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12.7: Age Related Changes to the Digestive System - Biology

12.7: Age Related Changes to the Digestive System - Biology


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Mouth

The most significant change to the mouth with age is the loss of teeth. This can result in a change of eating habits and long term deficits in nutrition.

Additional changes to the mouth include a decreased level of saliva production, thicker mucus production, and a diminished sense of taste.

Esophagus

Many other people experience difficultly in swallowing. Most often this is a result from incomplete relaxation of the lower esophageal sphincter, but it could be a result of a neurological disorder.

Other issues with esophagus include heartburn caused by stomach acid entering the esophagus through a weakened esophageal sphincter.

Stomach

The mucus membrane of the stomach thins with age resulting in lower levels of mucus, hydrochloric acid, and digestive enzymes. This reduces the digestion of proteins and may result in chronic atrophic gastritis.

Small Intestine

The walls of the small intestines atrophy with age. This alters the shape of the villi and reduces the surface area across which absorption occurs. Along with the atrophy these is a decrease in the production of digestive enzymes. Surprisingly these changes do not result in decreased rate of the absorption of digested food.

Large Intestine

The walls of the large intestines atrophy with age. The thinning of the walls results in outpockets from the wall, a condition known as diverticulosis.

Pancreas

The number of secretory cells in the pancreas decreases with age. This results in a decrease in the level of fat digestion.

Liver

While the liver reduces in size with age it does not show any significant reduction in the ability to perform its various functions in healthy elderly people.


Effects of Aging on the Liver

A number of structural and microscopic changes occur as the liver ages. (See also Overview of the Liver and Gallbladder for a discussion of normal function of the liver and gallbladder.) For example, the color of the liver changes from lighter to darker brown. Its size and blood flow decrease. However, liver test results generally remain normal.

The ability of the liver to metabolize many substances decreases with aging. Thus, some drugs are not inactivated as quickly in older people as they are in younger people. As a result, a drug dose that would not have side effects in younger people may have dose-related side effects in older people (see Aging and Drugs). Thus, drug dosages often need to be decreased in older people. Also, the liver's ability to withstand stress decreases. Thus, substances that are toxic to the liver can cause more damage in older people than in younger people. Repair of damaged liver cells is also slower in older people.

The production and flow of bile decrease with aging. As a result, gallstones are more likely to form.


Small intestine

Aging has only minor effects on the structure of the small intestine, so movement of contents through the small intestine and absorption of most nutrients do not change much. However, lactase levels decrease, leading to intolerance of dairy products by many older adults (lactose intolerance). Excessive growth of certain bacteria (bacterial overgrowth syndrome) becomes more common with age and can lead to pain, bloating, and weight loss. Bacterial overgrowth may also lead to decreased absorption of certain nutrients, such as vitamin B12, iron, and calcium.


12.7: Age Related Changes to the Digestive System - Biology

absorption passage of digested products from the intestinal lumen through mucosal cells and into the bloodstream or lacteals

accessory digestive organ includes teeth, tongue, salivary glands, gallbladder, liver, and pancreas

accessory duct (also, duct of Santorini) duct that runs from the pancreas into the duodenum

acinus cluster of glandular epithelial cells in the pancreas that secretes pancreatic juice in the pancreas

alimentary canal continuous muscular digestive tube that extends from the mouth to the anus

anal canal final segment of the large intestine

anal column long fold of mucosa in the anal canal

anal sinus between anal columns

appendix (vermiform appendix) coiled tube attached to the cecum

ascending colon first region of the colon

bacterial flora bacteria in the large intestine

bile alkaline solution produced by the liver and important for the emulsification of lipids

bile canaliculus small duct between hepatocytes that collects bile

bilirubin main bile pigment, which is responsible for the brown color of feces

body mid-portion of the stomach

bolus mass of chewed food

brush border fuzzy appearance of the small intestinal mucosa created by microvilli

cardia (also, cardiac region) part of the stomach surrounding the cardiac orifice (esophageal hiatus)

cecum pouch forming the beginning of the large intestine

cementum bone-like tissue covering the root of a tooth

central vein vein that receives blood from hepatic sinusoids

cephalic phase (also, reflex phase) initial phase of gastric secretion that occurs before food enters the stomach

chemical digestion enzymatic breakdown of food

chief cell gastric gland cell that secretes pepsinogen

chyme soupy liquid created when food is mixed with digestive juices

circular fold (also, plica circulare) deep fold in the mucosa and submucosa of the small intestine

colon part of the large intestine between the cecum and the rectum

common bile duct structure formed by the union of the common hepatic duct and the gallbladder’s cystic duct

common hepatic duct duct formed by the merger of the two hepatic ducts

crown portion of tooth visible superior to the gum line

cuspid (also, canine) pointed tooth used for tearing and shredding food

cystic duct duct through which bile drains and enters the gallbladder

deciduous tooth one of 20 “baby teeth”

defecation elimination of undigested substances from the body in the form of feces

deglutition three-stage process of swallowing

dens tooth

dentin bone-like tissue immediately deep to the enamel of the crown or cementum of the root of a tooth

dentition set of teeth

descending colon part of the colon between the transverse colon and the sigmoid colon

duodenal gland (also, Brunner’s gland) mucous-secreting gland in the duodenal submucosa

duodenum first part of the small intestine, which starts at the pyloric sphincter and ends at the jejunum

enamel covering of the dentin of the crown of a tooth

enteroendocrine cell gastric gland cell that releases hormones

enterohepatic circulation recycling mechanism that conserves bile salts

enteropeptidase intestinal brush-border enzyme that activates trypsinogen to trypsin

epiploic appendage small sac of fat-filled visceral peritoneum attached to teniae coli

