Toxins & Nutrition(1998) & Leber's

Learn more about Leber's.

Researchers have identified both exposure to toxins and nutritional deficiencies as been connected to incidence of mitochondria-mutated conditions such as Leber's.

In Cuba, in the 1990's an epidemic affected 50,000 patients with symptoms common to both lazy eye due to alcohol/tobacco toxins and Leber's. There was characteristic damage leading to these conclusions. The patients exhibited both vitamin deficiencies and mitochondrial damage from methanol and cyanide toxins.

The researchers were particularly interested in determining why impaired production of cellular energy led to this kind of damage, and why, within the nervous system, why the optic nerve's ganglion cells were especially vulnerable.

The researchers comprehensively evaluated both the patients via neuroophthalmologic exams, as well as blood, cerebrospinal fluid, DNA, and, from deceased patients, the nerves running down the back of the leg and the eye and optic nerve itself. Blood folic acid levels were low, and blood formate levels were high. These were then tested via animal models.

Finding: These patients' vision conditions improved when their nutritional deficiencies were corrected, and their exposure to toxins ceased.

The researchers concluded that mitochondria (noting that the mitochondria in cells of the eye are most vulnerable) can be damaged either genetically or by way of nutritional deficiencies or exposure to toxins. There is a threshold, once passed, which results in irreversable damage.

Researcher: Sudan, A., et. al

Published: Acquired mitochondrial impairment as a cause of optic nerve disease., Trans Am Ophthalmol Soc. 1998;96:881-923.