STEP 1 aging process : the process of growing old, is defined as the gradual biological impairment of normal function, probably

y as a result of changes made to cells (mitotic cells, such as fibroblasts and post-mitotic cells, such as neurons) and structural components (such as bone and muscle). These changes would consequently have a direct impact on the functional ability of organs (such as the heart, kidney and lungs), biological systems (such as the nervous, digestive and reproductive system) and ultimately the organism as a whole.

STEP 2 1. aging process There are three main factors that influence the body's aging process. First, as we grow older, the number of mistakes incurred by daily cellular reproduction increases. The body actually creates nonfunctional cells, leading to more rapid deterioration of the body's functions. With advancing age, a larger percentage of our cells, even though they're present, are useless. And worse yet, these nonfunctional cells sometimes interfere with normal cellular processes. The second part of the aging process relates to cellular damage that causes the shortening of DNA, eventually triggering a process called apoptosis or "programmed cell death." This is particularly important when we realize that there are DNA fragments in each of our cells' many mitochondria compartments. When these mitochondria serve as energy generators during normal cell functions, oxygen free radical by-products are produced, and damage can occur to healthy DNA, creating DNA fragments and triggering cell apoptosis. As time passes, increased damage to healthy DNA leads to accelerated cell death, and our old bodies simply cannot generate cells fast enough to compensate for the loss. This process is most visible and obvious in our skinthe older we get, the thinner our skin becomes.

The third part of the aging process involves the cellular down-regulation of our natural oxidative enzymes such as superoxide dismutase and catalase and glutathione perxoidase, making our antioxidant defenses less efficient with age. the most prominent theory accepted by the scientific community has been termed the Free Radical Theory of Aging. Free radicals are mostly oxygencontaining molecules with single electrons in the outermost orbital that are very eager to pair up with anything else that has electrons. These short-lived molecules, with an average life span of one-millionth of a second, are very potent toxins that afflict our bodies. By attacking the cell's DNA, free radicals destroy the cell, causing healthy cells to die prematurely. When we're young, our natural antioxidant defense system functions well by "mopping up" free radicals before they can cause damage. However, as we age, the antioxidant defense system becomes less efficient through down-regulation of

oxidative enzymes. The increase in free radical damage impairs cellular regulation and functioning and triggers aging symptoms as well as many diseases. Why do cells become susceptible to free radical damage? First, the daily energy production by the cell's mitochondria generates increased numbers of free radicals as by-products. The second reason is due to the constant access and utilization of nucleus DNA to make mRNA for production of functional protein, followed by repairing and rewinding the DNA back into chromosomes. These activities often cause a fault in the repair process, damaging DNA. The third reason is external free radical assault. This assault comes from sunlight (including UVA and UVB rays), pollution, stress, smoking, etc. Smoking a single cigarette generates trillions of free radicals. 2. theory of aging process There are various theories put forward to explain the above mentioned changes of agiing. The Neuroendocrine Theory: This theory elaborates on the complicated network of biochemicals that governs the release of our hormones. The hypothalamus sets off various chain reactions whereby an organ releases a hormone which in turn stimulates the release of another hormone, which in turn stimulates yet another bodily response. Aging causes a drop in hormone production leading to decline in our bodys ability to repair and regulate itself (23). The Genetic Control Theory: This theory focuses on the genetic programming encoded within our DNA.We are born with a unique genetic code, a predetermined tendency to certain types of physical and mental functioning. The genetic inheritance has a great deal to tell about how long we live. Each of us has a biological clock ticking away set to go off at a particular time. When that clock goes off it signals our body first to age and then to die. The timing on this genetic clock is subject to enormous variation (24). The Free Radical Theory: Free-radical are required for physiological functions, but free radicals also attack thestructure of our cell membranes, creating metabolic waste products like lipofuscins.An excess of lipofuscins in the body is shown as a darkening of the skin in certain areas, so-called aging spots. Lipofuscins in turn interfere with the cells ability to repair and reproduce themselves. They disturb DNA and RNA synthesis and interfere with synthesis of protein. They also lower the energy levels, prevent the body from building muscle mass and destroy cellular enzymes, which are needed for vital chemical processes. Free-radical disruption of cell metabolism is part of what ages our cells (21). Substance that combats free-radical damage is known as a free-radical scavenger. Free-radical scavengers actually seek out free radicals and harmlessly bind them before they can attach themselves to other molecules and/or cause crosslinking. Specialists in anti-aging medicine prescribe a host of natural and manufactured free-radical scavengers to help combat the effects of aging (25). Other theories of aging that have been proposed throughout the years are: Mitochondrial Theory: The free radical theory is supported by direct experimental observations of mitochondrial aging. Mitochondria are one of the easiest targets of free-radical injury because they lack most of the defenses found in other parts of the cell. This theory states that electrons leaking from the electron transfer chain (ETC) reduce molecular oxygen to form O2(superoxide anion radicals) which can cause the generation of other reactive oxygen species (ROS). The ensuing state of oxidative stress results in damage to ETC components and mitochondrial DNA (mtDNA), thus increasing further the production of ROS. Ultimately, this vicious cycle leads to a physiological decline in function or aging

