Anise and Human Health

(Pimpinella anisum) An HERB belonging to the PARSLEY family that originated in India and was cultivated in ancient China and Egypt. The fruit, aniseed, is dried and used as a seasoning. The distinctive, licorice-like flavor of anise extract adds to the taste of shortbread cakes, such as pizella (Italy) and pains á l’anis (France). Anise is used in certain candies. Crushed aniseed together with cinnamon and coriander is used to make a liqueur, anisette. Chopped anise leaves have been used in pickled vegetables and soups.

What is anion?

A negatively charged ion. Anions are the opposite of CATIONS, which carry positive charges. Important anions are formed when weak acids ionize. Anions, together with their cation counterparts, occur in blood and are called electrolytes. They are required to maintain the appropriate effective concentration of ions and PROTEINS in the
blood. Key anions in blood are chloride (Cl–), phosphate (H2PO4–), and bicarbonate (HCO3
–).
Chloride (Cl–) is the predominant anion in body fluids. Neither chloride nor phosphate can be made by the body; they are essential nutrients to be supplied by the diet. Phosphate and bicarbonate ions help buffer blood at nearly a constant pH. These anions are examples of “conjugate bases,” formed when weak acids ionize.

What is angiotensin?

A protein-like hormone formed in the blood that raises blood pressure. Angiotensin contracts the muscles of CAPILLARIES and ARTERIES (vasopressor), which increases resistance for blood flow. Angiotensin is liberated by the action of RENIN, an ENZYME formed by the kidneys, on a serum PROTEIN (angiotensinogen) produced by the liver. The release of renin by the kidneys is triggered when they experience lowered blood flow, for example, due to dehydration. Angiotensin also plays an important role in the regulation of blood pressure by stimulating the ADRENAL GLANDS to secrete ALDOSTERONE. Aldosterone, in turn, promotes SODIUM retention and water retention by the kidneys, to help regulate water balance.

What is pernicious anemia?

A form of ANEMIA caused either by a dietary deficiency of VITAMIN B12 or by inadequate B12 absorption. It is characterized by quite large red blood cells (macrocytic) that are overloaded in the hemoglobin (hyperchromic). Low vitamin B12 consumption is a concern for strict VEGETARIANS who avoid meat and meat products. Pernicious anemia is also caused by inadequate vitamin B12 uptake. Normally, the gastric lining secretes a PROTEIN called INTRINSIC FACTOR that’s needed to specifically bind vitamin B12. Because this protein is required for vitamin B12 absorption by the intestine, inadequate intrinsic factor production, even with adequate dietary B12, can cause pernicious anemia.
Pernicious anemia affects the nervous system as well as the blood. Symptoms include memory loss, weakness, personality and mood swings, and numbness and tingling in the hands and feet. If this anemia continues unchecked, nerve damage may be irreversible. Pernicious anemia is most common in males between the ages of 40 and 65 years who have a family history of the condition. Treatment for intrinsic factor defect involves vitamin B12 injections. Oral doses of vitamin B12 can remedy dietary deficiencies when intrinsic factor production is normal.

What is aplastic anemia ?

A form of ANEMIA in which the numbers of RED BLOOD CELLS as well as white cells are reduced. This type of anemia is caused by exposure to chemicals (such as solvents), toxic heavy metals, some drugs like chloramphenicol, or ionizing radiation (like X rays). Radiation therapy, chemotherapy, and lead poisoning can damage bone marrow, thus reducing red blood cell production. Both the blood platelet count and immunity decline, with a concomitant increased susceptibility to infection. Destruction of the bone marrow is potentially life-threatening.

Why Do You Have Anemia?

