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by Peter Stevenson

Disturbances of endocrine function can usually be divided into hyperfunction and hypofunction1. Each of which can be further classified as either primary or secondary dysfunction. Primary endocrine disorders originate within the target gland responsible for producing the hormone. In secondary disorders, the target gland is normal, but its function is altered by defective levels of releasing hormones or releasing factors from the hypothalamic-pituitary system.

Hypofunction can be caused by:

  • Congenital defects which can result in the absence of or impaired development of a gland or absence of any enzyme needed for hormone synthesis;
  • Destruction of a gland, which may occur because of disruption in blood flow, infection or inflammation, autoimmune responses or neoplastic growth (i.e. tumours);
  • Aging, which may result in: endocrine deficient states, absence of hormone receptors, defects in receptor binding of hormones, or impairment of cellular responses to hormones;
  • Inactive hormones: some glands may produce biologically inactive hormones, or active hormones may be destroyed by circulating antibodies before they can exert their action.

Hyperfunction can be caused by:

  • Excessive stimulation of a gland, for example in Graves’ Disease the thyroid is stimulated by antibodies that mimic the hormone Thyroid Stimulating Hormone (TSH);
  • Hyperplasia of a gland;
  • Hormone producing tumours of the gland – sometimes ectopic tumours will produce hormones.

Other reasons for gland and endocrine dysfunction include:

  • Bed rest – which results in a lowered Basal Metabolic Rate, decreased anabolic processes and increased catabolic processes which can lead to protein deficiency and negative nitrogen balance. All of which can impact hormone production;
  • Stress – which affects adrenocorticosteroid production particularly if sustained over long periods.

The remainder of this paper discusses five examples of specific endocrine dysfunction.

Growth Hormone (Somatotropin)

Special cells in the Anterior Pituitary called somatotropes secrete growth hormone (GH). GH is necessary for growth and regulation of metabolic functions. GH stimulates all aspects of cartilage growth, and its most obvious effect is on linear bone growth resulting from its action on epiphyseal cartilage plates of long bones.

GH also affects the growth of: visceral and endocrine organs; skeletal and cardiac muscle; skin and connective tissue. It facilitates the rate of protein synthesis by all cells, and enhances fatty acid mobilisation for use as fuel.

Two hypothalamic hormones regulate GH secretion: Growth Hormone Releasing Hormone (GH-RH) which stimulates release, and somatostatin which inhibits release. GH secretion can be stimulated by hypoglycemia, fasting, starving, increased blood levels of amino acids, and stress conditions (trauma, excitement, emotional stress, heavy exercise). Increased glucose levels inhibit GH, free fatty acid release, cortisol and obesity. Impairment of secretion, leading to growth retardation, is not uncommon in children with severe emotional deprivation 1.

Table 1 summarises the impact of deficiency and excess of GH.

Deficiency (Hypofunction)

Excess (Hyperfunction)



  • Tumors
  • Lack of somatotropes


  • Idiopathic lack of GH-RH with adequate somatotropes


Congenital GH deficiency

  • Normal birth length followed by decrease in growth rate
  • Normal intelligence
  • Short Stature
  • Obesity with immature facial features
  • Some delay in skeletal maturation
  • Puberty often delayed
  • Microphallus in males
  • May lead to hypoglycemia and seizures

Acquired GH deficiency

  • Occurs later in childhood
  • May be due to tumor


  • Adenoma (Tumor)


  • Pituitary adenoma



  • Occurs before puberty prior to fusion of epiphyses of long bone
  • Usually caused by adenomas in prepubutal children

Isosexual precocious puberty

  • Development of appropriate sexual characteristics and fertility at an early age
  • If puberty occurs in female before eight years of age and in boys before nine years of age then they are suspected of having this condition
  • Caused by early development of hypothalamic-pituitary-gonadal axis.