esophagus muscular tube that runs from the pharynx to the stomach

external anal sphincter voluntary skeletal muscle sphincter in the anal canal

fauces opening between the oral cavity and the oropharynx

feces semisolid waste product of digestion

flatus gas in the intestine

fundus dome-shaped region of the stomach above and to the left of the cardia

G cell gastrin-secreting enteroendocrine cell

gallbladder accessory digestive organ that stores and concentrates bile

gastric emptying process by which mixing waves gradually cause the release of chyme into the duodenum

gastric gland gland in the stomach mucosal epithelium that produces gastric juice

gastric phase phase of gastric secretion that begins when food enters the stomach

gastric pit narrow channel formed by the epithelial lining of the stomach mucosa

gastrin peptide hormone that stimulates secretion of hydrochloric acid and gut motility

gastrocolic reflex propulsive movement in the colon activated by the presence of food in the stomach

gastroileal reflex long reflex that increases the strength of segmentation in the ileum

gingiva gum

haustrum small pouch in the colon created by tonic contractions of teniae coli

haustral contraction slow segmentation in the large intestine

hepatic artery artery that supplies oxygenated blood to the liver

hepatic lobule hexagonal-shaped structure composed of hepatocytes that radiate outward from a central vein

hepatic portal vein vein that supplies deoxygenated nutrient-rich blood to the liver

hepatic sinusoid blood capillaries between rows of hepatocytes that receive blood from the hepatic portal vein and the branches of the hepatic artery

hepatic vein vein that drains into the inferior vena cava

hepatocytes major functional cells of the liver

hepatopancreatic ampulla (also, ampulla of Vater) bulb-like point in the wall of the duodenum where the bile duct and main pancreatic duct unite

hepatopancreatic sphincter (also, sphincter of Oddi) sphincter regulating the flow of bile and pancreatic juice into the duodenum

hydrochloric acid (HCl) digestive acid secreted by parietal cells in the stomach

ileocecal sphincter sphincter located where the small intestine joins with the large intestine

ileum end of the small intestine between the jejunum and the large intestine

incisor midline, chisel-shaped tooth used for cutting into food

ingestion taking food into the GI tract through the mouth

internal anal sphincter involuntary smooth muscle sphincter in the anal canal

intestinal gland (also, crypt of Lieberkühn) gland in the small intestinal mucosa that secretes intestinal juice

intestinal juice mixture of water and mucus that helps absorb nutrients from chyme

intrinsic factor glycoprotein required for vitamin B12 absorption in the small intestine

intestinal phase phase of gastric secretion that begins when chyme enters the intestine

jejunum middle part of the small intestine between the duodenum and the ileum

labium lip

labial frenulum midline mucous membrane fold that attaches the inner surface of the lips to the gums

lacteal lymphatic capillary in the villi

large intestine terminal portion of the alimentary canal

laryngopharynx part of the pharynx that functions in respiration and digestion

left colic flexure (also, splenic flexure) point where the transverse colon curves below the inferior end of the spleen

lingual frenulum mucous membrane fold that attaches the bottom of the tongue to the floor of the mouth

lingual lipase digestive enzyme from glands in the tongue that acts on triglycerides

liver largest gland in the body whose main digestive function is the production of bile

lower esophageal sphincter smooth muscle sphincter that regulates food movement from the esophagus to the stomach

major duodenal papilla point at which the hepatopancreatic ampulla opens into the duodenum

mass movement long, slow, peristaltic wave in the large intestine

mastication chewing

mechanical digestion chewing, mixing, and segmentation that prepares food for chemical digestion

mesoappendix mesentery of the appendix

microvillus small projection of the plasma membrane of the absorptive cells of the small intestinal mucosa

migrating motility complex form of peristalsis in the small intestine

mixing wave unique type of peristalsis that occurs in the stomach

molar tooth used for crushing and grinding food

motilin hormone that initiates migrating motility complexes


74 Age Related Changes to the Digestive System

The most significant change to the mouth with age is the loss of teeth. This is caused by a combination of bone loss from the jaw, which occurs with age, and gum disease. Both result in a loosening of teeth. While lost teeth can be replaced with dentures these are not equivalent to natural teeth. Dentures can make it difficult to chew comfortably. This can result in a change of eating habits and long term deficits in nutrition.

Additional changes to the mouth include a decreased level of saliva production, thicker mucus production, and a diminished sense of taste.

Esophagus

Many other people experience difficultly in swallowing. Most often this is a result from incomplete relaxation of the lower esophageal sphincter, but it could be a result of a neurological disorder.

Other issues with esophagus include heartburn caused by stomach acid entering the esophagus through a weakened esophageal sphincter.

Stomach

The mucus membrane of the stomach thins with age resulting in lower levels of mucus, hydrochloric acid, and digestive enzymes. This reduces the digestion of proteins and may result in chronic atrophic gastritis.

Small Intestine

The walls of the small intestines atrophy with age. This alters the shape of the villi and reduces the surface area across which absorption occurs. Along with the atrophy these is a decrease in the production of digestive enzymes. Surprisingly these changes do not result in decreased rate of the absorption of digested food.

Large Intestine

The walls of the large intestines atrophy with age. The thinning of the walls results in outpockets from the wall, a condition known as diverticulosis.

Pancreas

The number of secretory cells in the pancreas decreases with age. This results in a decrease in the level of fat digestion.

Liver

While the liver reduces in size with age it does not show any significant reduction in the ability to perform its various functions in healthy elderly people.


