Marketisation of Pet Health Care?
Traditional de-sexing protocols and methods typically result in the adrenal glands taking on more responsibility. Adrenal glands produce hormones that are directly or indirectly involved in most major bodily functions. One theory suggests that when de-sexed, the adrenal glands can be overwhelmed by the additional requirements and cannot maintain hormonal balance and may result in problems with the nervous system and immune systems, body composition difficulties, blood sugar irregularities, irregular androgen levels.
The mechanism by which all this damage can occur has not been specifically identified in any of the research we read or publicly available. However, given the challenges vets face today in addressing allergies, cancers and associated immune system anomalies in pets, we believe it might not be a simple task for the system to provide hormone replacement to resolve the imbalances. This is based on the observation that the hormone systems are a complex system of systems.
A theory that we do find interesting is that the mechanism might be related “broken communications” with the brain. The theory is based on the concept that a surgically neutered animals’ brain does not know that the sex organs are gone. So perhaps the brain keeps sending signals to those missing sex organs. In a non-neutered cat or dog the testicles or ovaries would then signal back to the brain and it in turn would reduce its output of hormones. This cycle is often referred to as a ‘negative feedback’ cycles. However, in a de-sexed cat or dog, without feedback from the sex organs, the poor old brain keeps pumping out hormonal signals. The adrenal glands are the innocent bystanders that end up mistaking these signals as meant for them, and pump out their own hormones to excess, resulting in adrenal disease or distress.
UC Davis has only recently produced peer reviewed studies which confirm:
- De-sexing can interfere with orthopedic development1 2 ;
- De-sexing can render dogs more susceptible to behavior problems 3 ;
- De-sexing can damage the immune system resulting in increased incidence of various cancers1 2.
Our theory revolves around the hypothesis that de-sexing introduces a very efficient endocrine disruptor in the body. By removing the glands associated with sex hormones, a similar situation is created as one would observe with endocrine disruptor chemicals in the body:
Read More: Endocrine Disrupting Chemicals (EDCs)(WHO)
- reduce the production of hormones in endocrine glands;
- affect the release of hormones from endocrine glands;
- copy or counteract the action of hormones at target tissues;
- speed up the metabolism of hormones and so reduce their action.
Pet parents familiar with Endocrine Disruptors will recognise:
- atrazine / herbicides
Read More: Endocrine Disruptors (ToxTown)
Did you know? “Virtually all classes of EDs can mimic or block effects of male and female sex hormones”
Read More: Endocrine Disrupting Chemicals EDCs (Hormone.Org)
When you compare the effects of de-sexing on the body, and the effects of endocrine disruptors, you will find an uncomfortable close correlation in symptoms and observations.
|ED / EDC Disease Related Symptoms||De-Sexing Correlating Impairments|
|Neurological changes||Increased cognitive impairment|
|Behavioral changes||Behavioral changes in females and males|
|Reduced ability to handle stress||Sex hormone production is additional burden on adrenal glands. When a de-sexed dog experiences high stress situations, the adrenal glands can become overwhelmed.|
|Compromised thyroid function||Three fold increased risk of hypothyroidism as compared to intact dogs|
|Weakened immune system||Increased risk of persistent or recurring urinary tract infections by a factor of 3 to 4. Increased risk of recessed vulva, vaginal dermatitis, and vaginitis. Increased incidence of allergic reactions.|
|Increased risk of Diabetes||Increased risk of Diabetes with hypothyroidism, Cushings and hyperestrinism, all emerging diseases|
|Increased risk of obesity||Increased risk of obesity by a factor of 1.6 to 2 in females, and triple the risk of obesity in males. It is common and associated with many health problems|
|Increased risk of Cancer||Increased incidence of Cancer|
The adrenal glands are responsible for producing cortisol in response to stress. However, because stress response is a primary responsibility for the adrenal glands, high levels of chronic stress will force the adrenals to devote their energy to cortisol production, and production of sex hormones will become secondary. If the stress is ongoing and significant, the production of sex hormones can be interrupted. In de-sexed pets this will deprive the body of adequate sex hormones.
Read More: 5 Ways That Stress Causes Hypothyroid Symptoms, Chris Kresser (Article)
The hypothalamus and pituitary glands direct both adrenal and thyroid gland hormone production. Chronic adrenal stress might be responsible for depresses hypothalamic and pituitary function. And since the hypothalamus and pituitary glands control thyroid production, anything that disrupts the Hypothalamus and Pituitary (HPA) systems will also suppress thyroid function. Stress will predictably cause inadequate production of DHEA (anabolic) and sex hormones, thyroid dysregulation, and a failure of the hypothalamus and pituitary to secrete numerous other hormones required for a stable metabolism. You can envision the hormonal disruption spreading outward to other body systems like a pebble’s wake when thrown into a pond.
