News & Updates
October 14, 2020
Sometimes I’m asked, “Caroline, how does your SARDS treatment protocol different from Dr. Plechner’s protocol?”
Before I reply, let me say that Dr. Plechner’s work was important to me, both personally and professionally. And despite some significant differences in our work, his work influenced mine.
Dr. Plechner’s work was unconventional. And because of this — rightly or wrongly— he endured professional attacks from other veterinarians. Some of these endocrinologists are still in practice today and maintain their opposition to Dr. Plechner’s practices. This might explain why veterinary endocrinology still ignores the concept of cortisol replacement as the treatment for elevated adrenal sex hormones.
For humans, cortisol replacement has been the standard medical treatment for elevated adrenal sex hormones for 65 years. Sixty-five years. That’s a stunning difference between the two fields. Countless other treatments have been adapted from human medicine to veterinary medicine, but this one remains ignored.
Difference in Dosing
There are several distinctions between my SARDS protocol and Dr. Plechner’s protocol. The first distinction is in the dosing. Dr. Plechner’s protocol recommends higher doses and more potent forms of cortisol replacement as compared to my SARDS protocol.
Dr. Plechner felt pressure to lower sex hormone levels quickly and show rapid results in his cases. Consequently, his doses supply more than a dog requires as a daily replacement dose. His doses are closer to anti-inflammatory or immunosuppressant levels. It’s not uncommon for dogs on his protocol to experience clinical signs/symptoms from the prescriptions in addition to the signs/symptoms they already experience from the elevated sex hormone steroids.
In my dealings with general practice veterinarians across the country these past 15 years, it’s become clear that most are not comfortable giving the Depo-Medrol injections recommended in Dr. Plechner’s protocol. That’s not a judgement, merely an observation.
Their main complaint is this. Depo-Medrol is a long-acting injectable that persist for several weeks. So, if the Depo-Medrol injection delivers an excess of cortisol, there is no way to mitigate the effects of that injection, no way to lower the dosage. Both dog and owner must “ride it out”.
On the other hand, my protocol stems from the work of Dr. Simpson, my general practice veterinarian. He ran a holistic practice and understood cortisol deficiency. Between 1999 and 2005, two of my dogs were diagnosed with elevated adrenal sex hormones. One was a Dachshund, the other a Boxer.
Dr. Simpson practiced a milder version of Dr. Plechner’s program. Dr. Simpson felt that his clients were troubled by the effects of Dr. Plechner’s dosing just as much as they were troubled by the original hormone problem — endless panting, accidents in the house, etc. Consequently, Dr. Simpson endeavored to replace only what the dog needed on a daily basis and no more.
This gentler approach is the basis for my SARDS protocol. It describes the methods holistic veterinarians use to replace only what cortisol the dog is missing, no more. It’s easier to get a dog’s general practice veterinarian on board with this dosing. After all, if you’re making the argument that, “We’re just replacing what the dog would normally make,” then low-dose treatment is understandable.
One can’t make the same argument, however, when discussing doses that are closer to anti-inflammatory levels (Dr. Plechner’s). It can’t be both ways. This is either seen as a hormone replacement issue requiring a low daily replacement dose or it’s seen as an inflammatory problem requiring a larger, anti-inflammatory dose. And this leads us to the second distinction between my work and Dr. Plechner’s.
Retinal Seizure or Auto-immune Disease?
In 2006 I recognized the connection between SARDS and adrenal exhaustion. When my SARDS research was published at the 2007 meeting of the American College of Veterinary Ophthalmologists (ACVO) I contacted Dr. Plechner. I sent him my papers and informed him that SARDS-affected dogs were testing positive for elevated sex-hormones, including elevated estrogen. And I further explained that they responded brilliantly to low-dose cortisol replacement therapy. This was Dr. Plechner’s introduction to SARDS.
2007 was also about the time that some veterinary ophthalmologists were investigating autoimmunity as a possible cause of SARDS. Dr. Plechner latched on to that theory. To this day his website asserts that SARDS is an autoimmune disease despite growing evidence to the contrary.
And therein lies the problem. If one claims SARDS is an autoimmune disease, one would expect that 40 years of high-dose, short-term prednisone (the standard in ophthalmic veterinary care) to have had some positive effect on vision. Furthermore, one would also expect that mycophenolate mofetil, a powerful immunosuppressant recently studied, would also have had some positive results. Neither has.
