Frankl was right After all

In this article Elisabeth Lukas Explorer modern Depression research, which confirms the logotherapeutic approach.

For almost 30 years, logotherapists had to be ridiculed for sticking to Frankl’s old classification of endogenous and reactive depression – and then naming noogenic, which no one else diagnosed.

Now it seems that Frankl has been rehabilitated. Katsuhito Fukuda, a Japanese biochemist, clearly writes of two distinct forms of depression based on his research.
He speaks of “genetic depression” (we called it “endogenous”), which is inherited, laid out in the genes. Inherited – but it does not necessarily break out.

He speaks of “stress-generated” depression – a broad term, but under it fit the suffering and existential vacuum. So we might find reactive and noogenic depression here.
Then he goes on to recognize certain inflammations in the intestinal tract that lower the mood toward depression – Frankl would have said “somatogenic pseudodepression” – because it would be gone with healing of the gut.

The scientist also writes that antidepressants work only for genetic depression (triptophan metabolism – an amino acid), but not for those produced by stress.
Frankl – and the logotherapists were callers in the desert for 30 years,
keeping old-fashioned terms – and now Frankl is rehabilitated.

Frankl was an excellent diagnostician – and looked closely at his patients. If you are trained on his criteria, you also notice the huge differences between a (endogenous) depressive who only says yes and no and otherwise hardly talks, one who cries his eyes out because his girlfriend left him (reactive) and one who doesn’t know what to do with his life (noogenic). I have all three in the practice, all three have had antidepressants on prescription.

Dr. Heidi Schoenfeld Bamberg, January 2022

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Elisabeth Lukas
Frankl was right after all About modern depression research

Viennese neurologist and psychiatrist Viktor E. Frankl (1905 – 1997) was an astonishingly accurate differential diagnostician for his time and its ́ state of science. He
claimed, among other things, that the mental illness called depression “is not the same as depression”, but that there are different types of this disorder, which must be neatly distinguished from each other and treated differently accordingly. In order to bring his list succinctly to the point, the following subdivision should be recalled:

Endogenous depression: this is primarily due to neurochemical disturbance factors, is largely hereditary, tends to occur in phases and is relatively independent (at most triggered) by external circumstances, and can be alleviated by administering antidepressants.

Reactive depression: This is primarily the result of suffering or severe strokes of fate, which the patient does not have sufficient skills to cope with. The therapy aims at increasing psychological resilience and load capacity.

Noogenic depression: This is primarily due to existential frustration, which makes one’s own life and survival seem indifferent and without perspective. In this case, a struggle to rediscover meaningful tasks is indicated.

Such a classification of depressive illnesses is, of course, subject to a dimensional ontological view of a human being, as Frankl designed it with his “personal union” of soma, psyche and nous. This means that one has to start therapeutically in the respective dimension that is currently affected in order not to bypass the core of the disease process. However, since many of Frankl’s colleagues knew only a two-dimensional view of humans with soma and psyche, they, towards the end of the last century, split into the “biologists” and “psychologists”, as I would like to call them. While the “biologists”, in the course of rapidly developing brain research, tended to interpret mainly neuronal and genetic processes as the basis of depression, the “psychologists” held to the origin stories of all mental problems due to various damaging influences. No agreement could be reached within the guild, so it was decided without further ado to exclude the question of origin and to distinguish only between mild, moderate and severe courses of depression (cf. DSM III, 1980). Almost everyone was satisfied with this, and the advantage of a simple formula was obvious: the more severe a depression manifests itself, the more medicinal support is to be arranged, and the milder a depression manifests itself, the more one can rely on the usefulness of accompanying conversations.

The logotherapy-trained specialists were not satisfied with this. It was not as if they denied the closely interconnected interactions between soma and psyche. Frankl himself spoke of a “psychophysical parallelism” (which he contrasted with the noopsychic antagonism). But the complete ignorance of the noogenic component as well as the omission of any dimensional criterion of distinction in relation to the depressive clinical picture was considered by the

students of Frankl to be a serious cardinal error. They tried to draw attention to it in publications and international bodies, but unfortunately with little success.

