic Tachycardia Syndrome (POTS) - see links below, or indeed during light exercise), a heavy heart beat, palpitations and even chest pains (if not enough oxygen or ATP is available for the cardiac muscle) when fatigued or when lieing down on the left side.
POTS may also be accompanied by Neurally Mediated Hypotension (NMH), which is a drop in blood pressure that occurs after being upright, e.g. a drop in systolic BP of 25mm Hg). It occurs when too little blood circulates back to the heart when people are upright and triggers an abnormal reflex interaction between the heart and the brain. It is also known as the fainting reflex, delayed orthostatic hypotension, neurocardiogenic syncope, vasodepressor syncope and vaso-vagal syncope. Syncope is the medical term for fainting.
What is the mechanism of the cardiomyopathy? How is heart function impaired exactly? Diastolic Dysfunction is the result of this low mitochondrial function. The heart has two phases, the relaxation/expansion phase, where the left venticle fills with blood (known as the diastolic phase); and the contraction or systolic phase. The expansion/relaxation (diastolic) phase is said to require more energy than the contraction phase, so this part of the cycle is not executed as well, resulting in only partial filling of the left ventricle. This creates a larger pressure difference than normal. This puts additional strain on the heart muscle.
Currently the most comprehensive article on the internet on Cheney's theory is shown below which was written by Carol Sieverling, based on a series of patient interviews with Paul Cheney between September and November 2004.
This article however does not go into sufficient detail in a number of areas, including the role of PFOs, the effects of oxygen on the heart, other treatments to support enzyme production (including animal stem cells) and promote heart function etc., which have been elaborated on by Cheney in his actual seminars and talks (and indeed more recent research papers), which were captured on video, and are listed below.
A 2003 video talk by Dr Cheney can be seen at the link below.
To purchase a 2 DVD set of Dr Cheney's seminar from 9 September 2006, University of North Texas, Health Science Center, Fort Worth, Texas, visit the links below. It appears that one batch of these DVDs features a corrupted section of the seminar which cannot be viewed properly.
I have attempted to integrate all of the above Cheney sources into one overall high level summary below, with my own commentary and critique. This was first written in January 2009, but I have since integrated a wide variety of other material and split the article into 3 pages, as mentioned above.
Cheney seems to have consistently changed the emphasis of his theory over the years, and refined it, and each year he seems to come up with new ideas for protocols, based on the studies of the patients at his clinic, whom do not seem to be truly representative of the diversity of CFS cases elsewhere. There are various areas of discrepency and contradiction in the ideas presented, which are discussed on this page and the other two related pages.
The related topic of homocysteine metabolism and glutathione production, and elevated homocysteine levels, which can contribute to an increased risk of heart attack in some CFS patients, is discussed elsewhere on the Nutritional Deficiencies page.
Cheney theories that the body has a special sequence of sacrificial prioritisation, sacrificing blood flow (perfusion) to organs in a sequence, rather than in an equal manner. This is a result of CFS patients having a low blood pressure, and the blood supply to the organs being shut down one by one, in order to maintain sufficient blood pressure (and effectively raise the blood pressure). The order of this proposed sequence is summarised below.
Skin and Compensatory Hypothyroidism: temperature sensitivity & regulation, decreased ability to detoxify the body through the skin (Multiple Chemical Sensitivities), downregulating the thyroid function to avoid overcompensating for temperature variations, etc. Perhaps cold extremities.
Muscles: mitochondrial depletion in muscles, fibromyalgia type pains, joint problems, etc. Decreased mitochondrial efficiency puts less of a demand on the heart at first.
Liver/gut: less stomach acid and digestive enzyme production, poor absorption of digested nutrients as less microcirculation, food allergies, dysbiosis etc.
Brain: toxification of brain tissue, cognitive problems (less reserve), hpothalamic problems (neurological/nervous system complaints, endocrine system problems/inefficiency) etc.
Exercise intolerance, unable to sustain cardiac output, perhaps developing into chest pain (heart muscles not getting adequate oxygen). Compensated Idiopathic Cardiomyopathy is theorised mechanism in CFS patients that prevents them moving to the next stage (known as the 'Event Horizon' or 'Point of No Return').
When microcirculation defect within the heart itself (produced by a low Q value) begins to affect Q itself, then a downward spiral occurs. This is referred to as the 'Event Horizon'.
Lung and Kidney: Both the lung and kidney share the Renin-angiotensin system (RAS), a hormone system that regulates blood pressure and water (fluid) blanace. The kidneys secrete renin when blood pressure is low to stimulate the constriction of blood vessels to bring up the blood pressure again. With renal failure (i.e. significantly decreased kidney function) comes an inability to control blood pressure adequately as well as abnormal fluid levels in the body, deranged acid levels, abnormal levels of potassium, calcium, phosphate, hematuria (blood in the urine) and (in the longer term) anemia. Long-term kidney problems have significant repercussions on other diseases, such as cardiovascular disease. Combined kidney and liver failure is known as Hepatorenal Syndrome.Congestive Heart Failure (CHF) (an inability to pump enough oxygen rich blood to meet the body's (reduced) needs), Pulmonary Edema/Oedema (swelling or fluid accumulation in the lungs, impairing gas exchange and even causes respiratory failure) is the ultimate progression (if things develop this far), resulting in death.
So to summarise, Cheney's theory is that CFS is a set of symptoms of Compensated Idiopathic Cardiomyopathy, that without it would otherwise mean those affected would likely die very young of a heart attack. The degree of compensation is said to vary hence showing variations in CFS severity and degree of symptoms. This does not mean that CFS patients will not develop fatal heart conditions, but that the onset is much later than it otherwise would be, at a slightly younger age than the rest of the population.
In the 2004 document, Cheney states that the cause of the Compensated Idiopathic Cardiomyopathy (CICM) or decreased cardiac output is a loss of muscle power on account of mitochondrial inefficiency. This is attributed to a number of causes:
Viral and Bacterial Infections
Heavy Metal Toxicity: An Italian study in a cardiology journal found that in all 13 cases of ICM studied, patients had 23,000 times more mercury than the 4 control patients (i.e. without ICM or any other heart condition), and 18,000 times more than the 24 patients with other types of heart disease studied.
Free Radical formation (Oxidative Stress) - the formation of the oxidising agent Peroxynitrite believed to be the chief culprit. I would like to add that free radical damage could equally come from external sources, i.e. processed and junk food, smoking and drugs, build up of heavy metals in the body, other environmental factors, coinciding with a lowering of the body's natural defences against free radicals and an insufficient antioxidant intake in one's diet.
However, in his 2006 seminar, Cheney's overall argument is that viral and bacterial infections are a result of poor mitochondrial function (and the knock on effects of lower oxygen requirements/levels).
He does not focus so much on heavy metal toxicity as a cause of mitochondrial dysfunction.
He does however examine DNA damage from elevated RNase-L levels (a cellular anti-viral response) as a cause of CICM and oxidative damage from free radicals from excessive oxygenation (which is a circular argument as this is a result and not a cause of mitochondrial dysfunction, i.e. a deficit of energy to actually produce protective antioxidants against the free radicals produced by metabolism). He did not really mention peroxynitrite or the roots causes of mitochondrial function at all, but rather their downstream effects and how to address mitochondrial dyfunction, how to accelerate reverse phenotype adaptation and how to boost the heart output.
Cheney states that reduced oxygen levels in the body and a more anaerobic metabolism results in lower oxygen levels in the cells, which attracts facultative anaerobes, e.g. candida, Lyme Disease (bacteria of the Borrelia genus) and Chlamydia bacteria etc. Thus Cheney postulates that they are the result and not the cause of CFS. Cheney postulates that the low oxygen levels and consumption are an adaptation to poor mitochondrial function, which 'cause' the CFS. There are of course other reasons for Candida overgrowth besides low oxygen levels, and these may include diets high in simple carbohydrates, excessive ingestion of mouldy-type foods, stress and a variety of other factors. Low oxygen levels are of course irrelevant to viral infections, which often play a part in CFS cases.
Cheney stated that for many years he believed that viral infections were the cause of CFS, rather than just the trigger, and that too high RNase-L levels were also party to blame. RNase-L production is an anti-viral response by the body to a viral trigger, which indiscriminately destroy viral RNA as well as human RNA (by inhibiting ability to replicate). Excess RNase-L production in CFS cases is thought to explain much of the cellular damage that occurs. Excessive RNase-L damages cellular and mitochondrial RNA and also impairs ATP production and according to Cheney is even thought to induce intracellular acidosis (through excessive lactate build up). RNase-L is examined in more detail on the Stealth Viruses page.
However, he stated in the 2006 seminar that he believes that the viral infection is merely a symptom of low mitochondrial function, and that fighting the viruses will not cure CFS. He believes that if the body does not have enough energy, then it cannot address all the other downstream issues that result from a lack of energy, i.e. enzymatic efficiency etc. Whilst in many patients, the viral and bacterial infections work synergistically with the low energy levels/availability to produce a more adverse situation, if one fixes the energy issue, Cheney believes the other issues will correct themselves. His logic being that all people have viruses floating around in the bloood stream and in the tissues, but not everyone has CFS. However, this slightly contradicts what he said in 2004 and also the 2006 recommendation he has given for the anti-viral drug Nexavir, discussed in the Other Treatments section.
One example given of the energy argument is taking the actual required vitamins in the form the body uses them rather than the precursors of those vitamins, as the body requires energy to convert them, and amino acid and other chemical conversion in the body in a CFS patient is already flawed, i.e. better to take folate rather than folic acid, as the body has to convert folic acid to folate (requiring ATP which is in short supply). How significant this actually is given the quantities involved is a matter of debate.
This logic is however somewhat flawed, and contradicts the 'synergistic' argument; as treatment may indeed require tackling all issues, including downstream effects (like viral or bacterial infections) as well as 'initial causes'; as the downstream effects of viral or bacterial infections put a strain on the immune system and require additional energy and ATP to combat, 24/7, which makes the job of fixing the energy deficit that much harder, as the energy requirement is much higher because of them. In addition, I believe that it is also a chicken and egg question, as to which was the initial cause, and they likely worked together synergistically from the start (in terms of the trigger).
Cheney states that by treating energy production (mitochondrial function), the thyroid and cardiac function will sort themselves out, but by targetting the thyroid and cardiac function and not the energy production issue, the patient may not make significant progress, or if he does, may be in a dangerous position (in terms of putting too much pressure on heart output and 'over oxygenation'). Clearly there is some merit to these statements, but logic would dictate treating all areas rather than just one.
