Dr. Cheney's Thoughts on CFIDS

The following article was written by Linda Sleffel for the CFIDS/FMS Support Group of Ohio, based on Dr. Cheney's June 2005 lecture in Dallas/Ft. Worth. The 2003 study by Peckerman which was the beginning of Cheney's investigation of the role of cardiomyopathy in CFIDS is available for download at http://www.cfids-cab.org/MESA/Peckerman.pdf

CHENEY VIDEO 2005: CFS AND DIASTOLIC CARDIOMYOPATHY

by Linda Sleffel


All of the theories, opinions, and recommendations in this report are those of Dr. Cheney, not of the CFIDS/FMS Support Group of Central Ohio, its members, or its steering committee. We recommend that you seek additional information, consult your own doctor, and consider carefully before beginning any treatment.

“Cardiopathy” means heart disease or heart dysfunction. “Cardiomyopathy” means disease or dysfunction of the heart muscle. “Cardio” means “heart;” “myo” means “muscle,” and “pathy” means disease or dysfunction, some physiological process that is abnormal.



DIASTOLIC CARDIOMYOPATHY

Dr. Cheney believes that CFIDS patients have a heart problem that reduces cardiac output. The body tries to compensate for the reduced blood flow, and compensatory mechanisms actually cause most of the symptoms of CFIDS. He no longer believes that viruses cause CFIDS; he thinks CFIDS patients have some underlying abnormality that allows a virus or other precipitating factor to make the heart problem worse and push them into the early stages of CFIDS.

The heart problem involved is called diastolic cardiomyopathy. “Diastolic” refers to the period between heartbeats when the heart is expanded, taking in blood for the next heartbeat; “systolic” refers to the period of the heartbeat, when the heart is contracted and is pumping blood.

Diastolic cardiomyopathy is NOT the kind of heart disease that causes heart attacks. It is NOT the kind of cardiomyopathy that caused Dr. Cheney to have to have a heart transplant. It has only been identified by the medical profession in the last ten years, and it can only be detected by highly sophisticated equipment.

First, a little review of heart function: Blood from the entire body enters the right atrium of the heart through the vena cava. From the right atrium, it passes through a valve to the right ventricle, which pumps it to the lungs for oxygenation. Oxygenated blood returns to the heart and enters the left ventricle. It then passes through the mitral valve to the left ventricle, the most powerful part of the heart, which pumps it out through the main artery of the body, the aorta, to the entire body.

Diastolic cardiopathy has not been studied extensively; it is not detected by the usual kinds of testing. Echocardiograms (sonograms) typically measure what is called the “ejection fraction,” the percentage of blood in the ventricle that is forced out by each heartbeat. The ejection fraction is completely normal in CFIDS patients; it may even be above normal. Further, cardiologists have not studied this dysfunction in detail, because testing for it is complicated; they don’t understand this abnormality, and they have no treatment for it. (Where have we heard this before?)

Even though the ventricle is pumping well, cardiac output, measured in liters per minute, can be far below normal. (A liter is a little more than a quart.) Normal output ranges between 4 and 24 liters per minute, with 4 being the output when resting and 24 the output of a well-trained athlete. Output capacity of 7 to 10 liters per minute is required for normal activities and for maintaining the health of the body.

Depending on the sensitivity settings of the equipment, as many as 20 percent of the population may be shown to have diastolic cardiomyopathy. There are two types of this disorder; people with the more serious form may die of it. CFIDS patients have a milder form, which is not life-threatening, and the compensations their bodies have made — which Dr. Cheney believes cause many CFIDS symptoms — protect them from progressing to a life-threatening form of diastolic cardiomyopathy.

The reason CFIDS patients have low cardiac output is not that the left ventricle is weak or is not performing properly. The problem is that not enough blood is entering the ventricle between heartbeats; the ventricle is not filling properly.

The process of expanding and filling with blood flowing from the left atrium actually requires more energy than pumping. In a very complicated process, the calcium in the muscle cells is forced out of the cells into the calcium channels, and the cells must actually expand so the ventricle can expand. The atrium provides some pumping action to push blood into the ventricle, but the ventricle must also suck the blood in. Dr. Cheney compares the energy aspect of ventricular filling to pushing a boulder uphill, and the pumping or release of the energy, to the boulder rolling down the hill.

He believes the mitochondria of the heart muscle cells cannot produce enough energy to allow the ventricle to fill properly. The mitochondria are the structures inside cells that metabolize glucose to produce energy. He doesn’t know the reason for the mitochondrial dysfunction, although the abnormal form of RNase-L, an immune system enzyme, contributes to cellular dysfunction and may damage the mitochondria.

Blood flow through the heart can be measured by impedance cardiography. A small electrical current is passed through the chest from the front to the back. Since blood is basically water, and since water conducts electricity, the more blood that is being pumped through the heart, the faster the electrical current will pass.

