tl;dr: Yes, there is a point at which recovery is not possible without significant medical intervention.
Death by starvation is not simply a matter of running out of energy to sustain life, so cannot be treated simply by providing additional energy. Various bodily systems are damaged during the process of starvation and may remain impaired afterward. Additionally, lack of adequate nutrients can lead to potentially-deadly chemical imbalances which the body is not able to recover from without assistance.
An extensive list of such effects can be found in section 3, "Medical", of the paper Refeeding the Patient with Anorexia Nervosa: Perspectives of the Dietitian, Psychotherapist and Medical Physician (DOI 10.12691/jnh-3-2-1). While the paper specifically provides a broad overview of the effects and treatment of anorexia nervosa, the "Medical" section primarily describes the effects of starvation in general.
I will specifically call out here the paper's discussion of "refeeding syndrome", as it relates directly to the question's claim that WW2 concentration camp survivors were simply "overfed to death" (emphasis mine):
The other main medical issue to be concerned with during the refeeding of patients with anorexia nervosa is the actual refeeding syndrome. This syndrome was first described in survivors of concentration camps who were liberated and then fed excessive amounts of high-dextrose containing foods by their well-intentioned liberators. Surprisingly, many died soon after their liberation despite receiving high quality nutrition and despite having lived under horrific conditions in the years prior. Then, further attention was called to this in the “Minnesota Experiment,” wherein conscientious war objectors were noted to have a marked decrease in the size, of their heart size as seen on chest radiographs during their periods of starvation. In 1969, with the invention of total parenteral nutrition (TPN) and its early administration to patients on a burn unit, this lesson was repeated when many of the patients died soon thereafter, and were noted to have critically low serum phosphorous levels. Anorexia nervosa now serves as a sobering model of the inherent calamity which can occur with the refeeding of starved patients if there is inattention to the metabolic responses to the renewed nutrition.
Briefly, phosphate is critical for glucose metabolism. When starved patients shift from a catabolic state to an anabolic state with the provision of calories anew, there is great demand for the production of high energy compounds for glycolysis, the Krebs cycle and the formation of adenosine triphosphate (ATP) and 2,3-diphosphoglycerate (2,3 DPG), resulting in marked utilization of serum phosphorous and a reduction in phosphorus levels.  The resultant hypophosphatemia, if severe (<1.5 mmole/L), causes the development of a group of serious adverse sequela including seizures, heart failure, hemolysis, rhabdomyloysis, respiratory failure, coma and sudden death. These phenomena, all or in part, are known collectively as the refeeding syndrome. In theory, any person who has been malnourished and without caloric intake for just a few weeks, is at risk for its development as they begin to reefed[sic] if there is lack of attention to their phosphorous, potassium, magnesium and glucose levels.  The risk for refeeding syndrome seems to mostly begin just 2-3 days after the initiation of refeeding and it lasts in general for 1-2 weeks with progressive calorie increases. It best correlates with the severity of malnutrition as defined by nadir percent of ideal body weight.  Different series have reported on the incidence of refeeding hypophosphatemia, varying from 15% to upwards of 35%. [7, 40] Prophylactic phosphorous is therefore not indicated, but rather, it is most important to closely monitor the patient during the first weeks of refeeding for clinical and laboratory changes.