{"id":21940,"date":"2026-05-20T21:07:14","date_gmt":"2026-05-20T19:07:14","guid":{"rendered":"https:\/\/www.ngdcare.nl\/uncategorized\/endocrine-support-bundle\/"},"modified":"2026-05-20T21:07:14","modified_gmt":"2026-05-20T19:07:14","slug":"endocrine-support-bundle","status":"publish","type":"post","link":"https:\/\/www.ngdcare.nl\/en\/blog-en\/endocrine-support-bundle\/","title":{"rendered":"Endocrine support bundle"},"content":{"rendered":"
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NGD Care: Scientific background<\/div>\n

The endocrine system as an adaptation system:
\n hormonal disorders in dogs and cats<\/h1>\n

Why endocrine disorders are systemic diseases, how the HPA axis and HPT axis work, what diagnostics and pitfalls are per condition, and how phased system support in addition to medication promotes recovery. Substantiated with literature. <\/p>\n

By Stefan Veenstra DVM<\/p>\n<\/div>\n

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The endocrine system as an adaptation system<\/h2>\n

The endocrine system is often described as a collection of glands that each produce their own hormone. Thyroid makes T4. Adrenal glands make cortisol and aldosterone. Pituitary gland controls. But this description misses the point: the endocrine system is primarily an adaptation system. It regulates how the body responds to change, internally and externally. <\/p>\n

Stress response, energy management, immune activation, growth, and repair are controlled via hormonal feedback mechanisms that are interconnected. Disruption of one axis almost always leads to secondary disruption of other systems. This is why endocrine disorders are rarely purely hormonal diseases: they are systemic diseases. <\/p>\n

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Background and clinical context<\/strong><\/p>\n

This article forms the scientific background to the NGD Care Endocrine Bundle. It covers the four most common endocrine disorders in dogs and cats, their common mechanisms, and the underpinnings of the phased supplementation approach. Always in addition to regular veterinary treatment. <\/p>\n<\/div>\n

The two central axes<\/h2>\n

The HPA axis: stress response and cortisol regulation<\/h3>\n

The hypothalamic-pituitary-adrenal axis (HPA axis) is the central neuroendocrine stress regulation mechanism. In a stress stimulus, the hypothalamus secretes corticotropin-releasing hormone (CRH), which triggers the pituitary gland to produce ACTH, which then stimulates the adrenal cortex to secrete cortisol. [1]<\/a><\/sup><\/p>\n

Cortisol prepares the body for the stress response via gluconeogenesis, immune modulation, and suppression of the parasympathetic nervous system. In acute stress, this mechanism is adaptive and functional. In chronic activation, as in Cushing’s, or in the event of failure of the adrenal gland, as in Addison’s, the feedback loop is structurally disrupted. <\/p>\n

The HPT axis: basal metabolic rate and energy<\/h3>\n

The hypothalamic-pituitary-thyroid axis (HPT axis) regulates basal metabolic rate via T3 and T4. The hypothalamus produces TRH that stimulates TSH secretion by the pituitary gland, which triggers the thyroid gland to produce T4. T4 is peripherally converted to the biologically active T3, largely in liver and kidneys but also via gut microbiome enzymes. [2]<\/a><\/sup><\/p>\n

T3 directly regulates the expression of mitochondrial genes and the activity of the electron transport chain. Deficiency of T3, as in hypothyroidism, decreases mitochondrial energy production in virtually every cell type. Excess T3, as in hyperthyroidism, chronically drives metabolism beyond its limits and causes protein catabolism. <\/p>\n

Diagnostics per condition: blood tests, pitfalls and interpretation<\/h2>\n

Hypothyroidism in the dog<\/h3>\n
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Primary tests<\/strong><\/p>\n

Total T4 as a screening test. TSH as confirmation: increased TSH at decreased T4 confirms primary hypothyroidism. Free T4 via equilibrium dialysis as gold standard in doubtful cases. <\/p>\n<\/div>\n

