Cancer

Image source: author unknown

General Description

Cancer can be defined as uncontrolled cell division. When cells in some areas of the body duplicate without control, the excess tissue that develops is called a tumor or neoplasm.
Tumors may be malignant and may spread (metastasize) to other parts of the body, or benign. Benign tumors are generally not harmful because they do not spread to other parts of the body. However, benign tumors may sometimes be removed to prevent disfigurement or interference with normal body function. (1)


Causes

Several factors may contribute to the loss of control of cell division. Agents which can can contribute to uncontrolled cell division are called carcinogens.

Chemical and other environmental factors (including lifestyle choices such as diet and smoking) are associated with an estimated 60 - 90% of all human cancers. Viruses may also initiate the cancer process. Ultimately, these mechanisms either directly or indirectly influence the cellular genetic program which control cell division.(1)

Much cancer research today is directed at understanding the genetic and biochemical mechanisms which cause the suppression of the normal cellular division process. Normally, if a cell becomes damaged by a carcinogen, there are mechanisms to eliminate these defective cells. However, when a cell becomes cancerous, many of these inherent mechanisms are also affected.(2)

At Risk

Both "lifestyle" and environmental factors play a major role in the risk for developing cancer. Lifestyle factors include diet, smoking, alcohol consumption and exposure to the sun. Environmental factors include air and water pollution.

The hydrocarbons in cigarette smoke are carcinogenic and it is not surprise that 90% of all lung cancer patients are or were heavy smokers.

Additionally, certain genetic predispositions may exist for certain cancers, but it is unclear how much is due to genetic susceptibitly and how much is due to similar lifestyles in related individuals. (1,2)

Prevention and Management

The best way to reduce the risk of cancer is to reduce or eliminate exposure to potential carcinogens. It is estimated that 80% of all cancers can be prevented by lifestyle changes such as diet, quitting smoking and reducing exposure to the sun.(1)

Diet may be a major factor in 30 to 40 percent of all cancers in men and for 60 percent of all cancers in women. Colon and breast cancer have a strong link to diet.(3,4)

Some of the foods we eat can contain cancer promoters. These include fat, alcohol and salt-cured and smoked foods.(2)

Many foods also contain compounds which help protect against cancer. There is a well established correlation between fruit and vegetable consumption and cancer risk. In particular, fruits and vegetables are sources of fiber, beta carotene, vitamin C, and other compounds associated with lower risk for cancer. However, individuals rarely consume enough of these to ward off potential carcinogens.(2,5)

Many plant-derived compounds (referred to as phytochemicals) show promise in both prevention and inhibition of the cancer process. Many of these phytochemicals operate as antioxidants and reduce the damage caused by free radicals. It is theorized that free radical damage to a cells genetic machinery may be one of the mechanisms of cancer promotion.(3,6,7)

These phytochemicals include allyl sulfides (onions, garlic, leeks, chives), indoles and isothiocyanates (cruciferous vegetables), isoflavones (soybeans), phenolic acids (tomatoes, citrus fruits, carrots), polyphenols (green tea, grapes, wine), saponins (beans and legumes) and terpenes (cherries, citrus fruit peels).

Eating a variety of vegetables and fruits is more important than concentrating on particular kinds to get the full gamut of phytochemicals found in nature. The following guidelines are recommended by the American Institute of Cancer Research (AICR):
1) eat more grains,
2) eat a variety of vegetables,
3) eat more fruit,
4) season with herbs and spices instead of salt,
5) decrease portions sizes of meat fish and poultry,
6) explore new foods and new recipes.

Additional Information
Disclaimer: These websites, addresses and/or phone numbers are provided for information purposes only. USANA, Inc. makes no claim, actual or implied, regarding the content or validity of the information obtained from these outside sources.