A condition characterized by subnormal levels of HEMOGLOBIN, the oxygen-binding PROTEIN in blood. Half a million Americans are at risk for anemia, including 40 percent of pregnant women, pre-menopausal women, vegans (those who eat no animal products), adolescents relying on JUNK FOOD diets, infants, and children with inadequate diets.
Anemia may result from either an inadequate number of RED BLOOD CELLS (erythrocytes) or an abnormally low hemoglobin content of red blood cells. With deficient functional red blood cells, the oxygen supply to tissues is inadequate for optimal RESPIRATION, causing shortness of breath, FATIGUE, weakness, pallor, headache, and lowered resistance to infection. There are two general types of anemia based on red blood cell size. Megaloblastic anemia is characterized by large red blood cells; their shortened life span results in a decreased number of cells. Microcytic anemia is characterized by small red blood cells with reduced hemoglobin content. Many nutritional deficiencies lead to anemia. Inadequate dietary IRON, COPPER, FOLIC ACID, PROTEIN,
VITAMIN B6, vitamin B12, VITAMIN C, VITAMIN A, VITAMIN E, and RIBOFLAVIN can cause this condition. Each of these nutrients is required for the production of red blood cells (ERYTHROPOIESIS). Iron deficiency anemia is the most common diet-related anemia in the United States and it represents the last stage of iron deficiency. It is characterized by small, pale red blood cells (microcytic anemia), due to chronic blood loss or inadequate iron intake. Symptoms include FATIGUE, pallor, and shortness of breath. Studies of the nutritional status of developed nations have routinely found up to 30 percent of a population with iron deficiency. Groups that are at highest risk are children under the age of two years, teenage women, pregnant women, and the elderly. Pregnancy drastically increases the requirement of iron. In terms of blood loss the most common causes of iron deficiency are excessive bleeding during menstruation and intestinal bleeding due to parasites, ulcers, or malignancy. Iron deficiency can be caused by impaired iron uptake by the intestine, due to a lack of stomach acid (ACHLORHYDRIA) or from chronic DIARRHEA. With iron deficiency, the resulting anemia can be treated by iron supplementation.
Deficiencies of either folacin or vitamin B12 can cause anemia because each is essential for DNA synthesis and deficiencies impair erythrocyte production. Folic acid deficiency is much more common because folic acid stores in the body are small, yet folic acid participates in many biosynthetic reactions. On the other hand, vitamin B12 is stored in the LIVER, and only trace amounts are required daily for a few specific functions. Anemia due to inadequate folic acid and vitamin B12 produces large (macrocytic) cells with a short life span. This form of anemia can occur when intake of fresh vegetables is very limited, or when the need for folic acid outstrips intake, as may occur during pregnancy or in ALCOHOLISM. Treatment with folic acid can ameliorate megaloblastic anemia, yet mask an underlying vitamin B12 deficiency. This point emphasizes that treatment of anemia requires expert medical supervision.
Anemia can also indicate a serious condition unrelated to diet. Non-nutritional causes of anemia include chronic blood loss and congenital defects in red blood cell formation, such as thalassemia or sickle cell anemia, due to mutant hemoglobins, and spherocytosis (spherical red blood cells). Hemolytic anemia is the result of excessive hemolysis (destruction of red blood cells) in susceptible people exposed to bacterial toxins, toxic chemicals, or drugs that may produce JAUNDICE.
Anemia also may result from reduced nutrient uptake due to the presence of parasites and chronic infections, gastrointestinal disease or bowel resection

Foods and anaphylaxis

An extreme reaction of the immune system in response to exposure to foreign substances. Insect bites, drugs, injected serum, and certain foods can create anaphylaxis. This abnormal response or immediate hypersensitivity is usually very rapid in susceptible individuals who may have been sensitized by previous exposure, and may produce shock (“anaphylactic shock”). The massive release of histamines and other inflammatory agents leads to spasming of smooth muscles, especially those of the air passageways, and to widespread swelling due to the increased water leaking out of capillaries. Symptoms range from asthma to fever, itching, hives, and flushed skin in mild cases, to chest constriction, irregular pulse, painful, labored breathing, and convulsions in severe cases. Anaphylaxis can be life-threatening and may require emergency room care.

What is anaerobic

Cellular processes that do not require oxygen. Energy can be produced in cells without oxygen. Anaerobic GLYCOLYSIS refers to an energy yielding process by which ATP, the energy currency of the cell, is produced from GLUCOSE without the participation of oxygen. As an example, skeletal muscle produces LACTIC ACID and ATP from glucose when oxygen supplied to muscle is inadequate to meet energy needs during strenuous physical exertion.
Accumulated lactic acid is then converted back to glucose during the recovery period following EXERCISE when the oxygen supply is again adequate.
Anaerobic processes are important for certain bacteria as well. Anaerobic bacteria in the intestine grow without oxygen and block the growth of potential disease-producing microorganisms. Anaerobic fermentation of SUGAR by yeast yields alcohol-containing products such as WINE and BEER.

What is anabolism (biosynthesis)?

