News & Updates
February 12, 2017 • Sticky Post
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.
May 13, 2017
Great question. I believe this must be addressed by dog owners and their local, home town veterinarians. Why your local vet? Because, to date, veterinary ophthalmologists maintain that they do not know the cause of SARD. Consequently, they have not identified any preventative measures.
Part 1: If you’ve been reading these pages, you are familiar with the unmistakable relationship between adrenal exhaustion (i.e.. elevated estrogen) and the onset of sudden blindness. 98% of SARD dogs tested demonstrate elevated estrogen. If the adrenal exhaustion could be promptly identified and treated, it might preempt the damage to the retina.
So, perhaps the most effective mode of prevention would be to educate general practice veterinarians and this might have to come from you, the dog owner. General practice vets should be educated:
- to recognize the signs of adrenal exhaustion and the breeds (Dachshunds, small terriers) most at risk
- how to test for adrenal exhaustion
- and how to treat it
Many dog owners make an appointment with their general practice veterinarian prior to the onset of blindness. The owners bring in the dog with signs of increased hunger and thirst, perhaps accidents in the house, and/or any of the other common signs such as, lethargy, depression, aggression, pacing, panting, etc. The general practice veterinarian may run a blood test to rule out Cushing’s disease (i.e.. a tumor growing on one of the glands that produces excess cortisol).
It seems logical to run a Cushing’s test, since the symptoms mentioned above can be signs of a tumor/excess cortisol. However, these are also signs of adrenal exhaustion (excess estrogen). How can this be? How can both excess estrogen and excess cortisol produce the same symptoms?
Both estrogen and cortisol are steroid hormones. And as two molecules go, they are very, very similar, so they both have similar effects on the body. They both cause: drinking, peeing, hunger, depression, infections, etc. So, if the Cushing’s test is negative, the veterinarian, should suspect adrenal exhaustion. And really, to prevent vision loss, the veterinarian should test for adrenal exhaustion along with, or instead of, Cushings, so that no time is wasted.
If the testing can be done and the treatment initiated immediately, how many dogs might retain their vision? How many dog owners could be spared their grief and pain!
Part 2: For your part, consider raising any future dogs in a more old-fashioned way… treating the dog as we did decades ago, before SARD first made it’s appearance. SARD was only first diagnosed in the late 1970’s-early 1980’s. Rather than type out this information a second time, I am giving you a link to another website of mine. Here, you will find information about homemade meals, why to minimize chemical exposures, and some thoughts about vaccines. We also have a DVD that covers these topics:
April 16, 2017
There are two times each year when I see an uptick in the occurrence of SARD. The first is in the fall. Around Thanksgiving. The second is in the spring. Around Valentines day. During these times, the adrenal gland typically experiences an increase in activity. Why?
In the autumn the adrenal gland helps the body prepare for the stress of the coming winter. It helps the animal grow a winter coat, deal with the cold weather and fewer calories, go into hibernation. In the spring, the adrenal gland is involved with the new seasonal changes: coming out of hibernation, preparing for breeding.
When an adrenal gland can no longer produce cortisol, it produces adrenal sex-hormones (most notably, estrogen) instead. So in the fall and in the spring, when the adrenal gland is being stimulated by the brain, it produces a spike in estrogen levels.
As you may know from my writings, my thesis is that elevated estrogen triggers a seizure in the retinas. During that time the retina cannot communicate with the brain. Since the brain is where visual images really occur, the dog loses vision suddenly.