American Institute of Cancer Research. 1759 R Street N.W., Washington, DC 20069, 1-800-843-8114

Abstracts
Ames BN, Gold LS, Willett WC. The causes and prevention of cancer. Proc Natl Acad Sci U S A 1995 Jun 6;92(12):5258-65. Epidemiological evidence indicates that avoidance of smoking, increased consumption of fruits and vegetables, and control of infections will have a major effect on reducing rates of cancer. Other factors include avoidance of intense sun exposure, increases in physical activity, and reduction of alcohol consumption and possibly red meat. A substantial reduction in breast cancer is likely to require modification of sex hormone levels, and development of practical methods for doing so is a high research priority. Resolution of the potential protective roles of specific antioxidants and other constituents of fruits and vegetables deserves major attention. Mechanistic studies of carcinogenesis indicate an important role of endogenous oxidative damage to DNA that is balanced by elaborate defense and repair processes. Also key is the rate of cell division, which is influenced by hormones, growth, cytotoxicity, and inflammation, as this determines the probability of converting DNA lesions to mutations. These mechanisms may underlie many epidemiologic observations.

References
1 Ruddon, RW. Cancer Biology. Oxford University Press. 1995.
2 World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition and the Prevention of Cancer: a global perspective. Banta Book Group, Menasha, WI. 1997.
3 Bidlack WR, Interrelationships of food, nutrition, diet and health: the National Association of State Universities and Land Grant Colleges White Paper. J Am Coll Nutr 1996 Oct;15(5):422-33
4 Bland JS. Phytonutrition, phytotherapy, and phytopharmacology. Altern Ther Health Med 1996 Nov;2(6):73-6
5 Fraser D. Nutrition and cancer: epidemiological aspects. Public Health Rev 1996;24(2):113-21
6 Halliwell B. Oxidative stress, nutrition and health. Experimental strategies for optimization of nutritional antioxidant intake in humans. Free Radic Res 1996 Jul;25(1):57-74
7 Cassileth BR and Chapman CC. Alternative cancer medicine: a ten-year update. Cancer Invest 1996;14(4):396-404

Source

Bipolar disorder/manic depression

Description
Bipolar disorder, also known as manic-depression, is a mood disorder in which the person experiences severe pathologic swings from hyperactivity and euphoria to sadness and depression.

Types
This disease may be dominated by manic or depressive episodes, or moods may be mixed.2

At Risk
According to the American Psychiatric Association, approximately 0.4% to 1.6% of adults have bipolar disorder. This disorder is equally common in women and men, more common in higher socioeconomic groups, and associated with high levels of creativity. Thirty years is the average age for the onset of bipolar disorder.3

Prevention and Management
General:
Mania is treated with lithium. About 14 days are required before improvement is noted. When manic symptoms are severe, lithium is usually administered in combination with an antipsychotic such as haloperidol, until the acute symptoms abate, allowing tapering and discontinuation of the antipsychotic. Lithium is slightly more effective in preventing manic than depressive episodes. The depressive phase is treated the same as for any major depressive disorder. 4

Nutritional Influences:
Folic acid, vitamin B12 or vitamin C may be deficient, and supplementation may be beneficial.5
Supplementation with omega-3 fatty acids may benefit some patients.6

Additional Information
Disclaimer: These websites, addresses and/or phone numbers are provided for information purposes only. USANA, Inc. makes no claim, actual or implied, regarding the content or validity of the information obtained from these outside sources.
http://www.psych.org/
http://www.mentalhealth.com/

Abstracts
Fava M, Borus JS, Alpert JE, Nierenberg AA, Rosenbaum JF, Bottiglieri T. Folate, vitamin B12, and homocysteine in major depressive disorder. Am J Psychiatry 1997 Mar;154(3):426-8.
OBJECTIVE: The authors examined the relationships between levels of three metabolites (folate, vitamin B12, and homocysteine) and both depressive subtype and response to fluoxetine treatment in depressed patients.
METHOD: Fluoxetine, 20 mg/day for 8 weeks, was given to 213 outpatients with major depressive disorder. At baseline, depressive subtypes were assessed, and a blood sample was collected from each patient. Serum metabolite levels were assayed. Response to treatment was determined by percentage change in score on the 17-item Hamilton Depression Rating Scale. RESULTS: Subjects with low folate levels were more likely to have melancholic depression and were significantly less likely to respond to fluoxetine. Homocysteine and B12 levels were not associated with depressive subtype or treatment response.
CONCLUSIONS: Overall, the results are consistent with findings linking low folate levels to poorer response to antidepressant treatment. Folate levels might be considered in the evaluation of depressed patients who do not respond to antidepressant treatment.