Anatomy and physiology of ageing 7: the endocrine system

Glands in the endocrine system produce a range of hormones that regulate our body’s activities by keeping substances such as blood glucose and electrolytes within their normal ranges. Like all other body systems, the endocrine system undergoes age-related changes that negatively affect its functioning. As a result of these changes, older people are more prone to disturbed sleep patterns, have a reduced metabolic rate, lose bone density, accumulate body fat, and show increases in blood glucose. As a consequence, they are at higher risk of health issues such as insomnia, fractures, type 2 diabetes and cognitive decline. This seventh article in our series about the effects of age on the body describes what happens, with advancing age, to endocrine glands and hormone production.

Citation: Knight J, Nigam Y (2017) Anatomy and physiology of ageing 7: the endocrine system. Nursing Times [online] 113: 8, 48-51.

Authors: John Knight is senior lecturer in biomedical science Yamni Nigam is associate professor in biomedical science both at the College of Human Health and Science, Swansea University.

  • This article has been double-blind peer reviewed
  • Scroll down to read the article or download a print-friendly PDF here to see other articles in this series

Introduction

The endocrine system works in conjunction with the nervous system to regulate, and coordinate the activities of, the body’s tissues and organs. It consists of a collection of glands located in different parts of the body – the main ones being the pituitary, pineal, thyroid, parathyroids, adrenals, pancreas, ovaries and testes (Fig 1). These glands produce a variety of blood-borne chemical signals called hormones, which play an essential role in maintaining balance (homoeostasis) in the body, helping to ensure that variables such as blood glucose and electrolytes are kept within normal ranges.

Pituitary gland and somatopause

The pituitary gland, often referred to as the master gland, produces several major hormones and regulates the activity of many other endocrine glands. It is split into a posterior portion, which is formed from neural tissue extending from the hypothalamus, and an anterior portion, which is formed from epithelial cells derived from the roof of the oral cavity.

The anterior pituitary secretes growth hormone (somatotropin), which promotes the growth of bone, muscle and most of the major internal organs. In early childhood, somatotropin is secreted in relatively small amounts, but during the teenage years there is a marked increase in serum somatotropin levels corresponding to the growth spurts of puberty. Around the age of 25-30, somatotropin secretion begins to decline in both men and women. In men it is estimated to halve every seven years – although there appears to be much variation between individuals (Gentili, 2015).

The decline in somatotropin secretion in later years is often referred to as the somatopause and is associated with a variety of physiological changes (Jonas et al, 2015 Veldhuis et al, 2005), including:

  • A general reduction in protein synthesis
  • A progressive reduction in lean body mass (muscle) contributing to a decline in metabolic rate
  • An increased deposition of adipose tissue, particularly abdominal fat (‘middle-age spread’)
  • A reduction in bone mass and density leading to an increased risk of osteoporosis and fractures
  • A general decrease in immune function and higher susceptibility to infection.

The somatopause can be hastened in people who lead a sedentary lifestyle and in those who already carry a high percentage of body fat. Conversely, in pre-menopausal women, oestrogen appears to slow its onset and progression (Gentili, 2015).

The exact causes of somatopause are yet to be fully established, however, the age-related decrease in somatotropin secretion mirrors the decrease of growth-hormone releasing hormone (GHRH) secretion by the hypothalamus. Recent research indicates that some of the negative physiological changes that come with declining levels of somatotropin can be reversed by growth hormone replacement therapy. In clinical trials, recombinant human growth hormone has been shown to improve lean muscle mass retention and quality of life scores in older people (Jonas et al, 2015).

Pineal gland and sleep disturbances

The pineal gland is slightly smaller than a pea and resembles a small pine cone – hence its name. Found in the diencephalon, towards the centre of the brain, it synthesises the hormone melatonin from the neurotransmitter serotonin. The pineal gland functions like an internal body clock: during the day, when there is a lot of light, melatonin secretion is inhibited, but as the day draws to a close and light diminishes, melatonin secretion increases, preparing the body for sleep.

As we age, the pineal gland undergoes a process of calcification, detectable even in young children. Melatonin levels progressively decrease: 60-year-olds have 80% less melatonin in their blood than teenagers. Some drugs commonly prescribed to older people, such as beta blockers and non-steroidal anti-inflammatory drugs, can reduce melatonin levels even further.

Decreased melatonin levels are linked to an increased prevalence of sleep disturbances and, in some people, may ultimately lead to geriatric insomnia (Bubenik and Konturek, 2011). Since sleep is essential for cognitive function, sleep disturbances can exacerbate age-related changes in the brain.

There is some evidence that exposure to bright light – either sunlight or artificial light – in the morning increases the speed of sleep onset by triggering an earlier release of melatonin in the evening. Similarly, the therapeutic use of prolonged-release melatonin has been shown to improve sleep onset time, sleep quality, morning alertness and quality of life in people aged 55 and over who have insomnia (Wade et al, 2007).

Thyroid gland and metabolism

The thyroid gland plays a major role in controlling metabolism and adjusting blood calcium levels. The hormones it secretes regulate a number of physiological processes, including:

  • The metabolism of carbohydrates, fats and proteins
  • Thermoregulation
  • Digestion
  • Muscle and nerve activity
  • Maintaining skin thickness and integrity
  • Maintaining normal bone density.

Changes to metabolic rate

The thyroid secretes the iodine-containing hormones T4 (tetraiodothyronine, which is also known as thyroxine) and T3 (triiodothyronine), which largely control cellular metabolism. T4 is released in greater quantities than T3, the typical ratio being 15:1. T4 is then rapidly converted into the more biologically active T3, which is around three times more potent in terms of increasing the metabolic rate.