3. skin looked more saggy/slacker,especially around the eyes The skin loses underlying fat layers and oil glands, causing wrinkles and reduced elasticity. There is increased susceptibility to cold, bruising and bedsores. In addition, the skin develops age spots due to deposits of melanin pigment. The hair gradually loses its pigmentation and turns gray. The nails become thicker due to reduced blood flow to the connective tissues. Theskin becomes somewhat less sensitive to sensations including heat, cold and injury The Free Radical Theory of Aging is particularly relevant to skin cells. The unstable free radical molecules vibrate in the skin, literally poking holes in the collagen fibers (the skin's support structure) of the dermis. After years of this free radical assault, the collagen, which is a critical structural element of skin, becomes weaker and eventually causes the skin to collapse and form wrinkles. The rapid rate at which skin cells divide causes a shorter life span for the cell, and as we mature, the number of skin cells in our bodies decreases. Over time, the process results in our skin becoming thinner and thinner. Essentially, the more skin cells in your body and the thicker these cells are, the healthier your skin will be and the less wrinkles you will have. The skin loses some of its elasticity, and becomes dry and wrinkled because the sweat and sebaceous glands function less effectively. As the circulation of the blood to the skin slows, cold is felt more readily. With aging the skin becomes thinner and may be more susceptible to being broken or cut. When broken, the skin may be more prone to infection.

With aging, the outer skin layer (epidermis) thins, even though the number of cell layers remains unchanged. The number of pigment-containing cells (melanocytes) decreases, but the remaining melanocytes increase in size. Aging skin thus appears thinner, more pale, and clear (translucent). Large pigmented spots (called age spots, liver spots, or lentigos) may appear in sun-exposed areas. Changes in the connective tissue reduce the skin's strength and elasticity. This is known as elastosis and is especially pronounced in sun-exposed areas (solar elastosis). Elastosis produces the leathery, weather-beaten appearance common to farmers, sailors, and others who spend a large amount of time outdoors. The blood vessels of the dermis become more fragile. This leads to bruising, bleeding under the skin (often called senile purpura), cherry angiomas, and similar conditions. Sebaceous glands produce less oil as you age. Men experience a minimal decrease, usually after the age of 80. Women gradually produce less oil beginning after menopause. This can make it harder to keep the skin moist, resulting in dryness and itchiness. 4. her weight decreased and her body shape got thinner The amount of muscle tissue (muscle mass) and muscle strength tend to decrease. This process is called sarcopenia, which literally means loss of flesh. Loss of muscle mass begins around age 30 and continues throughout life. By age 75, the percentage of muscle mass is typically half of what it was during young adulthood. Muscle mass decreases possibly because the muscles are used less and begin to shrink. Also, the levels of growth hormone and testosterone, which stimulate muscle development, decrease. Muscles cannot contract as quickly because more fast-

contracting (fast-twitch) muscle fibers are lost than slow-contracting (slow-twitch) muscle fibers. Sarcopenia can be defined as the age-related loss of muscle mass, strength and function the following factors play a role: Age-related reduction in nerve cells responsible for sending signals from the brain to the muscles to initiate movement A decrease in the concentrations of some hormones, including growth hormone, testosterone, and insulin-like growth factor A decrease in the body's ability to synthesize protein Inadequate intake of calories and/or protein to sustain muscle mass