References
1 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52-66.
2 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52.
3 Werbach M. Nutritional Influences on Mental Illness. Tarzana (CA):Third Line Press. p 52-53. 4 Cecil Textbook of Medicine. 20th ed. Philadelphia:WB Saunders Company; 1996. p 2002.
5 Rudin DO. The major psychoses and neuroses as omega-3 essential fatty acid deficiency syndrome: Substrate pellagra. Biol Psychiatry 1981;16(9):837-50.

Source

Nutritional health: ADD/ADHD

Image: Time Magazine, July 18, 1994: Attention Deficit Disorder

Description

* Attention Deficit Disorder and Attention Deficit/Hyperactivity Disorder are not well understood and have been difficult to define. The American Psychiatric Association describes ADD/ADHD as "a disease of infancy and childhood characterized by developmentally inappropriate inattention, impulsiveness, and hyperactivity." Affected children typically have problems in school because of their inability to persist with tasks or to organize their work. They do not appear to listen or to hear what is said, and are unable to sit still. The activity is haphazard and not goal-directed. Some children display the inattention component without hyperactivity.
* These disorders are far more common in boys than in girls, and half of all cases occur before age four.1
* Symptoms are grouped into inattention and hyperactivity-impulsivity categories. Diagnosis of attention-deficit hyperactivity disorder is based on the person demonstrating at least six symptoms from one or both of these categories. 2

Causes

* Although the causes are not clear, dopamine, a brain neurotransmitter, is thought to play a role in attention deficit hyperactivity disorder. People with ADHD may have malfunctioning D4 dopamine receptors. 3

Types

* A patient with symptoms mainly from the inattention category is classified as predominantly inattentive type.
* A patient with mainly hyperactivity-impulsivity symptoms is diagnosed as a predominantly hyperactive-impulsive type.
* Someone with at least six symptoms from both groups has combined-type attention-deficit hyperactivity disorder. This is the most common type. 4

At Risk

* It is thought that children are born with this disorder. It affects boys more than girls.5
* Complications during pregnancy, delivery and infancy are positively correlated with incidence of ADD/ADHD.6
* There may be a genetic element to this disorder. Diagnosing and treating family members may be helpful. 7,8

Prevention and Management

General:

* Because pregnancy, delivery and infancy complications may lead to higher incidence of ADD and ADHD, good prenatal care, including healthy behavior by the mother, is important. 9

Nutritional Influences:

* Contrary to popular belief, sugar does not seem to increase hyperactivity in children. 10
* Some researchers believe that essential fatty acid deficiency may play a role in ADD/ADHD in some children. 11

Additional Information
Disclaimer: These websites, addresses and/or phone numbers are provided for information purposes only. USANA, Inc. makes no claim, actual or implied, regarding the content or validity of the information obtained from these outside sources.

* http://members.aol.com/addcenter/page1.htm
* http://www.cpgs.com/add/

Abstracts

Stevens LJ, Zentall SS, Deck JL, Abate ML, Watkins BA, Lipp SR, Burgess JR. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. Am J Clin Nutr 1995 Oct;62(4):761-768. Attention-deficit hyperactivity disorder (ADHD) is the term used to describe children who are inattentive, impulsive, and hyperactive. The cause is unknown and is thought to be multifactorial. Based on the work of others, we hypothesized that some children with ADHD have altered fatty acid metabolism. The present study found that 53 subjects with ADHD had significantly lower concentrations of key fatty acids in the plasma polar lipids (20:4n-6, 20:5n-3, and 22:6n-3) and in red blood cell total lipids (20:4n-6 and 22:4n-6) than did the 43 control subjects. Also, a subgroup of 21 subjects with ADHD exhibiting many symptoms of essential fatty acid (EFA) deficiency had significantly lower plasma concentrations of 20:4n-6 and 22:6n-3 than did 32 subjects with ADHD with few EFA-deficiency symptoms. The data are discussed with respect to cause, but the precise reason for lower fatty acid concentrations in some children with ADHD isnot clear.