The clearance of T4 by the liver decreases with age, but this is offset by a gradual decline in T4 secretion, so T4 serum levels tend to remain constant. However, there is a clear age-related decrease in the levels of serum T3, as well as of thyroid-stimulating hormone (TSH) produced by the pituitary gland (Peeters, 2008 Chahal and Drake, 2007). This may contribute to the gradual reduction in basal metabolism that is apparent in many people in middle and old age (in which the decline in lean muscle mass described above also plays a role).

With advancing age, autoimmune reactions against one’s own thyroid gland are commonly seen. Indeed, the presence, in older people, of antibodies specific to thyroid tissue is so common that it is often considered a normal age-related change. A high concentration of such antibodies may herald the onset of autoimmune hypothyroidism, a disease affecting up to 5% of the over-60s and associated with low metabolic rates, a tendency to put on weight and low core temperature. Since this condition is autoimmune in nature, women are at greater risk of developing it (this is true for most autoimmune diseases): up to eight times more women than men experience autoimmune hypothyroidism.

The results of thyroid function tests should be assessed carefully in older people, as common long-term conditions (such as chronic obstructive pulmonary disease, hypertension, diabetes and arthritis) and dieting can lead to reductions in circulating thyroid hormones, particularly the more active T3. This phenomenon of reduced thyroid function in the absence of thyroid disease is referred to as non-thyroidal illness. Similarly, many drugs used to treat long-term conditions in older people (for example, lithium and glucocorticoids) can supress thyroid function or reduce the activity of circulating thyroid hormones, leading to a reduction in metabolic rate (Peeters, 2008).

Changes to calcitonin secretion

The thyroid gland also plays a role in calcium homoeostasis. When we consume foods rich in calcium, it releases calcitonin, which inhibits the activity of osteoclasts – bone cells that break down bone tissue (bone is a dynamic tissue continually being built and broken down). By inhibiting osteoclast activity, calcitonin indirectly increases bone density.

Few studies have examined the effects of ageing on calcitonin production in humans. The most comprehensive study, dating back to 1980, demonstrated an age-related decline in calcitonin production in 50 healthy women aged between 20 and 69 years (Shamonki et al, 1980). This decline may partially explain the reduction in bone mass seen in most women as they grow older. However, a later study has contradicted these findings, showing that although women appear to have lower levels of calcitonin secretion than men, there is no clear age-related decrease in serum calcitonin concentration (Tiegs et al, 1986).

Parathyroid glands and hyperparathyroidism

The posterior portion of the thyroid is the location of four tiny parathyroid glands, which secrete parathyroid hormone (PTH) whenever blood calcium levels fall. Since a normal concentration of calcium is essential to many physiological processes (including muscle contraction, nerve conduction and blood clotting), the reserves of calcium stored in the skeleton need to be mobilised. PTH triggers the release of calcium from the bones into the blood by indirectly stimulating osteoclasts.

Several studies have shown that most people, as they grow older, have significantly increased levels of circulating PTH (Portale et al, 1997). This hyperparathyroidism may well be one of the main causes of the reduction in bone density commonly seen in middle and old age. Recent studies have also shown a potential link with other pathologies, particularly age-related cognitive decline and dementia (Braverman et al, 2009).

Pancreas and diabetes risk

The endocrine regions of the pancreas (islets of Langerhans) regulate blood glucose levels. Beta cells in the islets secrete insulin in response to increased blood glucose – for example, after a carbohydrate-rich meal. Insulin binds to receptors present on most cells, triggering the uptake of glucose from the blood. Once inside the cells, glucose is either metabolised immediately to release energy, or stored and converted into glycogen.

Alongside race, genetic predisposition and a high body mass index, ageing is one of the many risk factors linked to the development of type 2 diabetes (Knight and Nigam, 2017). Ageing human cells become less sensitive to the effects of insulin. The most likely cause appears to be a reduction in the number of insulin receptors at the surface of cells. This gradual insulin resistance goes hand in hand with an increase in blood glucose concentrations.

As shown in a study of 6,901 non-diabetic people (Ko et al, 2006), fasting blood glucose levels rise by around 0.15mmol/L for each decade of life after the age of 20. Whether this rise is a normal age-related change or a sign of diabetes in its early stages is not always clear, but it is certainly seen in many older people with no other symptoms of diabetes.

With advancing age, the insulin-producing beta cells become less sensitive to the level of glucose in the blood, so higher blood glucose levels are needed to trigger insulin release. Since older people’s cells are less receptive to insulin, the pancreas often responds by producing more, leading to increased insulin levels in the blood (hyperinsulinaemia). This can put excessive stress on the beta cells, leading to their exhaustion.

Age-related depletion of the beta cell population in the pancreas also occurs as a result of increased programmed cell death (apoptosis) and a diminished ability of the pancreas to produce new cells. Beta cell exhaustion and depletion result in a drop of insulin secretion of up to 0.5% per year of life. Additionally, the clearance of insulin by the liver increases with age, so there is less insulin available to interact with cells and promote glucose uptake.

These age-related changes to insulin production, clearance and response contribute to the creation of a diabetogenic environment. This may partially explain why the risk of developing type 2 diabetes increases with age (Brown, 2012).

Abdominal fat

The accumulation of abdominal fat is a common feature of ageing, particularly in people who have a poor diet and/or a sedentary lifestyle. Many age-related changes to the endocrine system contribute to this accumulation of adipose tissue, including the somatopause, autoimmune hypothyroidism, insulin resistance, and reduced circulating sex hormones.

This abdominal fat accumulation is linked to heart disease, high blood pressure and type 2 diabetes. These conditions may occur in isolation or together in the form of metabolic syndrome (Gong and Muzumdar, 2012).

The adrenal glands

The two adrenal glands are located above the kidneys and each consists of two main regions: the adrenal medulla (inner region) and the adrenal cortex (outermost layer).