Processes involved in synthesizing the molecules needed for cellular growth and maintenance. Thus the formation of PROTEIN, DNA, RNA, LIPID, CARBOHYDRATE, FAT, and GLYCOGEN are anabolic processes. Anabolism consumes chemical energy in the form of ATP and NADPH (a reducing agent), which are supplied by CATABOLISM, the energy-yielding oxidative processes involved in degradation. Optimal function and health rely upon a balance of anabolic and catabolic processes (homeostasis). These two branches of metabolism are controlled by the ENDOCRINE SYSTEM, which in turn responds to external influences such as diet. Anabolic processes require small building blocks supplied by breaking down STARCH, PROTEIN, and FAT in foods to build larger molecules. GLYCEROL and FATTY ACIDS are the subunits of fat; AMINO ACIDS yield proteins; and glucose yields glycogen. Fat and carbohydrate degradation provides an energized form of ACETIC ACID (acetyl CoA) to synthesize fatty acids and cholesterol. Other specialized products are also assembled from several different types of smaller precursors. For example, heme, the iron-containing pigment of the oxygen transport protein HEMOGLOBIN, is synthesized from an amino acid (GLYCINE) and SUCCINIC ACID, a common intermediate in energy-producing pathways.
Growth and an anabolic state, seen as an increase in body mass and muscle mass, occur during childhood, adolescence, pregnancy, and strenuous physical activity, such as body building. The weight gained in these situations represents increased protein, bone, or fat, not fluids. Increased fat stores and accumulated body fat represent stored surplus energy in adults and can result from too little exercise, the over-consumption of FOOD, heredity, or a combination of the above factors.

Anabolic Steroids

A family of steroids related to the male sex hormone TESTOSTERONE. These are classified as prescription drugs used to make up for hormone imbalance and deficiencies. However, synthetic analogs of testosterone have been obtained illegally by athletes and by teenage males to build muscles, and the U.S. FDA has described steroid abuse as a drug epidemic. While testosterone stimulates growth during adolescence, the synthetic derivatives can cause many side effects. Athletes compound this unsafe practice by “stacking” anabolic steroids—taking a combination of brands at 10 to 100 times the recommended doses for weeks at a time.
In men, the side effects of anabolic steroid use include lowered sperm count, enlarged prostate gland, shrinking testicles, balding, and enlarged breasts. If taken before puberty, anabolic steroids can stunt growth. These effects seem to be reversible if anabolic steroids have been used for a short time. Some women body builders also use steroids to build muscle. Side effects in women do not seem to be reversible: masculinization, including increased muscles, increased size of clitoris, growth of facial hair, a deepening voice, shrinkage of breast size, uterine atrophy, and menstrual irregularities. Severe cases of acne and bouts of rage are signs of anabolic steroid use, especially in males. Anabolic steroid use can have more subtle, longterm detrimental effects; damage may show up years later as a HEART ATTACK, high blood pressure, CANCER, and LIVER damage in both men and women.

Amylose

A water-soluble form of STARCH found in seeds, tubers, and root vegetables. It is made up of long chains of GLUCOSE units, and often contains a thousand or more glucose units. Amylose differs from the other prevalent form of starch, AMYLOPECTIN, which is highly branched. Amylose forms large spiral configurations when dissolved in water and can react with iodide to form a characteristic blue-purple pigment. Amylopectin and amylose occur together in starch, and the relative amounts vary depending on the plant sources. During digestion, AMYLASE breaks down amylose to maltose, a disaccharide composed of two glucose units. An intestinal enzyme, MALTASE, then hydrolyzes maltose to the simple sugar glucose, the ultimate product of starch digestion.

Amylopectin

The water-insoluble form of STARCH. Plants synthesize this very long chain of GLUCOSE units as a storage form of energy, often to nurture the future embryo, seedling or sprout. It is often the major form of starch and it possesses a highly branched, bushy structure resembling liver GLYCOGEN (animal starch). In contrast, AMYLOSE is made up of single straight chains of glucose units.
Amylopectin forms a paste in hot water. Starch occurs in seeds, tubers, and root vegetables as both amylopectin and amylose, although the ratio of two forms varies with the source. Cooking softens starch granules, making them available to DIGESTION by AMYLASE. The ultimate product of amylopectin digestion is GLUCOSE. Commercial processing converts starch to glucose, then to HIGHFRUCTOSE CORN SYRUP, a major sweetener