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Pitfalls<\/strong><\/p>\n

Reduced T4 alone is insufficient. Disease of any kind, malnutrition, corticosteroids and phenobarbital reduce T4 without hypothyroidism. This is called euthyroid sick syndrome. TSH may be normal in secondary hypothyroidism via pituitary dysfunction. <\/p>\n<\/div>\n<\/div>\n

Hyperthyroidism in cats<\/h3>\n
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\n

Primary tests<\/strong><\/p>\n

Total T4 increased in most hyperthyroid cats. In case of borderline values: free T4, T3 suppression test or scintigraphy. Ultrasound of the thyroid gland for adenoma detection. <\/p>\n<\/div>\n

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Pitfalls<\/strong><\/p>\n

In concomitant CKD, T4 can be false normal because kidney disease lowers T4. This masks the hyperthyroidism. After treatment of hyperthyroidism, latent CKD can become visible because the increased renal blood flow through T4 normalizes. <\/p>\n<\/div>\n<\/div>\n

Cushing’s disease (hyperadrenocorticism)<\/h3>\n
\n
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Primary tests<\/strong><\/p>\n

ACTH stimulation test and low-dose dexamethasone suppression test (LDDST) as screening tests. Urine cortisol\/creatinine ratio as a simple home test. High-dose dexamethasone suppression test and endogenous ACTH to distinguish PDH versus adrenal tumor. <\/p>\n<\/div>\n

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Pitfalls<\/strong><\/p>\n

No test is 100% sensitive or specific. Atypical Cushing’s with elevated adrenal steroids, but normal cortisol is missed by standard cortisol tests. Stress temporarily increases cortisol and can give false positive results. Always take into account clinical signs: polyuria, polydipsia, bilateral alopecia, pendulum bend. <\/p>\n<\/div>\n<\/div>\n

Addison’s disease (hypoadrenocorticism)<\/h3>\n
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Primary tests<\/strong><\/p>\n

ACTH stimulation test is the gold standard: no cortisol response after ACTH confirms primary adrenocortical insufficiency. Electrolytes: sodium\/potassium ratio below 27 is highly suspect. Basal cortisol below 2 ug\/dl is very suggestive. <\/p>\n<\/div>\n

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Pitfalls<\/strong><\/p>\n

Atypical Addison’s with glucocorticoid deficiency alone without aldosterone deficiency has normal electrolytes, thus missing the diagnosis. Hyperkalemia has many causes: hemolytic samples, thrombocytosis, constipation. Always repeat when in doubt. A low sodium\/potassium ratio in an acutely ill animal is an emergency. <\/p>\n<\/div>\n<\/div>\n

The four disorders mechanistic<\/h2>\n
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Hypothyroidism (dog)<\/strong><\/p>\n

Most often autoimmune destruction (lymphocytic thyroiditis) or idiopathic atrophy of the thyroid gland, leading to deficiency of T4 and T3. T3 deficiency decreases the expression of mitochondrial genes, reduces the activity of complex I and II of the electron transport chain, and slows cell turnover in all tissues. Consequences: lethargy, weight gain despite normal food, muscle weakness, skin and coat problems and reduced stress resistance. The autoimmune component implies structural gut barrier attention: intestinal hyperpermeability is associated with autoimmune thyroiditis via molecular mimicry of gut proteins with thyroid antigens. [3]<\/a><\/sup><\/p>\n<\/div>\n

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Hyperthyroidism (cat)<\/strong><\/p>\n

Usually a benign functional thyroid adenoma that autonomously produces T4 independent of TSH regulation. Chronically elevated T3\/T4 drives metabolism beyond its physiological limits: mitochondria are overloaded and produce excess ROS, muscle proteins are catabolically broken down for energy, the heart is overloaded via positive chronotropic and inotropic effect. The result is weight loss despite hyperphagia, muscle loss, hypertension and tachycardia. After treatment, a mitochondrial exhaustion phase often occurs that can last for months. [4]<\/a><\/sup><\/p>\n<\/div>\n