Proper thyroid function depends on healthy adrenal glands. In case studies4 where adrenal hormones are abnormal, adrenal hormone replacement therapy returned the thyroid levels to normal without the need for thyroid hormone replacement.
In support of the theory that de-sexing is an endocrine disruptor (ED), and the likely basis for an endocrine disease syndrome (EDS), let us examine the five common diseases and the glands they impact as part of this endocrine disease syndrome.
The Thyroid Gland (Hypothyrodism)
Hypothyroidism, which is the failure of the thyroid gland to produce enough thyroid hormone, has been tied directly to de-sexing in at least one canine study. De-sexing was found to be correlated with a threefold increased risk of hypothyroidism compared to intact dogs 5 6 .
The Adrenal Gland (Cortisol and Cushings Syndrome)
The Hormone Health Network states that Cushings consists of the physical and mental changes that result from having too much cortisol in the blood for a long period of time. Cortisol is a steroid hormone produced by the adrenal glands. Hyperadrenocorticism7 (overproduction of cortisol in the adrenal gland) is due 15% of the time to a tumor in the adrenal gland (Cushings Syndrome), or 85% of the time to a tumor in the pituitary gland (Cushings Disease). Based on our theory of ED and research available, our observation is that the higher incidence of Cushings of both causes in the canine population is due to de-sexing and the additional stress inflected on the hormonal complex. This can result in overproduction of cortisol, a deficiency of sex hormones, hormonal imbalance, and the compromise of the immune system.
Read More: Cushing Syndrome (HormoneOrg)
The Pituitary Gland (Cushings Disease)
According to a 2009 study 8 , “Cushing’s disease (CD) is a common endocrinological disorder in dogs… in contrast to humans in whom CD is rare. The clinical presentation of CD, however, is highly similar between dogs and humans, with characteristic signs, such as abdominal obesity, weight gain, fatigue, muscle atrophy and skin changes. Canine CD may therefore serve as an animal model for human CD.”
In de-sexed male dogs, the data seem to suggest an increased incidence of overproduction of cortisol purportedly due to a pituitary tumor (microadenoma), or to enlargement (hyperplasia) of the pituitary gland and diagnosed as Cushings disease.
In studies among ancient human civilizations whom practiced castration of males at a very early age, the bone structure in the brain which houses the pituitary gland was enlarged, consistent with pituitary enlargement9 . In a 1979 study 10 conducted on patients with diseases that caused them to have low gonadal sex hormones (e.g. testosterone), the authors noted, “… results suggest that hyperplasia or microadenoma of the pituitary gland may occur secondary to gonadal failure … lack of awareness … may result in inappropriate surgical management of what may appear to be primary pituitary tumor.”
However, if the historical studies are correct, Cushings of a pituitary origin in neutered male dogs should be treated by testosterone, rather than drugs that destroy a normal adrenal gland. Researchers have long observed the presence of adequate levels of cortisol along with normal circulating levels of sex hormones serve to “turn off” the signal (ACTH) coming from the pituitary which stimulates the adrenal gland to produce more cortisol. The precise interactions are unclear, however a series of studies in the late ’90s evaluated the cortisol production of castrated male animals provided with subcutaneous implants supplying various levels of testosterone replacement 11 .
The pituitary gland also produces Growth Hormone, which can be compromised when the pituitary and adrenal glands are excessively stressed. Lack of growth hormone can cause altered glucose metabolism (precursor to diabetes), abdominal obesity, diminished muscle tone and function, and reduced vitality and energy. Because these symptoms seem so much like those of the other endocrine maladies we are discussing here, it serves as an example as to why it is so difficult to identify, and remedy hormone imbalance once incurred.
Read More: Adult Growth Hormone Deficiency , Morton et al (PNA)
Hyperestrinism (Atypical Cushings)
Atypical Cushings is defined in veterinary literature as overproduction of other adrenal steroids12 known as “sex steroids” with no excess cortisol (e.g. hyperestrinism). Atypical Cushings does not exist as a disease entity in humans. Hyperestrinism (excess estradiol) without elevated cortisol is an emerging disease entity in canines, with a side effect of insulin resistance in male dogs which can lead to type 2 diabetes.
