Natural Treatment

Menieres affects roughly 0.2% of the population. Ménière’s disease usually starts confined to one ear but it often extends to involve both ears over time so that after 30 years, 50% of patients with Meniere’s have bilateral disease (Stahle et al, 1991). There is some controversy about this statistic however — some authors, for example Silverstein, suggest that the prevalence of bilaterality is as low as 17% (Silverstein, 1992). We suspect that this lower statistic is due to a lower duration of followup and that the 50% figure is more likely to be correct. Other possibilities, however, are selection bias and different patterns of the disease in different countries. Silverstein suggested that 75% of persons destined to become bilateral do so within 5 years. 

Symptoms

The symptoms of Ménière’s disease occur suddenly and can arise daily or as infrequently as once a year. Vertigo, often the most debilitating symptom of Ménière’s disease, typically involves a whirling dizziness that forces the sufferer to lie down. Vertigo attacks can lead to severe nausea, vomiting, and sweating and often come with little or no warning.

Attacks of vertigo can be severe, incapacitating, and unpredictable. Some patients experience vertigo for hours or days, and this combines with an increase in volume of tinnitus and temporary, albeit significant, hearing loss. Hearing may improve after an attack, but often becomes progressively worse. Some sufferers experience what are informally known as “drop attacks” — a sudden, severe attack of dizziness or vertigo that causes the sufferer, if not seated, to fall. Patients may also experience the feeling of being pushed or pulled (Pulsion). Some patients may find it impossible to get up for some time, until the attack passes or medication takes effect.

Causes

The actual cause of the fluid accumulation in the inner ear, the condition which sets off the whole process to begin with in Meniere’s Disease, is not known. In animals, experiments have been done which show that if the sac that drains fluids from the inner ear is tied off, fluid will build up in the inner ear and cause changes comparable to those in humans. Because of the observation of fluid build up in the inner ear of animals, the most commonly performed operation in the past involved drainage of the endolymphatic sac in patients with Meniere’s.

Many experts on Ménière’s disease think that a rupture of the membranous labyrinth allows the endolymph to mix with perilymph, another inner ear fluid that occupies the space between the membranous labyrinth and the bony inner ear. This mixing, scientists believe, can cause the symptoms of Ménière’s disease. Scientists are investigating several possible causes of the disease, including environmental factors, such as noise pollution and viral infections, as well as biological factors. 

Treatment

Your doctor may recommend that you try to control the attacks by changing your diet. Since the disease is a result of a problem with fluid in canals of the inner ear, you may have to limit your salt intake. Controlling the level of salt in your body will indirectly control the amount of fluid in the inner ear canals. A medicine called a diuretic (water pill) may also help. You should limit the amount of caffeine and alcohol in your diet, and quit smoking if you smoke. Your doctor can prescribe medicines to help with feelings of dizziness and nausea. These medicines may cause you to feel sleepy. In difficult cases of Meniere’s disease (when attacks can’t be controlled by diet or medicines), surgery may be necessary.

A meningioma is a type of tumor that develops from the meninges, the membrane that surrounds the brain and spinal cord. There are three layers of meninges, called the dura mater, arachnoid and pia mater. Most meningiomas (90%) are categorized as benign tumors, with the remaining 10% being atypical or malignant. However, the word “benign” can be misleading in this case, as when benign tumors grow and constrict and affect the brain, they can cause disability and even be life threatening.

Meningiomas are the most common benign tumors of the brain (95% of benign tumors). However they can also be malignant. They arise from the arachnoidal cap cells of the meninges and represent about 15% of all primary brain tumors. They are more common in females than in males (2:1) and have a peak incidence in the sixth and seventh decades. Most cases are sporadic while some are familial. There has been some evidence that persons who have undergone radiation to the scalp are more at risk for developing meningiomas. The most frequent genetic mutations involved in meningiomas are inactivation mutations in the neurofibromatosis 2 gene (merlin) on chromosome 22q. 