Adrenal medulla and adrenaline

The adrenal medulla is the location of chomaffin cells, which secrete the catecholamines adrenaline (epinephrine) and noradrenaline (norepinephrine). These are the ‘fight or flight’ hormones that prepare the body for activity when it is threatened or in a state of excitement. The effects of adrenaline and nor-adrenaline include:

  • Increased heart rate
  • Increased vasoconstriction in the skin and gut
  • Increased blood pressure
  • Increased blood flow to the major skeletal muscle groups
  • Increased blood flow to the brain
  • Dilatation of pupils
  • Increased breathing rate and airway dilatation
  • Increased breakdown of liver glycogen resulting in increased blood glucose.

Ageing is associated with a decline in the secretion of adrenaline, but adrenaline plasma levels remain relatively constant as clearance by the kidneys is usually reduced. There is some evidence that older men secrete less adrenaline in response to acute stress than younger men (Seals and Esler, 2000).

Adrenal cortex, aldosterone and cortisol

The adrenal cortex synthesises a variety of steroidal hormones from cholesterol, mainly aldosterone and cortisol.

Aldosterone
Aldosterone is a mineralocorticoid that regulates plasma levels of sodium and potassium, and plays an important role in water balance and blood pressure control. Research has revealed an age-related decrease in serum aldosterone levels, effectively reducing the body’s ability to retain sodium.

Decreased aldosterone secretion may contribute to postural hypotension and the light-headedness that is often experienced by older people when they stand up. This is supported by research demonstrating significant reductions in serum aldosterone levels in older people when they are upright, as opposed to recumbent (Hegstad et al, 1983).

Since sodium attracts water into the cardiovascular system via osmosis, lower plasma sodium levels (hyponatraemia) can lead to reduced blood volume and blood pressure. Several medications commonly prescribed to older people – such as opiates, non-steroidal anti-inflammatory drugs, diuretics and antidepressants – can exacerbate hyponatraemia (Liamis et al, 2008). Blood volume and blood pressure may be further reduced by age-related increases in the secretion of atrial natriuretic hormone (ANH), a powerful diuretic produced by the heart (Miller, 2009).

Cortisol
Cortisol is a glucocorticoid and its release is triggered by biological stressors such as physical injury or starvation. It is a natural anti-inflammatory and plays an important role in the breakdown of protein and fat.

Research into how cortisol levels change with ageing is often contradictory. Initial studies suggested that there could be a 20-50% increase in the mean levels of cortisol secretion between the ages of 20 and 80 (Chahal and Drake, 2007). More recently, however, it has been shown that this is not necessarily true: in some people, cortisol secretion diminishes with age, in others levels remain relatively stable throughout life (Wolf, 2015).

There appears to be a link between increased cortisol levels, reduced bone density and increased risk of bone fracture. There is also growing evidence that a higher cortisol concentration can contribute to the loss of cells from the hippocampus, resulting in hippocampal atrophy. This is often associated with a reduction in cognitive function in older people (Chahal and Drake, 2007). Other studies have shown that age-related increases in cortisol may also be linked to memory loss and sleep disorders (Chahal and Drake, 2007 Wolf et al, 2005).

Ageing of the endocrine system

There is some evidence that exercising regularly and maintaining a low percentage of body fat may slow the onset of the somatopause, help maintain bone density and improve the control of blood glucose. Supplementation with synthetic growth hormone has recently been shown to increase lean muscle mass in older people. However, this kind of therapy is associated with many side-effects such as joint pain, oedema and impaired glucose tolerance (Jonas et al, 2015).

The most famous and most thoroughly researched hormone replacement therapies are those that are used to treat the complications of the menopause. These therapies will be explored in the next article in this series.

Key points

  • The endocrine system regulates our physiology via a complex cascade of chemicals called hormones
  • Hormones play an essential role in maintaining homoeostasis in the body
  • Age-related hormonal changes can lead to the build-up of body fat, lower bone density, impaired blood glucose control and sleep disturbances
  • Age-related changes to the endocrine system increase the risk of insomnia, fractures, type 2 diabetes and cognitive changes
  • Exercising regularly and maintaining a low percentage of body fat may slow down some of the effects of ageing on the endocrine system

Also in this series

Braverman ER et al (2009) Age-related increases in parathyroid hormone may be antecedent to both osteoporosis and dementia. BioMed Central Endocrine Disorders 9: 21, 1-10.

Brown JE (2012) The ageing pancreas. British Journal of Diabetes and Vascular Disease 12: 3, 141-145.

Bubenik GA, Konturek SJ (2011) Melatonin and aging: prospects for human treatment Journal of Physiology and Pharmacology 62: 1, 13-19.

Chahal HS, Drake WM (2007) The endocrine system and ageing. Journal of Pathology 211: 2, 173-180.

Gong Z, Muzumdar RH (2012) Pancreatic function, type 2 diabetes, and metabolism in aging. International Journal of Endocrinology 2012: 320482.

Hegstad R et al (1983) Ageing and aldosterone. American Journal of Medicine 74: 3, 442-448.

Jonas M et al (2015) Aging and the endocrine system. Postępy Nauk Medycznych 28: 7, 451-457.

Knight J, Nigam Y (2017) Diabetes management 1: disease types, symptoms and diagnosis. Nursing Times 113: 4, 40-44.

Ko GT et al (2006) Effects of age on plasma glucose levels in non-diabetic Hong Kong Chinese. Croatian Medical Journal 47: 5, 709-713.

Liamis G et al (2008) A review of drug-induced hyponatremia. American Journal of Kidney Disease 52: 1, 144-153.