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Cushing’s disease<\/strong><\/p>\n

Chronically elevated cortisol levels via pituitary adenoma (PDH, 85%) or adrenal tumor (AT, 15%). Cortisol induces a catabolic state via glucocorticoid receptors in almost every cell type: protein breakdown in muscle and connective tissue, inhibition of glucose uptake via GLUT4 downregulation, immune suppression and fat redistribution to visceral depot. Chronically elevated cortisol damages mitochondrial membranes via oxidative stress, induces insulin resistance via serine phosphorylation of IRS-1, and damages the gut barrier via tight junction-down regulation. The latter increases LPS load which further activates the HPA axis. [5]<\/a><\/sup><\/p>\n<\/div>\n

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Addison’s disease<\/strong><\/p>\n

Autoimmune destruction of the adrenal cortex leads to a deficiency of cortisol and in most dogs also aldosterone. Cortisol deficiency means the failure of stress adaptation: the body cannot respond to physiological, metabolic or emotional stressors. Aldosterone deficiency causes natriur loss and potassium retention with electrolyte disturbances and hypotension. The autoimmune component, as in hypothyroidism, implies intestinal barrier attention. The stress response dropout makes Addisonian dogs extremely vulnerable to triggers that pass by in healthy animals: infection, relocation, vaccination, or anesthesia can trigger an Addisonian crisis. [6]<\/a><\/sup><\/p>\n<\/div>\n

Two recognized drivers with the same endpoints<\/h2>\n

The four clinical conditions above are diagnosed via blood tests and hormone tests. But in practice, we regularly see animals with identical symptoms and blood values that do not receive a formal endocrine diagnosis, because two other drivers produce the same endpoints via a different route. They are rarely recognized as an endocrine problem, but they are mechanistically. <\/p>\n

Chronic stress: the sympathetic nervous system as an endocrine driver<\/h3>\n

An animal that is in a state of sympathetic activation 24 hours a day, 7 days a week does the same as an animal with early Cushing’s: it produces chronically elevated cortisol and adrenaline via the HPA axis and the sympathetic-adrenal medulla system. The physiological consequences are mechanistically identical to those of the clinical disorders. <\/p>\n

Chronic sympathetic dominance activates the hypothalamus via continuous CRH secretion, which prompts the pituitary gland to engage in sustained ACTH production and adrenal stimulation. In early stages, cortisol is structurally elevated. In late stages, after months to years of overload, the adrenal glands become exhausted and cortisol production drops. This is functional adrenal cortex depletion: not Addison’s autoimmune destruction, but the same functional endpoint of cortisol deficiency and stress response failure. [12]<\/a><\/sup><\/p>\n

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Early phase: overactivation<\/strong><\/p>\n

Increased cortisol via HPA axis overactivation. Increased heart rate and breathing. Polyuria and polydipsia via cortisol induction of diabetes insipidus-like leak. Skin problems via reduced skin barrier function due to cortisol. Low-grade ignition via NF-kB activation. Identical to early Cushing’s picture without adrenal pathology. <\/p>\n<\/div>\n

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Late phase: exhaustion<\/strong><\/p>\n

Decreased cortisol production due to adrenal cortex exhaustion. Fatigue, low energetic load capacity, reduced stress response. Electrolyte disorders in severe exhaustion. Increased infection sensitivity. Identical to subclinical Addison’s picture without autoimmune destruction. <\/p>\n<\/div>\n<\/div>\n

The diagnostic pitfall is real: a dog with chronic stress due to an unsafe home situation, an animal with a painful condition, or a cat that lives in a multi-cat house for a long time under social pressure, can show almost identical blood values and symptoms as an animal with early Cushing’s or subclinical Addison’s. Cortisol levels can be increased or decreased depending on the phase. ACTH stimulation test can provide a flat response in exhausted adrenal glands without autoimmune destruction. <\/p>\n