Meningiomas are benign tumors, although there are rare malignant meningiomas. The majority of meningiomas are classified as meningotheliomatous or syncitial, fibrous, transitional, or angioblastic. The World Health Organization has developed a grading system, which scores architecture, cellularity, nuclear pleomorphism, mitotic figures, necrosis, and brain infiltration. Using the WHO scoring system, tumors are graded as grade I (benign), grade II (atypical), grade III (anaplastic) and grade IV (sarcomatous). Over 90 percent of tumors are classified as benign based on this system. The grading system has prognostic significance for behavior.

Meninges are the three layers of tissue that cover and protect the brain and spinal cord. From the outermost layer inward they are: the dura mater, arachnoid mater, and pia mater. A meningioma grows from the arachnoid gap cells that form the middle layer, the arachnoid mater, and are usually attached to the dura. Some meningiomas contain cysts or calcified mineral deposits, and others contain hundreds of tiny blood vessels. Because meningiomas tend to grow inward, they commonly cause pressure on the brain or spinal cord. Although less common, meningiomas can grow outward, causing the skull to thicken. Meningiomas grow very slowly, and it is oftentimes many years before they cause symptoms. 

Meningiomas can invade the bone or muscle, but such invasion is not a sign of malignancy. Meningiomas can grow through the holes (foramina) at the base of the skull and grow outside the skull. As meningiomas grow, they compress the normal brain. Old hemorrhage may be present. En plaque meningiomas are flat and hard. They grow on the surface of the brain. Ventricular meningiomas grow in the lateral, 3rd or 4th ventricles, and may obstruct CSF (spinal fluid) flow. Meningoimas are rarely cystic (5% of cases).

Radiation therapy: If your meningioma can’t be completely removed, your doctor may recommend radiation therapy following surgery. The goal of radiation therapy is to destroy any remaining meningioma cells and reduce the chance that your meningioma may recur. During radiation therapy, your health care team positions you on a table. A large radiation machine moves around you aiming a high-powered energy beam at precise points on your body to target the meningioma cells and leave your healthy cells unharmed. You typically undergo radiation therapy daily for five or six weeks.

In 1861, the French physician Prosper Ménière described a condition which now bears his name. Ménière’s disease is a disorder of the inner ear which causes episodes of vertigo, ringing in the ears (tinnitus), a feeling of fullness or pressure in the ear, and fluctuating hearing loss. In figure 1, the area of the ear affected is the entire labyrinth, which includes both the semicircular canals and the cochlea.

No one knows the cause. Meniere’s disease has something to do with fluid in canals of the inner ear. Although it can be troublesome, Meniere’s is not contagious and it isn’t fatal. However, it’s a “chronic” problem, which means that it lasts a long time. People with Meniere’s disease don’t have symptoms all the time. When symptoms occur, it’s called an “attack.” Attacks may happen often, or only sometimes. Attacks usually last from 20 minutes to 2 hours or longer. Meniere’s disease usually occurs in only one ear. It affects both ears in only about 30% of patients.

The exact cause of Ménière’s disease is not known, but it is believed to be related to endolymphatic hydrops or excess fluid in the inner ear. It is thought that endolymphatic fluid bursts from its normal channels in the ear and flows into other areas causing damage. This may be related to swelling of the endolymphatic sac or other tissues in the vestibular system of the inner ear, which is responsible for the body’s sense of balance. The symptoms may occur in the presence of a middle ear infection, head trauma or an upper respiratory tract infection, or by using aspirin, smoking cigarettes or drinking alcohol.

The symptoms of Ménière’s disease are associated with a change in fluid volume within a portion of the inner ear known as the labyrinth. The labyrinth has two parts: the bony labyrinth and the membranous labyrinth. The membranous labyrinth, which is encased by bone, is necessary for hearing and balance and is filled with a fluid called endolymph. When your head moves, endolymph moves, causing nerve receptors in the membranous labyrinth to send signals to the brain about the body’s motion. An increase in endolymph, however, can cause the membranous labyrinth to balloon or dilate, a condition known as endolymphatic hydrops.