A detailed look at Peroxynitrite formation and methods of restraining Nitric Oxide and Peroxynitrite formation is found on the Nitric Oxide & Peroxynitrite page.
In Cheney's 2006 seminar, he postulates that in extreme cases of Diastolic Dysfunction in CFS patients, a Patent Foramen Ovale (PFO) may be present and exaccerbating the cardiac dysfunction. A PFO is a tiny hole in the heart, utilised in foetal physiology.
Let us examine what a PFO is first of all.
During a foetus' development, the heart's two atria chambers are connected by a hole through the wall of the muscle (formed roughly in the fourth week of gestation), which allows blood to be diverted away from the lungs.
In the primitive atrium it is known as the foramen ovale, the formane in the septum secundum. A drawing of the septum secundum in a foetal heart is shown below.
'The foramen ovale begins forming late in the fourth week of gestation. Initially the atria are separated from one another by the septum primum [shown below] except for a small opening in the septum, the ostium primum.'
'As the septum primum grows, the ostium primum narrows and eventually closes. Before it does so, bloodflow from the inferior vena cava wears down a portion of the septum primum, forming the ostium secundum...The ostium secundum provides communication between the atria after the ostium primum closes completely. Subsequently, a second wall of tissue, the septum secundum, grows over the ostium secundum in the right atrium. Bloodflow then only passes from the right to left atrium by way of a small passageway in the septum secundum and then through the ostium secundum.'
'This passageway is called the foramen ovale [ie. the foramen in the septum secundum]. Normally this opening closes in the first three months of life. When the lungs become functional at birth, the pulmonary pressure decreases and the left atrial pressure exceeds that of the right. This forces the septum primum against the septum secundum, functionally closing the foramen ovale. In time the septa eventually fuse, leaving a remnant of the foramen ovale, the fossa ovalis.'
In a foetus, the lungs are not working and are full of fluid in the womb, and are only used once the baby is born. Up to that point, the foetus relies on oxygen being supplied in the umbilical cord, which diffuses into the baby's own blood. At the point of birth, when emerging from the womb, the baby takes its first breath and this PFO valve shuts. The umbilical cord is cut and tied off shortly afterwards.
In most infants it grows shut, using scar tissue, but in 15-20% of the population it does not. i.e. in 15-30% of the population the PFO valve never grew shut, but opens and closes depending on the partial pressure of oxygen in the blood. This is the foramen ovale, specifically the foramen in the septum primum. 'Patent' literally meaning 'open'. This can potentially result in heart difficulties, e.g. laboured breathing or recurrent respiratory infections. Please see the link above for further details. The article is spread over 8 pages.
'Atrial septal defect (ASD) is a form of congenital heart defect that enables blood flow between the left and right atria via the interatrial septum. The interatrial septum is the tissue that divides the right and left atria. Without this septum, or if there is a defect in this septum, it is possible for blood to travel from the left side of the heart to the right side of the heart, or vice versa.'
The article 'Atrial Septal Defect, Ostium Secundum' by Ira H. Gessner, is shown at the link below.
'Fusion of the septum primum and the septum secundum closes the foramen ovale. Complete closure occurs in most individuals. In 25-30% of normal adult hearts, however, a probe can be passed from the right atrium to the left atrium via the foramen ovale and ostium secundum. This patent foramen ovale allows a tiny left-to-right shunt that can be detected by sensitive techniques, such as color Doppler echocardiography, in 15-20% of adults.'
'There are three major types of interatrial complications: ostium secundum, ostium primum and sinus venosus defects. Secundum Atrial Septal Defect (ASD), [i.e. a PFO], is by far the most common type. Adult patients with simple congenital heart disease, such as isolated atrial septal defects are rapidly becoming a relatively large population with a variety of clinical problems...more recently, MRI are mandatory to assess types and significance of ASDs. Standard echocardiography is the first-line imaging modality to confirm suspicion of such defects and 3D echo and MRIs are the most modern and more promising techniques in case of difficult diagnosis. Surgical or percutaneous repair should be offered at any age unless associated with pulmonary vascular disease, whereas surgery remains the only option for primum and sinus defects. Follow-up of operated patients is based on Holter ECG and echocardiography. Adults with isolated ASD are more likely to reach adult age without being diagnosed. This diagnosis should be kept in mind in presence of symptoms and signs of pulmonary overload. Unfortunately, I do not have any clear recommendations and some indications can be retrieved from the literature. Percutaneous device-based closure or conventional or mini-invasive surgery should be proposed on the basis of types of defects (secundum, primum or sinus defects). In case of secundum ASD, decision about surgery or device-based closure should be made on the basis of anatomical characteristics of the defect. Currently, percutaneous closure seems to be the first choice in uncomplicated defects, whereas mini-invasive surgery seems indicated in some cases (e.g. difficult control's arrhythmia, difficult anatomy, defects larger than 40 mm, etc.)'
Cheney suggests that it is one of the primary drivers behind cardiac insufficiency and the mechanism of CFS within severe CFS patients. A PFO may indeed exaggerate the symptoms of mitochondrial cardiac insufficiency in CFS patients. Cheney likens the PFO, an impaired cardiac function, to the foetal circulation, which is an immature function, the difference being that the foetus is not able to use its lungs but relies on the umbilical cord, whereas the adult with a PFO has no umbilical cord and relies on his lungs for oxygen requirements.
Cheney hypothesises that CFS sufferers (with no PFO) may actually rip/blow open this Formane Ovale valve, having formerly been sealed shut with scar tissue after birth, when sufficient pressure builds up in the right atrium. This valve thus remains open for much of the time, depends on the oxygen levels and pressure inside the right atrium. Cheney believes that Diastolic Dysfunction/CICM may greatly increase the likelihood of ripping open one's foramen ovale, if one does not already have a PFO. The further down the line of CICM is, and the weaker the heart function is (i.e. a reflect of poor mitochondrial function), then the more likely this scenario is to develop. One should take into account the decreased strength of the heart muscle, heart muscle wasting, decreased blood pressure being compensated for by sequential sacrifice of blood supply to the organs and increased heart rate; but also the increased pressures inside the heart resulting from diastolic dysfunction.
Dr Tatinha has also confirmed with me that it is indeed possible to blow/rip open one's Foramen Ovale and thus develop a PFO at any point in one's life. How frequent this actually is however is not fully understood. If one assumes that having a PFO in the vast majority of cases is a congenital (birth) defect which will never grow shut, then is it possible that those patients who are claimed to rip open a Foramen Ovale may be able to grow it shut again (with scar tissue) as they once did when they were infants? Is there a difference between doing so as an infant and as an adult? Clearly the adult heart is operating at much greater pressures. It is probably unlikely that it will self-correct in an adult.
In Cheney's clinic, he has observed the prevalence of PFOs to be approximately 80-90%, in contrast to the 15-30% of the population with one. There appears to be a little 'back pedalling' or at least more accurate quantification in Cheney's figures in 2006, as in his 2003 seminar video he states that 99% of his patients had a PFO, which is quite different. Was this based on a very small number of patients? Or just a moment of generalisation to emphasise the point? It would make sense to take his latest figures more seriously. Clearly not everyone who has a PFO develops CFS during his lifetime. And not every CFS patient has a PFO (yet). One can speculate as to the reason for this, whether these CFS cases simply arose from that 15-20% sub-segment of the population, or whether they blew/ripped open their Foramen Ovales in the course of Diastolic Dysfunction as a result of a progressed state of CFS.
Cheney has in his own research admitted that perhaps he receives only the most extreme and far gone (cardiac-related?) CFS cases in his clinic (i.e. those that have progressed to severe diastolic dysfunction and have 'developed' PFOs), and his own research and hypotheses, based upon those patients that visit his clinic, may indeed reflect this. Is it possible therefore that his test subjects are not representative of the CFS community as a whole? And that his hypotheses are based often on a small subset of the many routes and 'configurations' that CFS can manifest itself in? If Cheney is correct that ripping open one's Foramen Ovale is indeed one of the latter stages of CFS, which many/most CFS cases will progress to in less than ideal circumstances (lack of treatment, lifestyle/diet/environment/biochemical status conducive to deterioration of one's condition), then he is really looking at the worst case scenario of CFS. Otherwise, he is merely looking at a small cross section of cases that bear no relevance to the types and progression of CFS in most patients in general.
'The missing piece to this puzzle may be that we see a super-select group of CFS patients at our clinic.'
Cheney has observed the effect of oxygen on the PFO as described in the section above. Supply of oxygen enriched mixtures or oxygen under pressure as in hyperbaric oxygen therapy has shown mixed results. Whilst low oxygen doses (i.e. slightly enriched oxygen mixtures) has shown to improve most CFS patients with a PFO at Cheney's clinic, high oxygen doses (i.e. pure oxygen or oxygen mixtures under pressure) has resulted in a larger percentage of patients getting worse. Cheney claims that the cardiac muscle has an oxygen threshold, and below this the PFO stays shut, but above certain partial pressures of oxygen, the PFO opens and stays open. He therefore concludes that too much oxygen is not a good thing and can simply worsen the diastolic dysfunction of a person with a PFO. Of course, it is one thing breathing 90% O2 at atmospheric pressure, but it is quite another breathing O2 enriched air or pure O2 under pressure, and Oxygen becomes toxic and inflames the lungs at 1.6 and can cause CNS toxicity, and may also displace Nitrogen and CO2 in the blood, so it is not surprising that some problems can be observed with O2 under pressure in CFS patients.
Besides minor complications and constraints on one's lifestyle, there are more serious consequnces of having a PFO, both for younger and older patients (whether they have CFS or not), including an increased risk of a stroke from a paradoxical embolism is a cause of stroke in both age groups. The prevalence of a PFO has been shown to be much greater amongst patients who have had a cryptogenic stroke than amongst those with stroke of known cause in all age groups. There is also a very strong connection between the presence of a PFO with concomitant (simultaneous) atrial septal aneurysm and cryptogenic stroke (a stroke of unknown origin), compared with incidences of known/identifiable types of stroke.