LaHoste GJ, Swanson JM, Wigal SB, Glabe C, Wigal T, King N, Kennedy JL. Dopamine D4 receptor gene polymorphism is associated with attention deficit hyperactivity disorder. Mol Psychiatry 1996 May;1(2):121-4. Dopamine is believed to play a major role in the manifestation of attention deficit hyperactivity disorder (ADHD), which affects 3-6% of school-age children and shows evidence of familiarity. The dopamine D4 receptor, which is preferentially distributed in cortical and limbic regions of the brain, is currently of major interest because of the high degree of functionally relevant variability in its gene (DRD4), and the association of this gene with Novelty Seeking behavior. We examined the variability in the length of a region of DRD4 that contains a 48-bp repeat sequence in children with ADHD and controls matched for ethnicity. ADHD children differed from controls in that the 7-fold repeat form of DRD4 occurred significantly more frequently than in the control sample. This form of the receptor has previously been shown to mediate a blunted intracellular response to dopamine. Although ADHD is likely to be multifactorial in its etiology and its heritability is likely to be polygenetic, the present findings suggest that polymorphic variation in the gene encoding the D4 dopamine receptor may be a contributing factor in the expression of symptoms associated with ADHD.

References

1 Stevens LJ, Zentall SS, Deck JL, Abate ML, Watkins BA, Lipp SR, Burgess JR. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. Am J Clin Nutr 1995 Oct;62(4):761-768.
2 Diseases. Springhouse (PA):Springhouse Corporation; 1993 p 50.
3 LaHoste G. Dopamine DR receptor gene polymorphism is associated with attention deficit hyperactivity disorder. Mol Psychiatry 1996 May;1(2):83-4.
4 Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation; 1993. p 898.
5 Milberger S. Pregnancy, delivery and infancy complications and attention deficit hyperactivity disorder: issues of gene-environment interaction. Biol Psychiatry 1997 Jan 1;41(1):65-75.
6 Hechtman L. Families of Children with attention deficit hyperactivity disorder: a review. Can J Psychiatry 1996 Aug;41(6):350-60
7 Comings D. Genetic aspects of childhood behavioral disorders. Child Psychiatry Hum Dev 1997 Spring;27(3):139-50.
8 Milberger S. Pregnancy, delivery and infancy complications and attention deficit hyperactivity disorder: issues of gene-environment interaction. Biol Psychiatry 1997 Jan 1;41(1):65-75.
9 Kanarek R. Does sucrose or aspartame cause hyperactivity in children? Nutr Rev 1994 May;52(5):173-5.

Source

Nutritional health: asthma

Description

Asthma is a chronic disorder characterized by recurring attacks of airway obstruction. The breathing difficulty that results can range from mild wheezing to respiratory failure. The airway obstruction results from bronchospasms, increased secretion of mucous, and swelling of bronchial mucosa.

Causes

Asthma may result from sensitivity to specific external allergens or from other, nonallergenic factors. Asthma that is related to allergies is considered extrinsic, while asthma that does not seem to be related to allergies is called intrinsic asthma. Allergens that cause extrinsic asthma include pollen, animal dander, house dust or mould, kapok or feather pillows, food additives containing sulfites, and any other sensitizing substance.

Types

There are various types of asthma which are differentiated by cause (such as allergy or exercise) and the degree of severity.

At Risk

About half of all patients with asthma are under age 10.

About one-third of all patients with asthma share the disease with at least one immediate family member.

Prevention and Management

General:

The best prevention of asthma attacks is to identify and avoid the precipitating factors. People who have extrinsic (allergy-induced) asthma are advised to minimize their exposure to specific allergens.

Nutritional Influences:

There are a number of studies that indicate that determination of food sensitivities (even if none had been suspected), and avoiding the foods which test positive either reduced or eliminated symptoms in some people.,,, Of course, not all asthma is related to food sensitivities.