So when Dr. Plechner backed the autoimmune theory of SARDS, and since he was already recommending higher doses of Depo-Medrol and prednisone, he did himself a disservice. Ophthalmologists had been prescribing anti-inflammatory levels of prednisone since the 1980’s with no success. The way other practitioners saw it, Dr. Plechner was simply prescribing more of the same anti-inflammatories. His underlying principle —the idea of repairing a cortisol deficiency—was lost.
I’m unclear as to why Dr. Plechner embraced the autoimmune model so adamantly. In one of our conversations I made a strong case for a retinal seizure or “excitotoxicity” as the cause of SARDS. Both concepts (excitotoxicity versus autoimmunity) are explained by elevated estrogen. Both concepts are explained by a disruption in cortisol synthesis. Perhaps he wished to align himself with the university researchers at the time. I don’t know. But with respect, I think he was wrong on this point.
If elevated estrogen causes a seizure in the retina, it explains the sudden nature of vision loss and the reason vision can be restored. Ophthalmologists have long reported that retinal cells are not destroyed at the time of vision loss. Degeneration occurs in the weeks and months after vision loss. If retinal cells can be spared from destruction, and the seizure halted, vision often returns.
To that end, my SARDS protocol is divided into two parts. Part 1 addresses the elevated sex hormone production using the milder hormone replacement approach. Part 2 protects the retinal cells from destruction until sex-hormone levels decline.
Dr. Plechner dismissed the idea of retinal protection therapies and advised his clients to ignore them. His protocol addresses only the adrenal piece.
Dietary Sources of Estrogen
Some dog owners ask me to comment on Dr. Plechner’s dietary recommendations, specifically the recommendation to eliminate foods that contain phytoestrogens. He felt these contributed to the dog’s estrogen load.
It’s my opinion that vegetables did not contribute to the adrenal problem and eliminating them from the dog’s diet also deprives the animal of valuable anti-oxidants. Flax seed and soy are by far and away the leading sources of dietary phytoestrogens, and since dog owners typically do not feed these, this issue is of little concern.
Instead, my protocol recommends a diet that provides a variety of nutrients over time. This mimics the way animals eat in the wild. It’s good for the dog and easier for the dog’s owner.
Success Rates of the Protocols
In 2008 I reported that 23% of dogs following my protocol regained some vision. Functional vision was confirmed by general practice veterinary examination or by ophthalmic veterinary examination. I have always been careful not to overstate this figure, in fact, I typically describe it as 20%. Dr. Plechner reported that 80% of dogs on his protocol regained vision.
In 2019, a survey was conducted by a large online support group for the owners of SARDS dogs, a group with which I have no affiliation. 352 dog owners who had tried some type of treatment for their dogs were asked if treatment restored any vision. Respondents replied that the Levin protocol was successful 55% of the time and the Plechner protocol was successful 43% of the time.
Undeniably, this was an informal poll with no method of verification. Taken at face value, however, it suggests a significant increase in the success rate of my SARDS protocol —of which I was unaware— and a decline in that of Dr. Plechner’s.
Over time my SARDS protocol has been modified slightly. This may have improved outcomes. Furthermore, client compliance may have improved. Evidently, some dog owners implemented only bits and pieces of my protocol in the early years.
Here’s a quick review
LEVIN’S SARDS PROTOCOL
- Based on the seizure/excitotoxity model
- Low doses aim to replace daily needs, no more
- General practice vets more likely to implement
- Addresses both retinal and adrenal issues
- Diet is more relaxed
- Based on the autoimmune model
- Higher doses often exceed daily needs
- General practice vets less likely to implement
- Addresses only adrenal issue
- Diet is more restrictive
March 20, 2019
Many of my articles discuss estrogen levels in SARD dogs. Other sex-hormones are typically elevated as well. This article will focus on the effects of elevated androgens— testosterone and androstenedione.
As you read on, I’d like you to keep in your mind an image of the typical teenage boy. Maybe you can picture him standing in front of the refrigerator saying, “Mom, I’m starving!” He’s filling out and putting on weight. He may have acne, greasy skin or hair, maybe even body odor. These are some of the same problems we see in SARD dogs.
Other signs of elevated androgens include male and female pattern baldness. In SARD dogs we see bilateral flank alopecia (hair loss) and/or hair thinning along the spinal column.
Elevated androgens contribute to mood changes such as aggression, depression and anxiety. They may alter sleep patterns, contributing to insomnia—all problems we see in SARD dogs.
Since androgens are steroid hormones like estrogen, they too can aggravate heart disease, cause liver damage, raise serum cholesterol, blood pressure and blood sugar levels.