Chronic Stress vs Cushing’s<\/h3>\n

Chronic stress and early Cushing’s can give a strongly overlapping clinical picture: polyuria, polydipsia, increased cortisol, low-grade inflammation and behavioral changes. The distinction is primarily in the ACTH stimulation test and the urine cortisol\/creatinine ratio. In Cushing’s, the cortisol response after ACTH is extremely high and suppression via dexamethasone is absent. In chronic stress, the response is increased but the system does respond to dexamethasone. On ultrasound, the adrenal glands in Cushing’s are bilaterally enlarged (in PDH) or one adrenal gland shows a mass (in adrenal tumor). In chronic stress, the adrenal glands are normal to slightly enlarged but symmetrical without mass. History is distinctive: an identifiable chronic stress source, pain, social pressure, or environmental insecurity, points away from primary adrenal pathology. <\/p>\n

Chronic Stress Exhaustion vs Addison’s<\/h3>\n

This is the trickiest distinction because both can provide a planar ACTH stimulation test. The three most distinctive parameters are electrolytes, endogenous ACTH and ultrasound. In classic Addison’s, the sodium\/potassium ratio is reduced below 27 due to aldosterone deficiency. In functional stress exhaustion, electrolytes are almost always normal because aldosterone is regulated via angiotensin II and the zona glomerulosa is spared longer than the zona fasciculata. Endogenous ACTH is elevated in primary Addison’s because the pituitary gland works harder to stimulate the destroyed adrenal gland. In HPA axis exhaustion due to chronic stress, endogenous ACTH is low or normal. On ultrasound, the adrenal glands in autoimmune Addison’s are bilaterally atrophic. In case of stress exhaustion, they are normal in size. When in doubt and a clinically ill animal always the safe choice: prednisolone as a temporary support does not harm functional exhaustion, but the lack of cortisol in real Addison’s can be fatal. <\/p>\n

Ultra-processed food: dysbiosis as an endocrine disruptor<\/h3>\n

Ultra-processed diets, especially dry foods with simple protein sources, high glycemic load, synthetic additives and minimal fermentable fibers, cause the same four endpoints as the clinical endocrine disorders via an indirect but mechanistically well-documented pathway.<\/p>\n

Step 1: dysbiosis.<\/strong> Limited fiber content lowers the production of butyrate and other short-chain fatty acids. Pathogenic fermenters occupy the space of sacharolytic bacteria. The microbiome shifts to an LPS-producing profile. <\/p>\n

Step 2: leaky gut.<\/strong> LPS activates TLR4 on enterocytes and induces NF-kB-mediated cytokine production. Pro-inflammatory cytokines damage tight junctions. The intestinal barrier becomes permeable to bacterial fragments, LPS and undigested dietary proteins. <\/p>\n

Step 3: systemic low-grade inflammation.<\/strong> Systemic LPS loading activates the HPA axis directly via TLR4. This increases CRH production in the hypothalamus, which pushes the HPA axis into a chronic activation state. At the same time, the pro-inflammatory state lowers hormone receptor sensitivity: cortisol, thyroid hormone and insulin work less effectively at the same concentration. <\/p>\n

Step 4: neurotransmitter imbalance.<\/strong> The microbiome produces 90% of the body’s serotonin and significant amounts of GABA precursors. In dysbiosis, serotonin precursor production decreases, which influences behavior via the gut-brain axis: increased stress sensitivity, anxiety, sleep problems. This strengthens the HPA axis activation in a vicious circle. [2]<\/a><\/sup><\/p>\n

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The end result of chronic poor nutrition<\/strong><\/p>\n

An animal on ultra-processed dry food for years may develop the following symptoms that mimic all four endocrine endpoints: loss of adaptability via chronic HPA axis activation, mitochondrial exhaustion via increased oxidative stress due to LPS load, low-grade inflammation that lowers hormone receptor sensitivity, and gut-hormone-axis disruption that undermines T4-to-T3 conversion and cortisol regulation. Blood values may be normal. The vet finds nothing. The animal functions suboptimally. This is where the integrative history, nutritional analysis and gut recovery make all the difference. <\/p>\n<\/div>\n