Diets rich in antioxidants may have a modulatory effect on bronchial reactivity.

Inclusion of oily fish in the diet may protect against asthma in childhood.

Vitamin B6 levels in the blood have been found to be lower in asthmatics than the non-asthmatics. Positive results have been reported when B6 supplements have been taken.

Vitamin B12 therapy has been used to successfully treat asthmatics, especially those who suffer attacks after eating foods containing sulfites.

Vitamin C levels in asthmatics are often lower than in non-asthmatics. Vitamin C may also be beneficial to those who experience asthma during exercise.

Magnesium levels are lower in one out of two asthmatics during an attack. People with asthma also have lower magnesium concentrations in their white blood cells between attacks. Treatments by inhalation or injection have proven beneficial in stopping asthmatic attacks and improving lung function. At this time, however, the effect of oral supplementation remains unexplored.

Selenium supplementation might be beneficial to patients with intrinsic asthma, which may be at risk of selenium deficiency.

Additional Information

Disclaimer: These websites, addresses and/or phone numbers are provided for information purposes only. USANA, Inc. makes no claim, actual or implied, regarding the content or validity of the information obtained from these outside sources.

http://207.201.168.245/

Abstracts

Soutar A, Seaton A, Brown K. Bronchial reactivity and dietary antioxidants. Thorax 1997 Feb;52(2):166-70.
It has been postulated that dietary antioxidants may influence the expression of allergic diseases and asthma. To test this hypothesis a case-control study was performed, nested in a cross sectional study of a random sample of adults, to investigate the relationship between allergic disease and dietary antioxidants.

METHODS: The study was performed in rural general practices in Grampian, Scotland. A validated dietary questionnaire was used to measure food intake of cases, defined, firstly, as people with seasonal allergic-type symptoms and, secondly, those with bronchial hyperreactivity confirmed by methacholine challenge, and of controls without allergic symptoms or bronchial reactivity.

RESULTS: Cases with seasonal symptoms did not differ from controls except with respect to the presence of atopy and an increased risk of symptoms associated with the lowest intake of zinc. The lowest intakes of vitamin C and manganese were associated with more than fivefold increased risks of bronchial reactivity. Decreasing intakes of magnesium were also significantly associated with an increased risk of hyperreactivity.

CONCLUSIONS: This study provides evidence that diet may have a modulatory effect on bronchial reactivity, and is consistent with the hypothesis that the observed reduction in antioxidant intake in the British diet over the last 25 years has been a factor in the increase in the prevalence of asthma over this period.

References
1 Pelikan Z et al. Bronchial asthma due to food allergy. Paper presented at the XII International congress of Allergy and Clinical Immunology, Washington, D.C., October 1985.
2 Lindahl O et al. Vegan diet regimen with reduced medication in the treatment of bronchial asthma. J Asthma 1985;22:45-55.
3 Hoj L et al. A double-blind controlled trial of elemental diet in severe, perennial asthma. Allergy 1981;36:257-62.
4 Woods R et al. Patients perceptions of food induced asthma. Aust N Z J Med 1996 Aug; 26(4):504-12.
5 Soutar A, Seaton A, Brown K. Bronchial reactivity and dietary antioxidants. Thorax 1997 Feb;52(2):166-70.
6 Hodge L et al. Consumption of oily fish and childhood risk. med J Aust 1996 Feb 5;164(3):137-40.
7 Delport R et al. Vitamin B6 nutritional status in asthma:the effect of theophyline therapy on plasma pyridoxal-51-phospaht and pyridoxal level. In J Vitam Nurt Res 1988;58(1):67-72, 1988
8 Simon RA et al. Sulfite-sensitive asthma. Res. Instit. of Scripps Clinic Scientific Report 1982-83;39:57-58.
9 Rozanov EM et al. [Vitamin PP and C allowances and their correction in the treatment of bronchial asthma patients.] Vopr Pittan 1987;(6):21-24.
10 Schachter EN, Schlesinge A. The attenuation of exercise-induced bronchospasm by ascorbic acid. Ann Allergy 1982;49:146-150.
11 Haury VG. Blood serum magnesium in bronchial asthma and its treatment by the administration of magnesium sulfate. J Lab Clin Med 1940;26:340-4.
12 Fantidis P, Ruiz Cacho J, Marin M, Madero Jarabo R, Solera J, Herrero E. Intracellular (polymorphonuclear) magnesium content in patients with brochial asthma between attacks. J R Soc Med 1995 Aug;88(8):441-5.
13 Rolla G et al. Magnesium attenuates methacholine-induced bronchoconstriction in asthmatic. Magnesium 1987;6(4):201-4.
14 Skobeloff EM et al. Intravenous magneium sulfate for the treatment of acute asthma in the emergency department. JAMA 1989;262(9):1210-13.
15 Werbach M. Healing Through Nutrition. New York: HarperCollins; 1993.
16 Kadrabova J et al. Selenium status is decreased n patients with intrinsic asthma. Biol Trace Elem Res 1996 Jun;52(3):241
17 Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation; 1993. p 621.
18 Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation; 1993. p 621.
19 Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation; 1993. p 621.
20 Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation; 1993. p 621.