Ammonia (NH3) and Human Health

The nitrogen waste produced primarily from AMINO ACID metabolism. Ammonia is highly toxic to the nervous system and the brain. It may interfere with metabolic processes required for energy production in the brain. Normally the brain transforms ammonia into GLUTAMINE, a safe, neutral amino acid released into the bloodstream. Next, glutamine is absorbed by the intestine, which releases the ammonia for disposal by the LIVER. Normally the liver very efficiently metabolizes ammonia to UREA, the ultimate nontoxic waste product, via the UREA CYCLE to keep the level of ammonia in the blood at very low levels. Urea is excreted safely in urine. Ammonia is also produced in the intestinal tract by bacteria. Ammonia is absorbed by the intestine and transported directly via the portal vein to the liver for disposal. Liver disease, such as CIRRHOSIS, reduces urea production and leads to elevated blood levels of ammonia (ammonemia), which causes neurological abnormalities. Genetic defects in the ammoniadisposal mechanism of the urea cycle generally lead to brain damage.

What is amino sugars

A family of nitrogen-containing sugars. Cells attach NITROGEN to the simple sugars GLUCOSE and GALACTOSE to produce GLUCOSAMINE and galactosamine, respectively. These and similar amino sugars are used to produce carbohydratecontaining proteins (GLYCOPROTEINS) that coat cell surfaces, and for structural materials (MUCOPOLYSACCHARIDES) that help form the matrix of cartilage for ligaments and joints.

Understanding Amino Acids

Small organic acids that serve as raw materials of PROTEINS. The 50,000 to 100,000 different proteins in the body are combinations of just 20 different types of amino acids. During protein synthesis, amino acids are linked together like beads on a string to form long chains (polypeptides). Each type of protein possesses a unique amino acid sequence, specified by the cell’s genes.
As the name implies, each amino acid possesses an amino group and a carboxylic acid functional group, and therefore amino acids behave as both ACIDS and BASES. They also possess side chains with different properties. For example, certain amino acids, like ASPARTIC ACID and GLUTAMIC ACID, are acidic; others like ARGININE and LYSINE are basic;
METHIONINE and CYSTEINE contain SULFUR. Another group repels water and has the branched chains:
VALINE, LEUCINE, and ISOLEUCINE. Just as hands and feet are mirror images of each other, amino acids occur as mirror-image forms (optical isomers). The left-hand forms are desigamino nated as “L,” and the right-handed opposites are designated as “D.” Only L-amino acids are supplied by food and synthesized in the body, and only the “L” forms occur in proteins. Therefore, unless indicated otherwise, an amino acid can be assumed to be the “L-” form when mentioned in nutrition literature. The only common amino acid that does not exist as optical isomers is glycine, the simplest of amino acids.
DIGESTION of food proteins releases amino acids, which are absorbed in the INTESTINE. Depending on the person’s body size and the type of protein that is consumed, 55 g to 65 g of protein a day supplies adequate amino acids for an adult. Few Americans are likely to be protein-deficient, because the typical U.S. diet generally supplies twice as much protein as needed. With a varied diet, neither a meat eater nor a knowledgeable VEGETARIAN needs extra protein to obtain adequate amino acids.
MEAT, FISH, POULTRY, and DAIRY products like EGGS are the best sources of essential amino acids. Proteins that provide ample amounts of essential amino acids are said to be COMPLETE PROTEINS. Several plant proteins approach the quality of animal protein: soy, AMARANTH and QUINOA are examples. However, most plant proteins are deficient in at least one essential amino acid. For example, LEGUMES are low in methionine; CORN is low in lysine. These foods can be balanced during the day by eating “complementary” protein foods that provide ample amounts of those amino acids deficient in another food. Surplus dietary amino acids may be used for energy, and amino acids from the breakdown of cellular protein can be important fuel sources when food intake is inadequate. After 12 to 24 hours without food, MUSCLE protein breaks down rapidly, releasing amino acids into the bloodstream and processing them in the LIVER. The liver removes NITROGEN and converts it to UREA, while converting the amino acids to GLUCOSE and releasing it into the bloodstream to maintain blood sugar levels. In this way, most amino acids can contribute to blood glucose; consequently, muscle protein can help fuel the brain during STARVATION when the glucose supply becomes critical.
Ten amino acids are designated as dietary “nonessential” amino acids because they are synthesized by the body and do not need to be supplied in food. On the other hand, the diet must provide the other eight amino acids to prevent malnutrition. These dietary “essential” amino acids are lysine, valine, PHENYLALANINE, TRYPTOPHAN, isoleucine, leucine, METHIONINE, and THREONINE. Two other amino acids may be conditionally essential. HISTIDINE may not be formed in adequate amounts by infants and growing children, and arginine may be inadequately synthesized by adults with liver disease and by BREAST-FEEDING mothers.
Amino acids like phenylalanine and arginine, thought to stimulate GROWTH HORMONE release and thus promote FAT loss, are neither safe nor effective methods for weight control. Large amounts (several grams per day) of single amino acids used as supplements or additives, can drastically affect the body and damage the KIDNEYS. The therapeutic use of amino acids is still in experimental stages. The U.S. FDA removed amino acids from the GENERALLY RECOGNIZED AS SAFE list of FOOD ADDITIVES, and it is prudent to consult a health care provider before supplementing with individual amino acids.