Four common endpoints<\/h2>\n

Despite the different causes and mechanisms per condition, all four endocrine disorders share four common endpoints that the bundle targets.<\/p>\n

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1. Loss of adaptive capacity<\/strong><\/p>\n

The HPA axis is dysregulated in all four disorders: chronically overactive (Cushing’s), dropped out (Addison’s) or secondarily suppressed by HPT axis dysregulation. The body cannot respond adequately to allostatic load, resulting in chronic sympathetic dominance or parasympathetic insufficiency. <\/p>\n<\/div>\n

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2. Mitochondrial Exhaustion<\/strong><\/p>\n

T3 regulates mitochondrial biogenesis via PGC-1alpha. Cortisol damages mitochondrial membranes in chronic elevation. Chronic overactivity in hyperthyroidism overloads mitochondrial capacity. In all four, cellular energy production is structurally reduced, with fatigue, muscle loss and reduced recovery capacity as a clinical consequence. [7]<\/a><\/sup><\/p>\n<\/div>\n

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3. Increased oxidative stress<\/strong><\/p>\n

Hypothyroidism lowers endogenous antioxidant capacity via decreased superoxide dismutase expression. Hyperthyroidism increases ROS production via overloaded mitochondria. Cortisol in Cushing’s induces oxidative stress via lipid peroxidation of mitochondrial membranes. All four lead to reduced glutathione reserves. <\/p>\n<\/div>\n

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4. Gut-hormone-axis disruption<\/strong><\/p>\n

The gut microbiome produces deiodinase enzymes that convert T4 to T3. In dysbiosis, peripheral T3 production also decreases with adequate levothyroxine dosing. LPS through a disrupted intestinal barrier activates the HPA axis and undermines hormone receptor sensitivity. Bowel repair is mechanistically indicated in all endocrine disorders. [2]<\/a><\/sup><\/p>\n<\/div>\n<\/div>\n

Nutrition for endocrine disorders<\/h2>\n

In endocrine disorders, nutrition is rarely discussed as a therapeutic tool in regular practice. However, from integrative systems biology, there are mechanistic links between food quality and hormonal function that are clinically relevant. <\/p>\n

Ultra-processed dry food increases LPS-producing dysbiosis via limited fibre content and activates the HPA axis via TLR4. This is a direct external trigger for HPA-axis dysregulation in both Cushing’s and Addison’s. In hypothyroidism, tyrosine, iodine and selenium are the essential cofactors for T4 synthesis and T4-to-T3 conversion: fresh varied protein sources provide these cofactors in bioavailable form that ultra-processed feed lacks. <\/p>\n

In Cushing’s and hyperthyroidism, muscle loss via catabolic hormone action is a primary clinical problem. Adequate protein intake is the most direct dietary intervention to inhibit muscle breakdown. Protein restriction in these conditions directly worsens cachexia. <\/p>\n

The supplements in the bundle mechanistically worked out<\/h2>\n

Phase 1: Prebiotics, Enzyme Mix 2, Liposomal Vitamin C, Liposomal Curcumin<\/h3>\n

Prebiotics<\/strong> promote sacharolytic fermentation and the production of short-chain fatty acids that modulate the HPA axis via cortisol reactivity dampening. In all four endocrine disorders, the HPA axis is dysregulated and microbiome repair is mechanistically indicated. Specific to hypothyroidism: Prebiotics promote the bacterial species that produce deiodinase enzymes for T4-to-T3 conversion, which improves active thyroid hormone status also at adequate levothyroxine dosing. <\/p>\n