A PFO also has a potential impact on scuba divers. If one does have a PFO, then one is at considerable risk of getting the 'bends' or decompression sickness from a non-decompression dive well within the non-decompression limits, let alone a very deep dive or decompression dive. During a scuba dive one is breathing in air or other gases at a pressure equal to the surrounding water (i.e. at a greater pressure the deeper one goes). This pressure forces nitrogen into the blood which is then absorbed by the tissues of the body. The lungs are the place where nitrogen under pressure is absorbed into the blood, but also where nitrogen escapes from the blood and is removed from the body during one's ascent. Depending on the depth and bottom time, the ascent has to be adjusted accordingly, to allow the nitrogen to escape from the tissues at a controlled rate and be removed from the body without forming too big bubbles which can occur if one ascends too quickly. If a diver has a PFO, then some blood full of fine bubbles of nitrogen bypasses the lungs and goes directly to the brain and onwards to the rest of the body, where a bubble getting stuck in a blood vessel will cause the symptoms of DCS and at worst death.
The usual method for testing for a PFO is a transthoracicechocardiogram with a a saline bubble infusion. This is performed by aggitating a saline solution with air bubbles by squirting saline with air in it from one syringe to another, both connected via a tube. This aggitated saline, containing very fine air bubbles, is injected into a vein in the arm. The patient is then required to perform the valsalva manoevre (i.e. blowing into a closed tube), which increases the pressure in the heart and will open up the PFO if it present. The heart is monitored on the echocardiogram (ultrasound) on the screen and any bubbles that pass directly from the right atrium to the left can be observed on the screen. The exact method of counting/recording bubbles that do pass through a PFO varies. Clearly it depends on the competence of the cardiologist, and evidently many people have been misdiagnosed because the practitioner was not paying attention to he bubbles properly and perhaps missed a few that passed across. The procedure is not painful and is akin to a slightly aggressive scuba diving ascent in terms of bubble formation. If no PFO is present, all the bubbles in the blood will be transported to the lungs for removal.
Other methods for PFO testing include a transesophageal echocardiogram, transcranial doppler (TCD) and even MRI. The exact method used will depend on the consultant in question.
I myself have been involved in recreational scuba diving and technical/decompression diving, and one of the recommended practices in certain fields of the technical diving (DIR) community is to have a PFO test, to check that one definitely does not have a PFO before embarking on any serious decompression diving. So if one is found to have a PFO, then one should desist from diving immediately and write off one's diving career. Knowing one does not have a PFO also gives one assurance that doing aggressive but accurate decompression dive profiles will not result in the bends. Some technical divers argue that if a diver has gone to the stage where he is performing deep diving and decompression diving, and has not had the bends, then in all likelihood he does not have a PFO and thus a test is not necessary. However this is not strictly true in all cases.
I had a PFO test performed by a private specialist in London in 2000 and his results were negative. Please see the links page for details. My CFS developed around the end of 2002, however, I had always had minor mitochondrial, endocrine, digestive and immune system problems for many years prior. The onset of my condition cannot therefore be explained by a PFO, although it is possible according to Cheney that I may have ripped open his foramen ovale when my CFS condition deteriorated, although I consider this unlikely. As a PFO does not necessarily lead to CFS, then having a PFO concurrent with CFS does not necessarily mean that one cannot overcome one's CFS and get back to how one was before, i.e. a non-CFS suffering person who happens to have a PFO.
Most doctors do not bother to test for PFOs as it is not regarded as important, and finding a doctor or specialist who is willing to get involved or knows anything about it is quite difficult.
There are two medical procedures for PFO closure, transcatheter closure and surgical closure. Transcatheter closure involves having a 'plug' pushed up one of your blood vessels until it reaches the heart, where it is pushed into the hole of the foramen ovale to effectively plug it shut. The exact shape and size of the plug will depend on the individual. The surgical closure involves open heart surgery and 'sewing' the foramen ovale shut. I have heard of one of two DIR technical divers that have had their PFOs sewn up as they refused to give up diving. So if you do have a PFO and want to have it plugged or sewn up, then it is really no big deal. Do not write yourself off as 'doomed' if you have bad CFS and a PFO as both can be corrected (independently or together).
The adaptation is genetically coded as a DNA and RNA phenotype shift. This tends to happen over 2-3 years. This locks in the dysfunction (or metabolic function and level of enzymatic activity etc.) at the genetic level, and means that the longer one's condition goes on for, or the worse it becomes, the harder it is to recover as the mechanisms and biochemical problems becoming increasingly coded on a genetic level. This does not mean that one is genetically programmed to develop CFS, or that one's CFS is incurable, but that one's body adapts, and it is not solely the hypothalamic dysfunction that is driving the problems. Of course, as one treats CFS, the genetic coding and phenotype adaptation will work in reverse, to return to 'normal', but this process may slow down one's recovery that would otherwise have been much swifter. According to Cheney, it may take up to 2-3 years for one's body to readjust back to normal, even after one has seemingly removing all the barriers to full health and is supplementing the body. This he cites is not a disease issue any longer but an adaptation issue, and the more one can do to help the adaptation process along by providing optimal conditions for the body, and indeed to accelerate it the better, rather than keeping the adaptation locked in by continuing to abuse the body or over-stress it. He also believes that a rapid recovery from a body that was phenotypically adapted to CFS or a very severe state of CFS is in an 'unstable state', and one may either be suppressing the body's natural defence mechanism which will come back to exert its purpose to protect the body again; or equally (my comment) that the body's natural tendency is to return to the previous state of adaptation (if it has not had time to phenotypically adapt to a new, healthy pattern) with the slightest 'push'. As stated, in the latter case, it is important not to overdo it as soon as one starts to feel better, but let the body naturally adjust over time to this healthy state.
Cheney cites his heart transplant operation, that took place during 2003/2004 at the peak of his CFS condition (and diastolic failure), presumably having been extremely ill with CFS himself in the many years of his research prior to this, when he still felt fatigued after receiving a new heart; although of course this was in part due to his mitochondrial function still being poor and being unable to 'fuel' his 'new' heart, as well as phenotype shift (the body not being used to a stronger, more youthful heart with a higher potential peak output).
Cheney in his 2006 seminar was rather vague as to whether it was reflected in the RNA or DNA, and mentioned both.
In the Other Treatments section below, Cheney cites stem-cell related treatments or compounds that promote stem cell growth and production may assist in accelerating the reverse of this phenotype adaptation to CFS.
How much truth is there in this theory? Clearly the results speak for themselves, but is phenotype encoding just another way of saying that the longer the symptoms persist for, the more complex the underlying biochemical problems become underneath, and thus take more unravelling and time to address?
One might argue that herbal medicine, diet, emotional state and indeed energetic state (in terms of 'qi') are also very important, and may greatly progress the rate of one's recovery. Are oriental medicine and energetic therapies in general describing the same thing? Or is Cheney pointing to the wrong/different cause, both of which are acting on the rate of recovery? Can energetic therapies like oriental medicine etc. actually speed up phenotype adaptation?
Some miscellaneous medical and cardiac information web site links are listed below, containing up to date medical news and articles.
Cheney (in 2004) has suggested some other approaches to assist in our Cardiac function, day to day, increase one's 'Preload (blood volume)' in the heart and reduce one's 'Afterload blood volume' (reducing the resistance the blood encounters). This is not intended as a 'cure' but more as a way of alleviating symptoms associated with cardiac insufficiency. The trick to preloading is not to 'preload' too much or the effect is counterproductive in absolute terms.
lying down. Lying down seems to increase cardiac output by an average of 2 litres per minute. One could lie down prior to engaging in any demanding activity even if one is not going to sleep or is not tired. A short lie down of 20 minutes can really help one's energy levels. Those who feel worse when lying down (i.e. are over-'preloading') should avoid it during the day.
the endocrine system tends to retain fluids better during the day and lose fluids more readily at night. Some patients should avoid drinking too much closer to bed time as they may over-'preload'.
Using Vitalyte brand isotonic drinks. Cheney believes this can help restore blood volume readily and is easily absorbed. However, I am not convinced about isotonic drinks, as they contain large amounts of sugar, and may potentially exaccerbate harmful micro-organism overgrowth issues and also put strain on the adrenal glands. Most holistic practitioners advise against consuming simple carbohydrates, unless in small doses, e.g. fresh fruit (which also contain a variety of other nutrients and enzymes), for a variety of reasons.
Adaptogenic herbs like Licorice root, help to stimulate adrenal hormone levels, like cortisol. Licorice root is a vasodilator and may help increase cardiac efficiency. Vasodilators tend to lower blood pressure by enlarging/relaxing blood vessels and decreasing flow resistance. Vasoconstrictors conversely raise blood pressure by constricting the blood vessels and creating increased flow resistance. Only Licorice root containing Glycyrrhizin, the principle active ingredient, will have this adaptogenic effect. There is of course a huge array of adaptogenic herbs, fish extracts, minerals and vitamins, which are not mentioned, and much more than can be done here, to help normalise the endocrine system. Exactly which adaptogenic herbs will be most effective and in what dosage varies and changes over time, on a continuous basis, which is not really delved into by Dr Cheney, and betrays perhaps a slight lack of knowledge in this area.
The glycyrrhizin in licorice extract is an inhibitor of 11 beta hydroxysteriod dehydrogenase and can elevate cortisol levels. In many CFS patients, cortisol levels are depressed. Cortisol aids in Sodium retention and tends to increase blood pressure. Thus, be aware that some adaptogenic herbs, particularly licorice, can raise blood pressure more than one wants, and excessive usage has been associated with hypertension and even death (on account of excessive hypertension). So take note of what adaptogenic herbs your adrenal supplements contain, and in what quantities, and the dosage you are taking, whether they have a tendency to induce hypertension or not, and the relative effect it has on your heart. Perhaps buy a Blood Pressure Monitor, which are relatively inexpensive.
Magnesium. Magnesium is an adaptogenic vasodilator that opens/relaxes the blood vessels as needed. Cheney recommends Mg/Taurine injections as above and/or oral Magnesium Glycinate.
