Correspondence (letter to the editor): When Does Long Term Damage Develop?

With regard to the role of the allelic variant 4 of apolipoprotein E (APOE), it should be added that Jordan et al showed as early as in 1997 in a study in boxers a high risk of encephalopathy in carriers of the APOE 4 feature. Later, it was found in victims of accidents that the prognosis of cerebral damage was relatively unfavorable if they were of the APOE4 genotype (2).

The biological involvement of APOE also includes the lipid transport into the central nervous system and involvement of neural regeneration after injuries. The genotype 4 was unfavorable for repair processes. In carriers of this genotype, the brain's recovery mechanism is therefore deficient and they are therefore particularly at risk of developing boxer's encephalopathy. Other genetic factors have also been mentioned in this setting (3).

What does this mean for clinical practice?

Even today, genetic screening is possible in order to identify persons in boxing who are at particular risk of encephalopathy. Determining the APOE genotype would be sufficient to do so. Neuron specific Enolase (NSE) or S100B follow-up are also possible. Such an approach, however, would entail fundamental ethical questions.

• Should sports clubs be allowed to force their members to undergo genetic/biochemical screening?

• Should athletes with a characteristic genotype (and/or abnormal development of the destruction markers NSE and S100B) be excluded from boxing?

• Is there a right to ignorance specifically with regard to these matters?

• Is there a “right to inflict self harm”?

Basically, the time has come to rethink all these questions with regard to boxing.