The fluid-filled hearing and balance structures of the inner ear normally function independent of the body’s overall fluid/blood system. In a normal inner ear, the fluid is maintained at a constant volume and contains specific concentrations of sodium, potassium, chloride and other electrolytes. This fluid bathes the sensory cells of the inner ear and allows them to function normally.With injury or degeneration of the inner ear structures, independent control is lost, and the volume and concentration of the inner ear fluid fluctuates with changes in the body’s fluid/blood.

Medical treatment of Meniere’s Disease is aimed at decreasing the amount of fluid in the inner ear. This is accomplished by following a low salt diet and taking a diuretic (water pill). Salt (sodium chloride) causes water to be retained by the body; therefore, by reducing the amount of salt in the diet less fluid will be retained. A diuretic is taken on a routine basis to further reduce the amount of fluid in the body. The above treatments are aimed at controlling the disease process and can be used for many months or years.

Colitis usually begins in the lower part of the colon and spreads upwards. The first symptom of the trouble is an increased urgency to move the bowel, followed by cramping pains in the abdomen and, sometimes, bloody mucus in the stools. As the disease spreads upward, the stools become watery and more frequent and are characterised by rectal straining. The loss of blood and fluid from the bowels results in weakness, fever, nausea, vomiting, loss of appetite, and anaemia.

Ulcerative colitis is defined as mild, moderate or severe, according to the frequency of diarrhoea, the presence of blood and how generally unwell the person is. Ulcerative proctitis, which is confined to the rectum, is a very common and relatively benign form of ulcerative colitis. Ulcerative colitis is more common than Crohn’s disease. The disease may involve the entire colon (pancolitis), only the rectum (ulcerative proctitis) or, more commonly, somewhere between the two.

Diarrhea, abdominal pain and cramping are the main symptoms of this disease . Anemia, rectal bleeding, loss of appetite, fever, eye irritation, dehydration, painful spasms and fatigue, ulceration in the digestive tract, bloating, and mucus in the stool are certain other symptoms. About 2 million of the total population in the U.S. suffer from this disease which is rarely found in Asia and South America. It has also been found that Jewish people tend to have more incidence of colitis than non-jewish people.

Ischemic colitis involves an area of inflammation caused by interference with the blood flow to the colon. Most of the classifications of intestinal ischemia in the literature are based on the major causative factors. This is a potentially serious condition and requires care from your doctor. Patients may present with colicky abdominal pain, which becomes continuous. The extent of IBD can range from mild to severe based on the amount of damage from lack of oxygenated blood. The sooner IBD is treated, the more favorable the outcome.

Causes 

No one knows for sure what causes inflammatory bowel disease. A number of theories have been developed to explain the condition. Some researchers believe that the disorder is caused by some organism, such as a bacterium or virus. No such organism has been found, however. Other researchers think the body’s immune system becomes confused and begins to attack the body’s own cells as though they were foreign invaders that needed to be killed.

The Facts on Ulcerative Colitis

Ulcerative colitis a type of inflammatory bowel disease (IBD) that causes inflammation and sores in the lining of the rectum and large intestine (colon). It’s a chronic condition although symptoms can disappear for months at a time, only to flare up again unexpectedly. It typically first appears in men or women between the ages of 15 and 40, but occasionally this condition first occurs in people in their 60s.

Treatment

The goals of therapy are to control the infection and relieve symptoms. Medicines to fight the virus (antiviral medications) are prescribed. The medicines may be given through a vein and sometimes by mouth for several weeks. In some cases, long-term therapy may be needed. A medication called CMV hyperimmune globulin may be used when other drugs don’t work.

Colitis (also called ulcerative colitis) is an acute or chronic inflammation of the membrane lining the colon—your large intestine or bowel. Colitis causes inflammation and sores, called ulcers, in the top layers of the lining of the large intestine. Ulcerative colitis rarely affects the small intestine except for the lower section, called the ileum.

Colitis means inflammation of the colon. The colon, also known as the large intestine or large bowel, constitutes the last part of the digestive tract. The colon is a long, muscular tube that receives undigested food from the small intestine. It removes water from the undigested food, stores it and then eliminates it from the body through bowel movements. The rectum is the last part of the colon adjacent to the anus. The common symptoms of colitis include:

• abdominal pain,
• diarrhea, and
• sometimes, rectal bleeding. 