Epidemiological studies indicate that the increased presence of endocrine disrupting chemicals (EDCs) in the environment may also play an important part in the incidence of metabolic diseases 13 . Among these compounds, polychlorinated biphenyls (PCBs), dioxins, phthalates and bisphenol-A (BPA), have been correlated with alterations in blood glucose homeostasis in humans. This altered blood glucose homeostasis may enhance the development of type 2 diabetes14 . The data linking EDCs with obesity, metabolic syndrome and diabetes are strong and the number of studies finding positive association is growing 15. If de-sexing acts in the manner of endocrine disruptors you would expect to see an increase in type 2 diabetes in dogs.
“The prevalence of diabetes mellitus in dogs increased from 13.1 cases per 10,000 in 2006 to 23.6 cases per 10,000 in 2015—a 79.7 percent increase.”
The veterinary community in general is acknowledging the emergence and rapid rise of diabetes in dogs, however it generally fails to classify it as type 2 diabetes, which is an important distinction to make. Low thyroid, Cushings, hyperestrinism, and low testosterone are all increasing in incidence due to the endocrine disruption brought on by de-sexing, and all are associated in some manner with an increased likelihood of developing type 2 diabetes.
EDCs can disrupt the thyroid’s normal processes, and therefore, can disrupt day to day metabolism. Recent (2016) studies in human populations have linked low thyroid hormones to type 2 diabetes. In one study it was found that low thyroid function is associated with a 1.2-fold increased risk of type 2 diabetes 16 . In another study, it was concluded that there appears to be a correlation between serum thyroid hormone levels and the prevalence of type 2 diabetes in the general population 17 .
Type 2 diabetes 18 is often associated with Cushings syndrome in the human environment. A review published in Trends in Endocrinology & Metabolism suggests that 36% of human patients with overt Cushing’s syndrome and 22% of patients with subclinical Cushing’s syndrome had diabetes while another 17% to 23% have impaired glucose tolerance.
With the emergence of these endocrine diseases, new tests must be devised to diagnose these illnesses as well as explore avenues of treatment. Once a dog has been de-sexed, their endocrine system has been forever altered. There is no going back to optimal health; de-sexing permanently damages your dog’s ability to respond to physical and / or psychological stress; leaving your dog increasingly susceptible to cancer, metabolic disease including diabetes, immune-related disease, infection and anxiety 19 .
What have we learned to date?
It is difficult to explain why the veterinary community continues to treat de-sexing and the associated glands and hormones only relevant to reproduction. It is no exaggeration to say that in modern human medicine and endocrinology testosterone is no longer a marginal hormone. Neither is it a lifestyle hormone for those men seeking eternal youth. Its deficiency leads to a serious deterioration of the health of men expressing itself in the metabolic syndrome and its sequels: diabetes mellitus type 2 and atherosclerotic disease, osteoporosis and sarcopenia20 , all strongly limiting physical independence in old age and accelerating morbidity and mortality 21 . It is not a stretch to apply the same principles to our fur kids.
More research needs to be undertaken to confirm the specifics of endocrine disruption as well as the exact mechanism by which failure to respond to stress appropriately, has resulted in the emergence of hypothyroidism, Cushings, Atypical Cushings, hyperestrinism and Type 2 diabetes in dogs, but with what we have learned to date, traditional de-sexing will no longer be an option in our household.
Articles and Videos
We will add research, articles and opinion pieces to the post as we find them.
- The Neutering Controversy: Understanding Data on Hormones, Behavior and Neoplasia (TVP);
- Baldness and Hormone-Related Skin Disorders in Dogs (PetMD);
Dr. Becker and Dr. Valente Talk About Spaying and Neutering
Dr. Becker: The Truth About Spaying and Neutering
Research and References
- 1.Hart B, Hart L, Thigpen A, Willits N. Long-term health effects of neutering dogs: comparison of Labrador Retrievers with Golden Retrievers. PLoS One. 2014;9(7):e102241. doi:10.1371/journal.pone.0102241
- 2.Hart BL, Eckstein RA. The role of gonadal hormones in the occurrence of objectionable behaviours in dogs and cats. Applied Animal Behaviour Science. April 1997:331-344. doi:10.1016/s0168-1591(96)01133-1
- 3.Hart B. Effect of gonadectomy on subsequent development of age-related cognitive impairment in dogs. J Am Vet Med Assoc. 2001;219(1):51-56. doi:10.2460/javma.2001.219.51
- 4.Abdullatif H, Ashraf A. Reversible subclinical hypothyroidism in the presence of adrenal insufficiency. Endocr Pract. 2006;12(5):572. doi:10.4158/EP.12.5.572
- 5.Panciera D. Hypothyroidism in dogs: 66 cases (1987-1992). J Am Vet Med Assoc. 1994;204(5):761-767. https://www.ncbi.nlm.nih.gov/pubmed/8175472.
