Jump to comment:

• Neuropathy by overachieved rapid glycemic oral control
  San M
  Published on: 14 September 2019
• Grounds for abandoning "diabetes" as a diagnosis?
  Richard G Fiddian-Green
  Published on: 9 March 2005

• Published on: 14 September 2019

  Neuropathy by overachieved rapid glycemic oral control

  • San M, Engineer Patient self

  Letter response to the article "Under-recognised paradox of neuropathy from rapid glycaemic control."

  I am a data point of what the author says is elusive example of neuropathy (albeit in initial stages) by rapid glycemic control using only oral medication.
  My A1c reduced by about 1 point ( 7.7 to 6.8) in 3 months and further down to 6.1 in 3 more subsequent months.

  From the initial 7.7 A1c date, I was started on a higher oral dosage, as well as serious diet modification.

  Two months later, I had a rapid onset of feet burning symptoms. The symptoms came on and off. With subsequent tighter diet control that included episodes of low glucose levels, feet burning was still present and became more frequent. After reading up on this subject and its counter intuitive conclusions, I loosened diet control and also had my doctor reverse the last medication increase to previous levels. This seems to have helped and my left foot has been free of burning for a few days now, and the right foot also improving. Continuing monitoring and hoping for the best. Thanks to your and similar articles for highlighting this controversial and elusive phenomenon.

  Conflict of Interest
  None declared

  Conflict of Interest:
  None declared.

  • Back to top
• Published on: 9 March 2005

  Grounds for abandoning "diabetes" as a diagnosis?

  • Richard G Fiddian-Green, FRCS, FACS

  Dear Editor,

  Unlike peripheral tissues where insulin promotes, and indeed is necessary for cellular glucose uptake and utilisation, that is not true for the brain and presumably, therefore, peripheral nerves. The inference is that changes in the rate of glucose uptake by the brain and peripheral nerves are a function of its concentration in blood and are driven by mass action independently of insulin. In which ca...

  Show More

  Dear Editor,

  Unlike peripheral tissues where insulin promotes, and indeed is necessary for cellular glucose uptake and utilisation, that is not true for the brain and presumably, therefore, peripheral nerves. The inference is that changes in the rate of glucose uptake by the brain and peripheral nerves are a function of its concentration in blood and are driven by mass action independently of insulin. In which case rapid glycaemic control in a patient who has had a chronic hyperglycaemia might induce an acute decline in intraneuronal energy charge [1] sufficient to cause a neuropathy.

  A progressive decline in energy charge induces dysfunction first, then apoptosis and finally necrosis. Unlike apoptosis, which does not induce inflammatory changes andmight even be a stimulus for cell renewal, necrosis does. If, therefore, the neuropathy is sustained it might be due either to a persistent decline in energy charge insufficient to cause apoptois or necrosis or irreversible damage with inflammatory changes which might even be visible in histological preprations of nerve biopsies.

  The first of these raises the possiblity that chronic hyperglycaemia in a "poorly controlled" diabetic is an indication of a compendatory cytoprotective response to a decline in energy charge that is not being met by and might even be being exacerbated by the therapeutuc interventions chosen. In which case the failure of treatment might lie in the failure to have identified and addressed the causes of the decline in energy charge. In other wwords the widespread assumption that the metabolic defect in diabetics is simply an intracellular deficiency of glucose might be false.

  The large number of people developing late complications from "diabetes" is testimony to the continued failure of modern diabetic treatment. The failure might have been promoted by the diagnostic labels that have been used for so many decades for the inference is that the metabolic defect is confined to distrubances of insulin/glucose metabolism. Hence the commercial initiatives and various forms of transplantation that have evolved in an effort to develop better ways of achieving glycaemic control. If a different label, such as the intermittent or sustained energy deficit syndrome, were used physicians would be encouraged to look for other causes for the decline in energy charge. More importantly, perhaps, they would b encouraged to jettison glycaemic control as their sole manegement objective in favour of achieving energy control.

  The etymology of diabetes reveals the antiquity of the diagnotic label and its inappropriateness today. "Diabetes comes from the word for “siphon,” as people with diabetes urinate like a siphon draining water. Mellitus comes from the word for honey, since people with diabetes mellitus have a sweet smelling (and tasting) urine, from the excess glucose in it. Insipidus comes from insipid, meaning “lacking flavor or zest; not tasty,” since diabetes insipidus has non-sweet urine" [2].

  The move to call type II diabetes the metabolic syndrome might be viewed as a step in the right direction but as this includes metabolic variables other than the energy charge it is unlikely to redirect attention to the energy charge per se. Even if it did it might encourage a rush to incorporate nuclear magnetic resonance spectroscopy as the means of detecting and monitoring "diabetics". This could be jumping from the frying pan into the fire for, as addressed in a series of eLetters concerning a paper in Chest [2], this may have serious limitations. Not the least of these is its potential to divert attenton even further from the central metabolic issue with a series of new red herrings,

  References

  1. Hardie DG, Hawley SA. AMP-activated protein kinase: the energy charge hypothesis revisited. Bioessays. 2001 Dec;23(12):1112-9.

  2. Medical Etymology. www.grahamazon.com/2004/12/medical-etymology/

  3. Dantzker DR. Monitoring tissue oxygenation : the quest continues. Chest. 2001 Sep;120(3):701-2.

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top