The most important research on diastolic cardiomyopathy, Dr. Cheney believes, is described in a 2003 article: Peckerman, et al., “Abnormal Impedance Cardiography Predicts Symptom Severity in Chronic Fatigue Syndrome,” The American Journal of the Medical Sciences, 2003; 326(2):55-60. Dr. Peckerman’s findings are described in the CFS Research Review, Vol. 4, Issue 2, Fall 2003, pp. 1-3.

Using impedance cardiography, Peckerman found that the patients he had identified as being extremely disabled by CFIDS had low cardiac output, and that the degree of disability was correlated with the degree of reduced output.

Although not life-threatening, the diastolic dysfunction prevents the heart from pumping enough blood to supply all the tissues with the oxygen and nutrients they need to be healthy. It could lead to dangerously low blood pressure if it were not for the fact that the body tries to compensate for the reduced blood flow and maintain adequate blood pressure.



COMPENSATORY MECHANISMS

The first way the body tries to compensate for reduced blood flow is to constrict the capillaries, the smallest blood vessels. Constricting blood vessels will increase blood pressure, just as using a nozzle to constrict the flow of water from a hose will increase water pressure and make the stream strong enough to reach farther.

While blood vessel constriction can maintain blood pressure, it reduces blood flow to the cells, which are then starved of oxygen and nutrients. This will affect every organ system in the body. It also sets up several vicious circles, in which dysfunction in one system will affect another, which in turn will cause further dysfunction in the first.

Good circulation depends not only on cardiac output, but on the rhythmic constriction of blood vessels, which helps keep the blood moving. This aspect of circulation is also impaired in CFIDS.

When organ systems aren’t getting enough blood and enough oxygen and nutrients, the body compensates in a second way. It further reduces the blood supply to organ systems less essential for maintaining life, in order to send more to essential systems.

The first organ system whose blood flow is sacrificed for the benefit of others is the skin. When you go out on a 100-degree day, the skin needs 3 liters of blood per minute to dissipate heat and cool your body. But if your heart output is low, possibly as low as 4 liters per minute, your body cannot send 75 percent of blood flow to the skin and still maintain the functioning of other systems. So the blood is not directed to the skin to cool you off, and you become unable to tolerate heat or to adjust to changes in temperature.

The second organ system to be affected by reduced blood flow is the gut, the tissue of the intestines. The digestive system is the system that exposes your body to the greatest amount of foreign substances. Along with nutrients, your food contains toxic substances, which enter the gut. Your gut also contains billions of bacteria, more bacteria than you have cells in your body. Many of them are actually needed to maintain the health of the gut, but they all produce waste products from their own metabolism. When gut cells don’t get enough oxygen, they secrete a substance called vascular endothelial growth factor of VEGF. VEGF causes leaks in capillaries, which leads to leaky gut syndrome. This allows toxins produced by the bacteria to pour into the bloodstream instead of remaining inside the gut and being eliminated in the feces.

At one time Dr. Cheney believed liver function was impaired in CFIDS patients. Now he thinks the liver is simply overwhelmed by the amount of toxins in the blood, and is unable to detoxify them all.

The constriction of capillaries impairs microcirculation throughout the body. It prevents the brain from getting enough oxygen. It means that hormones can’t reach the cells, so the patient can experience a variety of hormonal imbalances, including thyroid problems and derangement of female hormones. The immune system is not necessarily impaired, but it is ineffective because immune cells and chemicals aren’t transported to the cells and tissues that need them. Lack of an effective immune system allows viruses and intracellular bacteria to become active. This, in turn, can lead to further increases in RNase-L and further cell damage.

Impaired oxygen and nutrient supply to the muscles causes extreme muscle fatigue.

Some CFIDS patients have hypercoagulability — their blood coagulates faster than normal, and this also contributes to poor microcirculation. These patients may be helped by anti-coagulants such as heparin.

Reduced levels of 2,3 DPG can further impair oxygen transport. 2,3 DPG is necessary to allow hemoglobin molecules to release oxygen molecules into the tissues. So blood oxygen levels may be normal, but tissues may still be starved of oxygen.

There is a breath-holding exercise that can increase 2,3 DPG levels: Inhale through your nose for four seconds. Hold your breath for seven seconds. Exhale through tightly pursed lips for eight seconds, creating back-pressure. You should be able to hear the air being forced out of your mouth. Do this eight times in a row, twice a day. If you feel light-headed, just do it six times, or until you begin to feel light-headed, and then build up to eight times.

Poor microcirculation can cause pain, because the blood cells cannot squeeze their way through the tiniest blood vessels. Adrenaline can increase cardiac output, but pain decreases adrenaline production, so people suffering from pain will not have enough adrenaline in their systems to benefit heart function.

