February 12, 2017
Here, in a nutshell is my thesis as to the cause of SARD. You can read the details, below.
- These dogs develop elevated estrogen levels
- That estrogen permits excessive levels of calcium to enter the retinal cells
- This calcium causes a seizure (vision loss)
- and ultimately retinal cell death
Now for further details, I’m including an excerpt from one of my papers. For those of you who want to check my references, click the link. For those of you who don’t like reading medical jargon, there is a plain English translation down below.
Dogs affected with SARD routinely present with signs suggestive of hypercortisolism (1,2,3,4,5) but only a minority are diagnosed with Cushing’s disease. (2,6) Early on, researchers speculated that this hypercortisolism was the physiological response to some unidentified stress. (5) SARD- affected dogs also demonstrate elevated levels of adrenal sex hormones (androstenedione, estradiol, progesterones, and testosterone) within the first year of blindness. (7,8) One explanation for this pattern of events is Selye’s model of stress adaptation, which describes the progression from adrenal gland hyperactivity to adrenal gland exhaustion (cortisol insufficiency and excessive estrogen production).
Apoptosis is a common final pathway in multiple retinal disorders including SARD. (33) It is also prevalent in other systems such as the central nervous system and immune system. Apoptosis is modulated in these systems is by steroid hormones such as cortisol and sex hormones. (34,35)
Retinal photoreceptor cell membranes contain gated ion channels, which control the influx of calcium ions (Ca++) into these cells. In photoreceptor outer segments, Ca++ controls light adaptation. In photoreceptor inner segments, Ca++ regulates cell metabolism, glutamate release, gene expression, and cell death. (36)
In pathological conditions of steroid hormone excess, Ca++ influx increases. Elevations in intracellular calcium, along with pro-oxidants, neurotoxins, and ishchemia damage the cell mitochondria. Caspases and other apoptosis-inducing factors are then released, degrading cellular components. (37) In SARD cases, retinal abnormalities typically do not develop until weeks or months after SARD onset, indicating that apoptosis is not immediate. (2,3)
And here’s the translation in plain English
There are little doors into each retinal cell. These doors are called calcium channels. Normally, the doors open up for a split second, a small amount of calcium enters the cell, and the door closes. That small amount of calcium creates an electrical signal to the brain that we know as vision.
When estrogen levels are high, as they are in SARD dogs, the calcium channels remain open longer and much more calcium enters the cells. This excessive calcium causes an extensive electrical signal to move through the retina, throwing it into a seizure. This is when communication to the brain is interrupted and vision is suddenly lost. The retinal cells are not dead at that point. They are simply unable to communicate with the brain. Over time, the overabundance of calcium damages the mitochondria, the little organs inside the cell. Once the mitochondria are damaged a self-destruct message called apoptosis is initiated, and the retinal cells are finally destroyed.
My thesis is actually supported by much research published by the veterinary ophthalmology community, as you can see by the other works I reference. It’s likely, however, that your veterinary ophthalmologist did not inform you about my work. That will be a topic for another blog post.
I have followed hundreds of SARD cases in the past 15 years. There is a clear correlation between the incidence of SARD and elevated levels of adrenal estrogen. The estrogen levels can be brought down to normal levels with hormone replacement therapy. This offers the best chance for a comfortable life. You and your dog should not have to suffer.