Nutritional Diseases of Great Apes and Cheetahs: The Potential Role of Sodium Depletion
World Small Animal Veterinary Association World Congress Proceedings, 2014
Adrian S.W. Tordiffe, BVSc, MSc
National Zoological Gardens of South Africa, Pretoria, South Africa


Sodium is the most important cation of the extracellular fluid (ECF) compartment and plays a critical role in the regulation of extracellular osmolality and volume. Sodium is maintained within very narrow limits within the ECF, as its concentration is the major determinant of water movement across cellular plasma membranes. The fraction of ECF in the vascular compartment partially determines arterial and venous blood pressure.

Plants generally contain low sodium concentrations and many omnivores and herbivores actively seek out and ingest sodium-containing soils and other substances to supplement their intake. It is well known that a sodium deficiency in herbivores can reduce appetite and food intake. Despite its physiological importance, sodium is often neglected as a key component in many animal diets. The anti-salt propaganda in human nutrition may be partially responsible for this.

Regulation of Total Body Sodium

Various regulatory mechanisms involved in sodium homeostasis are well described; however, a complete understanding of the feedback control system capable of maintaining total body sodium (TBS) is still lacking. Maintenance of TBS requires balancing sodium intake and excretion. This is achieved by mechanisms that either control sodium intake (hunger for salt), or others that reduce renal sodium excretion. An increase in dietary sodium intake will expand extracellular volume and decrease renin secretion, whereas sodium deprivation will result in contraction of extracellular volume and stimulate renin secretion, activating the renin-angiotensin-aldosterone system (RAAS). Renin, a proteolytic enzyme released from the juxtaglomerular cells in the afferent arterioles in the kidney, converts angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II causes sodium retention directly and indirectly. It has a direct action on the proximal tubule increasing sodium reabsorption. Indirectly, angiotensin II stimulates the adrenal cortex to synthesize and secrete aldosterone. Aldosterone acts on the distal tubule to promote sodium reabsorption. Through these physiological mechanisms, sodium is retained and extracellular volume expands.


Aldosterone produced by the adrenal cortex glomerulosa cells is essential in the regulation of electrolyte balance, but it has also been shown that it has proinflammatory and/or profibrotic effects through mineralocorticoid receptor activation, particularly in cardiac and renal tissues. Aldosterone seems to play an active role in wound healing through its activation of an important kinase pathway called mTOR (mammalian target of rapamycin). Excessive and prolonged activation of mTOR seems to promote interstitial inflammation and fibrosis. This profibrotic effect has been shown to be activated at fairly low aldosterone concentrations in the upper physiological range.1 Low salt intake, obesity, insulin resistance, hyperkalaemia, hyperparathyroidism, and to some extent elevated ACTH have all been shown to be associated with increased aldosterone secretion. In addition to causing elevated aldosterone levels, reduced-sodium diets have also been shown to result in significant elevation of blood lipid (triglycerides and cholesterol) and catecholamines.2


Chronic renal disease is a common cause of morbidity and mortality in older captive cheetahs (Acinonyx jubatus). The incidence of non-immune-mediated glomerulosclerosis often exceeds 80%, characterised by thickening of the glomerular and tubular basement membranes. The lesions have been shown to increase in severity with age. Generalised adrenocortical hyperplasia is also very common and strongly associated with glomerulosclerosis.3 Cardiac fibrosis was also noted in 28% (12/43) cheetahs on postmortem from captive facilities in South Africa.4

Wild cheetahs consume a wide variety of vertebrate prey, often eating the abdominal organs first before moving on to eat the skeletal muscle and other parts. In captivity, cheetahs are often fed supplemented beef, chicken, or horse meat from exsanguinated and eviscerated carcasses. As sodium is particularly concentrated in the blood, removal of this component from the cheetah diet may result in a significant reduction in sodium intake. If the minimum daily sodium requirement of domestic cats (both adult and young) is extrapolated to cheetahs, it can be seen that cheetah in captivity are fed a diet that is potentially sodium deficient. In 20 out of 31 (65%) urine samples collected from captive cheetahs in July 2013, no sodium could be detected. Urine sodium levels below 10 mmol/L are considered to be indicative of inadequate intake in humans.

Great Apes

Around the world, cardiovascular disease is common in all the great ape species in captivity and has been reported to be responsible for 41% of adult western lowland gorilla (Gorilla gorilla gorilla), 23% of adult orang-utan (Pongo pygmaeus), 77% of adult chimpanzee (Pan troglodytes), and 46% of adult bonobo (Pan paniscus) deaths in zoos and other captive facilities.5 The most common lesions are replacement fibrosis with atrophy and hypertrophy of cardiac myocytes with sudden death or dilative cardiomyopathy being the most common clinical presentation. Renal disease was found to be the second most common cause of death in one captive chimpanzee population.6 Hypercholesterolaemia and hypertriglyceridaemia are also commonly seen in captive great apes7 even though they receive little or no saturated fat in their diet. These clinical features resemble metabolic syndrome seen in humans. Although lack of exercise, psychological stress, unknown viral infections, or genetic factors may have an impact, nutritional factors are likely to play a central role in the pathogenesis of great ape cardiomyopathy. Captive diets are generally higher in carbohydrates, often due to the addition of biscuited formulations, fruit, bread, and other starchy food items. Salt is very rarely added to the diet of captive great apes.

Many great ape species are primarily herbivorous and live in areas where high rainfalls have leached the soils of their mineral content. Plants also generally do not require sodium in large quantities and many primates must actively seek alternative sources of sodium. Mountain gorillas in Uganda consume decaying wood. Wood represents only 3.9% of their wet weight food intake, but contributes over 95% of their dietary sodium.8 Western lowland gorillas have also been shown to specifically select plants with high sodium content in swampy forest clearings.9

The feeding of high-carbohydrate/energy-dense captive diets that are low in sodium provides a plausible explanation for possible chronic RAAS overactivation resulting in cardiac fibrosis. This hypothesis deserves further investigation.


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6.  Lammey ML, Lee DR, Ely JJ, Sleeper MM. Sudden cardiac death in 13 captive chimpanzees (Pan troglodytes). J Med Primatol. 2008;37(s1):39–43.

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8.  Rothman JM, Van Soest PJ, Pell AN. Decaying wood is a sodium source for mountain gorillas. Biol Lett. 2006;2(3):321–324.

9.  Magliocca F, Gautier-Hion A. Mineral content as a basis for food selection by western lowland gorillas in a forest clearing. Am J Primatol. 2002;57(2):67–77.


Speaker Information
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Adrian S.W. Tordiffe, BVSc, MSc
National Zoological Gardens of South Africa
Pretoria, South Africa

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