Some Further Doubts about Grossarth-Maticek's Data Base

Some Further Doubts about Grossarth-Maticek's Data BaseAuthor(s): Henk M. van der Ploeg and Wim Chr. KleijnSource: Psychological Inquiry, Vol. 4, No. 1 (1993), pp. 68-69Published by: Taylor & Francis, Ltd.Stable URL: http://www.jstor.org/stable/1449601 .

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COMMENTARIES

Some Further Doubts About Grossarth-Maticek's Data Base

Henk M. van der Ploeg and Wim Chr. Kleijn Vrije UniversiteitAmsterdam

Van der Ploeg and Vetter (this issue) showed that, in the Grossarth-Maticek interview data base for 110 cases, the response pattern on the first 58 interview questions was found twice, mostly once in the normal Heidelberg sample and once in the stressed sample. They concluded that the interviews were used twice deliberately or by some systematic accident.

In order to explore the "systematic accident" hypoth- esis and address some dubious results reported by Vet- ter (1991) about the values of blood cholesterol in several subjects from the Heidelberg 1972 studies, we performed computer analyses to reinspect some raw data files with somatic data.

In the Heidelberg 1972 studies, as many as seven consecutive measurements were taken of blood cholesterol and of the number of leukocytes and lymphocytes in blood. The interval between the measurements was about 6 months, according to Grossarth-Maticek, Vet- ter, and Heller (1986). The counts of blood cholesterol, leukocytes, and lymphocytes seem to be among the essential elements in the theorizing and research of Grossarth-Maticek (see, e.g., Eysenck, 1991; Eysenck & Grossarth-Maticek, 1991; Grossarth-Maticek & Eysenck, 1989; Grossarth-Maticek & Eysenck, 1991).

At first measurement, blood cholesterol in the normal sample averaged 225, which is 5.9 mmol/liter (SD = 60, N = 1,017), and blood cholesterol in the stressed sample averaged 290, which is 7.6 mmol/liter (SD = 60, N = 1,493). At first measurement, the number of leukocytes in the normal sample averaged 5,494 (SD = 1,805), and the number of leukocytes in the stressed sample averaged 4,795 (SD = 626). Last, the percentage of lymphocytes in the normal sample averaged 31% (SD = 7.2%), and the percentage of lymphocytes in the stressed sample averaged 24% (SD = 3.5%).

Over the seven measurements, these average values were more or less the same, despite the fact that the number of probands with valid measurements de- creased to n = 676 in the normal sample and to n = 294 in the stressed sample.

We computed Pearson correlations between the individual values obtained at first measurement with the values obtained at second measurement, third measurement, and so on up to the seventh measurement. In the normal sample, first-measurement blood cholesterol correlated with that of the next measurements .83, .81, .70, .66, .62, and .62, respectively. In the stressed sample, these correlations were .49, .50, .52, .56, .60, and .52, respectively. In the normal sample, the correlations for the number of leukocytes were .09, .06, .00,

.05, .07, and -.01; in the stressed sample, these correlations were .56, .42, .41, .39, .47, and .22. The correlations for the percentages of lymphocytes are correspondingly close to zero in the normal sample and vary from .45 to .33 in the stressed sample.

This suggests that these somatic data "behave" differently according to the sample studied.

As was done for the interview data base, we analyzed whether, for two (or more) individuals, identical series of somatic data could be found in the two samples.

The cases in the files with raw data-respectively, blood cholesterol measurement in the normal and stressed samples and leukocyte and lymphocyte data for these same samples-were ordered from low to high values using the values of the seven measurements, starting with the first measurement, then the second, then the third, to the seventh measurement. For each of these (rank) ordered files, every case was com- pared with its preceding case. The number of consecutive identical values (starting from the first measurement) was counted. On the condition that the first four measurements were identical, eventual additional missing values were also counted as being identical (if this was the case). Table 1 shows the results of these procedures.

In the normal sample, no identical series of seven consecutive measurements could be found, which means that, in this sample, almost all individuals had idiosyncratic and different series of values for blood cholesterol, leukocytes, and lymphocytes. Respec- tively, 6.4% and 0.5% of the cases had three or more identical, consecutive values for cholesterol or leukocytes. In the stressed sample, the pattern is completely different.

For the blood cholesterol variable, in 74 cases an identical series of seven consecutive values could be observed for another proband in the stressed sample (e.g., 285, 240, 160, 190, 285, 180, and missing were observed for Subjects 37 and 364); three or more identical, consecutive values were found in 25% of the cases.

For the leukocyte variable, 89 identical, consecutive series of seven values could be observed in the stressed sample (e.g., 4,900, 4,350, 4,800, 5,000, 5,100, 5,150, and missing were observed for Subjects 976 and 1,509); 35% of all cases had three or more identical, consecutive values.

