Chronic fatigue, internationally known as Chronic Fatigue Syndrome (CFS), has long been referred to by physicians as a physical and mental fatigue state that does not improve even after long and deep sleep or after a rest cure. At the end of the 19th and beginning of the 20th century, respectively, the term “neurasthenia” was used for this. At that time, it mainly affected the “weaker” sex. Today, hundreds of thousands of members of both sexes complain equally of CFS. There is much evidence that these symptoms are of psychosomatic origin.
The Canadian historian and medical sociologist Edward Shorter dealt with CFS in his extensive study published in 1992 under the title “From Paralysis to Fatigue. A History of Psychosomatic Illness in the Modern Era“(in 1994 in German under the title “Moderne Leiden. Zur Geschichte der psychosomatischen Krankheiten“). He refers to the frequent hysterical paralysis in upper class women described in the last third of the 19th century by the notorious Parisian neurologist Jean-Martin Charcot (1825-1893), chief physician of the Salpêtrière Clinic, which still exists today. However, these and other allegedly hereditary psychosomatic complaints disappeared after Charcot’s death, just like other fads, as quickly as they had appeared. In other words, the patients had put on the performance they believed the doctor wanted to see. Shorter also considered CFS to be a fashionable disease in some ways, positing it as a consequence of the individualistic postmodern lifestyle. He suspected that CFS was caused by the somatisation of depression, especially as for a long time it was regarded as a good thing that mental symptoms were attributed to organic causes.
Prof. Øystein Fluge from Haukeland Hospital in Bergen, Norway sees things differently. He postulates that CFS patients have permanently lost the ability to extract energy efficiently from sugar or carbohydrates via the citrate cycle and the subsequent mitochondria’s respiratory chain due to a defect in their immune system. Instead of carbohydrates, these people would then have to cover their energy requirements mainly by digesting amino acids and fats, which is less efficient.
In order to test this hypothesis, Fluge and his team analyzed the blood of 200 patients with CFS and 102 subjects without symptoms of fatigue. They found that the concentration of a-amino acids, which are suitable as an energy source, was extremely low in the blood of female CFS patients. This finding was lacking in male CFS patients. Fluge therefore suspects that men take the energetically utilizable a-amino acids from the muscles rather than from the blood. In the blood of CFS patients of both sexes, however, abnormally high concentrations of enzymes inhibiting pyruvate dehydrogenase (PDH) activity were measured. PDH is the key enzyme for the introduction of carbohydrates into the citric acid cycle via acetyl coenzyme A. If the PDH is missing, pyruvate (pyruvate) produces lactic acid (lactate) instead of acetyl-CoA with some unpleasant side effects such as muscle aches. And only two molecules of adenosine triphosphate (ATP) are formed from one glucose molecule, which is regarded as the cells’ “pocket change energy”. By contrast, a total of 30 ATP molecules can be obtained from a glucose molecule via the citrate cycle and the subsequent respiratory chain. This huge difference would explain why CFS patients feel so weak.
Fluge and his colleagues base their hypothesis on the observation that CFS symptoms are first observed in most patients after a cold or similar mild infection. Therefore, they suspect that some of the antibodies produced by the immune system to fight the infection may miss their targets and block PDH instead. This assumption is substantiated by the observation that CFS patients seem to feel better when the antibody-forming B-cells (white blood cells) of their immune system are eliminated with the cancer drug rituximab. But this would have to be confirmed by a large-scale test, the results of which will not be available until next year. Fluge, however, is already certain: “CFS is a physiological effect, not a psychosomatic one”.
Has he really got enough for a convincing argument? The fact is that acetyl-CoA can be formed not only from pyruvate, but also by the oxidation of fatty acids to ketones. This is what the followers of the keto diet, who consciously refrain from carbohydrates, take advantage of. Among these are many successful competitive athletes. There is no question of CFS. The only side effect is an unpleasant smell because ketones circulate in their blood instead of glucose. Fluge also admits that the causal chain of CFS is probably much more complex than initially assumed. He refers to a publication by Robert Naviaux from the University of California at San Diego, which has also shown a lack of fatty acids in the blood of CFS patients.
All of this cannot rule out the theory that CFS is a somatised depression. It is a well-known fact that depression does not only occur in the heads of patients, but also affects their entire organism, which in a way reduces its performance. Disturbances of the immune system and low mood can have common (internal or external) causes. This leads to the age-old unresolved question of the temporal order of the chicken or the egg. However, patients are faced with the question of whether they should trust chemotherapy (according to Prof. Fluge) more than psychotherapy.
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