Understanding amino acid metabolism

Chemical processes by which amino acids are either synthesized or are broken down and are used for energy in the body.
Amino acid synthesis is important because approximately half of the different amino acids used as PROTEIN building blocks can be made from CARBOHYDRATES.
Amino acids such as ALANINE, GLUTAMIC ACID, and GLUTAMINE made by the brain and MUSCLE help transport NITROGEN waste products via the bloodstream to the LIVER for disposal. When amino acids are degraded, the first step (transamination) releases nitrogen with the help of VITAMIN B6. The final nitrogen-containing waste product is UREA. The second step of amino acid degradation requires the oxidation of the carbon atoms of amino acids to produce ATP, the energy currency of cells. The waste product is CARBON DIOXIDE. An alternative route permits the liver to convert most amino acids to blood sugar (GLUCOSE) when the diet does not provide adequate carbohydrates that can be digested to glucose to fuel the brain. This process is called GLUCONEOGENESIS. HEME (the pigment of red blood cells), neurotransmitters (brain chemicals that carry nerve impulses), purines (building blocks of RNA and DNA), and HORMONES represent important amino acid derivatives.

What is Amine?

A very large family of basic organic compounds that contain nitrogen. Amines become positively charged ions (cations) in the blood.
Physiologically important amines include the hormones EPINEPHRINE (adrenaline) and norepinephrine, and neurotransmitters such as ACETYLCHOLINE and SEROTONIN, chemicals released by activated nerve cells. CHOLINE serves as a raw material for both acetylcholine and LECITHIN, a common LIPID of cell membranes. All AMINO ACIDS used to build PROTEINS have properties of amines. Tyramine found in fermented foods is an amine that can cause headache and food sensitivities. A variety of amines in food can react with the food additive nitrite to produce cancer-causing substances (nitrosoamines).

Nutritional Value of Amaranth (Amaranthus cruentus; grain amaranth)

A nutritious alternative to WHEAT. The tiny spherical seeds are the size of poppy seeds. Originally grown in Mexico as a staple food of the Aztecs, it was eaten in rituals of Native Americans until the Spanish conquest of Mexico, when its cultivation was outlawed.
Amaranth is now cultivated in the United States, and its excellent nutritional qualities account for its present popularity. Amaranth possesses a higher PROTEIN content than most CEREAL GRAINS; the nutritional value of amaranth protein approaches that of MILK. Its protein contains a high percentage of the essential AMINO ACID lysine, which is low in other grain proteins like wheat. Amaranth does not contain typical wheat ALLERGENS, nor does it contain GLUTEN; therefore, people allergic to wheat can often eat amaranth because it belongs to an unrelated plant family. Amaranth is available in health food stores as a whole grain, a FLOUR, and as CRACKERS and breakfast cereals. Amaranth flour has a nutty flavor and can be used to supplement wheat flour. Popped amaranth seed is mixed with honey to make a Mexican confection known as alegria. Amaranth species have also been cultivated in Asia as a source of greens (een choi in China, hiyu in Japan, and CHAULAI in India). One hundred grams of amaranth provides protein, 15 g; carbohydrate, 66 g; fiber, 4.5 g; fat, 5.7 g; and fat, 4.5 g.