Enzyme mix 2<\/strong> supports digestion and absorption of nutrients in the disturbed parasympathetic nervous system that suppresses digestion in all endocrine disorders. In Cushing’s, gastrointestinal ulceration is a known side effect of chronically elevated cortisol. Enzyme support reduces the fermentation of undigested food residues that feed LPS-producing bacteria. <\/p>\n

Liposomal vitamin C<\/strong> is a cofactor for cortisol synthesis in the adrenal cortex via hydroxylation of steroid precursors. In Addison’s, the adrenal cortex is destroyed, but vitamin C supports the oxidative stress that is increased in cortisol deficiency due to reduced antioxidant enzymes. In Cushing’s case, vitamin C protects against the oxidative damage caused by chronically elevated cortisol. In hypothyroidism, vitamin C is a cofactor for the peroxidase reaction in T4 synthesis. <\/p>\n

Liposomal curcumin<\/strong> inhibits NF-kB activation and modulates the HPA axis via reduction of CRH expression in the hypothalamus. This is mechanistically relevant in Cushing’s and Addison’s where the HPA-axis feedback loop is disrupted. Curcumin additionally modulates thyroid peroxidase activity and has demonstrated modulating effects in both hypothyroidism and hyperthyroidism in animal models. [8]<\/a><\/sup> The autoimmune component in hypothyroidism and Addison’s is addressed aditionally via gut barrier repair and immune modulation. <\/p>\n

Phase 2: Myco Adaptogen Complex, Adaptogen Complex, PEA & Boswellia, Omega-3 Calanus Oil<\/h3>\n

Myco Adaptogen Complex<\/strong> contains Reishi, Lion’s Mane, Cordyceps and other medicinal mushrooms with adaptogenic and HPA axis modulating effects. Reishi modulates the HPA axis via inhibition of cortisol secretion and has demonstrated anxiolytic effects in animal models. Cordyceps supports adrenal function via adrenocortical stimulation, relevant in Addison’s for optimizing residual adrenal capacity. The beta-glucans act as prebiotics and support the microbiome that influences the hormonal feedback loop via the gut hormone axis. [9]<\/a><\/sup><\/p>\n

Adaptogen Complex (ashwagandha and rhodiola)<\/strong> restores the HPA axis through two complementary pathways. Ashwagandha withanolides modulate the HPA axis via inhibition of cortisol production and improvement of glucocorticoid receptor sensitivity in the hippocampus, the key structure for HPA axis negative feedback. This is mechanistically relevant in Cushing’s for HPA axis normalization in addition to trilostane, and in Addison’s for optimization of the residual stress response. Rhodiola modulates serotonergic and dopaminergic neurotransmission and improves energetic resilience in the event of exhaustion due to chronic stress stress. [10]<\/a><\/sup><\/p>\n

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Contraindication Adaptogen Complex in Hyperthyroidism<\/strong><\/p>\n

Ashwagandha has potential thyroid-stimulating effects via increasing T4 production in animal models. In untreated or unstable hyperthyroidism, Adaptogen Complex is contraindicated. After successful treatment and stabilization of T4 values, the complex can be used for HPA axis recovery and energetic load capacity. <\/p>\n<\/div>\n

PEA & Boswellia<\/strong> addresses neuroinflammation that is present in all four endocrine disorders via the HPA-axis-immune axis. In Cushing’s disease, chronic cortisol suppresses the immune system but at the same time increases neuroinflammation via direct glucocorticoid receptor activation in neuronal cells. PEA modulates mast cell activation and microglia response via PPAR-alpha. Boswellia inhibits leukotriene B4 synthesis via 5-lipoxygenase, which is increased in chronic endocrine dysregulation. <\/p>\n

Omega-3 Calanus oil (EPA and DHA)<\/strong> protects cell membranes and hormone receptors. Hormone receptors are transmembrane proteins whose signaling efficiency depends on the fluidity of the lipid bilayer. In chronic omega-6\/omega-3 imbalance, almost universal in animals on ultra-processed feed, membranes become stiffer and hormone receptor sensitivity decreases. EPA additionally modulates the eicosanoid balance towards resolvins and protectins that dampen HPA axis reactivity. <\/p>\n