Pathogenesis Motor Unit Remodeling Age related changes in the neuromuscular system may play a role in the onset of sarcopenia. With age the number of spinal cord motor neurons and functioning motor units decline (Roth, Ferrel & Hurley 2000, Roubenoff 2001). This is a continuous process throughout life and is considered irreversible (Roubenoff 2001). Human nerve cells have a predetermined life span and the decline in these cells is dependent on the location in the body, age, and presence of disease (Vandervoort & Symons 2001). It is interesting to note that nerve cells can still remain present in aged individuals yet be impaired because of biochemical changes (Vandervoort & Symons 2001). The motor neurons are responsible for sending signals from the brain to the muscles to initiate movement. A motor unit consists of the motor neuron and all of the muscle fibers that it connects to or innervates. The number of fibers that a motor neuron innervates depends on the function of that specific muscle. For example, a muscle that requires precise movements, such as muscles of the eye, will have motor units with a motor neuron innervating a few muscle fibers. Muscles that require less precise movements, such as the quadriceps muscles, will have motor units with a motor neuron innervating hundreds and possibly over a thousand muscle fibers.

The loss of muscle fibers begins with the loss of motor neurons. Motor neurons will die with age resulting in a denervation of the muscle fibers within the motor unit. This denervation causes the muscle fibers to atrophy and eventually die, leading to a decrease in muscle mass. (Roth, Ferrel & Hurley 2000). When a motor neuron dies, an adjacent motor neuron, usually a slow twitch (ST) motor neuron, may reinnervate the muscle fibers, preventing atrophy. This process is called motor unit remodeling. When compared to FT motor units, ST motor units have slower firing rates, are slower to contract, produce less muscle force and are smaller in size and fiber number. Motor unit remodeling by ST motor neurons leads to less efficient motor units. The remodeled ST motor unit will have less precise control of movements, less force production and slowing of muscle mechanics (Roth, Ferrel & Hurley 2000; Roubenoff 2001; Waters, Baumgartner & Garry 2000). This may help explain the loss of balance and speed of movement with age. In addition, denervation rates of FT muscle fibers may exceed

reinnervation rates by ST motor neurons, further explaining atrophy of FT muscle fibers in the elderly (Roth, Ferrel & Hurley 2000).

Protein Synthesis/Regeneration Another factor affecting sarcopenia is the rate of muscle protein synthesis. The quality and quantity of protein in the body is maintained by a continuous repair process, which involves both protein breakdown and synthesis (Nair 1995). The balance of protein synthesis and breakdown determines the protein content in the body (Nair 1995). With age, the changes in whole-body protein turnover reflect a decreased synthesis rate rather than an increased catabolic rate (Vandervoort & Symons 2001). Additionally, research has consistently reported that muscle protein synthesis rates are lower in older adults when compared to younger adults (Nair 1995; Yarasheski et al. 1999; Hasten et al. 2000; Roth, Ferrel & Hurley 2000). A decrease in muscle protein synthesis will result in the loss of muscle mass. It is important to note that the ability of the muscle to regenerate following injury or overload is also decreased with age. Muscle regeneration and growth of muscle tissue require the assistance of satellite cells (Roth, Ferrel & Hurley 2000). Satellite cells are specialized cells located in the basal membrane of the muscle cell and are necessary for the development of new muscle tissue. The number of satellite cells in skeletal muscle decreases as an individual ages, providing a possible mechanism for the loss of muscle mass and strength (Roth, Ferrel & Hurley 2000). All of the above are physiological explanations of why resistance training in the elderly should follow a progressive overload prescription.

Hormones Aging is associated with several changes in hormonal levels, including a decrease in the concentrations of growth hormone (GH), testosterone (T), and insulin-like growth factor (IGF-1). A decrease in the concentrations of these hormones may be linked to the development of sarcopenia. GH and IGF-1 play a dominant role in the regulation of protein metabolism; GH and T are required for protein maintenance; and IGF-1 levels are positively correlated with muscle protein synthesis rates, specifically myofibrillar protein (actin and myosin filaments) and myosin heavy chain synthesis (part of the myosin containing cross-bridges) (Waters, Baumgartner & Garry 2000). A sustained decrease in these hormones is linked to a decrease in muscle mass and an increase in body fat (Waters, Baumgartner & Garry 2000). Although these hormones are involved in protein metabolism and maintenance, there is conflicting evidence whether hormone replacement is effective in maintaining or gaining muscle mass (Roubenoff 2001). Studies examining hormone replacement effects on lean body mass have mainly focused on GH. These studies have reported that GH replacement has not always been effective in increasing muscle mass and strength in older subjects (Roubenoff 2001; Waters, Baumgartner & Garry 2000). It has also been suggested that changes in female estrogen levels may play a role in the development of sarcopenia during menopause. However, limited research on this topic exists. 5. her vision was getting blurred When you are young, the lens in your eye is soft and flexible. The lens of the eye changes its shape easily, allowing you to focus on objects both close and far away.