Ulcerative colitis is closely related to another condition of inflammation of the intestines called Crohn’s disease. Together, they are frequently referred to as inflammatory bowel disease (IBD). Ulcerative colitis and Crohn’s diseases are chronic conditions that can last years to decades. They affect approximately 500,000 to 2 million people In the United States. Men and women are affected equally.

Ulcerative colitis affects the large intestine (also known as the colon) and the rectum. It causes inflammation of the colon’s inner lining and the rectal wall, which become red, swollen, and ulcerated, resulting in abdominal pain or cramping, rectal bleeding, and diarrhea. Less common are fatigue, appetite loss, and anemia. Some people also have joint pain, redness, swelling, and liver problems.

The immune system is composed of immune cells which protects the body from bacteria, fungi and other foreign invaders. In a normal case, exposure of the human body to harmful foreign bodies and parasites leads to the activation of the immune system. But it is not so in the case of a person suffering from ulcerative colitis. Here activation of the immune system takes place in the absence of any known invader. This results in inflammation and ulceration.

Ulcerative colitis can occur in people of any age, but it usually starts between the ages of 15 and 30, and less frequently between 50 and 70 years of age. It affects men and women equally and appears to run in families, with reports of up to 20 percent of people with ulcerative colitis having a family member or relative with ulcerative colitis or Crohn’s disease. A higher incidence of ulcerative colitis is seen in Whites and people of Jewish descent.

Inflammation is a process that occurs when the body’s immune system begins to fight off foreign invaders, such as viruses, bacteria, and fungi. The immune system is a network of organs, tissues, cells, and chemicals designed to kill invading organisms. Some of the chemicals produced by the immune system irritate the body’s own tissues. They cause heat, redness, swelling, and loss of function. These changes are all characteristic of inflamed tissue.

The infection is spread by saliva, urine, respiratory droplets, sexual contact, and blood transfusions. Most humans are exposed to the virus in their lifetime, but it usually produces no symptoms in healthy people. However, serious CMV infections can occur in people with weakened immune systems. This includes patients receiving chemotherapy for cancer treatment and patients on immune-suppressing medicines following an organ transplant.

Foot pain is a really popular trouble. Foot pain in the “baseball of your foot,” that region between your archway and the toes, is mostly called metatarsalgia. The pain normally centers on one or much of the five bones (metatarsals) in this mid-portion of the foot. About 75% in the U. S. get foot pain at some moment in their lives. Most foot pain is caused by shoes that do not equip decently or push the feet into stilted shapes (such as pointed-toe, high-heel shoes. Foot pain can be caused by bunions hammer toes plantar warts from pressure on the soles of your feet and fallen arches also called flat feet.

The most common cause of heel pain is plantar fasciitis. Many patients with plantar fasciitis have a heel spur on the front and bottom of their heel, but heel spurs do not cause pain.  The common name is “heel spur” because it’s easier to pronounce than “plantar fasciitis” and doctors are able to point to the spur on an x-ray. 

Plantar fascia is the fibrous ligament below the heel bone that gets inflamed causing heel pain. Plantar Fasciitis is often known as a heel spur as it’s easy to say. Heel spur is the bony growth on the calcaneal bone. Due to similarity in the site of pain in plantar fasciitis and heel spur, these conditions may be misdiagnosed.

Heel spurs are common in patients who have a history of foot pain caused by plantar fasciitis. In the setting of plantar fasciitis, heel spurs are most often seen in middle-aged men and women, but can be found in all age groups. The heel spur itself is not thought to be the primary cause of pain, rather inflammation and irritation of the plantar fascia is thought to be the primary problem. A heel spur diagnosis is made when an X-ray shows a hook of bone protruding from the bottom of the foot at the point where the plantar fascia is attached to the heel bone.