In his 2006 seminar, Cheney discusses the concept of using sublingual Magnesium (i.e. under the tongue drops), subcutaneous Magnesium injections (under the skin injections, directly into fatty tissue) and also applying Magnesium Sulphate cream to the skin; rather than actual Magnesium injections. In these applications, he suggests using minute quantities, the reason being that often it is not a case of physically magnesium being deficient in the body but the 'energy signature' of magnesium being deficient, and application of that 'energy signature' (EM?) is said to be what the body, and specifically what the heart requires. The effect on the heart of sublingual Mg is thought to last 5-10 minutes; Mg cream 1 hour; and subcutaneous Mg up to 8 hours. Whilst I can see some benefit in these forms of supplementation, from a 'homeopathic' perspective, I believe the argument that the body is not physically deficient in Magnesium is not always/often true. I have myself tried Kirkman Laboratories Magnesium Sulfate (Sulphate) cream, and found that applying a small amount to the skin on the first occasion produced a major improvement in energy levels for a few hours. However, subsequent applications with a similar small amount produced a small if any noticeable improvement, suggesting that the body perhaps no longer had a need for the 'energy signature' of Magnesium, and if anything required larger amounts to actually absorb enough physical Magnesium (if applicable). An associate of mine, John, noticed the exact same pattern also.
Another alternative to Kirkman Labs Magnesium Sulfate cream is a Dea Sea Salts lotion, for example, Yarden J.Malki Products' Dead Sea Natural Mineral Body Lotion. Dea Sea Salt (MAris Sal) is chiefly comprised of Magnesium. It also has the added benefit of containing a variety of other minerals, including potassium. Yarden also offer shower cream and shampoo products. Also consider a dead sea salts or epsom salts foot bath or bath. Please see the Nutritional page for more information.
This may perhaps explain why patients with related conditions like Fibromyalgia and Multiple Chemical Sensitivities (MCS) have been shown in recent studies to have less blood flow to certain parts of the brain.
However, Dr Cheney believes that a problem with 'Q' is what differentiates CFS and PVFS from Fibromyalgia and MCS, as the latter groupings do not have a problem with Q according to him - unless the patients also have CFS. Dr Cheney has historically not differentiated between CFS and ME.
Perhaps this is a circular argument (a chicken and egg situation), as many of the diosorders, imbalances and deficiencies in question actually have an impact/are active agents in both. All Fibromyalgia and ME cases in my experience have some component of mitochondrial inefficiency, endocrine system dysfunction and also toxicity behind them.
In Cheney's 2006 seminar, he additionally recommends the following treatments.
Hawthorn. Hawthorn leaves and flowers (tops) are generally believed to contain a higher concentration of the active chemicals than Hawthorn berries. Hawthorn has been used for heart conditions for thousands of years, and recent studies have shown it be effective in supporting heart function and increasing cardiac output. It is a cardio-protector, a cardio-tonic, antioxidant (an SOD inducer), anti-inflammatory and bad (LDL) cholesterol reducing agent. It helps to raise cardiac output and improve the maximum workload by up to 7W. It is generally considered beneficial for those with high blood pressure (hypertension), cardiac insufficiency, heart failure and for preventing strokes. It is even a powerful chelating agent, and can assist in heavy metal detoxification. Cheney recommends Hawthorn to nearly all his CFS and ME patients.
The two classes of compound that are the key ingredients in Hawthorn are flavonoids and oligomeric procyanidins (OPCs). OPCs are a class of flavinol. Hawthorn is an Angiotensin Converting Enzyme (ACE) Inhibitor. Other sources of OPCs include Grape Seed Extract and Pycnogenol. The active flavinoids in Hawthorn include vitexin 4--rhamnoside, O-glycosides, luteolin-7 glucoside, hyperoside, quercetin and rutin.
ACE Inhibitors (such as Hawthorn) 'slow (inhibit) the activity of the enzyme ACE, which decreases the production of angiotensin II. As a result, the blood vessels enlarge or dilate, and blood pressure is reduced. This lower blood pressure makes it easier for the heart to pump blood and can improve the function of a failing heart.'
Myocardial contractions are increased/made easier by reducing periperhal resistance. Hawthorn also acts to strengthen the actual myocardial contractions. So whilst Hawthorn is used to treat high blood pressure, CFS sufferers in general tend to have too low a blood pressure, the sequential sacrifice of organs an attempt to compensate for this. Increasing the strength of the contractions may encourage the heart to pump more blood and oxygen to the organs that were sacrificed previously, hopefully turning around the symptoms of CFS without putting a strain on the heart, but rather supporting the heart. In addition, it is expected that Hawthorn will help the heart to cope with the increased pressure differences arising from Diastolic Dysfunction, where the left ventricle does not fill with blood properly during the relaxation/diastolic phase, prior to contraction/systolic phase. By strengthening the heart muscle and dilating the blood vessels, perhaps it might ease the diastolic dysfunction by allowing more blood to enter the left ventricle during the diastolic/relaxation phase.
Procyanidins slow the heart rate and also have a mild depressant effect on the Central Nervous System. OPC a.k.a. pcynogenol is also found in a number of other plant extracts such as grape skin, cocoa, cinnamon, apples, green tea, black tea and especially black chokeberry. Please see the Antioxidants section on the Nutritional page for more information.
As it is a CNS Depressant, the effects will be amplified if taken with alcohol or mood stabilising medication.
Hawthorn should not be taken in conjunction with the medications Digoxin or Phenylephrine.
I have observed that a number of Hawthorn products exist on the market, in the form of herbal capsules and tinctures, with considerable differences in quality and the amount of Hawthorn per capsule. Some rely more on leaves and flowers and others more on berries. Hawthorn leaves and flowers can of course be purchased from a quality organic herbal supplier in bulk, to make one's own tinctures, if need be (if it is being taken regularly), which is hugely cheaper than purchasing a manufactured Hawthorn supplement. A typical tincture dosage is 1-2ml. The effects of Hawthorn may be slow to come on, typically taking several hours. Please see the Recipes page for more information. Hawthorn is the genus known as Crategus. There are many different species of Hawthorn, but the most commonly used is Crategus monogyna.
As mentioned above, Hawthorn is a chelating agent. This means that if enough is taken, then one may begin to experience detoxification side effects, such as headaches, fatigue and perhaps even blotches or boils on the skin. Clearly, taking a certain amount of Hawthorn can be beneficial in certain cardiac cases, but if one takes too much, then the ingestion of the herb becomes counter productive, and its beneficial effects are overrided by the negative effects of over-detoxification. In severe cases of cardiac dysfunction, the body may become more sensitive to over-detoxification (meaning that one's mitochondrial function may become severe impaired near or at the limits of detoxification, and also the actual limit of one's detoxification capability itself may be significantly reduced compared with normal), meaning that one has to exercise more caution. As with many things, more is not necessarily better!
I have personally found Hawthorn to be a 'lifesaver' and have used it during periods where I experienced chest pains. Specifically, if I was experiencing severe cardiac-related chest pains, due largely to insufficient energy availability in the cardiac muscle, I have found that taking enough Hawthorn together with the mitochondrial supplements Acetyl-L-Carnitine, Co-enzyme Q-10 and NADH (Active Vitamin B3) and perhaps Lipoic Acid, combined with pacing one's breathing to try to relax, has helped to greatly alleviate such symptoms. This is over and above the 'normal' or regular dosages of these supplements that are taken throughout the day - i.e. extra.
D-Ribose. This is a sugar that is a constituent part of DNA, RNA and above all ATP molecules. It can directly assist with impaired cardiac function by being directly used by the body to create ATP (and not simply oxidised like glucose). Cheney asserts that in a small number of patients it seems to be converted to glucose and metabolised by both the patient and his bad bacteria (resulting in increased wind); also in a small number of patients it is metabolised anaerobically resulting in a build up of lactic acid in the body. Cheney believes that the bottleneck in glutathione production is the lack of energy rather than the lack of precursors (like NAC) and so believes that D-Ribose is the most effective means of boosting the body's Glutathione levels (indirectly via boosting mitochondrial function?) However, the most common experience is of some ATP production benefit overall. Please see the Mitochondrial page for more information. Cheney states that D-Ribose is a precursor to NADPH in the Krebs cycle, although this is not strictly correct, as the active form of Vitamin B3, NAD+, is phosphorylated by the NAD+ kinase enzyme, with ATP, to form NADP+ and ADP. D-ribose is a precursor to ATP. ATP is created from scratch and also converted from ADP in the body.
In Dr Cheney's Fairfax, Virginia seminar from 25 April 2009, he states that D-ribose is 'toxic' to CFS patients and that it simply makes the energy problem worse. Clearly this is a 360 degree turnaround.
Cheney has also recently been involved in research to see whether low molecular weight, cell signalling peptides or factors (CSFs) from human bone cell cultures (a.k.a. stem cell infusion) can help assist in CFS patients, and the results, on a small number of patients, showed marked improvement in most, but not all patients, 2 patients showing intolerance to the CSFs.
This type of therapy is thought to encourage stem cell growth in the human body, and thus accelerate the reverse process of phenotype adaptation that may have occurred in a particular patient. I have himself heard various claims for certain natural plant-based nutrients and food sources to be rich in chemicals that promote stem cell growth. Examples include wild blueberry, green tea extract, carnosine, vitamin D3, Spirulina and/or an AFA-Omega (EtOH). Both Spirulina and Aphanizomenon flos-aquae (AFA - or Lake Klamath algae) are types of blue-green algae, examined on the Digestive Disorders page.
Dr Myhill has suggested that although cardiac function and output capability in CFS patients is impaired, the traditional tests such as ECG, ECHOs and angiograms used by cardiologists will produce normal results. Dr Peckerman has proposed to the USNIH that an Impendence Cardiography type test for CFS be developed based on the principles of decreased 'Q' (cardiac output in litres per minute).
Dr Myhill's recommendations for mitochondrial and cardiac support are based on the cardiologist Dr Sinatra's recommendations. These are similar to Dr Cheney's suggestions, but also include D-ribose and L-Carnitine (of course other animo acids or organic acids may be deficient causing the problems rather than just Carnitine). Beta blockers, tricyclic antidepressants and phenothiazines actually block CoQ10 production in the body and way worsen the situation.
The book 'The Sinatra Solution: Metabolic Cardiology' by Dr Stephen T. Sinatra can be viewed at on line by clicking here.
Dr Myhill is also a strong advocate of cellular detoxification, particularly using methods such as phospholipid therapy and FIR saunas. She views toxicity as one of the major stumbling blocks in proper mitochondrial function in CFS patients. These techniques are explored more on the Toxicity page.
Additional Articles about Cardiac Insufficiency and CFS:
A list of related research articles by Dr Peckerman, Dr Martin Lerner, Dr Myhill and Dr Paul Cheney and many others, some of which have already been listed on this page, are available at the link below.