After the age of 40, the lens becomes more rigid. Because the lens cant change shape as easily as it once did, it is more difficult to read at close range. This normal condition is called presbyopia.

In the fourth decade, the pupil begins to decrease in size and there is decreased response to light. Because of these changes, older people require three times the amount of illumination to see as compared to a younger person. Focusing takes longer with an increase in nearsightedness, making small print harder to read. There is loss of accommodation which makes reading and close work difficult. This condition, which is known as presbyopia, can be corrected by wearing glasses with convex lenses. There is thickening and yellowing of the lens of the eye. This results in light diffraction, increased sensitivity to glare, decreased depth perception and more difficulty distinguishing pastel colors, especially blues and green

As people age, the following occur:

The lens stiffens, making focusing on close objects harder. The lens becomes denser, making seeing in dim light harder. The pupil reacts more slowly to changes in light. The lens yellows, changing the way colors are perceived. The number of nerve cells decrease, impairing depth perception. The eyes produce less fluid, making them feel dry.

A change in vision is often the first undeniable sign of aging. Changes in the lenses of the eye can cause or contribute to the following:

Loss of near vision: During their 40s, most people notice that seeing objects closer than 2 feet becomes difficult. This change in vision, called presbyopia, occurs because the lens in the eye stiffens. Normally, the lens changes its shape to help the eye focus. A stiffer lens makes focusing on close objects harder. Ultimately, almost everyone with presbyopia needs reading glasses. People who need glasses to see distant objects may need to wear bifocals or glasses with variable-focus lenses. Need for brighter light: As people continue to age, seeing in dim light becomes more difficult because the lens tends to become less transparent. A denser lens means that less light passes through to the retina at the back of the eye. Also, the retina, which contains the cells that sense light, becomes less sensitive. So for reading, brighter light is needed. On average, 60-year-olds need 3 times more light to read than 20-year-olds. Changes in color perception: Colors are perceived differently, partly because the lens tends to yellow slightly with aging. Colors may look less bright and contrasts between different colors may be more difficult to see. Blues may look more gray, and blue print or background may look washed out. These changes are insignificant for most people. However, older people may have trouble reading black letters printed on a blue background or reading blue letters.

The pupil of the eye reacts more slowly to changes in light. The pupil widens and narrows to let more or less light in depending on the brightness of the surroundings. A slow-reacting pupil means that older

people may be unable to see when they first enter a dark room. Or they may be temporarily blinded when they enter a brightly lit area. Older people may also become more sensitive to glare. However, increased sensitivity to glare is often due to darkened areas in the lens or to cataracts.

Fine details, including differences in shades and tones, become more difficult to discern. The reason is probably a decrease in the number of nerve cells that transmit visual signals from the eyes to the brain. This change affects the way depth is perceived, and judging distances becomes more difficult. Older people may see more tiny black specks moving across their field of vision. These specks, called floaters, are bits of normal fluid in the eye that have solidified. Floaters do not significantly interfere with vision. Unless they suddenly increase in number, they are not a cause for concern. The eyes tend to become dry. This change occurs because the number of cells that produce fluids to lubricate the eyes decreases. Tear production may decrease. The appearance of the eyes changes in several ways:

The whites (sclera) of the eyes may turn slightly yellow or brown. This change results from many years of exposure to ultraviolet light, wind, and dust. Random splotches of color may appear in the whites of the eyes, particularly in people with a dark complexion. A gray-white ring (arcus senilis) may appear on the surface of the eye. The ring is made of calcium and cholesterol salts. It does not affect vision. The lower eyelid may hang away from the eyeball because the muscles around the eye weaken and the tendons stretch. This condition (called ectropion) may interfere with lubricating the eyeball and contribute to dry eyes. The eye may appear to sink into the head because the amount of fat around the eye decreases.