Miller M (2009) Fluid balance disorders in the elderly. American Society of Nephrology online curricula: geriatric nephrology.

Peeters RP (2008) Thyroid hormones and aging. Hormones 7: 1, 28-35.

Portale AA et al (1997) Aging alters calcium regulation of serum concentration of parathyroid hormone in healthy men. American Journal of Physiology 272: 139-146.

Seals DR, Esler MD (2000) Human ageing and the sympathoadrenal system. Journal of Physiology 528: 3, 407-417.

Shamonki IM et al (1980) Age-related changes of calcitonin secretion in females. Journal of Clinical Endocrinology and Metabolism 50: 3, 437-439.

Tiegs RD et al (1986) Secretion and metabolism of monomeric human calcitonin: effects of age, sex, and thyroid damage. Journal of Bone and Mineral Research 4: 339-349.

Veldhuis JD et al (2005) Joint mechanisms of impaired growth-hormone pulse renewal in aging men. Journal of Clinical Endocrinology and Metabolism 9: 7, 4177-4183.

Wade AG et al (2007) Efficacy of prolonged release melatonin in insomnia patients aged 55-80 years: quality of sleep and next-day alertness outcomes. Current Medical Research and Opinion 23: 10, 2597-2605.

Wolf OT (2015) Effects of Stress on Memory: Relevance for Human Aging. Encyclopedia of Geropsychology. Singapore: Springer Science.

Wolf OT et al (2005) Subjective memory complaints in aging are associated with elevated cortisol levels. Neurobiology of Aging 26: 10, 1357-1363.


Effects of Aging on the Respiratory System

In healthy people, these age-related changes seldom lead to symptoms. These changes contribute somewhat to an older person's reduced ability to do vigorous exercise, especially intense aerobic exercise, such as running, biking, and mountain climbing. However, age-related decreases in heart function may be a more important cause of such limitations.

Older people are at higher risk of developing pneumonia after bacterial or viral infections. Thus, vaccines for respiratory infections such as influenza and pneumococcal pneumonia are particularly important for older people.

Importantly, age-related changes in the lungs are compounded by the effects of heart and lung diseases, especially those caused by the destructive effects of smoking.

Did You Know?

In healthy people, age-related reductions in lung function seldom lead to symptoms, but they can contribute to an older person's reduced ability to do vigorous exercise.

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OTHER TOPICS IN THIS CHAPTER


Examples of the Autonomic Nervous System Response

Fight or Flight Responses

The autonomic nervous system is often described using the response to imminent physical danger and the recovery of the body after the threat has receded. For instance, when faced with a predator, the body increases heart rate and breathing, reduces digestive secretions and activity, and preferentially diverts blood towards skeletal muscles to enable the body to physically combat the challenge. This is usually accompanied by piloerection to conserve body heat.

This is why the sympathetic nervous system is said to mediate the fight-or-flight response. Once the situation has become calmer, the parasympathetic nervous system restores the body towards normal functioning, resuming digestion and excretion, reducing blood pressure and restoring normal circadian rhythms.

General Activity

However, even in the absence of an external threat, the two branches of the autonomic nervous system undergo changes and interact closely with the endocrine system to minutely monitor the internal and external environment. For instance, sympathetic activation can lead to an increase in circulating plasma levels of epinephrine and norepinephrine secreted from the adrenal gland.

Usually, heart rate increases during inspiration and decreases during expiration. This variation is normal and is influenced by the vagus nerve, and thus the autonomic nervous system. When heart rate variability decreases, it indicates reduced parasympathetic activity.

Hormones and the Autonomic Nervous System

Hormones can alter the autonomic nervous system response as well. In fertile, reproducing mammalian females this interaction between the ANS and the endocrine systems is particularly interesting. Estrogen is involved in increasing the activity of a crucial part of the parasympathetic nervous system – the vagus nerve. Estrogen simultaneously dampens sympathetic nervous system activity. The hormone progesterone appears to have the opposite effect.

In the follicular phase of the menstrual cycle, there is increased estrogen concentration within the bloodstream. Under the influence of increased plasma estrogen concentrations, there is an increase in parasympathetic nervous activity, which causes an increase in heart rate variability. On the other hand, during the luteal phase of the menstrual cycle, heart rate variability points towards a decrease in vagal activity. This suggests another shift in the sympathovagal balance. The importance of these changes to the cardiovascular microenvironment is not fully understood, but it is hypothesized that this could explain the differences in the risk faced by men and women for heart disease.

However, it is important to note that gross cardiovascular parameters such as blood pressure or heart rate remain mostly unaffected by the phase of the menstrual cycle due to other compensatory mechanisms.

Autonomic Nervous System and the Cardiovascular System

The interaction between the autonomic nervous system and the cardiovascular system becomes even more important during pregnancy as there are large-scale changes to hemodynamics. Blood volume, basal oxygen consumption, red cell mass, cardiac output, and the heart rate increase in pregnant women. Both systolic and diastolic blood pressure drop and there is extensive remodeling of all blood vessels. While the changing hormonal environment primarily mediates these changes, the autonomic nervous system is also an important player.

Again, heart rate variability becomes a relatively sensitive and non-invasive measure of autonomic nervous system activity. Studying the variability in heart rate of pregnant women at different gestational ages shows an increase in vagal activity in the first trimester, coupled with a decrease in sympathetic nervous system activation. This reverses as gestational age increases, with great spikes in neural activity of the sympathetic nervous system and the release of adrenal hormones as the woman nears term.