  • Result of GH excess in adulthood, or after epiphyses of long bones are fused
  • Chronic, debilitating disorder of body growth and metabolic disorder
  • Person cannot grow taller but soft tissue continues to grow
  • Results in enlargement of hands, feet, and membranous bones of the face and skull
  • Appearance of broad bulbous nose, protruding lower jaw, slanting forehead, splayed teeth, deepening of voice due to enlarged larynx
  • Kyphosis results due to enlarged vertebrae
  • Virtually every organ in the body is enlarged

Enlarged heart and accelerated atherosclerosis may lead to an early death

Table 1 A summary of the causes and manifestations of excess and deficient GH.

Other effects of inappropriate levels of GH include: alterations in fat and carbohydrate metabolism, and a diabetagenic effect (insulin agonist). Enlargement of the pituitary glands may lead to many secondary problems, headaches, visual field defects, and hypothyroidism.

Thyroid Disorders

The thyroid hormones T3 (triiodothyronine) and T4 (thyroxine) affect several functions of the body especially the basal metabolic rate. Table 2 summarises the actions of the thyroid hormones and the impact of excess or deficient levels.

Affected Area/System Hypothyroidism Hyperthyroidism
Basal Metabolic Rate Decreases Increases
Sensitivity to Catecholamines Decreases Increases
General Features Myxedamatous features

Deep Voice

Impaired growth in children


Lid lag

Decreased blinking

Blood cholesterol levels Increased Decreased
General behavious Mental retardation (infant)

Mental and physical sluggishness


Restless, irritable, anxious



Cardiovascular function Decreased Cardiac Output


Increased Cardiac Output

Tachycardia and palpitations

GIT Function Constipation

Decreased appetite


Increased appetite

Respiratory function Hypoventilation Dyspnea
Muscle tone and reflexes Decreased Increased with tremors and fribillatory twitching
Temperature tolerance Cold intolerance Heat intolerance
Skin and hair Decreased sweating

Coarse and dry skin and hair

Increased sweating

Thin and silky skin and hair

Weight Increases Decreases

Table 2 Affects of Hypo and Hyperthyroidism.

Parathyroid Hormone

The Parathyroid hormone (PTH) is produced by the parathyroid glands which are nodular glands that are closely associated with the thyroid. This hormone has two major target organs: bones and kidneys. The hormone activates vitamin D in the intestine, and ultimately causes an increase in blood calcium concentration. In the kidneys PTH works at two sites. At the distal tubule it increases the reabsorption of calcium ions, and at the proximal tubule it causes inhibition of reabsorption and thus increases the excretion of inorganic phosphate. In bone it acts to release both calcium and phosphate.

Hypoparathyroidism results in hypocalcaemia (low circulating levels of calcium), and it is often caused by surgery for hyperthyroidism (thyroidectomy). Hyperparathyroidism results in hypercalcaemia (high levels of circulating calcium), and is usually caused by a benign tumor. A condition called Psuedohypoparathyroidism also exists. It refers to a group of X-linked dominant genetic disorders characterized by hypocalcaemia in the presence of high levels of PTH.

Table 3 summarises the affects of hyper and hypocalcaemia resulting from parathyroidism.

Deficiency of PTH (leading to Hypocalcaemia) Excess of PTH (leading to Hypercalcaemia)
  • Signs and symptoms are related to neural activity and cardiovascular function
  • Tetany, laryngeal spasm, seizures & death
  • Chvostek’s and Trousseau’s sign
  • Hypotension, cardiac insufficiency, dysrhythmias
  • Hyperactivity
  • Numbness, tingling
  • Cramp
  • Decrease in neuromuscular activity
  • Resorption of Calcium from bone causing bone pain
  • Exposure of kidney to high levels of calcium
  • Neural excitability may be decreased
  • Dulling of consciousness, stupor, weakness and muscle flaccidity
  • Acute psychoses
  • Cardiovascular increased contractility, ventricular arrhythmias
  • Increased calcium in the urine resulting in impaired kidney function and ability to concentrate urine by interfering with the action of ADH leading to predisposition to renal calucli

Table 3 Results of Hypo and Hyperparathyroidism.


