The only time I'm a doctor is when I'm talking to a hot chick at a bar... But, from what I recall the actual doctor saying, the hyperoxia (oxygen poisoning) theory explains that breathing (in this case) 95% oxygen on the ground when usually we'd be breathing ~21% might be a bad thing. Our OBOGS-equipped platforms we fly are able to deliver 95-100% O2 on the ground, and in military flight, the mask is supposed to be on during checks/taxi. So on the ground, this leads to "absorption atelectasis". (From Wikipedia) Since oxygen is exchanged at the alveoli-capillary membrane, nitrogen is a major component for the alveoli's state of inflation. If a large volume of nitrogen in the lungs is replaced with oxygen, the oxygen may subsequently be absorbed into the blood, reducing the volume of the alveoli, resulting in a form of alveolar collapse known as absorption atelectasis.
In flight, this leads to acceleration atelectasis and pulling G's can cause the base of the lung to collapse. So basically, drastically changing the composition of your alveoli on the ground, then going up and being exposed to O2 concentrations that vary between 60-80% during flights where you do multiple altitude changes is causing hypoxia (that's the theory at least).
Now take a jet like the F-15 where LOX and a diluter-demand regulator is used... At 10k' altitude, 25-50% O2 (by volume). At 20k' altitude, 40-65% O2. Finally, around 28-30k' altitude, the regulator stops diluting the incoming oxygen from the LOX bottle and 100% O2 is delivered for those altitudes and higher. LOX jets historically have a MUCH lower (reported) percentage of hypoxia events per flight hour.
Anyways, none of this is my research, but I just thought those basics were very interesting especially given the OBOGS issues in the T-6 (and across multiple other platforms as well).