Toxicity of Amanita

A genus of MUSHROOM that includes many poisonous species, along with a few edible ones. Amanita species can be confused with edible mushrooms. The most common cause of mushroom poisoning is the ingestion of A. phalloides (death cap) and A. virosa (destroying angel). These species produce specific toxins called amatoxins and phallotoxins, compounds with cyclic AMINO ACID structures. A single mushroom may contain enough of these poisons to kill an adult. Eating the mushroom can cause LIVER, HEART, and KIDNEY damage, as well as symptoms of common shock and delirium.

Alzheimer’s disease and Nutrition

A progressive, degenerative disease of the brain and the leading cause of SENILITY in the United States. About 4 million Americans have Alzheimer’s disease, roughly 10 percent of the U.S. population over the age of 65 and nearly half of the population over 85. The disease can also strike younger adults (a small percentage of people in their 30s and 40s have Alzheimer’s). On average, a person lives between eight and 20 years after the onset of symptoms, which include short-term memory loss, difficulty performing simple tasks, and disorientation to time and place. Alzheimer’s disease results from the death of nerve cells in the forebrain and the hippocampus responsible for memory and learning. Patients also have a deficiency of ACETYLCHOLINE, a NEUROTRANSMITTER made by neurons that helps carry nerve impulses between cells. Currently, diagnosis of Alzheimer’s disease is very difficult, yet a comprehensive diagnosis is critical in treating the senile patient. Symptoms occurring before the age of 65 are designated early-onset Alzheimer’s; after 65, it is called late-onset Alzheimer’s.
Despite intensive research over the last decade, it is not known whether Alzheimer’s disease is a function of AGING, or whether it is the result of a specific disease process. Alzheimer’s seems to be a multifaceted disease, with environmental and genetic factors contributing. There is an association with Down’s syndrome and thyroid disease. Smoking a pack of cigarettes a day increases the odds of developing Alzheimer’s disease. Diet also plays a part. A healthy diet with low fat intake may reduce the risk of developing Alzheimer’s disease; studies also suggest that a high-fat diet during early and mid-adulthood may be associated with an increased risk of developing Alzheimer’s, especially in people with a genetic marker called apoE-4. In a retrospective study that examined food eaten by 304 men and women (72 with Alzheimer’s disease and 232 healthy individuals), researchers found that people with the apoE-4 gene who also ate the most fat were seven times more likely to develop Alzheimer’s than were people with the marker who ate lower-fat diets. In a separate 2000 study of Americans between the ages of 40 and 50, those who carried the apoE-4 gene and whose diet consisted of 40 percent fat calories had 29 times the risk for Alzheimer’s compared to non-apoE-4 carriers on the same high-fat diet.
Some population studies have reported an association between low-fat diets and a lower incidence in Alzheimer’s. For example, in China and Nigeria, where fat intake is low, the risk of developing Alzheimer’s is 1 percent at age 65 compared to 5 percent in the United States. In the Netherlands researchers reported an association between dementia and diets high in total fat, saturated fat, and cholesterol.
Scientists have identified four genes that increase the risk of developing Alzheimer’s. APOE-4 is implicated in late-onset cases. This gene can be passed down from one or both parents. Patients who have one copy of the gene have a three times greater risk of developing the disease than do patients who do not. Patients who inherit two copies have an eight times greater risk of developing Alzheimer’s. The other three genes—presenilin 1, presenilin 2, and amyloid precursor protein—are associated with early-onset cases. Nearly everyone who carries one or more of these genes will develop early-onset Alzheimer’s.
Another hypothesis for Alzheimer’s links
chronic CALCIUM deficiency to increased uptake of ALUMINUM and silicon by the brain. Aluminum concentrates in the brains of patients with the disease; whether this is a cause or an effect is unknown. In postmenopausal women, estrogen (hormone) replacement therapy may help prevent Alzheimer’s. The importance of estrogen in brain health is gradually being recognized. Alternatively, there may be alterations in nerve cell membranes. Other evidence links immune system activation with the disease process.
Research points to the following possible causes of senility: exposure to toxins, oxidative damage due to FREE RADICALS, abnormal protein metabolism, slow viruses, the narrowing by cholesterol deposits of arteries feeding the brain, ZINC and VITAMIN B12 deficiencies, head trauma, and adverse drug reactions that decrease blood and oxygen supply to the brain.