Meanwhile, the tide is likely to turn. Nowadays, there are highly topical research results on the enzymes of the tryptophan metabolism, which confirm Frankl’s theses. One of the leading biochemists in this field is Katsuhito Fukuda from the Soka Clinic for Psychosomatic Medicine in Saitama/Japan. He has been pointing out since 2014 in “Open Access Articles” and similar publications that there are indeed different etiologies of depression, which require a more precise classification of depression forms. After all, more than one third of all severely depressed patients do not respond to administrations of antidepressants, whereas a reorientation of ill-adapted thought patterns and behaviors, as can be initiated by therapeutic reasoning, turns out to be helpful in such cases. In other patients, however, similar discussions remain completely fruitless. Why? Because they have a different kind of depression.

Fukuda and his colleagues were able to show in the laboratory that genetically determined tryptophan release abnormalities in conjunction with their consequences in the further amino acid balance make the persons concerned susceptible to depression. These would carry a vulnerable constitution from the outset. What the psycho-pioneers called “endogenous depression” is thus a fact that can no longer be ignored, including the observation of phase progressions and the typical symptoms of sleep-disruptions, loss of appetite, lack of

focus, loss of interest, and irrational negative evaluations, as confirmed by statistics.

It is exciting that Fukuda has found a second type of depression, not genetic but caused in the gastrointestinal tract, which is virtually fueled by inflammation in the gut, Crohn’s disease, etc. As a side effect of the internal disease, it considerably dampens the ability to enjoy of life. Even the genius Frankl had an inkling of the possibility of such processes when he created the term “somatogenic pseudoneuroses” and emphasized that hormonal, vegetative and other purely organic disorders can lead to psychiatric-like crises. Following this, we could speak of “somatogenic pseudodepressions” in Fukuda’s second finding.
Fukuda and his team of scientists have clearly distinguished “reactive depression,” which they are not afraid to call by this time-honored name. For their explanation, they draw on stress factors, namely long-lasting or unforeseeable sudden stress, which only gradually impairs the tryptophan metabolism of the affected persons in an impact process. In this regard, no genetic predisposition could be determined, and the symptoms also deviate from the above description. Worry, anxiety, sadness, despair dominate and if sleep is affected, rather the ability of falling asleep. Taking antidepressants is of little or no use.
One can subsume many things under the word “stress”. It is a pity that in the reactive
area the same attention was not paid as in the endogenous area. Otherwise the researchers would have noticed that besides all the pressure and agony that painful events produce, there is also a “suffering from seemingly meaningless life,” and that this suffering reveals a specifically human component that Frankl christened “noogenic.”

What a strange stress it is when, for example, members of the older generation, including wealthy, well-off people in secure positions, draw (the wrong) balance and ask themselves, “What have I gotten out of my life so far? Quite a few disappointments, plenty of toil and trouble! And what can I expect from the rest of my life? To grow old, to become weaker, to die! Is my life even worthwhile then?” What a stress it is when members of the younger

generation, including top-fit and educated ones with excellent career options, slip right out of their youthful exuberance into hopelessness, lose their confidence in the future, and say to themselves, “It’s all going to pieces anyway. The world is getting hotter and hotter, more and more brutal, our life prospects are getting worse and worse, our opportunities are fading away … What’s the point of getting involved in anything at all?” These are basic existential and principled questions that reach far beyond individual loss and inconvenience. If no valid and, above all, meaningful answers are found to them, the slip into a “noogenic depression” is not unlikely – despite the complex balance of tryptophan enzymes in the body still continuing to function perfectly for a long time.

Soma and psyche are not “the whole story of the human being”, as Frankl taught. Even if modern findings “rehabilitate” him in tidbits (as the mentioned results of Fukuda et alii do), the “nous”, the human spirituality, should not be overlooked again and again. After all, it constitutes our freedom, responsibility, creative power and inalienable personal dignity – and these cannot be found under the electron microscope.

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