I am largely in agreement with the hypothesis of mitochondrial dysfunction being behind the cardiac symptoms as described by Dr Cheney and Dr Myhill. This observation is not unique to Cheney by any means. I have observed a similar pattern in my own condition, whereby a significant decline in mitochondrial function, to very low levels, was quickly followed by noticeable chest pains and poor cardiac adaptation to stress and physical and mental exercise of very low levels. These mild cardiac pains and elevated heart rate were greatly helped by taking ATP supplements and mitochondrial assisting supplements. Indeed the symptoms became much worse when insufficient sleep was obtained (i.e. less recycling of ADP to ATP during deep sleep) and also when insufficient levels of the correct neurotransmitters present in the body (i.e. GABA). I firmly believe that mitochondrial function is behind the observed cardiac problems, assuming no congenital cardiac conditions are present, when in those cases, then clearly these will be a contributary factor also.
Cheney has himself stated that mitochondrial inefficiency is behind the reduced cardiac function or capability. The bottle neck here is not the cardiac function but the mitochondrial capability and the efficiency of the biochemical steps and enzyme production associated with the Krebs cycle in the mitochondria. So perhaps the heart is not really protecting the body but is merely responding to the circumstances it finds itself in, i.e. doing as much as it can given its mitochondrial efficiency. How much of this adaptation is phenotype related, how much is brainstem related, and how much is merely responding to a reduced mitochondrial capability based on specific causes such as toxicity and insufficient nutrient levels, pH and so on?
If the bottle neck was the heart, i.e. mitochondrial function was sub-normal but not affecting the heart significantly, and the cardiac muscle was failing for another reason, then and improving mitochondrial capacity of the body as a whole put more strain on the heart. In this scenario, then decreased metabolism would in a sense be a protective mechanism for the heart. But as mitochondrial function is the bottleneck and not the heart, then in a sense this protective mechanism idea is perhaps not valid.
Cheney's suggestions for improving mitochondrial function is a global type of treatment, improving the mitochondrial function of the body as whole including the heart, so as the body's mitochondrial capability and O2/nutrient and blood demands increase, so does the heart's output increase also. Exactly if they improve together or not, or if one lags behind the other is another matter - if Cheney is right, then the body will prioritise the heart over the body if necessary.
His argument is that increasing oxygen levels in the tissue will by default increase respiration in the tissues which is not what you want, but this cannot occur without an increase in blood supply. Cheney's findings show that increasing oxygen supply through supplemental oxygen ends to improve mitochondrial function slightly, but not enough in most patients to pose any problems for the heart. Introducing more O2 into the bloodstream and target tissues by correcting some of the problems in the oxygen delivery system, as discussed on the Tissue Oxygenation page, can only increase respiration rates and metabolism by so much, because the Krebs Cycle and blood sugar availability would still be impaired. In my opinion, there is no 'protective mechanism' per se, it just appears that way. Of course, I am no expert in mitochondrial function and would welcome any clarifications or commentary to the contrary.
Of course increasing blood demand without providing the heart with any more fuel or a significant advantage can lead to chest pains. The cardiac function will improve with mitochondrial function, but it cannot happen overnight. One cannot put unreasonable demands on the heart during this process of recovery. So I believe that Cheney is half right in certain respects.
Whilst the body is reputedly 'protecting itself' by slowing down its metabolism and pumping less blood around the body, even if more oxygen was being supplied to the tissues, However, raising metabolism globally (i.e. improving mitochondrial function) would be a good thing as it would not put a strain on the heart as the heart would have more energy to operate closer to normal in a healthy manner. If any extra 'strain' was put on the heart would of course depend on what tissues were increasing their metabolism relative to the others (i.e. if the heart was improving its metabolism more than the other tissues, or the other way around).
Perhaps then the argument as to why the body is trying to keep metabolism lower mainly resides on impaired glutathione production and other antioxidant availability in the body, as increasing metabolism increases the level of superoxide production, which can damage the mitochondrial inner and outer membranes as well as the mitochondrial DNA; and also the chance of superoxide leaking out out of the mitochondria (and creating Peroxynitrite), and this causing damage to the outer membrane and to proteins and cell membranes thoughtout the body. However, increased metabolism should result in an increase in glutathione production and cofactor production - is this always the case? It depends on the availability of ATP and what the ATP is being allocated to - to increase energy output or to produce more glutathione and SOD. Of course, glutathione production is often a problem in CFS patients, but lowering metabolism doesn't necessarily prevent Peroxynitrite formation for the previously stated reasons. The only way the body is going to produce more glutathione is through increased metabolism (more energy) in conjunction with increased levels of the relevant nutrients. The argument that the body is protecting itself from oxidative stress by lowering metabolism/mitochondrial efficiency is also in doubt, as stated below as increased antioxidant intake can alleviate and even eliminate signs of inflammation from oxidative stress, but still the body 'chooses' to keep metabolism low. However, as Cheney stated, perhaps this is down to phenotype adaptation.
However, I am doubtful that Peroxynitrite is the main factor in bringing on impaired mitochondrial function, but believes there are other equally significant causes. As examined on the Tissue Oxygenation page, there seem to be some contradictions in his understanding of the role of Peroxynitrite and other factors in low oxygenation levels. The main precepts of his theory could be largely explained also simply by general, blanket reduced efficiency in all systems caused by mitochondrial function, toxic overload and immune system overload.
I however believe that this proposed sequential sacrifice sequence is not the only mechanism for the development of CFS. Indeed, another theory, described on the Liver Inefficiency page suggests that overloading the liver over a period of time, with toxins, from a variety of sources, as well as poisoning the liver itself, and wearing down the immune system with toxins, which in turn gives the liver more work to do, can result in a massive build up of toxins in the body, which has a knock on effect on mitochondrial function, the endocrine system, and further downstream effects on the digestive system, nutrient absorption and utilisation and even cardiac function. Diet is also very important, and a poor diet devoid of nourishment will also gradually reduce mitochondrial efficiency and endocrine system performance by a lack of necessary nutrients, for example Magnesium, and B-vitamins etc. and an intake of endocrine disrupting substances (from food and toxin sources).
Hypothyroidism is generally considered to be caused by an Iodine deficiency in one's diet - which could perhaps relate to decreased blood flow to the Thyroid, according to Cheney's model, supplying less Iodine to the Thyroid - or simply be a dietary problem. Hypothyroidism is also considered to be caused by auto-immune disorders where the Thyroid gland is attacked by the immune system; or genetic causes. Indeed some CFS cases do not involve a depressed thyroid. So it is perhaps not as clear cut as Cheney suggests.
One case study of hypothyroidism that does seem to back up Cheney's hypothesis is a friend of mine who has hypothyroidism. Her mother and sister had had hypothyroidism for many years and both had had operations to remove thyroid tumors. My friend was found to have a thyroid covered with numerous nodules. She found that when she either increased the amount of Thyroid hormone T4, or when she attempted to increase the blood circulation to the thyroid using Hydrotherapy, rather than improve her condition, it actually put a noticeable strain on her heart, and caused a variety of possibly thyroid related symptoms including head to toe hot flushes, a rash and swelling of the neck and face (where the hydrotherapy was carried out). She also had a history of intolerances to most types of treatment, supplement or environmental factor, including sunlight. Whilst this picture is clearly a little complex, with many other factors acting, probably an immune system disorder (and hence the immune system perhaps attacking the thyroid with an increase in blood supply) the connection between decreased thyroid function and cardiac capacity is fairly clear.
I also believe that to view the development of CFS in terms of sequential sacrifice up to the 'Event Horizon' or 'Point of No Return' is perhaps giving the body more credit than it perhaps deserves. I admit that this is plausible, but at the same time, believes that the sequence is not always so clear cut, as described above. It could just be that the heart is affected by mitochondrial, endocrine system and nutritional/cofactor deficiency just as all the other organs and a number of biochemical pathways are, and that the heart's reduction in capacity is merely just a reflection of that. Either way it doesn't really change the treatment protocols significantly to that already discussed elsewhere on this web site. The basic treatments are also very similar to those for assisting with Homocysteine metabolism and the Endocrine system in general. The heart is one organ of many in the body and they are all interdependent and reliant on core pathways and processes in the body to function properly.
It is fairly safe to assume that if heart insufficiency is not resolved, then over time one is somewhat more likely to be susceptible to a heart attack. Statistically speaking CFS patients tend to die younger of causes such as cancer and heart attacks, but this is not an overnight process, and may take 20-30 years to develop. However, this is an additional reason why CFS sufferers should be looking to try to address the root causes of their conditions and not 'mess around and waste time' in their overall programme of treatment if they can avoid it.
Dr Cheney has made many valid points, but I feel that what is being described in one possible route to CFS and progression in CFS, that Cheney has himself experienced and fully recovered from, and not one that is necessarily universally applicable, not a 'unifying theory of CFS'. In other words, we know that CFS and ME sufferers have an increased risk of earlier heart failure and/or cancer than the rest of the population. However, not all CFS cases progress to the ultimate stage of heart failure, or indeed cancer. These are just probabilities. It may well be that those patients that do eventually die of cancer have some degree of diastolic dysfunction, and indeed that those who die of neither eventually did also have some degree of diastolic dysfunction also. Whilst the order and sequence of Cheney's hypothesis may be debatable, it does bring together many areas of dysfunction very well and sheds light on a huge array of different aspects of the underlying mechanisms for CFS and is worth examination and consideration.
Sacrificial Prioritisation can be considered as creating a second problem in order to fix the first problem. The various protocols described on this site can work to prevent this from occurring, given careful personal management, but even if one does end up sliding down the ladder to a very difficult place to recover from, it is still possible, but might just take more time and skill to resolve.
Cheney emphasises the sequential sacrifice of the organs and systems of the body on account of reduced mitochondrial function, mainly a result of excessive Peroxynitrite formation. He cites various 'protective mechanisms' of the body to prevent normal levels of respiration and oxygenation. However, whilst he may be correct in his observations of the effect of O2 on PFO patients, these two conclusions do not seem to be correct to me. For example, excessive Peroxynitrite formation can surely not be both a cause and a solution at the same time? Peroxynitrite along with NO oxidise Hemolglobin into its non-O2 binding form, Methemoglobin. Surely the body cannot be purposely wanting to have free radical damage occur generally within it and in particular to damage the oxygen tranport capability of the body (along with everything else)? A reduction in Hemoglobin or RBC production, not limited by bottlenecks in Heme production or Methylation would be a more logical route. Of course, one cannot say that Hemoglobin levels are lower than in a healthy subject 'on purpose' if it would not be possible to produce more even if the body wanted to, on account of biochemical bottlenecks and inefficiency. It strikes me that Cheney has included a number of contradictory themes in his overall theory which he cites as being congruent and proof of a wider scheme of things regarding O2 and respiration management.