Cellular metabolic dysfunction plays a major role in CFIDS. RNase-L activation and mitochondrial dysfunction prevent the cell from carrying out normal aerobic metabolism. When aerobic metabolism is not functioning, the cell reverts to anaerobic metabolism, which produces only about one tenth as much energy as aerobic metabolism, and produces many more toxins.

Aerobic metabolism normally produces superoxide, one of the most destructive free radicals found in the body. However, in normal aerobic metabolism, SOD, superoxide dismutase, further metabolizes superoxide, and it is eventually converted to water. When cellular metabolism is highly dysfunctional, superoxide can leak out of the mitochondria, and this creates a serious risk.

The body naturally produces nitric acid, which is a normal chemical in the body and is necessary for certain body functions. It is necessary for the immune response; it is the chemical most important for memory function, and it is essential for penile erections. Nitric acid is produced by three forms of the enzyme NOS or nitric oxide synthetase. iNos is produced when the immune system perceives an infectious process. Microbes, mold toxins, and allergies trigger production of iNOS, with allergies triggering the greatest amount.

nNOS is produced by nerve cells, and it is triggered by thinking, having an emotional response, or smelling chemicals. Any of these contributes to the production of nitric acid in the brain.

eNOS is primarily triggered by VEGF, the chemical that contributes to leaky gut syndrome.

The real problem is that when a molecule of nitric acid encounters a molecule of superoxide, they combine instantly to produce a molecule of peroxynitrite, the very most destructive free radical produced in the body. Peroxynitrite causes damage in all cells, and in a very destructive vicious circle, cell damage caused by peroxynitrite increases the cellular metabolic function that causes production of peroxynitrite.

Dr. Cheney believes the body responds to the production of destructive free radicals by reducing energy output from the mitochondria. This contributes to fatigue and makes cellular metabolic dysfunction worse, but it protects the body from even greater cell damage caused by peroxynitrite.

Peroxynitrite damages the cells through oxidation, and many researchers consider free radicals and oxidation to be the cause of aging and of many diseases that can cause death. However, oxidation in the form of metabolism of sugar is also necessary for life. So oxidation keeps us alive, but eventually it contributes to almost every cause of death.

Substances that remove nitric oxide from the body are vitamin B-12, co-enzyme Q-10, taurine, and hawthorn.

Substances that remove peroxynitrite are essential fatty acids, HDL cholesterol (the “good cholesterol”), plant bioflavonoids found in the skin of fruits and vegetables, uric acid, and carbon dioxide. Uric acid comes from protein, especially from meat. Carbon dioxide not only helps remove peroxynitrite, but it can also reduce the abnormally alkaline condition outside the cells caused by cellular metabolic function and abnormally high acid levels within cells. You can increase carbon dioxide in your system by periodic breath-holding.



REDUCING THE EFFECTS OF DIASTOLIC CARDIOMYOPATHY

The simplest way to increase effective cardiac output is to put your feet up. Raising your feet, even when you are sitting up, is the equivalent of increasing output by 3 liters per minute.

If you have to stand up, step slowly backwards and forwards. The action of the leg muscles will help to keep the blood moving, and it is also the equivalent of increasing cardiac output by 3 liters per minute.

Increasing pre-load. A very important factor in cardiac output is pre-load, which is the amount of blood that enters the left ventricle to be pumped out to the body. Pre-load is highly dependent on the amount of blood returning to the heart through the veins, so it is also dependent on blood volume.

One way to increase blood volume is to drink Gookinaid (Gookinaid.com). Or you can drink Dr. Cheney’s home-made equivalent that doesn’t contain the sugar in Gookinaid. (1 cup spring water or filtered water, 1/8 teaspoon sea salt, and 1/8 teaspoon of “No Salt” salt substitute containing potassium. Add lime juice, an herbal tea bag, or stevia for taste.) Dr. Cheney recommends four to eight glasses of Gookinaid or the home-brew every day.

For patients with low blood pressure, Dr. Cheney recommends 1 to 2 teaspoons of licorice root extract every other day. Only the type with glycorrhizin is effective for this purpose.

To augment pre-load, lie down. This is equivalent to increasing cardiac output by 2 liters per minute in most CFIDS patients. However, some CFIDS patients feel worse when they lie down. For reasons not addressed in the video, lying down apparently decreases pre-load in these patients.

Reducing After-Load. After-load is the resistance the blood encounters in the circulatory system, and it is important to reduce after-load. Dr. Cheney recommends magnesium, which relaxes and opens up blood vessels. For oral magnesium, take magnesium glycinate capsules. Dr. Cheney also recommends injected magnesium.

**The following flowchart is an attempt to integrate the complex interplay of factors impacting mitochondrial function and, by extension, cardiac output. To view full size, right click on the diagram, open it in a new browser window, and then resize to full size using the controls of your particular browser.**

# posted by thevitaminkid @ 3:42 PM