In 43 cases (of the 74 and 89 cases, respectively), identical series were found for the blood cholesterol variable and for the leukocyte variable (e.g., for Sub-

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COMMENTARIES

Table 1. Number of Cases With Identical, Consecutive Measurement Values for Another Proband

Cholesterol Leukocytes

Normal Stressed Normal Stressed Number of Sample Sample Sample Sample Identical Values n % n % n % n %

0 73 7.1 106 6.9 105 10.2 103 6.7

1 519 50.6 577 37.5 776 75.6 378 24.6

2 368 35.9 471 30.6 140 13.6 525 34.2

3 60 5.8 200 13.0 5 0.5 299 19.5

4 6 0.6 87 5.7 - - 122 7.9

5 - - 22 1.4 - - 19 1.2

6 - - - - - - 2 0.1

7 - - 74 4.8 - - 89 5.8

Total 1,026 lOOWo 1,537 100% 1,026 100% 1,537 lOOWo

jects 188 and 713, 1,230 and 1,395 identical series were found for both somatic variables). Upon comparing the subject code numbers for which seven identical, consecutive somatic responses were found with the subject code numbers for which 58 identical, psychosocial interview responses were found (see van der Ploeg & Vetter, this issue), no systematic overlap between these two sets of code numbers was found. So, we did not observe for a subgroup of probands identical somatic and identical psychosocial responses. Only occasion- ally for a subject, identical somatic and identical psychosocial responses were found in the data base.

For the somatic data, blood cholesterol, and the number of leukocytes, the possible range of values was large. One might expect a standard measurement error up to 10%; within one individual, two measurements based on the same tube of blood usually produce different figures.

Given the standard error and standard deviations, the question may be raised whether these identical, consecutive somatic data may have arisen by chance. As was written for the identical interview responses (van der Ploeg & Vetter, this issue), "This question can easily be answered with statistics showing that the null hy- pothesis about the chance model can be rejected at a remarkable significance level."

In addition, it is a puzzle why these identical, consecutive values were found only in the stressed sample and not also in the normal sample. Furthermore, the somatic data in the two samples "behaved" differently and showed additional different characteristics.

Based on all this, we can safely conclude that it is extremely unlikely that these identical, consecutive series of somatic data-to be a precise series of seven consecutive values of blood cholesterol and the number of leukocytes-could have been found twice among the subjects of the Heidelberg 1972 stressed sample by chance. These somatic data could have been used twice by some "systematic accident" or by intent.

These identical series of values of somatic data oc- curred also among the subjects in the extended individual-therapy study (Eysenck & Grossarth-Maticek, 1991), which did not contribute to the credibility of the reported results and the reported effects of the creative novation therapy.

Note

Henk M. van der Ploeg and Wim Chr. Kleijn, De- partment of Medical Psychology, Vrije Universiteit Amsterdam, Van der Boechorststraat 7, D-558, 1081 BT Amsterdam, The Netherlands.

References

Eysenck, H. J. (1991). Cancer and personality. In C. L. Cooper & M. Watson (Eds.), Cancer and stress: Psychological, biological and coping studies (pp. 73-94). Chichester, England: Wiley.

Eysenck, H. J., & Grossarth-Maticek, R. (1991). Creative novation behaviour therapy as prophylactic treatment for cancer and coronary heart disease: II. Effects of treatment. BehaviourRe- search and Therapy, 29, 17-31.

Grossarth-Maticek, R., & Eysenck, H. J. (1989). Length of survival and lymphocyte percentage in women with mammary cancer as a function of psychotherapy. Psychological Reports, 65, 315- 321.

Grossarth-Maticek, R., & Eysenck, H. J. (1991). Creative novation behavior therapy as a prophylactic treatment for cancer and coronary heart disease: I. Description and treatment. Behaviour Research and Therapy, 29, 1-16.

Grossarth-Maticek, R., Vetter, H., & Heller, W. D. (1986). Kausale Pradiktoren fiir Krebserkrankung, Herzinfarkt und Hirnschlag: Theorie, Methode und Ergebnisse der Heidelberger pro- spektiven psychosomatischen Interventionsstudie (1972-1982). Ein Beitrag zur Atiologieforschung in der interdisziplinaren Epidemiologie [Causal predictors of cancer, cardiac infarct and stroke: Theory, methods and results of the Heidelberg prospec- tive psychosomatic intervention study (1972-1982). A contri- bution to the study of etiology in interdisciplinary epidemiology]. In E. D. Hager (Ed.), Biomodulation und Biotherapie des Krebses (pp. 87-117). Heidelberg: E. Fischer.

Vetter, H. (1991). Some observations on Grossarth-Maticek's data base. Psychological Inquiry, 2, 286-287.

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Some Further Doubts about Grossarth-Maticek's Data Base