Cheney does not believe that Sacrificial Prioritisation has anything to do with hypothalamus or brainstem function. He does not consider observations made by Neurologists such as Dr Peter Julu that Abnormal Spontaneous Brainstem Activations and an inflamed brainstem may result in a variety of adverse cardiac effects. Some of these are examined in the following section. In the Phenotype Encoding of CFS section above, I describe Cheney's hypothesis that it is not the hypothalamus that is driving the shift in physiology. Perhaps if Cheney was party to all the latest research in this area, he might revise his opinion slightly.
Cheney has proposed several mechanisms or rather drivers behind the sequential sacrifice of organs and systems of the body. The main drivers suggested or implied are superoxide production and its control (affecting mitochondrial function), the phenotype adaptation and finally the PFO (in those CFS cases that have one).
Is Cheney's theory akin to the tail wagging the dog rather than the dog wagging the tail? It does not appear that he has actually identified a specific mechanism and controlling factor for the sequential sacrifice. Some possibilities have been suggested, e.g. phenotype adaptation. However, the general controlled deterioration down the pathway towards cardiac failure over the long term is much less chaotic in some patients than his theory would suggest. Of course, there is very little equilibrium in the latter stages, but further up, there is a distinctive level of control and management occurring in my view, which would suggest Brainstem involvement. Has Cheney just viewed patients embodying different levels of deterioration and simply joined the dots together to produce a theory and connection between the different levels of condition where they may not always be one? Or such a clear one at any rate? He states that his hypothesis was based on his own personal experience of heart failure.
The hard evidence he relies on include red blood cell irregularities and other isolated trends amongst those patients he has studied himself. Coping with one's heart insufficiency is of course a practical reality whilst one is undergoing treatment to resolve the condition. However, if the cure is to fix the 'core problem' of mitochondrial dysfunction and toxicity, then in a sense perhaps the final destination is irrelevant? Of course, if it is indeed a distinct possibility, which statistics seem to suggest (if you ignore the cancer statistics) - being killed by cancer prematurely does not fit in with this model - then knowledge is power. However, for every person that may use this theory as motivation and leverage, there may be ten others who are scared to death by it, and are unnecessarily fixated on PFOs and Cardiac Arrest, and becoming needlessly stressed - which makes their overstimulated conditions even worse.
It is perhaps a chicken and egg question (to really mix metaphors!) The history of the patient and progression of the condition is in some respects irrelevant, but the actual current scenario is what matters, and how to treat it now. If most or all CFS patients have progressed to the latter stages of his sequence, is there statistical evidence for patients at the former end of the sequence? Or is the progression actually very rapid or indeed simultaneous? If the sequence is more of less correct, it is probably much more complicated than has been theorised, as there are a huge number of biochemical processes involved and steps in between. Of course Cheney is trying to distill the mechanics of Cardiac insufficiency down to a simple high level formula, but it is not really possible to separate many of the body's pathways out like this, as they are highly complex in nature and can be affected by a number of other systems and other biochemical problems.
In Cheney's clinic, he has observed the prevalence of PFOs to be approximately 80-90% (2006 figures?), in contrast to the 15-30% of the population with one. There appears to be a little 'back pedalling' or at least more accurate quantification in Cheney's figures in 2006, as in his 2003 seminar video he states that 99% of his patients had a PFO, which is quite different. Was this based on a very small number of patients? Or just a moment of generalisation to emphasise the point? It would make sense to take his latest figures more seriously.
One could complain that he does not attempt to examine the patients that do not fit his profile or research purpose and the reason for failure adequately, which takes away from the validity and usability of his research. As he stated himself, his patients are maybe represent only a certain type of CFS case and he could perhaps make more effort to collaborate with other doctors and clinics to study a wider variety of CFS cases. So for all the criticisms of Cheney's 2003 Heart Insufficiency theory, I have found it very interesting and very useful conceptually in certain respects, and this is why I have dedicated a page to it on this web site.
Just to what extent Formane Ovales are ripped open in CFS cases one can only speculate, and unless sufficient testing is performed on patients during the course of their illness from a wide variety of populations, then we will never know. Of course, this is hardly practical, as most patients don't report their CFS to their GP until it the pattern has firmly set in, and most people have never and will never have a PFO test performed. But perhaps it is an added incentive to seek early treatment, to keep the risk of bursting one's Foramen Ovale open down to near zero if possible; as well as having a life as soon as possible! Assuming one follows the correct course of treatment and does not do anything grossly irresponsible with one's health, then the chances of having a PFO-related complication or indeed diastolic failure are extremely low and no more significant than the average member of the population - i.e. nothing to worry about! It is not even certain that many if any CFS cases develop/rip open their Foramen Ovale during the course of their illness, and like Cheney admitted himself, he may well be seeing the most ill CFS patients at his expensive clinic, which perhaps were those CFS patients that have had a PFO all their lives, and having that PFO meant that their condition deteriorated more than most CFS sufferers. It is never wrong to have a PFO test, but this should be no more pressing than for the next person who does not have CFS. Cheney's theory is plausible in parts but is not intended to scare CFS sufferers and increase their stress levels. It contains many positive treatment ideas to return to you full health; and if one considers these ideas in the context of the other ideas and facts presented on this site, and indeed elsewhere, you have a significant arsenal of tools on your side to fully restore your health and beyond - to the pinnacle of health and vitality.
I had made a near full recovery through adrenal stimulation through herbs, and vitamin and mineral supplementation; and at another time, made a near full recovery when he began an EM stimulation/detoxification programme using FIR saunas and phospholipid therapy. Whilst these treatments may have indirectly stimulated the heart, I believe that by treating the body as a whole, and working on stimulating mitochondrial and endocrine function by various means, the heart is simultaneously treated (directly or indirectly).
At various points in the evolution of one's condition, then, certain inputs can lead to a full recovery if one does not overdo things too much. To me, this suggests that the overall picture is more complex that Cheney and Dr Myhill would have us believe. The solutions to mitochondrial inefficiency are also presented in a somewhat simplified manner - perhaps to make the concepts easier to grasp. However, as previous stated, simply throwing some specific cofactor, vitamin and mineral supplements at the body is not going to miraculously cure mitochondrial function in all patients. A more rigorous analysis is required of the levels of these cofactrs, nutrients and vitmains in the body; in addition to observing what else has been going on in the patient's life, the level of AMP formation and ATP depletion, as well as the stage of detoxification and overall liver health etc.
Traditional Chinese Medicine (TCM) probably views the problem in a similar manner, as it deems that Qi/Chi leads the blood flow, and that those patients with CFS have very low, stagant Chi which affects proper blood flow in the body. At various points when I have seen an acupuncturist, besides the stomach and spleen meridians being very weak, the heart and lungs were also found be deficient. This does not of course prove anything, but suggests that the heart does indeed play an important part of the picture in CFS, in addition to the other factors and deficiencies.
Cheney has himself stated that improving mitochondrial function is the 'cure' to cardiac insufficiency (assuming no congenital heart factors are at play) and CFS in general, so clearly boosting metabolism and mitochondrial function is considered good by him if it boosts BOTH the heart's capability as well the body's general demand for blood. Perhaps a similar argument could be made for oxygenation. Clearly each case is different and generalising about CO2 levels, peroxynitrite levels, superoxide levels, glutathione levels, oxygen demand and oxygen levels is not clever unless one takes into account the exact picture in a given individual and the exact bottle neck in mitochondrial function - as it is a hugely complex area. In amny cases, one has to support a number of other pathways in the body, repair cell membranes and remove heavy metal toxicity before mitochondrial function can effectively recover. Simply throwing mitochondrial support supplements at someone may only get you so far. It is doubtful that Cheney's studied patients are actually representative of the cross section of CFS in general but perhaps just one particular subset of it.
What sequence does Cheney actually propose for the recovery from CICM? Does mitochondrial function in general improve, resulting in increased demand from the tissues and also increased capability of the heart (both at the same time)? Followed by a gradual return to normal breathing (through instinct or through conscious practice)? Or does the breathing return to normal together with the other stages of improvement? There are clearly many assumptions being made here.
The heart is impaired as are many othe systems, and they all need to be supported and worked with and not abused until one's overall condition is resolved. From his comments on adrenal/circulation stimulation using licorice, as stated above, it is clear that Cheney is very much in the world of conventional medicine, which is of course not necessarily a bad thing, perhaps on the fringes of it, but he is clearly no holistic specialist. He appears to have a very rudimentary understanding of herbal medicine and indeed little or no understanding (demonstrated or discussed) electromagnetic stimulation and energetic therapies. His treatments recommendations appear to be a mixture of cutting edge biochemical supplementation, methods of which are generally agreed upon by most practitioners in the know, and slightly 'show off' and expensive approaches to a problem that could be solved using a cheap and tried and tested natural method instead.
I am somewhat cynical of doctors who charge exhorbitant sums for their often broke patients, but this criticism could perhaps be levelled at most private medical consultants and holistic practitioners, who often tend to run clinics in the most exclusive and expensive addresses in major cities. At the end of the day, if they get results and do not waste anyone's time, that is what is important, not prestige, money or who has been proven right or wrong.
I believe that my observed pattern in myself and others suggests that the deficiencies behind CFS, typically mitochondrial function and also hormonal function are stimulated by regular light exercise to some extent, if mitochondrial capacity allows it, and that such factors are really the root cause behind some patients conditions. As each case is different, one cannot really assume anything, but must try to determine the exact picture with each patient on a case by case basis.