Aldosterone is the main mineralocorticoid hormone 2 produced in the adrenal cortex by zona glomerulosa cells. It acts on the renal tubules to promote the retention of sodium ions and the increased secretion of potassium ions 3. Hypersecretion of aldosterone can lead to hypertension 3.

Primary hyperaldosteronism (Conn’s syndrome) or simply primary aldosteronism 4, usually arises because of autonomously secreting adrenal cortical adenoma 3. It can also arise from bilateral adrenocortical hyperplasia 4. In rare instances, adrenal carcinomas and ovarian malignancies have been reported to cause primary aldosteronism 4.

Increased sodium and lowered potassium levels in the blood characterize it. There is an excessive retention of sodium ions and water, and the increased water volume leads to an increase in blood volume and hypertension. If potassium depletion is great then hypokalemia results. This can cause neurons and muscle fibres to hyperpolarize, which makes them less responsive to stimulation. Flaccid paralysis, mental confusion, and changes in the electrocardiogram may result 2.

There is little reference found to hypoaldosteronism. It is expected that a deficiency of aldosterone will lead to loss of sodium and water and a reliance on the action of ADH for fluid retention. Hyperkalemia may also result, causing irritability, anxiety, and paraestheasia.


Insulin is secreted by pancreatic islet b -cells. It has a diversity of actions on a range of tissues, chiefly in the liver, muscles and adipose tissue 3. Actions can be grouped into two broad categories: as a growth factor to promote cellular growth and differentiation, and as a regulator of ‘intermediary metabolism’ 3. Insulin acts directly on muscle and adipose tissue to increase the ability to take up glucose, and thus lowers the level of circulating glucose (regulation). It also promotes the storage of glycogen in the liver and muscles, and inhibits the release of fatty acids and glycerol from adipose tissue.

Hyperinsulism may occur through insulin overdose, or (rarely) from a malignant tumor or hyperplasia of the pancreatic islet cells 2. An excess of insulin will cause blood glucose levels to drop (hypoglycemia) and cause the release of adrenaline, glucagon, and hGH. A drop in blood glucose levels is particularly dangerous to brain function and can lead to mental disorientation, convulsions, unconsciousness and shock 2.

Hypoinsulinism results in diabetes mellitus, of which there are two types: type I and type II. Type I, or insulin dependent diabetes mellitus, appears to be an autoimmune disease where the pancreatic islets cells are destroyed by antibodies 2. Type II diabetes is more common and usually arises not due to a lack of insulin but to a decreased cellular sensitivity due to a down regulation of receptors 2.

Table 4 presents some of the actions of insulin on macronutrient metabolism.

Nutrient Action of Insulin
  • Increased glucose transport into skeletal muscle and adipose tissue
  • Increased glycogen synthesis
  • Decreased gluconeogenesis
  • Increased glucose transport into fat cells
  • Increased fatty acid transport into fat cells
  • Increased triglyceride synthesis
  • Increased active transport of amino acids into cells
  • Increased protein synthesis by accelerating translation of RNA by ribosomes and increased transcription of DNA in nucleus to form increased amounts of RNA
  • Decreased breakdown by enhancing the use of glucose and fatty acids as a fuel source

Table 4 Affect of insulin on macronutrient metabolism 1


1. Porth, C.M., Pathophyisology: Concepts of Altered Health States 4th Edition, JB Lippincott Company, Philadelphia, 1994.

2. Tortora, G.J., Grabowski, S.R., Principles of Anatomy and Physiology - 8th Edition, Harper Collins, NY, 1996.

3. Wills, E.D., Biochemical Basis of Medicine, John Wright & Sons Ltd, Bristol, 1985.

4. Willis Hurst, J (Ed.), Medicine for the Practicing Physician – 3rd Edition, Butterworth-Heinemann, USA, 1992.

Copyright © The Australian Naturopathic Network 1998-2002. All rights reserved. 
Revised: May 18, 2002 .


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Copyright © The Australian Naturopath. All rights reserved.
Revised: May 18, 2002.