- 6.Panciera D. Is it possible to diagnose canine hypothyroidism? J Small Anim Pract. 1999;40(4):152-157. doi:10.1111/j.1748-5827.1999.tb03780.x
- 7.Greco DS. Cushing Disease (Pituitary-dependent Hyperadrenocorticism) in Animals. MSD. 2000. https://www.merckvetmanual.com/endocrine-system/the-pituitary-gland/cushing-disease-pituitary-dependent-hyperadrenocorticism-in-animals.
- 8.de B, Meij B, Kooistra H, Hanson J, Lamberts S, Hofland L. Cushing’s disease in dogs and humans. Horm Res. 2009;71 Suppl 1:140-143. doi:10.1159/000178058
- 9.Wilson JD, Roehrborn C. Long-Term Consequences of Castration in Men: Lessons from the Skoptzy and the Eunuchs of the Chinese and Ottoman Courts. The Journal of Clinical Endocrinology & Metabolism. December 1999:4324-4331. doi:10.1210/jcem.84.12.6206
- 10.Samaan N, Stepanas A, Danziger J, Trujillo J. Reactive pituitary abnormalities in patients with Klinefelter’s and Turner’s syndromes. Arch Intern Med. 1979;139(2):198-201. https://www.ncbi.nlm.nih.gov/pubmed/434974.
- 11.Viau V, Meaney M. The inhibitory effect of testosterone on hypothalamic-pituitary-adrenal responses to stress is mediated by the medial preoptic area. J Neurosci. 1996;16(5):1866-1876. https://www.ncbi.nlm.nih.gov/pubmed/8774455.
- 12.Zimmerman K, Panciera D, Hoeschele I, et al. Adrenocortical Challenge Response and Genomic Analyses in Scottish Terriers With Increased Alkaline Phosphate Activity. Front Vet Sci. 2018;5:231. doi:10.3389/fvets.2018.00231
- 13.Alonso-Magdalena P, Quesada I, Nadal A. Endocrine disruptors in the etiology of type 2 diabetes mellitus. Nat Rev Endocrinol. 2011;7(6):346-353. doi:10.1038/nrendo.2011.56
- 14.Alonso-Magdalena P, Ropero A, Soriano S, Quesada I, Nadal A. Bisphenol-A: a new diabetogenic factor? Hormones (Athens). 2010;9(2):118-126. doi:10.1007/BF03401277
- 15.Schug T, Janesick A, Blumberg B, Heindel J. Endocrine disrupting chemicals and disease susceptibility. J Steroid Biochem Mol Biol. 2011;127(3-5):204-215. doi:10.1016/j.jsbmb.2011.08.007
- 16.Chaker L, Ligthart S, Korevaar TIM, et al. Thyroid function and risk of type 2 diabetes: a population-based prospective cohort study. BMC Med. September 2016. doi:10.1186/s12916-016-0693-4
- 17.Gu Y, Li H, Bao X, et al. The Relationship Between Thyroid Function and the Prevalence of Type 2 Diabetes Mellitus in Euthyroid Subjects. J Clin Endocrinol Metab. 2017;102(2):434-442. doi:10.1210/jc.2016-2965
- 18.Barbot M, Ceccato F, Scaroni C. Diabetes Mellitus Secondary to Cushing’s Disease. Front Endocrinol (Lausanne). 2018;9:284. doi:10.3389/fendo.2018.00284
- 19.Feingold K, Anawalt B, Boyce A, et al. Endotext. January 2000. http://www.ncbi.nlm.nih.gov/books/NBK278943/.
- 20.Santilli V, Bernetti A, Mangone M, Paoloni M. Clinical definition of sarcopenia. Clin Cases Miner Bone Metab. 2014;11(3):177-180. https://www.ncbi.nlm.nih.gov/pubmed/25568649.
- 21.Saad F, Gooren LJ. The Role of Testosterone in the Etiology and Treatment of Obesity, the Metabolic Syndrome, and Diabetes Mellitus Type 2. Journal of Obesity. 2011:1-10. doi:10.1155/2011/471584