Dr Cheney's theory does not appear to explain why moderate exercise actually helps some CFS patients, both in the short term and also long term, but makes others extremely ill, even in small amounts. Perhaps this 'training' of the heart muscle is why these patients get better, but what about the other patients? Do CFS patients really have weak heart muscles, i.e. less muscle mass, or is it merely just an inability for the same muscle mass to function as it normally should, on account of mitochondrial and endocrine system insufficiency, which over time, and a lack of heavy exercise and training, leads to a gradual deterioration of the heart muscle? Those patients that use gentle exercise and show a sign of improvement (rather than deterioration) often do not completely recover; I myself at various points was able to build up my cardiovascular fitness over time, and hike up to 5 hours of vigorous walking, three times a week, week in, week out, but still the other actual aspects of my condition, i.e. mental energy and ability to concentrate hardly showed any improvement at all. This was odd as in some respects I was probably fitter than the average member of the public, but had very little mental energy and of course disrupted sleep patterns and impaired digestion etc.
Cheney's theory seems to suggest in some respects a binary or reductionist view of CFS rather than its heterogenous and complex reality, although this may be just a result of the way he presents topics and tends to exaggerate the importance of a given factor over all others at the point in time. He appears to have a penchant for the over-dramatic and theatrical in his claims and statements, and betrays the tell-tale signs of excessive ego that he likes to in a sense 'replace' all research that went before him. This is however not uncommon amongst researchers. Perhaps he has been searching for the 'Holy Grail' of CFS, like Physicists are searching for the 'Unifying theory of physics'. Given the heterogeneity of CFS, such a theory would only cover certain aspects and could never be applied to all aspects of CFS.
Dr Cheney's recommendations for treatment protocols of CFS patients have also varied and changed greatly over the years. Whether his ideas have evolved or actually changed and performed a complete U-turn many times is a matter of debate. Cheney has had a rather pharmaceutical medicine bias as opposed to a truly holistic approach, mixing holistic medicine with pharmaceutical drugs in his treatment protocols over the years. He has on occasion given arguably inappropriate advice or recommendations on occasion in the past too, and the same seems to be true of some of the protocols described in the 2004 document (e.g. rebreathing etc.) In some cases, whilst his grip on causality seems to be razor sharp, some of his recommendations for actual treatment based on these principles seem to be off the mark. For example, in his October 2001 seminar, he recommends the use of the drug Klonopin (aka Clonazepam) for promoting GABA production, and insists that it is not addictive. However, a friend of mine was addicted to Klonopin during his time of usage of it and had many extremely adverse effects from it. Documented withdrawal symptoms include severe anxiety and psychosis. I generally believe that Cheney has a great deal of useful things to say, but that some of his ideas/suggestions should be taken with a pinch of salt and interpreted correctly (or indeed modified).
It should be noted, that whilst Cheney's hypotheses about CFS treatment have changed greatly over the years, they are still evolving. Whether they are becoming more refined or not or more haphazard is a matter of debate. Perhaps a mixture of the two. In 2006, Cheney was strongly advocating the use of D-ribose and Coenzyme Q10 to improve mitochondrial function and thus assist the heart, yet in 2009 he stated that D-ribose and CoQ10 were 'toxic' to CFS patients and would only make them worse (i.e. increase oxidative stress and oxygen toxicity on cardiac muscle). In 2006, Cheney was promoting the idea of boosting reduced Glutathione production naturally, and his contemporaries were promoting methylation cofactors such Methyl-B12 and 5-MTHF (active B3), but in 2009 he declared them similarly 'toxic' to CFS patients. I am less than convinced by this revised position on these substances, although I am not particularly keen on D-ribose for a variety of reasons (but each individual reacts differently of course). That is the fundamental flaw here, Cheny has a predilection to making absolute statements and then making contradictory absolute statements later on in some cases. However, CFS is not a binary condition and it requires the practitioner to examine what the core problems, imbalances and deficiencies are in each case, rather than prescribe a generalised approach which 'supplements most of the cofactors' that might possibly affect a given individual - rather than finding out what is deficient and addressing those areas specifically.
Dysautonomia and Abnormal Spontaneous Brainstem Activation (ASBA)
An analysis of autonomic system profiling, and the types of parameters and reflex mechanisms of the sympathetic (fight or flight) and parasympathetic (rest and digest) nervous system that can be tested, can be found on the Tests page in the Neurophysiological Tests section. It is worth reading through this section in order to put this discussion of Abnormal Spontaneous Brainstem Activation into context.
Dysautonomia in general can be regarded as a shift in the body's normal automatic, unconscious regulatory functions that control many adaptations of the body that we do not consciously have to concern ourselves with regulating with our minds to ensure we stay alive throughout the day, in response to changing demands on the body. Fluctuations or instability in the baroreflex (Blood Pressure maintenance) and heart rate affect the provision of a steady and reliable blood flow to the organs and muscles of the body which can result in fatigue, dizziness, difficulty in exercising, quick depletion of energy and other symptoms.
During severe illness, especially infections, the body's autonomic system undergoes a shift in its normal baseline of functioning in order to prepare the body to fight off the infection. The brain stem and hypothalamus are involved in the body's immune system response. The problem lies when the autonomic nervous system does not return to its original equilibrium and normal baseline - it seemingly having 'forgotten' where or what it is, and being trapped in a pattern of dysautonomia or misregulation of the body. The autonomic functions of the brain are generally controlled by the Brainstem and the Pituitary Gland in the Hypothalamus. After a severe viral episode, or other mechanism, the brainstem itself can become overstimulated and over-interpret stimuli from the nervous system and also behave erratically itself.
'The brain stem (or brainstem) is the lower part of the brain, adjoining and structurally continuous with the spinal cord.'
As well as abnormal fluctuations or instability in the blood pressure and heart rate, Dr Peter Julu argues that the actual heart beat itself may be impaired. The heart beat may take the form of a 'stop-start' cycle, where the cardiac muscle receives energy and inotropics (compounds that help to strengthen the heart beat), which run out half-way through the beat cycle. This prevents a smooth heart beat and may be comparable to what Paul Cheney describes in his Diastolic Cardiomyopathy theory.
Abnormal Spontaneous Brainstem Activation (ASBA) is a condition whereby the brainstem is inflamed, irritated or overstimulated, and the neurons are 'misfiring' and sending signals to the nervous system, including the heart, in an abnormal or erratic manner. This can result in what we observe as cardiac arrhythmia and instability. This cardiac arrhythmia of the blood pressure and heart rate is manifested in random fluctuations in the heart rate and blood pressure, within certain limits, and abnormal responses to various physiological changes in the body, e.g. posture, bodily movements etc. (i.e. dysautonomia). ASBAs can be indirectly measured by abnormal spontaneous cardiac behaviour.
According to Dr Peter Julu, ASBAs are generally found in:
The Premature Brain
In the context of CFS and related conditions, it is the Allergic function that appears to be operating.
There are various possible causes of ASBAs in CFS patients. These could be:
Too low carbon dioxide levels in the blood and tissues (alkalosis)
Excessive immune system response, e.g. allergies*
Neurotoxin build up*
Multiple Chemical Sensitivies*
Abnormal Calcium/Magnesium Metabolism
Dr Peter Julu believes the emphasis is on Allergies rather than Heavy Metal Toxicity, which he believes has other types of effects on the body.
Those marked with a '*' above are all tied to the Nitric Oxide / Peroxynitrite cycle and the self-perpetuating cycle of free radical production and oxidative stress. These tend to inflame the nervous system, and upregulate the allergic response, which itself generates more Peroxynitrite (via Nitric Oxide and Superoxide). Excessive immunity activation is just one cause of the Peroxynitrite cycle, and there are many others, including stress and toxicity. In my opinion, ASBAs, caused by brainstem inflammation and improper brainstem functioning, are largely a result of excessive Peroxynitrite formation. This is a characteristic of inflammatory diseases in general. More information on this topic can be found on the Nitric Oxide/Peroxynitrite Cycle page.
Thermoregulatory Vasomotor Function (TVF) is the ability of the nervous system to control body temperature in response to changes in the external environment. It relates to the regulation of the blood vessels in the body. In a healthy person, if the left hand is exposed to cold, then the blood vessels in both hands are expected to constrict to stop heat loss, rather than each hand operating independently. Abnormal TVF may result in no response in the blood vessels in the rest of the body to a cold input one one of the extremities, or even the opposite response, e.g. vasodilation in both hands when vasoconstriction is expected. Examples of poor or abnormal TVF function include temperature sensitivity and maladaptation to temperature changes, e.g. a sensitivity to drafts. TVF problems can also result in the body running slightly too warm during certain times of the day, burning off more energy than it should be for heat, which is badly needed in the organs or tissues of the body. Certain individuals with TVF problems may find that they do not need such thick blankets at night, for example. TVF problems may arise for a number of reasons. One of these could be damage to the valves in the blood vessels in question by toxins. These valves can however repair once the sources of the toxicity is removed from the body. Another parallel mechanism for poor thermoregulatory problems may be decreased thyroid function. Another possible cause of systematic cellular temperature increase is the accumulation of Lipofuscin deposits in cells.
It is of interest that the Brain Stem and Hypothalamus have been identified by Neurologists such as Dr Peter Julu as being responsible for much of the dysautonomia observed in CFS patients and patients of related disorders. These parts of the brain are inflamed and irritated, and overstimulated. In contrast, the NLP practitioner Ashok Gupta, who treats CFS patients himself, has identified the Amagdala, in the Pre-Frontal Cortex, as being responsible for the problems of CFS. The Amagdala is the primitive part of the brain involved in interpretation of external conscious stimuli and dealing with the baser emotions, often associated with digust, fear and the fight or flight response. Ashok Gupta argues that this part of the brain is overstimulated and 'burnt out' and proposes a series of brain calming measures in order to calm the Amagdala and restore better quality sleep patterns and general relaxation. Please see the Stress Management and CFS page for more information.
A programme geared towards treating dysautonomia depends on the exact cause.
Supplemental Oxygen - to assist the body in supplying necessary O2 to the tissues.
Alteration of one's breathing technique depending on the ratio of CO2 to O2 in the blood and tissues, in order to maintain the correct balance of O2 and CO2 in the body.
One should examine and consider the possibility of allergic inflammation and aberrant allergic response, either to food, or the chemical compounds in the body. This may involve taming/retraining/reconditioning the body's allergic response and cellular inflammation, and perhaps also excluding certain irritating food types from one's diet temporarily. And most certainly an antioxidant treatment programme to deal with Peroxynitrite formation. Please see the Immune System page and Peroxyntrite page for more information.
A healthy liver and toxin-free body is also of key importance. Look at ways to support the liver and potentially detoxification protocols (carried out in such a manner as to support the bodily functions rather than just wear out the body).