But perhaps the most common problem facing these dogs (second to vision loss) is the increased appetite and weight gain. Excess androgens interfere with insulin, leptin, and ghrelin activity. All of which communicate with the appetite center in the brain.
Women with Polycystic Ovary Syndrome—a condition in which women suffer elevated testosterone levels—report a constant and overwhelming urge to eat, sometimes to the point of disrupting their sleep. They share comments such as, “I’m always hungry, I never feel full,” or “I have an insatiable appetite.” They report extreme difficulty keeping their weight at normal levels saying, “I can’t get the weight off no matter what I do,” and “The struggle never ends. It is so hard to walk into the kitchen and not want to stuff myself.”
So, when a SARD dog owner asks me, “What can I do to curb my dog’s appetite?” the answer is simple. Treat the elevated sex-hormones. Dietary measures such as calorie restrictions, adding green beans or canned pumpkin are simply band-aids that don’t address the underlying problem.
Ask your general practice veterinarian to test for adrenal exhaustion here or here. The protocol is here. Odds are excellent that your dog will feel better when elevated sex hormone levels are corrected.
Effects of androgens on insulin action in women: is androgen excess a component of female metabolic syndrome? A. Corbould. Diabetes Metabolic Research Review, 2008 Oct;24(7):520-32.
Obesity and Polycystic Ovary Syndrome
Obesity Management, 2007 Apr; 3(2): 69–73.
Polycystic ovary syndrome: syndrome XX?
S. Sam, A Dunaif
Trends in Endocrinology and Metabolism, 2003 Oct;14(8):365-70.
Impaired cholecystokinin secretion and disturbed appetite regulation in women with polycystic ovary syndrome
A. Linden Hirschberg, S. Naessen, M Stridsberg, B. Bystrom, J. Holte
Gynecological Endocrinology 2004; 19(2): 79-87.
Sex hormones, appetite and eating behaviour in women.
Maturitas, 2012 Mar;71(3):248-56.
Long-Term Testosterone Administration Increases Visceral Fat in Female to Male Transsexuals Jolanda M. H. Elbers Henk Asscheman Jacob C. Seidell Jos A. J. Megens Louis J. G. Gooren. The Journal of Clinical Endocrinology & Metabolism, July 1997; 82(7): 2044–2047.
March 20, 2019
Last week a general practice veterinarian asked me the following question. “Why is the daily replacement level dose of cortisol higher for SARD dogs than the physiological dose for Addison’s dogs?” This is a good question but I doubt it’s of interest to the average dog owner. Therefore, my comments are directed to the prescribing veterinarian.
Peripheral synthesis of glucocorticoid hormones
Because the adrenal gland is the primary producer of glucocorticoids, less attention has been paid to steroidogenesis in peripheral tissues. A wide range of peripheral tissues are reported to synthesize cortisol in humans and rodents. Mucosal, pulmonary, cardiovascular, epidermal and central nervous system tissue demonstrate local glucocorticoid production. While these levels have not been quantified, they are described in the literature as important sources of glucocorticoid synthesis.
The adrenal pathophysiology in Addison’s disease
Autoantibodies to steroid 21-hydroxylase are characteristic of autoimmune Addison’s disease. Autoantibodies are specific to the adrenal gland unless a poly-glandular syndrome exists. In that case, antibodies may also target organs such as the thyroid, pancreas, or gonads. Celiac disease has been reported in poly-glandular syndrome. I can find no reports, however, describing peripheral tissue such as lung, cardiovascular, epidermal or other mucosa as autoimmune targets. Cortisol production in peripheral tissue may remain intact.
The adrenal pathophysiology in SARD-affected dogs
In comparison, the adrenal dysfunction in SARD-affected dogs is similar to late-onset CAH due to 11-beta hydroxylase type 1 (11-BHD1) in humans. This genetic mutation results in a failure to produce 11-BHD1— the enzyme that reduces deoxycortisol to cortisol. It’s possible that unlike Addison’s disease which specifically targets adrenal tissue, the loss of 11-BHD1 affects systemic cortisol production including that of peripheral tissue.
This difference may explain why Addison patients may be maintained on lower doses of daily cortisol replacement when compared to SARD-affected dogs. Addisonian dogs may retain some peripheral cortisol production whereas SARD-affected dogs may not. Consequently, a slightly higher dose is necessary to suppress adrenal sex hormone excess in SARD-affected dogs.
March 9, 2019
Some people take issue with the way I describe the underlying hormone problem in SARD dogs. In this article I’m going to tell you why I use the phrase adrenal exhaustion.