Endocrine Function in Aging

The endocrine system in higher mammals represents one of the most complex and fundamental systems that regulates nearly all of an organism’s biological functions. This system is composed of multiple organs, tissues, hormones, and receptor modalities. Its ability to regulate critical functions such as reproduction, development, metabolism, stress responses, blood pressure, wakefulness, and digestion places it as one of the most important regulators of life-long physiology. Therefore, at any one point in time the physiological status of the majority of organs in the body is a function of the activity of the whole endocrine system. However, while appreciating the role of the endocrine system in such “frozen” points in time is important, the temporal variation in endocrine function across one’s lifespan is of crucial interest to researchers investigating age-related disorders. The importance of gerontological research is becoming more and more evident, given the ever-increasing proportion of aged people in Western countries.

Aging is a natural process that involves a general decline in many physiological functions with time. Aging is generically associated with a reduced capacity to maintain homeostasis and effective repair mechanisms, resulting in loss of function, senescence, and eventually death. It is obvious that the functions of endocrine organs alter during the aging process, resulting in a higher prevalence of endocrine malfunction-related disorders in the elderly population. Enhanced knowledge and appreciation of endocrine functions in aging will likely lead to the development of successful pharmacological or lifestyle therapies to treat endocrine-related diseases in elderly patients. The discovery and development of novel endocrine-targeted remedies will hopefully result in an improvement of quality of life and also overall lifespan. Thus, endocrine functions in the aging context are important fields of intense clinical and scientific interest and form the focus of this special issue.

The papers in this special issue are focused upon original research papers and review papers concerning several important molecular and tissue systems vital to the maintenance of the endocrine system in aging, that is, pancreatic function and type 2 diabetes mellitus (T2DM) testosterone deficiency and depression metabolic and endocrine alterations in muscle dystrophies and sarcopenia serum adipokines and osteocalcin in older patients with hip fracture gerontological neuroendocrine axis organization and disruption correlation of thyroid hormones and lipid profiles in elderly T2DM patients minimally invasive approaches to parathyroid surgery in elderly patients the proper interpretation of hormones and tumor marker measurements in the geriatric population.

As we have stated, aging is an important risk factor for metabolic disorders, including obesity, impaired glucose tolerance, and type 2 diabetes. Aging has long been associated in multiple animal species with the insulin/insulin-like growth factor-1 (IGF-1) signaling system. Z. Gong and R. H. Muzumdar summarize in their paper the current evidence on how aging affects pancreaticβ-cell function, β-cell mass, insulin secretion, and insulin sensitivity. They also review the effects of aging on the relationship between insulin sensitivity and insulin secretion. Accelerated insulin resistance appears to be one of the strongest hallmarks of advanced physiological aging therefore, a comprehensive understanding of all the defects that impair glucose homeostasis in the elderly will likely lead to the development of novel treatments that may substantially improve life quality and lifespan.

Testosterone deficiency, or hypotestosteronemia, is a widely recognized hormonal alteration strongly associated with male aging. The review paper by M. Amore et al. comprehensively summarizes the current understanding of the correlation between depressive symptoms with a syndrome called partial androgen deficiency of the aging male (PADAM). This paper highlights the potential benefits of testosterone treatment upon mood and affective disorders. While supplementation with testosterone fails to show sound evidence of effectiveness in the treatment of depression, testosterone supplementation has proved to be effective, on some levels, for improving quality of life of aged patients with PADAM.

In addition to the gerontological effects upon steroid hormone activity, aging also significantly affects thyroid function. These age-related effects, acting through the thyroid hormone system, greatly impact both lipid profiles and somatic metabolic parameters. The study conducted by F. Strollo et al. investigates the correlation between free thyroxine (FT4), free triiodothyronine (FT3) levels and total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels in euthyroid elderly T2DM patients. They found that TC and LDL-C correlate negatively with FT4 and positively with FT3. When divided according to treatment by oral hypoglycemic agents (OHA) and insulin (IT), they, however, reacted differently with respect to investigated associations.

Primary hyperparathyroidism (pHPT) is one of the most common endocrine diseases in the elderly and the chance of developing pHPT increases with age. Elderly patients with pHPT are often not referred for surgery because of their associated comorbidities that may increase surgical risk. The study by C. Dobrinja et al. demonstrates that minimally invasive approaches to parathyroid surgery seem to be safe and curative in elderly patients, with few associated risks because of the combination of modern preoperative imaging, advances in surgical technique, and advances in anesthesia care.

One of the most important factors related to the maintenance of health and independence in the elderly is endocrine-mediated control of the musculo skeletal system. An inability to maintain independence as well as increased morbidity due to elevated fall episodes are both likely to severely impact the cost of widespread healthcare in aging Western societies. Therefore, we have included several sections that contend with the effects of aging upon the endocrine regulation of musculo-skeletal tissues.

Common metabolic and endocrine alterations exist across a wide range of muscular dystrophies. The paper by O. del Rocío Cruz Guzmán et al. expertly reviews the current knowledge concerning the metabolic and endocrine alterations in diverse types of dystrophinopathies including childhood and adult dystrophies. K. Sakuma and A. Yamauchi also review the vital pieces of data concerning our current understating of the endocrine contribution to the age-related declines in muscle mass, muscle strength, and sarcopenia. These authors also investigated the current hormonal interventions designed to improve endocrine defects related to sarcopenia. Myostatin inhibition seems to be an intriguing strategy for attenuating sarcopenia as well as muscular dystrophy. The authors discussed how therapeutic supplementation with growth hormone, IGF-I, or estrogen had a minor sarcopenia-inhibiting effect, and that testosterone supplementation in large doses had several side effects, even though it significantly improved muscle defects. Ghrelin mimetics could also potentially be beneficial and reverse the dysfunctional catabolic state associated with sarcopenia in the elderly population.