Heel pain is normally caused by a biomechanical imbalance which over time creates tension in the planter fascia region of the foot, eventually causing pain in the heel. Spurs of the heel are soft calcium deposits that result from inflammation and tension in the planter fascia region of the foot. The heel spur itself does not cause pain. Instead, the heel spur is an indication that a patient may have planter fascilitis. Since heel spurs is mainly caused by improper biomechanics while walking, heel spur may actually be a repetitive stress disorder, similar to carpal tunnel in the wrists.

Skin Creams and Foot Baths

Skin creams can help maintain skin softness and pliability. Taking a warm footbath for 10 minutes two or three times a week will keep the feet relaxed and help prevent mild foot pain caused by fatigue. Adding 1/2 cup of Epsom salts increases circulation and adds other benefits. Taking footbaths only when feet are painful is not as helpful. A pumice stone or loofah sponge can help get rid of dead skin.

Megalencephaly, also called macrencephaly, is a condition in which an infant or child has an abnormally large, heavy, and usually malfunctioning brain. By definition, the brain weight is greater than average for the age and gender of the child.  Head enlargement may be evident at birth or the head may become abnormally large in the early years of life. Megalencephaly is thought to be related to a disturbance in the regulation of cell production in the brain.  In normal development, neuron proliferation - the process in which nerve cells divide to form new generations of cells - is regulated so that the correct number of cells is produced in the proper place at the appropriate time.

Symptoms of megalencephaly include delayed development, seizures,   and corticospinal (brain cortex and spinal cord) dysfunction.  Megalencephaly affects males more often than females. Unilateral megalencephaly or hemimegalencephaly is a rare condition that is characterized by the enlargement of one side of the brain. Children with this disorder may have a large, asymmetrical head accompanied by seizures, partial paralysis, and mental retardation. Megalencephaly is different from macrocephaly (also called megacephaly or megalocephaly), which describes a big head, and which doesn’t necessarily indicate abnormality.  Large head size is passed down through the generations in some families. 

Unilateral megalencephaly or hemimegalencephaly is a rare condition characterized by the enlargement of one-half of the brain. Children with this disorder may have a large, sometimes asymmetrical head. Often they suffer from intractable seizures and mental retardation. The prognosis for those with hemimegalencephaly is poor.

Megalencephaly is thought to be related to a disturbance in the regulation of cell reproduction or proliferation. In normal development, neuron proliferation - the process in which nerve cells divide to form new generations of cells - is regulated so that the correct number of cells is formed in the proper place at the appropriate time. Symptoms of megalencephaly may include delayed development, convulsive disorders, corticospinal (brain cortex and spinal cord) dysfunction, and seizures. Megalencephaly affects males more often than females. Unilateral megalencephaly or hemimegalencephaly is a rare condition and is characterized by the enlargement of one-half of the brain.

Megalencephaly affects males more often than females. Unilateral megalencephaly or hemimegalencephaly is a rare condition and is characterized by the enlargement of one-half of the brain. Children with this disorder may have a large, sometimes asymmetrical head. Often they suffer from intractable seizures and mental retardation.

This disorder can present as a seperate disease or syndrome while other times it may be a component of another syndrome (e.g. neurofibramatosis I or von Recklinghausen Disease). This variation of megalencephaly can also be inherited as an autosomal dominant disorder. If you wish your child (I assume this is what the question is in relation to) to be evaluated for reassurance purposes, I would recommend you make an appointment at the CCF Department of Pediatric Neurology or a pediatric neurologists recommended by your family pediatrician.

There is no standard treatment for megalencephaly. Treatment will depend upon the disorder with which the megalencephaly is associated and will address individual symptoms and disabilities. The prognosis for individuals with megalencephaly largely depends on the underlying cause and the associated neurological disorders. The prognosis for those with hemimegalencephaly is poor.

Macular degeneration affects your central vision, but not your peripheral vision; thus it doesn’t cause total blindness. Still, the loss of clear central vision — critical for reading, driving, recognizing people’s faces and doing detail work — greatly affects your quality of life. The condition tends to develop as you get older, hence the “age-related” part of its name. Macular degeneration is the leading cause of severe vision loss in people age 60 and older.