Here is a graphic representation of adrenal exhaustion. Bold text indicates areas of excess activity. Small text indicates an area of insufficient activity. Please note that all of the charts on this page differ only by the lab test performed.
In human healthcare there’s a condition that has some similarities to the symptoms SARD dogs suffer — fatigue, lethargy, depression, insomnia, weight gain, etc. Patients are typically middle-aged females. It was dubbed Chronic Fatigue Syndrome (CFS) in the 1980s. It has a neurological component. It has an endocrine component. And nowadays patients are treated with low-dose cortisol and thyroid hormone.
When I first began writing, I could have used this to illustrate and explain the adrenal dysfunction in SARD dogs. However, the allopathic medical community was quick to dismiss this term and these patients. Doctors told patients the problems were all in their head. They called it “a new-age illness.” They prescribed psychiatric and anti-anxiety medications. So, I couldn’t use this as a teaching tool. Your veterinarian would have scoffed at it just as MDs did in the 1980s.
We see another condition in humans that shares similarities with SARD dogs called Congenital Adrenal Hyperplasia (CAH). Specifically, it’s a version called “Adult-onset CAH due to 11-beta hydroxylase type 1 (11-BHD1)”. In this condition the adrenal glands become enlarged as they fail to produce cortisol. The result is a rise in adrenal sex hormones just as we see in SARD dogs. Management consists of low-dose cortisol replacement.
As the name implies, CAH is a congenital disease and is often apparent at birth. I might have used this terminology to illustrate and explain adrenal dysfunction in SARD dogs. But veterinarians said, “CAH is congenital. These dogs were not born with SARD!” And the discussion was ended.
In the field of veterinary medicine, a general practice vet named Alfred Plechner pioneered the use of low-dose cortisol in animals without a standard Addison’s diagnosis. He developed a laboratory test that assayed cortisol and total estrogen. He dubbed the scenario of low cortisol plus elevated adrenal estrogen Plechner’s syndrome.
I might have used this terminology to describe the adrenal dysfunction in SARD dogs, but veterinarians were quick to reject it. The treatment included aggressive cortisol replacement which was objectionable to most. Concerted efforts by the mainstream veterinary community resulted in a smear campaign against Dr. Plechner.
At the University of Tennessee, a veterinary endocrinologist named Jack Oliver developed a laboratory test that assayed cortisol and adrenal sex hormones. When dogs exhibited elevated sex hormones without elevated cortisol — essentially the same scenario described by Dr. Plechner — it was dubbed atypical Cushing’s disease.
To this day, endocrinologists at the University of Tennessee’s College of Veterinary Medicine do not supplement the cortisol in these dogs. Instead, they recommend therapies that further disrupt adrenal function. General practice veterinarians dutifully follow these recommendations. If I had used this terminology to describe the adrenal problem in SARD dogs, dogs would have received cortisol-reducing therapies rather than cortisol-replacing therapies.
In yet another camp of veterinarians — primarily holistic veterinarians — the very same adrenal condition garnered a third name. Atypical Addison’s disease. Practitioners realized that unlike typical Addison’s patients that exhibited low cortisol plus low aldosterone, these dogs exhibited low cortisol only, earning the atypical Addison’s label.
Atypical Addison’s might be a good description of the adrenal problem that SARD dogs experience. However, the veterinary establishment was quick to dismiss this phrase, claiming, “there is no such thing.” So, once again, the terminology was not entirely useful in securing treatment for these dogs.
So, to recap
• Chronic Fatigue Syndrome was written off as bogus.
• Congenital Adrenal Hyperplasia was too dissimilar to accept.
• Plechner syndrome was written off as bogus.
• Atypical Cushing’s disease results in treatments that further disrupt cortisol production.
• Atypical Addison’s disease was written off as bogus.
With veterinarians at such odds with each other, I returned to research done in human medicine. Hans Selye MD, famed author and the “father of endocrinology” detailed various phases of adrenal gland activity in his book, “The Stress of Life” (1956). In the phase called adrenal exhaustion, he described a failure of cortisol production.
This phrase carried with it the least baggage, was instructive, and offered the best chance for securing a dog’s treatment. I hope you now understand why I use this phrase. I also hope you’ve come to understand that institutional, mainstream medicine periodically promotes a false narrative.
If the phrase I’ve chosen still bothers you, simply refer to the problem in its simplest form. Call it “elevations-in-adrenal-sex-hormones-resulting-from-insufficient-cortisol-production.” That would do it.