Low bone mass density, a classical age-related health issue and a known health concern for fair-skinned, thin, postmenopausal Caucasian women, is found to be common among individuals with developmental/intellectual disabilities. The review paper by J. Jasien et al. provides a comprehensive overview of bone health of adults with developmental/intellectual disabilities, their risk of fractures, and how this compares to the general aging population. The authors contend that gaining a greater understanding of how bone health affected in individuals with developmental/intellectual disabilities could lead to better customized treatments for these specific populations.

The paper by A. Fisher et al. reveals the interactions between serum adipokines and osteocalcin in older patients with hip fracture. The authors found that serum osteocalcin concentration was inversely associated with resistin and positively with leptin, leptin/resistin ratio, and adiponectin/resistin ratio after adjustment for multiple potential confounders. Osteocalcin was found to be an independent predictor of serum leptin, resistin, leptin/resistin, and adiponectin/resistin ratios, which suggests bidirectional interactions (crosstalk) between leptin, resistin, and osteocalcin as a part of a complex homeostatic system regulating bone and energy metabolism.

The accuracy of analytical measurements of different biochemical parameters is of vital importance for the proper diagnosis and treatment monitoring of elderly patients. The paper by K. Sztefko et al. discusses important points to be considered in the interpretation of hormone and tumor marker measurements in the geriatric population using immunochemical methods, including general lack of immunoassay standardization, presence of cross-reacting substances in patients’ samples, limitation of free hormone measurements due to abnormal analyte binding protein concentrations, assay interferences due to a patient’s autoantibodies, heterophilic antibodies, and proper interpretation of very low- and very-high-sample analyte levels.

While the endocrine system is classically associated with the regulation of autonomic hormonal functions, many lines of recent evidence have demonstrated that cognitive central nervous function in the elderly is significantly affected during the aging process by endocrine control of somatic metabolism. Hence, both normal and pathophysiological aging, as well as neurodegenerative disorders, are all influenced by this “neurometabolic” interface. This functional connection between these two important systems (neuronal and endocrine) is primarily mediated through hormonal communication between the brain and the metabolic organs. The review paper by S. Siddiqui et al. discusses the physical structure and molecular components of this fundamental “neurometabolic” axis in aging. The authors then elaborate upon this by discussing how the connection of these two major functional domains is likely to be created by multifunctional “keystone” signaling factors, such as the epidermal growth factor receptor (EGFR). This paper draws together evidence to aid the appreciation of the truly multidimensional role of EGFR, at the systemic level, in neurometabolic processes and in the neurodegenerative trajectories seen in the aging process.

In another paper that discusses the functional interface between neuronal and endocrine systems during the aging process, A. M. Stranahan et al. investigate the effect of two well-characterized antiaging interventions (caloric restriction or exercise) upon hypothalamic function. The hypothalamus forms a vital bridge between higher neuronal activity and the status of the peripheral endocrine hormone system. Age-related changes in hypothalamic activity appear to be strongly connected to both endocrine and neuronal pathophysiological mechanisms. A. M. Stranahan et al. employ both caloric restriction and voluntary wheel running paradigms in diabetic and nondiabetic animals to investigate the contextual sensitivity of hypothalamic transcriptomic responses to these antiaging lifestyle strategies. The authors found that caloric restriction and physical exercise were associated with distinct hypothalamic transcriptional signatures that differed significantly between the host physiological contexts of the diabetic or nondiabetic mice.

In conclusion, our understanding of endocrine function in aging is making great strides. Several timely topics concerning endocrine function in aging were purposefully included in this special issue. However, it is clear that further efforts are needed to gain a greater appreciation of the mechanisms underlying endocrine alterations in aging, which will aid the development of more effective interventions for the treatment of endocrine defects during the aging process.

Acknowledgment

This work was supported entirely by the Intramural Research Program of the National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.

Huan Cai
Alan S. Mcneilly
Louis M. Luttrell
Bronwen Martin

Copyright

Copyright © 2012 Huan Cai et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Footnotes

Daniel Greenberg, Ph.D., F.A.C.N., is a Food Forum member and was a member of the workshop planning committee.

This section summarizes the presentation of Timothy Moran, Ph.D., Johns Hopkins University School of Medicine, Baltimore, Maryland.

The myenteric plexus and submucosal plexus are networks of neurons located in different areas of the wall of the digestive tract. The myenteric plexus is located between the layers of longitudinal and circular muscle (two layers of muscle involved with propulsive activity within the intestine), while the submucosal plexus is located between the circular muscle layer and the mucosa.

Sham feeding involves providing an animal with a liquid diet, which descends through the esophagus but immediately drains out from the stomach, thereby eliminating gastric stretch and intestinal stimulation.

This section summarizes the presentation of Robert Margolskee, M.D., Ph.D., Monell Chemical Senses Center, Philadelphia, Pennsylvania.

Papillae are small structures on the upper surface of the tongue.

G protein-coupled receptors are proteins located in the cell membrane that bind extracellular substances and transmit signals from those substances to an intracellular molecule known as a G protein.

ENaC is the epithelial sodium channel, a membrane-bound channel permeable to sodium ions and other substances.

L and K cells are types of intestinal enteroendocrine cells. L cells secrete GLP-1 K cells secrete gastric inhibitory peptide (GIP).

This section summarizes the presentation of Robert Ritter, V.M.D., Ph.D., Washington State University, Pullman.

This section summarizes the presentation of Laurette Dubé, Ph.D., M.P.S., M.B.A., McGill University, Montreal, Quebec, Canada.

A pyloric cuff is a device used to tighten the pylorus and prevent food from leaving the stomach, allowing researchers to separate gastric from intestinal factors.

The cephalic phase is a phase of gastric secretion that occurs before food enters the stomach.


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