Clinical trials of an experimental vaccine for the disease, called AN-1792, were halted abruptly in early 2002 when several participants developed brain inflammation after taking it. The drug was a form of beta-amyloid, a protein fragment found in the amyloid plaques that grow over the brain tissue of Alzheimer’s patients. Researchers had hoped exposure to the protein would trigger participants’ IMMUNE SYSTEMs to produce antibodies to the amyloid plaques.
Experiments in mice have shown that FOLIC ACID—a vitamin found in high amounts in dark green, leafy VEGETABLES, CITRUS FRUITS and JUICES, whole wheat BREAD, and dry BEANS—may help ward off Alzheimer’s disease. Since 1998 the U.S.
FDA has required the addition of folic acid to enriched breads, CEREALS, FLOURS, CORNMEAL, PASTA, RICE, and other GRAIN products.
There is limited evidence that antioxidants may help fight or prevent some of the brain cell damage in Alzheimer’s disease that may be attributed to free radicals, thus slowing the progression of the disease. In particular, some evidence suggests that vitamin C or vitamin E supplements can slow the course of Alzheimer’s over several years. In a National Institute on Aging study, the antioxidant vitamin E delayed by six months the progression of some symptoms of Alzheimer’s disease. In another National Institute on Aging study, people in the middle to late stages of Alzheimer’s who took vitamin E at levels 70 times higher than the recommended daily dose noticed some beneficial effects. At a dose of 2,000 IU daily, vitamin E was able to slow the expected rate of decline compared to patients who did not take the vitamin. Other studies suggest that taking antioxidants (vitamins C and E) might significantly lower the risk of developing Alzheimer’s. In one preliminary Massachusetts study, none of the 50 subjects who used either vitamin C or E developed Alzheimer’s at follow-up studies. In a Dutch study of 5,000 people, a diet high in antioxidants reduced the risk of developing Alzheimer’s.
Other antioxidants, such as GINKGO biloba and PHOSPHATIDYLSERINE, melatonin, flavonoids (chemicals found in many plants, including fruits and vegetables), and carotenoids (pigments found in plants such as carrots) also may help ease symptoms of Alzheimer’s disease. Small studies of ginkgo did find slight improvement among patients with Alzheimer’s who took the herb. Although German physicians have approval to use ginkgo to treat Alzheimer’s, and it has been used for thousands of years in Chinese medicine, North American physicians disagree as to its benefits as a memory treatment.
According to several studies, eating plenty of dark-colored fruits and vegetables may slow brain aging. Extracts of blueberries and strawberries reversed age-related decline in lab animal brain function. Blueberries may be the best anti-Alzheimer’s antioxidant of all. When Tufts University researchers analyzed more than 40 fruits and vegetables, they found that raw blueberries contained the highest level of antioxidants (nearly 60 times the recommended daily levels)—more than blackberries, beets, spinach, and garlic. Animals fed an antioxidant-rich blueberry extract diet showed fewer age-related motor changes and outperformed their study counterparts on memory tests. Some studies on wine have reported a lower risk, but they have not been consistent. It might be that wine may increase even more risk of developing Alzheimer’s for people who carry the apoE-4 gene that has been linked to Alzheimer’s—while protecting people who do not carry the gene. However, supplements containing high doses of antioxidants can cause adverse effects. In addition, high doses of vitamin E are potentially harmful if combined with blood-thinning drugs. No one should take these or any supplements without consulting a doctor.
It is safer to consume antioxidants as part of a healthy diet; antioxidants are found in most dark colored fruits and vegetables, whole grains, legumes, nuts, and wheat germ.
Nutritional approaches to treatment employ CHOLINE and LECITHIN (phosphatidylcholine) supplements. The rationale for their use is based on the fact that the brains of diseased patients do not make enough acetylcholine, and supplying this building block could boost acetylcholine production. Results of clinical studies have not shown consistent improvements. Researchers have used drugs that help maintain acetylcholine levels with mixed results. A growth promoter called nerve growth factor may enhance brain function in aged experimental animals. Preliminary research suggests that GINKGO biloba, a leaf extract, is known to have antioxidant and anti-inflammatory properties and to enhance NEUROTRANSMITTER function, alleviates the symptoms of Alzheimer’s disease. Scientists are currently studying whether a lowfat, high-fiber diet may reduce the risk of developing Alzheimer’s disease just as it lowers the risk of other diseases associated with aging, like cardiovascular disease and cancer. Finnish researchers who studied 1,500 patients for 21 years found that subjects with high CHOLESTEROL and high blood pressure had a corresponding higher risk of developing Alzheimer’s. French researchers noted a link between high blood pressure and Alzheimer’s risk.