I wish you and your dog all the best,
February 7, 2019
I received this note recently from the owner of a darling little dog named Milo. You can read our conversation below and you can read more about Milo’s recovery here.
January 29, 2019
Our dog has been on the SARD protocol since August and regained vision in his left eye soon after the treatment started. Within the last week I noticed he now has some vision in his right eye as well! The vet said structurally his eyes still appear normal. I would like to start weaning him off the steroids, but I’m worried about him having a rebound reaction. Do you have any advice for long term therapy maintenance?
This was my reply:
I’m happy to hear the good news!
The short answer is that the underlying adrenal condition does not repair itself. The adrenal exhaustion — the low cortisol production — is a lifelong problem that requires lifelong treatment (i.e. low-dose daily cortisol replacement via either low-dose Medrol or low-dose prednisone.)
It is not an anti-inflammatory medication. It is not an anti-inflammatory dose. It is a hormone replacement for a hormone that is no longer being produced.
There is every chance that if you wean off the hormone replacement therapy that your dog will experience a rise in the adrenal sex-hormone steroids (including estrogen) and will experience a resurgence of all his original symptoms including vision loss.
Hormone replacement — low dose prednisone or Medrol— is simply replacing what his body would make if it were healthy. This is why the treatment does not require “weaning off”.
Please, please read the following three articles carefully.
Here’s another way to think of this. Perhaps you know someone who is an “insulin diabetic”, a person who takes insulin injections to treat his or her diabetes. Insulin is a hormone that controls blood sugar. That person takes insulin daily because the pancreas no longer makes it. Once the blood sugar is controlled, the insulin is NOT discontinued. Similarly, low-dose cortisol replacement is typically NOT discontinued because it is simply replacing what the body can no longer make.
Another example is thyroid hormone. Perhaps you know someone who takes a small daily dose of thyroid hormone each day. Once the symptoms improve, the hormone is NOT discontinued, it is necessary for life just as cortisol is necessary for life.
Remember, the typical result of discontinuing low-dose cortisol replacement is a rise in sex-hormone STEROIDS.
I wish you all the best,
January 20, 2019
Also, please remember I am not dispensing veterinary advice. I am sharing my observations with you. And I’m sharing information that my holistic veterinarian once shared with me. If you find this information to be complex and counterintuitive, you’d be right. I’ll try to explain it all in plain English and I’ve made some graphs to help, as well.
The center portion of each graph represents normal hormone activity. The top third represents abnormally high activity. The bottom third represents low activity. Sex-hormone activity is represented via estrogen.
Please note that “activity” does not necessarily equate with blood test results, especially in terms of cortisol. Lab tests often lump precursor hormones into the “cortisol” reading, pushing it into the normal range or even above normal when in fact, true cortisol production (activity) is low. For further reading, click here and scroll to page 8.
In addition, most cortisol readings do not identify prescription cortisol replacements. Consequently, even with therapy it’s common for cortisol readings to remain low for the duration of the dog’s life despite obvious clinical improvement. This is why it is more important to evaluate adrenal estrogen levels rather than cortisol levels.
Patterns of Adrenal Activity
Insufficient cortisol production increases adrenal sex-hormone production. For further reading, click here and scroll to page 6.
The adrenal glands periodically experience spikes in activity. If an adrenal gland can no longe
r produce cortisol, it produces a surge of sex-hormone steroids at such times.
Even dogs receiving appropriate hormone replacement therapy may show an increase in steroid signs/symptoms during these spikes.
Some dog owners and practitioners assume that the increase in steroid signs/symptoms is a result of the daily low-dose cortisol replacement when in fact, it is a spike in sex-hormone steroids that’s to blame.
Twice a year there can be noteworthy spikes in adrenal activity. Not all dogs experience these spikes but many do. Those that do may experience varying degrees of severity.
The first spike occurs in autumn when the adrenal glands prepare an animal for winter—colder temperatures, fewer calories, hibernation, etc. The body does this by increasing cortisol production. Individuals that cannot produce sufficient cortisol however, experience a spike in sex-hormone levels instead. In the northern hemisphere this spike often occurs around late November and then subsides.
A secondary, smaller spike in adrenal activity occurs in early spring when the adrenal gland increases sex-hormone production. This is meant to help an animal shed its winter coat and enter breeding season. In the northern hemisphere this often occurs around mid-February and then subsides.
Perhaps you’ve recognized seasonal problems in your own dog. Problems such as seasonal skin and eye allergies, seasonal ear or bladder infections, seasonal hair loss on the flanks. Perhaps your dog was diagnosed with SARD during one or the other of these spikes.