Few people are aware that macular degeneration is an incurable eye disease and that it is the leading cause of blindness for those aged 55 and older in the United States, affecting more than 10 million Americans. Macular degeneration is caused by the deterioration of the central portion of the retina, the inside back layer of the eye that records the images we see and sends them via the optic nerve from the eye to the brain. The retina’s central portion, known as the macula, is responsible for focusing central vision in the eye, and it controls our ability to read, drive a car, recognize faces or colors, and see objects in fine detail.

Age-related macular degeneration (AMD) is a common eye disease that causes deterioration of the macula, the central area of the retina, the paper-thin tissue at the back of the eye where light-sensitive cells send visual signals to the brain. Sharp, clear, “straight ahead” vision is processed by the macula. Damage to the macula results in the development of blind spots and blurred or distorted vision. When the macula becomes damaged, many daily activities such as driving and reading become increasingly difficult. AMD usually affects individuals older than 50 years of age, and scientific evidence shows that genes may play a role in the development of nearly three out of four cases of this devastating eye disease.

Once dry AMD reaches the advanced stage, no form of treatment can prevent vision loss. However, treatment can delay and possibly prevent intermediate AMD from progressing to the advanced stage, in which vision loss occurs.  The National Eye Institute’s Age-Related Eye Disease Study (AREDS) found that taking a specific high-dose formulation of antioxidants and zinc significantly reduces the risk of advanced AMD and its associated vision loss. Slowing AMD’s progression from the intermediate stage to the advanced stage will save the vision of many people.

Multiple, small, round, yellow-white spots called drusen are the key identifiers for the dry type. The spots are located in the back of the eye at the level of the outer retina and are detected by examination of the retina with an ophthalmoscope Spots typically become visible when a person reaches his or her late 30s or older. People with these spots may have excellent vision and no symptoms. Most people with age-related macular degeneration begin with the dry form. The dry form of macular degeneration is much more common than the wet form.

Most people with macular degeneration have the dry form. In fact, macular degeneration almost always starts out as the dry form. The dry form may initially affect only one eye but, in most cases, both eyes eventually become involved. Dry macular degeneration occurs when the RPE cells begin to atrophy and lose their pigment. The normally uniform reddish color of the macula takes on a mottled appearance because of the patchy loss of pigment. Drusen, which look like yellow dots, are fatty-like deposits that appear under the light-sensing cells in the retina.

A macular hole is a small hole in the macula which is in the centre of the retina. The macula is the part of the retina which is responsible for our sharp, detailed, central vision. This is the vision we use when we are looking directly at things, when reading, sewing or using a computer. Macular holes usually only affect one eye, though there is a 10 per cent, one in ten, chance that the other eye will eventually be affected.

Causes of Macular Hole

The most common cause of a macular hole is localized pulling on the retina by the vitreous — the clear, gel-like substance that normally fills the inside back of the eye. This tugging may initially cause mild blurring of vision as the retina becomes thinner. If an actual hole develops, people are aware of a small blind spot in their central vision.

Macular holes develop in stages, including: foveal detachments (stage I), partial-thickness holes (stage II), and full-thickness holes (stage III). A stage IV macular hole is an advanced full-thickness hole, with vitreous separation from the optic disc and macula.

Most of the eye’s interior is filled with vitreous, a gel-like substance that fills about 80 percent of the eye and helps it maintain a round shape. The vitreous contains millions of fine fibers that are attached to the surface of the retina. As we age, the vitreous slowly shrinks and pulls away from the retinal surface. Natural fluids fill the area where the vitreous has contracted. This is normal. In most cases, there are no adverse effects.

Symptoms of Macular Hole

Macular holes often begin gradually. In the early stage of a macular hole, people may notice a slight distortion or blurriness in their straight-ahead vision. Straight lines or objects can begin to look bent or wavy. Reading and performing other routine tasks with the affected eye become difficult. 

In very rare instances, trauma or other conditions lead to the development of a macular hole. In the vast majority of cases, however, macular holes develop spontaneously. As a result, from traditional thinking there is no known way to prevent their development through any nutritional or chemical means, nor is there any way to know who is at risk for developing a hole prior to its appearance in one or both eyes. 