Source

Nutritional health: anxiety

Anxiety is a feeling of apprehension, worry, uneasiness, or dread, especially of the future. A certain amount of anxiety is normal and stimulates the individual to purposeful action. Excess anxiety interferes with efficient functioning of the individual.

Diagnosed anxiety disorders are classified into five basic types: phobias, generalized anxiety disorders, panic disorders, obsessive-compulsive disorders, and posttraumatic stress disorder.

Causes

The causes of clinical anxiety range from drug withdrawal (some phobias) to alterations in the brain's biochemistry (panic disorders) to conflict (generalized anxiety disorder). Because of the complexity of the brain and a person's psychological make up, diagnoses and causes may overlap.

Types

The severity of a person's anxiety can range from mild to very severe. Anxiety is a problem when the severity is inappropriate or when it interferes with normal daily functions.

At Risk

Drug abusers including alcoholics are susceptible to anxiety attacks especially during withdrawals. People with a wide variety of psychological or medical disturbances are at risk.

Prevention and Management

General:

It is often important to address any psychological factors underlying anxiety.
Physicians often prescribe various medications to help control severe anxiety.

Nutritional Influences:

Anxiety may be associated with elevated blood lactate level and an increased lactate to pyruvate ratio. This ratio is increased by alcohol, caffeine, and sugar, and deficiencies in niacin, thiamine, or magnesium.
Avoiding or reducing consumption of alcohol6, caffeine7, and sugar 9 may reduce anxiety.
Vitamin B Complex: In an observational study, 7 of 12 agoraphobia (fear of open spaces) patients were deficient in the vitamin B complex.
Calcium: Several case reports suggest low calcium levels may be associated with an organic anxiety syndrome.
Inositol: Inositol may have a calming effect.
Magnesium: Deficiency is often associated with anxiety.

Additional Information

Disclaimer: These websites, addresses and/or phone numbers are provided for information purposes only. USANA, Inc. makes no claim, actual or implied, regarding the content or validity of the information obtained from these outside sources.

http://www.npadnews.com/

Abstracts

Rudin DO. The major psychoses and neuroses as omega-3 essential fatty acid deficiency syndrome: substrate pellagra. Biol Psychiatry 1981 Sep;16(9):837-50. Pellagra was once a major cause of three behaviorally different mental disorders-schizophreniform, manic-depressive-like, and phobic neurotic - plus drying dermatoses, autonomic neuropathies, tinnitus, and fatigue. In this preliminary study all three of the corresponding present-day mental diseases are found to exhibit, statistically, the same pellagraform physical disorders but to ameliorate not so much with vitamins as with supplements of a newly discovered trace omega-3 essential fatty acid (w3-EFA), which provides the substrate upon which niacin and other B vitamin holoenzymes act uniquely to form the prostaglandin 3 series tissue hormones regulating neurocircuits en block. Since present-day refining and food selection patterns, as well as pure corn diets, deplete both the B vitamins and W3-EFA, the existence of therapeutically cross-reacting homologous catalyst and substrate deficiency forms of pellagra are postulated, the first contributing to the B vitamin deficiency epidemics of 50-100 years ago, the second to the more recent endemic "Diseases of Western Civilization" which express in certain genetic subgroups as the major mental illnesses of today.