In addition to seasonal cycles, activities of daily life may also cause smaller spikes in adrenal sex-hormones. Stressors such as home remodeling or adding a new family member may increase stress and sex-hormone steroids. Such events are not the cause of SARD, but these events may be more apparent in dogs already suffering adrenal exhaustion.
Estrogen is a catabolic steroid that breaks down organs such as the liver, kidneys, and cardiac muscle. It damages ligaments and tendons. It raises blood glucose levels initiating the equivalent of gestational diabetes. It raises cholesterol and triglyceride levels. It increases mast cell activity, histamine levels, and allergies. It suppresses immunoglobulin levels and the immune system. It is an excitotoxin that causes seizures, tremors, and head tics.
During such a spike, dog owners may report that the treatment doesn’t seem to be working as well as it did initially. Or, they may assume that the therapy is the cause of the problems. If it is wrongly assumed that the steroid signs are from the low-dose cortisol replacement, a practitioner may discontinue therapy. In that case, one of two things may happen:
- the dog may deteriorate rapidly. Cortisol is, after all, necessary for life and its absence is akin to an Addisonian crash.
- more often, the dog will ride out the seasonal spike of sex-hormones and the natural decline that follows the spike. Steroid signs/symptoms will dissipate. This may lead the practitioner and owner to believe that terminating the low-dose cortisol replacement was the correct course of action. The long-term outcome, however, is a different story. Untreated adrenal exhaustion (elevated sex-hormone production) contributes to long-term physical deterioration.
Please sit with that last point for a moment: By discontinuing low-dose daily cortisol replacement during an estrogen spike, the typical outcome is a gradual deterioration caused by elevated sex-hormone steroids.
Rather than discontinue therapy during an estrogen spike, holistic veterinarians will initiate a slightly more aggressive approach during these times. (That’s the counterintuitive part.) Holistic veterinarians accomplish this in one of two ways. They will either:
- repeat the initial SARD protocol injections at 70% of the original dosing. This statement applies to this protocol, no others.
- or instruct the client to pulse the oral cortisol replacement at a slightly higher dose for 1-2 weeks. No longer.
The chart above depicts only one spike, but such spikes may reoccur year after year. SARD-dog owners are encouraged to mark their calendars and plan ahead.
NOTE: On rare occasions, a dog’s adrenal glands may heal and cortisol replacement is no longer necessary. However, this is very uncommon and it generally occurs only after many years of hormone replacement.
Starting on the left side of the chart we see insufficient cortisol production resulting in rising sex-hormone levels (A). Once low-dose cortisol replacement therapy is initiated, sex-hormone levels begin to normalize (B).
As the seasons change, however, the dog may experience a seasonal spike in adrenal activity and a rise in sex-hormone levels (C). This translates to increased drinking, urination, appetite, liver enzymes, cholesterol levels, pancreatitis, blood glucose, seizures, lethargy, etc.
Concerned that it is the low-dose cortisol replacement therapy causing these signs/symptoms, the practitioner discontinues therapy. The seasonal estrogen spike naturally dissipates (D), and so do steroid signs. This may lead the owner and practitioner to believe that discontinuing the low-dose cortisol replacement therapy was the correct course of action.
Without therapy, however, sex-hormone steroids may:
- remain just slightly elevated
- climb gradually (E)
- or they may exhibit repeated spikes over time (F)
Rather than discontinue therapy, holistic veterinarians will provide slightly more aggressive therapy during an estrogen spike and then continue baseline therapy thereafter (G).
Is is possible that sex-hormone levels return to normal without intervention? Anything’s possible but observation would suggest otherwise. SARD-dog owners generally report ongoing health concerns with their dogs…not every one, but many do. Year after year, email after email, owners from every corner of the world describe their dogs’ health problems.
Some dogs appear to tolerate the mildly elevated estrogen. Their owners report that they “have no symptoms” other than the vision loss. But if a dog has SARD it’s almost guaranteed that he/she also has some degree of elevated sex-hormone steroids. It can be difficult to accept these connections. However, these connections still exist.
I present this information not to upset you, but rather in the hopes that every owner is made aware of their options and that every SARD dog can experience optimum health. I really do wish you and your dogs all the best.
For Part 4 click here.
November 7, 2018
If you haven’t read Part 1, please click here.