6. her hearing began to decline There is a decrease in sensitivity to high frequency tones and decreased discrimination of similar pitches because of changes in the bones and cochlear hair cells of the inner ear. Approximately 30% of all elderly persons have some hearing impairment. It is an invisible disability which is often covered up or denied by a person who may then be mislabeled as senile, dumb or uncooperative Most changes in hearing are probably due as much to noise exposure as to aging. Exposure to loud noise over time damages the ear's ability to hear. Nonetheless, some changes in hearing occur as people age, regardless of their exposure to loud noise. As people age, hearing high-pitched sounds becomes more difficult. This change is considered age-associated hearing loss (presbycusis). For example, violin music may sound less bright. The term presbycusis refers to sensorineural hearing impairment in elderly individuals. Characteristically, presbycusis involves bilateral high-frequency hearing loss associated with difficulty in speech discrimination and central auditory processing of information. Patofisiologi prebyscusis

Sensory presbycusis: This refers to epithelial atrophy with loss of sensory hair cells and supporting cells in the organ of Corti. This process originates in the basal turn of the cochlea and slowly progresses toward the apex. These changes correlate with a precipitous drop in the high-frequency thresholds, which begins after middle age. The abrupt downward slope of the audiogram begins above the speech frequencies; therefore, speech discrimination is often preserved. Histologically, the atrophy may be limited to only the first few millimeters of the basal end of the cochlea. The process is slowly progressive over time. One theory proposes that these changes are due to the accumulation of lipofuscin pigment granules. Neural presbycusis: This refers to atrophy of nerve cells in the cochlea and central neural pathways. Schuknecht estimated that 2100 neurons are lost every decade (of 35,000 total). This loss begins early in life and may be genetically predetermined. Effects are not noticeable until old age because pure-tone average is not affected until 90% of neurons are gone. Atrophy occurs throughout the cochlea, with the basilar region only slightly more predisposed than the remainder of the cochlea. Therefore, no precipitous drop in the high-frequency thresholds on audio is observed. A disproportionately severe decrease in speech discrimination is a clinical correlate of neural presbycusis and may be observed before hearing loss is noted because fewer neurons are required to maintain speech thresholds than speech discrimination. Metabolic (ie, strial) presbycusis: This condition result from atrophy of the stria vascularis. The stria vascularis normally maintains the chemical and bioelectric balance and metabolic health of the cochlea. Atrophy of the stria vascularis results in hearing loss represented by a flat hearing curve because the entire cochlea is affected. Speech discrimination is preserved. This process tends to occur in people aged 30-60 years. It progresses slowly and may be familial. Mechanical (ie, cochlear conductive) presbycusis: This condition results from thickening and secondary stiffening of the basilar membrane of the cochlea. The thickening is more severe in the basal turn of the cochlea where the basilar membrane is narrow. This correlates with a gradually sloping highfrequency sensorineural hearing loss that is slowly progressive. Speech discrimination is average for the given pure-tone average. 7. she was so easy to fall off Muscle mass is a primary source of metabolic heat. When muscles contract, heat is generated. The heat generated by muscle contraction maintains body temperature in the range required for normal function of its various chemical processes. As early as the third decade of life there is a general reduction in the size, elasticity and strength of all muscle tissue. The loss of muscle mass continues throughout the elder years. Muscle fibers continue to become smaller in diameter due to a decrease in reserves of ATP, glycogen, myoglobin and the number of myofibrils. As a result, as the body ages, muscular activity becomes less efficient and requires more effort to accomplish a given task. The elderly are less efficient at creating the heat necessary to drive the important biochemical reactions necessary for life. Changes in musculo-skeletal system: There is generalized atrophy of all muscles accompanied by a replacement of some muscle tissue by fat deposits. This results in some loss of muscle tone and strength.Somespecific implications of this are reduced ability to breathe deeply and reduced gastro-intestinal activity which can lead to constipation or bladder incontinence, particularly in women. Calcium is lost and bones become less dense. This can result in osteoporosis and a reduction of weight bearing capacity, leading to the possibility of spontaneous fracture. Thinning of the vertebrae also results in a reduction in height. In addition, the vertebrae can calcify, resulting in postural changes. The joints also undergo changes. In fact, arthritis, the degenerative inflammation of the joints, is the most common chronic condition in the elderly

As a person becomes older, the bone mass decreases by as much as 10 percent after the age of 35. For example, the spinal discs in the backbone compress, causing a bowed back. In addition, the bones lose elasticity and become more brittle, making breaks more likely. Osteoporosis is a significant concern to older people. The older a person is, the more at risk they are. In particular, older women have very high rates of osteoporosis. Estrogen has a protective effect on bones, yet they no longer produce it in levels effective to protect them from brittle bones. Osteoporosis accentuates the decrease in bone mass, resulting in additional breaks and fractures. There may also be slight changes in the bone angles, causing new stresses and a higher probability of breaks. These changes make an older person more vulnerable, and perhaps more cautious in moving around and traveling.