Treatment for Macular Hole

Although some macular holes can seal themselves and require no treatment, surgery is necessary in many cases to help improve vision. In this surgical procedure–called a vitrectomy–the vitreous gel is removed to prevent it from pulling on the retina and replaced with a bubble containing a mixture of air and gas. The bubble acts as an internal, temporary bandage that holds the edge of the macular hole in place as it heals. Surgery is performed under local anaesthesia and often on an out-patient basis.

Macular hole surgery with silicone oil tamponade is an option worth considering in cases with previous failed surgery (Group B), particularly in the presence of fellow eye pathology and if there are difficulties with posturing. This is because good anatomical closure rate can be achieved for these patients and there is substantial variability in visual improvement among eyes with successful closure of macular hole. Perhaps in future if we are able to predict the visual outcome for individual cases one can be more selective regarding candidates for reoperation.

Lactose intolerance is the inability to digest significant amounts of lactose, the major sugar found in milk. Lactose intolerance is caused by a shortage of the enzyme lactase, which is produced by the cells that line the small intestine. Lactase breaks down milk sugar into two simpler forms of sugar called glucose and galactose, which are then absorbed into the bloodstream. Not all people deficient in lactase have the symptoms commonly associated with lactose intolerance, but those who do are said to have lactose intolerance.

The normal mammalian condition is for the young of a species to experience reduced lactase production at the end of the weaning period (a species-specific length of time). In non dairy consuming societies, lactase production usually drops about 90% during the first four years of life, although the exact drop over time varies widely. However, certain human populations have a mutation on chromosome 2 which results in a bypass of the common shutdown in lactase production, making it possible for members of these populations to continue consumption of fresh milk and other dairy products throughout their lives.

The cells that line your small intestine produce an enzyme called lactase. Lactase breaks down lactose into two simple sugars — glucose and galactose — which can be absorbed into your bloodstream. Without lactase, the unprocessed lactose moves on to the colon, where the normal intestinal bacteria contend with it. This causes the hallmarks of lactose intolerance — gas, bloating and diarrhea.

Lactose, a disaccharide, is present in milk and processed foods. Dietary lactose must be hydrolyzed to a monosaccharide in order to be absorbed by the small intestinal mucosa. A deficiency of intestinal lactase prevents hydrolysis of ingested lactose. The osmotic load of the unabsorbed lactose causes secretion of fluid and electrolytes until osmotic equilibrium is reached. Dilation of the intestine caused by the osmosis induces an acceleration of small intestinal transit, which increases the degree of maldigestion. Within the large intestine, free lactose is fermented by colonic bacteria to yield short-chain fatty acids and hydrogen gas. 

When lactose moves through the large intestine (colon) without being properly digested, it can cause uncomfortable symptoms such as gas, belly pain, and bloating. Some people with lactose intolerance cannot digest any milk products, while others can eat or drink small amounts of milk products or certain types of milk products without problems.

Lactose intolerance is fairly common. It seems to affect guys and girls equally. Some ethnic groups are more likely to be affected than others because their diets traditionally include fewer dairy products: Almost all Asians and Native Americans are lactose intolerant, and up to 80% of African Americans and Hispanic Americans also have symptoms of lactose intolerance. Their ancestors did not eat dairy foods, so their bodies were not prepared to digest dairy, and they passed these genes on from generation to generation.

Many people who have gas, belly pain, bloating, and diarrhea suspect they may be lactose-intolerant. The best way to check this is to avoid eating all milk and dairy products to see if your symptoms go away. If they do, then you can try adding small amounts of milk products to see if your symptoms come back.

The common symptoms of lactose intolerance are gastrointestinal, primarily, abdominal pain, diarrhea, flatulence (passing gas), and, less commonly, abdominal bloating, abdominal distention, and nausea. Unfortunately, these symptoms can be caused by other gastrointestinal conditions or diseases, so the presence of these symptoms is not very good at predicting whether a person has lactase deficiency or lactose intolerance.