In that article we discussed how the term “steroid” has mistakenly come to mean cortisone and prednisone. And we noted that SARD dogs routinely develop high levels of steroids internally, called sex-hormone steroids. Here in Part 2 we’re going to address another misconception.
A Quick History
For decades, prednisone has been typically been prescribed in what’s called an anti-inflammatory or immuno-suppressant dose. These are the large doses that suppress the immune system response.
When a dog develops sudden blindness, it’s been the standard practice to rule out inflammatory activity. Veterinary ophthalmologists prescribe oral prednisone in a large, anti-inflammatory dose. The dog generally shows no improvement and in fact, may experience MORE hunger, thirst and lethargy than before.
Why? Because not only are these dogs producing high levels of sex-hormone steroids internally, they’ve been prescribed high levels of prednisone, another steroid, on top of that. No wonder these dogs feel worse than when they started!
The Difference is in the Dose
If you’ve read any of my work you know that sex-hormone levels rise when adrenal glands can no longer make sufficient cortisol. And you also know that when these dogs are given (and I cannot emphasize this enough) LOW DOSE, DAILY REPLACEMENT-LEVEL cortisol, it corrects the over-production of those sex-hormones.
A LOW, DAILY REPLACEMENT-LEVEL DOSE of cortisol (prednisone or Medrol) is very different than the large, short-term, anti-inflammatory dose that SARD dogs are typically prescribed at diagnosis. The large, anti-inflammatory dose is discontinued after a couple of weeks. In cases of adrenal exhaustion, cortisol replacement is typically necessary for life. So, the anti-inflammatory dose is both too high, and of too short a duration.
Understanding the difference in these dosages is crucial. An anti-inflammatory dose suppresses the immune system response and may worsen signs / symptoms. A low dose acts as a hormone replacement, corrects the sex-hormone problem, and improves signs / symptoms.
Let’s take the example of a 20-pound dog. Holistic veterinarians would typically give a 20-pound dog about 2mg of prednisone or Medrol as a daily replacement dose. On the other hand, an anti-inflammatory dose can range from 5mg-20mg per day. That’s double, triple, or even 10-fold as much as a daily replacement dose!
Here’s another way to look at it. Do you know someone who takes thyroid hormone? That person takes a tiny dose each day. It’s a lifelong treatment to replace the amount of thyroid hormone a body would normally make. If that person took 10 times what they actually needed, there would be some serious medical consequences very quickly.
So, when a SARD-dog owner says to me, “We tried the prednisone treatment and our dog felt even worse,” in all likelihood their dog was given a high, anti-inflammatory dose rather than a LOW, DAILY REPLACEMENT-LEVEL DOSE as described in the SARD protocol.
In Part 3 we will discuss some nuances of low-dose cortisol replacement therapy. I hope this has been helpful. Good luck.
November 7, 2018
We’ve all been taught that the term “steroid” means cortisol and its cousins cortisone, prednisone, methylpred, etc. Medical and veterinary personnel fall into this trap, as well. Doctors say things like, “I’m going to write you a prescription for a steroid.” So, we all tend to equate “steroid” with cortisone and prednisone.
When we discuss SARD dogs it becomes clear just how inaccurate and impractical this description is.
A steroid is a molecule with a particular shape — four rings of carbon atoms. More importantly, it’s a molecule with a mission. A steroid signals cells to do their work. It’s called a signaling molecule. There are hundreds of steroids produced by the body in addition to cortisol and cortisone.
Surely, you’ve heard stories of bodybuilders taking testosterone injections. They do this because testosterone is a steroid that signals muscle development. In fact, all of the sex-hormones are steroids: androgens, progesterones, and estrogens.
We know that when SARD dogs are tested, there is a high incidence of elevated sex-hormone production. These steroids signal many cells in the body. It’s the reason these dogs suffer such a wide variety of problems including hunger, thirst, obesity, lethargy, seizures, liver degeneration, etc.
So, when a SARD-dog owner says, “I would never put my dog on steroids” as though it’s a dirty word — Guess what!? — that dog is already experiencing high levels of steroids circulating through its body.
This information may make some readers angry. Other readers will ignore it. These are normal methods of coping with grief and loss of control. A few readers will have questions. Please see Part 2. And a very few will “be in a place” where they are ready to address the problem. I truly wish all of you the best. Click here for Part 2.
November 7, 2018
After some thought I’ve decided to write this article in plain English for the benefit of the average dog owner. If you wish to see a more thorough explanation or bibliography, click here.
As you may know, cortisol is our natural anti-inflammatory hormone. It plays a role in essentially all body functions and is necessary for the body’s survival.