References

1 Tabers Cyclopedic Medical Dictionary. 16th ed. Philadelphia:FA Davis Company; 1985. p 120.
2 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52-66.
3 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52.
4 Roelofs SM. Hyperventilation, anxiety, craving for alcohol: a sub acute alcohol withdrawal syndrome. Alcohol 1985;2(3):501-5.
5 Buist RA. Anxiety neurosis: The lactate connection. Int Clin Nutr Rev 1985;5(1):1-4.
6 Abbey LC. Agoraphobia. J Orthomol Psychiatry 1982;11:243-259.
7 Werbach M. Nutritional Influences on Mental Illness. Tarzana (CA):Third Line Press. p 52-53.
8 Pfeiffer C. Mental and Elemental Nutrients. New Canaan (CT):Keats Publishing Company; 1975.
9 Seelig MS et al. Latent tetany and anxiety, marginal Mg deficit and normocacemia. Dis Nerv Syst 1975;36:461-65.

Source

Nutritional health: Alzheimer's

General Description
Alzheimers disease is a progressive neurodegenerative disorder which primarily affects brain structures involved in memory processes and motor skills. Alzheimers disease is the most common form of dementia, which generally refers to a progressive decline in mental function, memory and acquired intellectual skills.(1)

Pathologically, the brain is reduced in size (atrophy), especially in the frontal occcipital and temporal regions. Histologically, it is characterized by thickening, conglutination, and distortion of the intracellular neurofibrils (neurofibrillary tangles) and by plaques composed of granular or filamentous masses, found predominately in the nerve cells of the cerebral cortex, amygdala, and hippocampus. (1)

Major clinical criteria for the clinical diagnosis of probable Alzheimer's include:
1) deficits in two or more areas of cognition;
2) progressive worsening of memory;
3) absence of other medical or psychological disorders that could account for memory impairment; and
4) clear consciousness despite memory impairment.

Causes
The exact cause of Alzheimers is unknown. The etiology is complex and may involve several genes and possible environmental factors.(2)
Chronic exposure to aluminum has been suggested as a possible causative agent in Alzheimers. However, clinical evidence for this link is inconclusive.(3)
Oxidative stress may play a role in the pathogenesis of neuron degeneration and death in Alzheimers (4,5) An increase in free radical production has been demonstrated in Alzheimers disease brain tissue.
In particular, iron has been shown to be a significant component of senile plaques in Alzheimers disease (6) and may contribute to the disease process by initiating lipid peroxidation, leading to membrane damage and ultimately cell death.(7)

At Risk
Alzheimer's disease is obviously related to age, - that is, the older you get the more likely you are to develop Alzheimer's disease or dementia. For instance, the prevalence of dementia is roughly 3% for individuals aged 65 to 74, whereas it is 18.7% for individuals between the ages of 75 and 84 and nearly 50% for those over age 85. In addition, there is evidence to suggest that genetic factors may play a part in some forms of AD.
Clinical manifestations of mental deterioration, memory loss, confusion, and disorientation may begin in late mid-life (>45 years old). Death usually results in about 5 to 10 years after diagnosis.

Prevention and Management

Nutrition influences:
Nutritional support is important in the treatment of Alzheimers.(2)
In patients with moderately severe impairment from Alzheimer's disease, treatment with alpha-tocopherol (vitamin E) or selegiline slows the progression of disease.(8)
There is an association between Alzheimers and low serum cobalamin (vitamin B12) levels.(9)
Deficiency of choline, an important component of membrane phospholipids and the neurotransmitter acetylcholine, may play a role in the etiology of Alzheimers(10)

Source

Nutritional health: allergies

Description
Allergic disorders are characterized by potentially harmful reactions to extrinsic materials or allergens. They include allergic rhinitis (hay fever), atopic dermatitis, anaphylaxis, hives, and blood transfusion reactions.(1)

The immune response is the bodys defense mechanism which identifies and destroys harmful foreign organisms. Allergic reactions are an overreaction of the bodys defense mechanism. This overreaction can lead to swelling, itching and many other symptoms all with varying degrees of severity.