8. she felt so dizzy and got balance disorder CAUSES OF DIZZINESS IN OLDER PEOPLE System Peripheral Vestibular (Otologic) Brainstem/Cerebellum (central) Proprioceptive (peripheral neuropathy) Visual Psychological Unknown

Contribution (Davis, 1994) 56 22 7 1 3 14

Dizziness or lightThe heart does not pump enough blood to the head headedness when standing because the heart is less able to respond to changes in position. The nervous system signals the heart to increase blood flow less effectively. The blood vessels do not constrict enough to maintain normal blood pressure when a person stands.

Causes of imbalance in older people Balance in walking and standing is dependent on many factors. Good balance requires reliable sensory input from the individuals vision, vestibular system (the balance system of the inner ear), and proprioceptors (sensors of position and movement in the feet and legs). The elderly are prone to a variety of diseases that affect these systems, including cataracts, glaucoma, diabetic retinopathy, and macular degeneration, which all affect vision; diabetic peripheral neuropathy, which affects position sense in the feet and legs; and degeneration of the vestibular system. Balance is also dependent on good muscle strength and joint mobility. A sedentary lifestyle and arthritis or diseases of bones and muscles can compromise strength and mobility.

The aging vestibular system Most people are familiar with the problems associated with the aging of senses such as vision and hearing. However, the vestibular system is another sensory system that can also begin to function poorly with age, leading to a diminished quality of life. The vestibular system is a complex structure of fluid-filled tubes and chambers that constitutes part of the inner ear. Specialized nerve endings inside these structures detect the position and movement of the head and also detect the direction of gravity. The signals sent from the nerves of the vestibular system are critically important to the brains ability to control balance in standing and walking and also to control certain types of reflexive eye movements that make it possible to see clearly while walking or running. Anatomical studies have shown that the number of nerve cells in the vestibular system decreases from about age 55. Blood flow to the inner ear also decreases with age. Idiopathic bilateral (occurring on both sides) vestibular loss becomes more severe as age progresses. When the vestibular system is damaged by any cause, an individual may experience dizziness and balance problems. However, the gradual, age-related loss of vestibular nerve endings can result in severe balance problems without any associated dizziness. This type of slow loss of vestibular function may be first noticed as difficulty walking or standing, especially in the dark while on soft or uneven surfaces (such as thick carpet or a forest path). Specific vestibular disorders in older adults

Sumber : Ko CW, Hoffman HJ, Sklare DA. Chronic Imbalance or Dizziness and Falling: Results from the 1994 Disability Supplement to the National Health Interview Survey and the Second Supplement on Aging Study. Twenty-ninth MidWinter Meeting of the Association for Research in Otolaryngology (ARO); National Institute on Deafness and Other Communication Disorders (NIDCD). Feb. 2006. 9. hasn't got menstruastion anymore since 5 years ago, menopause : is commonly used to describe any of the changes a woman experiences either just before or after she stops menstruating, marking the end of her reproductive period. Natural or physiological menopause occurs as a part of a woman's normal aging process. It is the result of the eventual atresia of almost all oocytes in the ovaries, causing an increase in circulating follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels as there are a decreased number of oocytes responding to these hormones and producing estrogen. This decrease in the production of estrogen leads to the perimenopausal symptoms of hot flashes, insomnia and mood changes. Long term effects may include osteoporosis and vaginal atrophy. A woman is born with a finite number of eggs, which are stored in the ovaries. The ovaries also produce the hormones estrogen and progesterone, which regulate menstruation and ovulation. Menopause occurs when the ovaries are totally depleted of eggs or no amount of stimulation from the regulating hormones can force them to work.

Menopause, when it occurs between the ages of 45 and 55, is considered "natural" and is a normal part of aging. But, some women can experience menopause early, either as a result of a surgical intervention, such as hysterectomy, or damage to the ovaries, such as from chemotherapy. Menopause that occurs before the age of 45, regardless of the cause, is called

premature menopause