One should also consider relaxation and brain calming techniques, which most likely affect the Amagdala primarily, but this may well have some knock on effect to other parts of the brain. Stress and hyperexcitation do appear to correlate quite strongly to a worsening of allergic response and related functions so this is worth exploring too.
Lip Trainer Patakara - a new product that is claimed to increase cerebral blood flow and boost parasympathetic nervous system responses. I have tried this product and it does seem to help, most so initially.
Anti-ageing, nootropic drugs such Centrophenoxine, that help to remove Lipofuscin deposits from the brain and heart, helping to increase cellular efficiency and communication, and allow better nervous system and cardiac function.
Neuronal Membrane stabilising prescription drugs such as Pregabalin (marketed by Pfizer as 'Lyrica'. These may help to reduce ASBAs. It has been recently marketed as a treatment for Fibromyalgia, which has received mixed reviews (presumably as there are many other factors involved in Fibromyalgia on a biochemical level). Pregabalin is not without side effects and are not something I would recommend considering unless only to be used for a short, disciplined period of time rather than regular, continual and long term usage. Pregabalin use can result in dependency and withdrawal symptoms if one discontinues it after long term usage.
Palpatations (Extrasystole or Cardiac Arrhythmia) can take the form of fluttering in the chest, skipped beats, heavy, thumping or pounding heart beats. It is not a fault with the heart per se, but a fault with the electrical signals or impulses going to the heart through the nervous system, from the brain stem. Whilst palpitations can be serious, in most cases they are relatively harmless. However their manifestation can cause considerable anxiety and stress in some patients, and can interrupt regular sleeping patterns etc. if experienced whilst lying down. Palpitations are therefore a pattern of irregular electrical signals to the heart. To alleviate the palpitations (in the short term) and return the beating pattern and electrical signalling from the brainstem to normal, a variety of methods can be employed.
Avoid caffeine, nicotene, alcohol, spicy foods (e.g. curries or chillies), high salt (Sodium) intake and recreational drugs as these can be triggers for palpitations. This is something you should be doing anyway to avoid putting excessive strain on your adrenal glands and interfering with your circadian rhythm in general.*
Relax - often over-mental exertion or stress can excite the neurons that are responsible for controlling one's pulse. If you have been busy for a while working or concentrating, and your palpatations are getting worse, then take some time out to relax and calm the mind. Various exercises to calm the mind and neuronal activity include energetic therapies (e.g. Quantum Touch and Reiki may be particularly effective), meditation, breathing exercises, certain types of relaxed distractions, binaural beats (delta at night, delta or theta range in the evening, alpha range in the morning) or perhaps relaxing herbs such as Valerian (close to bed time) etc. If you are experiencing palpitations in the middle of the night it may be useful to listen to 30 minutes or so of binaural beats, focussing on delta and perhaps theta frequencies, before going back to bed again.
Focus - use focus/distraction to your advantage, not to your detriment. If your palpitations have gone away, then if you focus on yourheart beat, then it is very easy to bring the palpitations back again. So it is wise not to focus on your heart beat, but to distract the mind. The mind likes to prove that it has to power to choose to do something, because it can, and usually it is easiest to choose the lowest level, negative choice, which in this case is to bring back the palpitations.
Supplementation with brain calming neurotransmitters and their precursors may help if the levels are low or tend to drop off during the night, e.g. 5-HTP, L-Theanine and/or GABA.
Some people may find sexual activity relaxing after orgasm, but it does elevate the heart rate and excite the nervous system, and can cause severe palpitations afterwards in some individuals - in which case any sexual activity should be ceased or drastically reduced until the cardiac arrhythmia has corrected itself in your treatment programme. Taking a little extra Pregnenolone (the prohormone) may potentially help alleviate such symptoms.*
Cough - coughing during palpitations may interrupt the rhythm and shift it back to normal. May only work whilst experiencing palpitations if they are body position specific.
Splash cold water in your face or immerse your face into cold water briefly (using a snorkel without a mask perhaps for prolonged exposure). This engages the mammalian diving reflex, which is used by humans and animals to prepare for extended times underwater - including Bradycardia, or the slowing down of the heart rate. This may help to bring your heart rate and palpitations back to their normal, proper rhythm. May only work whilst experiencing palpitations if they are body position specific.
Valsalva Manoeuvre - as described on the Tests page - can help to raise your abdominal pressure and effectively drain the heart of blood. It may also help to interrupt your current cardiac arrhythmia and restore proper heart function and rhythm from the brainstem. Of course, the Valsalva Manoeuvre should only be performed for short periods of time and if your heart is comfortable doing this. May only work whilst experiencing palpitations if they are body position specific.
Avoid Overexertion - if you had been exerting yourself too much physically or mentally immediately prior or cumulatively during the day, your brainstem pulse control may become disturbed and settle into the incorrect rhythm causing palpitations. In addition, such over-exertion can delete your mitochondrial reserves. You may want to consider pacing yourself and/or resting for the rest of the day and the next few days. Mitochondrial depletion may have an instant effect on the heart or a delayed effect on cardiac symptoms. The former scenario is clearly a sign of deterioration.*
Supplemental Oxygen - if Cardiac pain or palpitations are on account of Hypercapnia (too much CO2) and too little O2 in the blood, both of which are alleviated to some degree by breathing O2 and/or deeper breathing techniques. This is caused by a inefficient gas perfusion from the blood, often in certain body positions more than others. If you are already using supplemental oxygen (in a certain body position, e.g. supine) and it is not helping enough, you may need to increase the flow rate.* You may find sucking on the actual prongs of the cannula a useful short term way of breathing close to pure oxygen (rather than simply mixing O2 with inhaled air through your nose as per normal).
Change of body position temporarily to improve tissue oxygenation and lower carbon dioxide build up. If you tend to have palpitations when you are lying down, then it may be advisable to get up when your palpitations are worsening, either if you cannot sleep or have just woken up from a short period of sleep and perhaps also do some of the others on this list. A full bladder can sometimes make this worse (requiring change of body position and urination before trying to go back to bed again). Sometimes a change in body position actually brings on the palpitations, for example if you are half asleep, and perhaps moderately need to urinate, if you get up to go to the toilet, you may find that when you go back to bed again, it brings on the palpitations, which otherwise if you had just laid there and tried to go back to sleep would not have arisen. Making sure you urinate before going to bed at night however is a sensible idea and a partly full or full bladder when going to bed may bring on palpitations.*
Empty your bowels. Whilst on the toilet! A full colon may well be full of highly toxic substances and holding it when you could feasibly go to the toilet and empty your bowels, may well help stop or ease palpitations, as well as make you feel more relaxed and generally better. Whether in the middle of the night or during the day. It is best to empty the bowels before going to bed if possible.
Stop overeating. If you are overeating at meal times, then try to work on not doing so. An overful stomach may result in palpitations, especially when in the supine position..
If these methods still don't work (including those mentioned below), then there is likely another underlying chronic nutritional requirement. e.g. if you have been detoxifying the body with a chelation programme, you may well be chronically low on Calcium, Potassium, Sodium and/or Magnesium; or the ratios of Potassium, Calcium and Magnesium may be sub-optimal. Too high Sodium intake may deplete Potassum and interrupt electrical signals to the heart muscle. Another possible explanation is that there is a chronic B-vitamin deficiency such as Biotin deficiency etc. which may also result in excessive palpitations and low energy levels if present.
Chest pains are somewhat different to palpatations and are usually indicative of a slightly different type of problem, more localised in the cardiac muscle, typically in the right atrium in Diastolic Cardiomyopathy. Sometimes they are indistinguishable from palpatations and may occur at the same time and share some similar causes. Often palpitations can lead to chest pains as the heart is beating harder and using up more energy, and may become strained in mitochondrial terms (hence the pain). The methods for alleviating chest pain are similar to those for alleviating palpitations, but with the emphasis more on supporting the heart muscle and mitochondrial function in general. These are listed below. These may also help with palpitations. Some examples that help both chest pains and palptations are listed above and marked with a '*'.
Mitochondrial support supplements, e.g. Acetyl-L-Carnitine, Coenzyme Q-10, NADH (Active B3), Lipoic Acid - if Cardiac pain is on account of lack of cofactors for energy production. Possibly Peak ATP or D-Ribose if an emergency!
Cardiac support, e.g. Hawthorn (in the first instance, perhaps considering beta blocking drugs in the second instance). Hawthorn is a chelating/mobilising agent, and if significant levels of heavy metals are in the tissues, then taking it may make one feel very ill (depending on what stage of a chelation/detoxification programme one is in). Alternative antioxidants to Hawthorn to help lower blood pressure, that are not chelating agents, include: Co-Enzyme Q10, Grape Seed Extract (high in polyphenols and resveratrol), Pomegranate Extract (high in polyphenols), Quercetin, Bromelain, Nattokinase (the enzyme from Natto), Arjuna Bark, Hibiscus, Motherwort, Garlic, Vitamin E (Gamma Tocopherol), DHA (Omega 3 fatty acid in fish oil), Casein Peptide, etc. It should be noted that whilst Vitamin E, as well as being a blood pressure lowering nutrient, also increases the strength of the heart beat. Dosages should be increased slowly as a rapid increase in dosage may temporarily elevate blood pressure. High dosages may increase symptoms of heart palpitations so you may need to find the dosage that works best for you. If one suffers from palpitations at night, whilst in the supine position, then one may elect to take one's dosage of Gamma E in the morning and possibly mid-afternoon only (avoiding the evening). Those who are suffering from Rheumatic Fever or Rheumatic Cardiac Disease (damaged valves in the heart muscle) should avoid dosages of over 100 IU per day. Vitamin E is a powerful peroxynitrite scavenger and NMDA inhibitor, lowering excitotoxicity. It may also help to recycle oxidised Glutathione into reduced Glutathione, as other antioxidants tend to do.
If your heart muscle is overstrained, it may require muscle repair, like other strained muscles in the body if they are overexercised. The amino acid Glutamine constitutes a large part of the muscle tissues, and supplementation may be useful in relieving chest pains over a period of days. Be careful to keep your amino acid supplementation balanced so as not to throw your natural amino acid balance out of step.
Don't wait too long between meals. Going on an empty stomach for too long may worsen any palpitations or chest pains you are experiencing, especially in your most susceptible body position. Mitochondrial supplements may not be so effective if you have an empty stomach (i.e. no fuel to actually 'burn'. Too much food may also have an adverse effect.