Phase 3: Longevity Support, Liposomal CoQ10, Liposomal Glutathione<\/h3>\n

Longevity Support (NAD\u207a, resveratrol, ergothioneine)<\/strong> restores mitochondrial biogenesis compromised in all four conditions. NAD\u207a is a cosubstrate for SIRT1 and SIRT3 that regulate mitochondrial gene expression via PGC-1alpha. In hypothyroidism, PGC-1alpha activity is decreased by T3 deficiency. NAD\u207a supplementation restores this mechanism partly independently of T3. Resveratrol activates SIRT1 directly and has anti-inflammatory action via NF-kB inhibition. Ergothioneine selectively accumulates in tissue with high oxidative load, particularly in adrenal cortex and thyroid tissue itself. [7]<\/a><\/sup><\/p>\n

Liposomal CoQ10<\/strong> restores the electron transport chain that is structurally impaired in hypothyroidism via T3 deficiency and in Cushing’s via cortisol damage. CoQ10 is also essential for steroidogenesis in the adrenal cortex: the synthesis of cortisol and aldosterone requires functional mitochondria in the adrenal cortex cells. In Addison’s, adrenal cortex is destroyed, but CoQ10 supports the remaining steroidogenic capacity and the heart muscle in Addison’s that is vulnerable to hyperkalemia-induced arrhythmias. [11]<\/a><\/sup><\/p>\n

Liposomal glutathione<\/strong> restores the intracellular antioxidant capacity that is depleted in all four conditions. The thyroid gland has the highest glutathione requirement per gram of tissue of all organs due to the hydrogen peroxide-dependent thyroid peroxidase reaction in T4 synthesis. In hypothyroidism, this system is chronically underperforming. In Cushing’s disease, glutathione is depleted by cortisol induction from oxidative stress. Liposomal delivery form for maximum intracellular availability even in case of compromised intestinal barrier. <\/p>\n

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Why phasing is mechanistically compelling<\/strong><\/p>\n

Stabilizing the gut-hormone axis before adaptogenic support is not random. LPS from a disrupted gut barrier activates TLR4 and NF-kB, which keeps the HPA axis hyperreactive and lowers hormone receptor sensitivity. As long as this LPS load is active, adaptogens such as ashwagandha have less effect on HPA axis normalization. Phase 1 lowers the external trigger so that phase 2 can work optimally. Mitochondrial repair in Stage 3 is also not optimal if the oxidative load from LPS endotoxemia has not been reduced in Stage 1 and the HPA axis has not been normalized in Stage 2. <\/p>\n<\/div>\n

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When does this bundle apply?<\/h3>\n

Hypothyroidism in dogs supplemental to levothyroxine. Hyperthyroidism in cats after treatment and stabilization. Cushing’s in addition to trilostane. Addison’s supplements lifelong hormone replacement. Fatigue and muscle loss despite good hormone setting. Subclinical hormonal dysregulation without formal diagnosis. <\/p>\n

For specific conditions, we refer to the disorder blogs on hypothyroidism, hyperthyroidism, Cushing’s and Addison’s in the knowledge base.<\/p>\n<\/div>\n

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Conclusion<\/h2>\n

Endocrine disorders are not isolated glandular disorders. They are systemic diseases that affect metabolism, immune system, gut, mitochondria and behavior. Medication restores hormonal control, but not the secondary damage caused by the dysregulation. <\/p>\n

The NGD Care Endocrine Bundle supports the body’s ability to adapt in addition to the necessary medication. Phased, mechanistically substantiated, always in consultation with the treating veterinarian. <\/p>\n

We don’t send hormones. We support how the body adapts. <\/p>\n<\/div>\n

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View the NGD Care Endocrine Bundle<\/p>\n