Cortisol is created when the brain sends out a fancy chemical call adrenocorticotropic hormone (ACTH) into the bloodstream. ACTH stimulates the adrenal gland to convert precursor hormones (building blocks) into cortisol. It’s like an assembly line. One hormone molecule Is converted into another until it’s turned into cortisol.
When the brain senses that sufficient cortisol has been produced, it decreases ACTH production, thereby decreasing adrenal gland activity. This feedback loop is a little like the thermostat in your home. When the house is warm enough, the thermostat turns off the furnace.
Adrenal exhaustion is a condition where the body can NO LONGER CONVERT the precursor hormones into cortisol. This may be due to chronic stress, chemical damage, and/or genetic abnormality. Over the years, the veterinary community has called this condition by various names: hyperestrogenism, atypical Cushing’s disease, and Plechner’s syndrome.
When the glands can no longer convert precursors into cortisol, it creates a break or interruption in the assembly line. The precursor hormones pile up behind that break. With nowhere else to go, they are rerouted down an alternate assembly line to produce hormones called adrenal sex-hormones.
Furthermore, because the glands are no longer producing sufficient cortisol, the brain never receives the message to turn off ACTH production. This causes chronically elevated sex-hormone levels. Since the sex-hormones are steroids, the resulting symptoms look almost exactly like those of cortisol excess (Cushing’s disease). This is why a dog in adrenal exhaustion can mistakenly appear to be suffering from Cushing’s disease.
Low dose cortisol supplementation can reestablish the feedback loop. The brain recognizes the presence of the cortisol replacement and reduces ACTH production. Once the ACTH production is normalized, levels of sex-hormones begin to normalize as well. This is how low-dose cortisol replacement therapy reduces elevated sex hormone levels and the symptoms so common in SARD dogs.
Because low dose cortisol replacement simply replaces what the body would normally make, we do not expect to see the side-effects produced by high, anti-inflammatory doses of prednisone or other glucocorticoids.
On the other hand, if aggressive treatments for Cushing’s disease are implemented — treatments that destroy what little cortisol production exists — there can be life-threatening results. When dealing with a SARD dog, test sex-hormone levels, especially estrogen.
I hope this helps you and your dog.
October 28, 2018
Since we’re heading into the autumn SARD season, I thought I’d try again to offer a few words of advice. I know SARD dog owners struggle emotionally with this diagnosis. There are feelings of grief and loss and anger. I know the dogs struggle, too. For over a decade I’ve received emails or read posts that start like this.
“My dog is doing great but…”
• She was just diagnosed with an enlarged liver
• She is ravenous
• He is drinking a lot of water and has accidents in the house
• The snoring keeps me awake at night
• She’s put on a lot of weight and has trouble getting around
• He is acting kind of confused
• She is panting hard
• He’s so lethargic, he’s just a bump on a log
• She wet her bed during the night
• Her belly is so bloated
• She recently had a seizure and was taken to the emergency room
• She wakes up every 2-3 hours wanting to eat or go out
• Her liver values are high
• She constantly licks between her toes
• She’s lost her sense of smell
• She has stomach issues and diarrhea
• She’s just been diagnosed with kidney failure
• He has awful skin sores
• She gets chronic bladder infections
The list goes on and on. Year after year after year. These same dog owners also write:
• A few tests have ruled out Cushings
• Cushings blood work is completely normal
• ACTH and LDDS tests and are negative for Cushing’s
• They are still trying to find Cushings. She has a biopsy and an ultrasound scheduled
• We had our girl tested for Cushings. It came back negative
If you are “in a place” where you can accept that there is an underlying problem and that the problem is not Cushing’s disease [1,2], then simply ask your vet to run an adrenal estrogen level. That’s all. You don’t have to believe in my work. Just run an adrenal estrogen level and see what it says. NVDS is the more affordable option and requires only a single blood draw. UTCVM recommends an ACTH component. This can be more expensive and invasive but your general practice vet might prefer it.
 Van der Woerdt A, Nasisse MP, Davidson MG. Sudden Acquired Retinal Degeneration in the dog: clinical findings in 36 cases. Progress in Comparative Ophthalmology 1991; 1: 11-18.
 Gilmour MA, Cardenas MR, Blaik MA, Bahr RJ, McGinnis JF. Evaluation of a comparative pathogenesis between cancer-associated retinopathy in humans and sudden acquired retinal degeneration syndrome in dogs via diagnostic imaging and western blot analysis American Journal of Veterinary Research 2006; 67, 5; 877-881