To the bundle<\/a><\/p>\n<\/div>\n

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Literature<\/h2>\n
    \n
  1. Chrousos GP. Stress and disorders of the stress system. Nat Rev Endocrinol.<\/em> 2009; 5(7):374-381.<\/li>\n
  2. Virili C et al. Gut microbiota and Hashimoto’s thyroiditis. Rev Endocr Metab Disord.<\/em> 2018; 19(4):293-300. doi:10.1007\/s11154-018-9467-y. <\/li>\n
  3. Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol.<\/em> 2012; 42(1):71-78.<\/li>\n
  4. Mooney CT. Hyperthyroidism. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine.<\/em> 7th ed. St. Louis: Elsevier Saunders; 2010:1761-1779. <\/li>\n
  5. Sow Wetter FK et al. Cushing’s syndrome in dogs. Fat Clin North Am Small Anim Pract.<\/em> 2017; 47(2):309-327.<\/li>\n
  6. Scott-Moncrieff JC. Hypoadrenocorticism. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine.<\/em> 7th ed. St. Louis: Elsevier Saunders; 2010:1798-1810. <\/li>\n
  7. Canto C & Auwerx J. PGC-1alpha, SIRT1 and AMPK, an energy sensing network that controls energy expenditure. Curr Opin Lipidol.<\/em> 2009; 20(2):98-105.<\/li>\n
  8. Shukla S et al. Curcumin and thyroid disorders: a comprehensive review. Phytomedicine.<\/em> 2022;104:154256. <\/li>\n
  9. Matsuzaki H et al. Antidepressant-like effects of a water-soluble extract from Ganoderma lucidum mycelia in rats. BMC Complement Altern Med.<\/em> 2013;13:370. <\/li>\n
  10. Chandrasekhar K et al. A prospective, randomized double-blind study of safety and efficacy of a high-concentration full-spectrum extract of ashwagandha root. Indian J Psychol Med.<\/em> 2012; 34(3):255-262. <\/li>\n
  11. Crane FL. Biochemical functions of coenzyme Q10. J Am Coll Nutr.<\/em> 2001; 20(6):591-598.<\/li>\n
  12. McEwen BS. Stressed or stressed out: what is the difference? J Psychiatry Neurosci.<\/em> 2005; 30(5):315-318.<\/li>\n<\/ol>\n<\/div>\n

    This information is educational in nature and based on available scientific literature. The studies mentioned are not always directly veterinary or specific to the formulation described here. This text does not replace a veterinary consultation and does not contain any therapeutic claims. <\/p>\n<\/div>\n","protected":false},"excerpt":{"rendered":"

    NGD Care: Scientific background The endocrine system as an adaptation system: hormonal disorders in dogs and cats Why endocrine disorders are systemic diseases, how the HPA axis and HPT axis work, what diagnostics and pitfalls are per condition, and how phased system support in addition to medication promotes recovery. Substantiated with literature. By Stefan Veenstra … Read more<\/a><\/p>\n","protected":false},"author":2,"featured_media":21942,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"wds_primary_category":0,"footnotes":""},"categories":[178,8537],"tags":[11635,11631,11639,11630,11637,11634,11632,11633,11629,11628,11636,7747,11638],"class_list":["post-21940","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-blog-en","category-integrative-veterinary-medicine","tag-adaptogens","tag-addison","tag-cortisol-regulation","tag-cushings","tag-diagnostics","tag-gut-hormone-axis","tag-hpa-axis","tag-hpt-axis","tag-hyperthyroidism","tag-hypothyroidism","tag-mitochondria","tag-stefan-veenstra-dvm","tag-t4-t3-conversion","infinite-scroll-item"],"_links":{"self":[{"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/posts\/21940","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/comments?post=21940"}],"version-history":[{"count":0,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/posts\/21940\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/media\/21942"}],"wp:attachment":[{"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/media?parent=21940"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/categories?post=21940"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.ngdcare.nl\/en\/wp-json\/wp\/v2\/tags?post=21940"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}