It is important to remember that the immune response is vital for protecting the body from foreign invaders and when working correctly its importance cannot be understated. Asthma and allergies are among the most common health problems, with as many as 50 million Americans afflicted with asthma, hay fever or other allergy-related conditions.

The preponderance of food allergies are caused by eggs, milk, wheat, fish, shellfish, nuts, peanuts, soybeans and rice.

One of the most severe allergic reactions is anaphylaxis, which is "marked by the sudden onset of rapidly progressive urticaria (a vascular reaction of the skin) and respiratory distress." (2)

Causes
The reasons that the body overreacts to a particular antigen are not well understood. It is known that it takes time and repeated exposure to an antigen for an allergic response to take place. There is also evidence that susceptibility to allergies have a hereditary component.

At Risk
There is a genetic predisposition for atopic allergies, but not for any particular allergy itself. (3)

Prevention and Management
General: Avoid the materials or organisms that initiate the allergic reaction. This may mean avoiding certain foods or environments.

Nutritional Influences:

Avoid foods that contain ingredients which cause allergic reactions.

Vitamin A deficiencies may increase inflammatory responses.(4)

Nicotinamide has been shown to enhance the effectiveness of glucocorticoids in the treatment of allergic reactions. (5)

Pantothenic Acid: In one clinical trial the majority of more than 100 patients with allergic rhinitis who took pantothenic acid had almost instant relief. (6)

Vitamin C: May have a protective effect on airway hyperactivity in some patients with exercise induced asthma.(7)

Vitamin E: In elderly patients vitamin E supplementation reduced hypersensitivity reactions to various antigens and vaccines.(8)

Selenium: Selenium supplementation may be beneficial to patients with intrinsic asthma. (9)

Zinc, Selenium and Copper: Levels may be low in children with allergic colitis. (10)

Iron: High body iron stores may increase free radical production and may also elevate asthma risk.(11)

Proanthocyanidins: May reduce adverse allergic and inflammatory responses.(12)

Additional Information Disclaimer: These websites, addresses and/or phone numbers are provided for information purposes only. USANA, Inc. makes no claim, actual or implied, regarding the content or validity of the information obtained from these outside sources.

http://acaai.org/allergist/Pages/default.aspx

http://allergy.hno.akh-wien.ac.at/allergy/

http://www.foodallergy.org/

Abstracts
Meydani SN, Meydani M, Blumberg JB, Leka LS, Siber G, Loszewski R, Thompson C, Pedrosa MC, Diamond RD, Stollar BD. Vitamin E supplementation and in vivo immune response in healthy elderly subjects. A randomized controlled trial. JAMA 1997 May 7;277(17):1380-6.OBJECTIVE: To determine whether long-term supplementation with vitamin E enhances in vivo, clinically relevant measures of cell-mediated immunity in healthy elderly subjects. DESIGN: Randomized, double-blind, placebo-controlled intervention study. SETTING AND PARTICIPANTS: A total of 88 free-living, healthy subjects at least 65 years of age. INTERVENTION: Subjects were randomly assigned to a placebo group or to groups consuming 60, 200, or 800 mg/d of vitamin E for 235 days. MAIN OUTCOME MEASURES: Delayed-type hypersensitivity skin response (DTH); antibody response to hepatitis B, tetanus and diphtheria, and pneumococcal vaccines; and autoantibodies to DNA and thyroglobulin were assessed before and after supplementation. RESULTS: Supplementation with vitamin E for 4 months improved certain clinically relevant indexes of cell-mediated immunity in healthy elderly. Subjects consuming 200 mg/d of vitamin E had a 65% increase in DTH and a 6-fold increase in antibody titer to hepatitis compared with placebo (17% and 3-fold, respectively), 60-mg/d (41% and 3-fold, respectively), and 800-mg/d (49% and 2.5-fold, respectively) groups. The 200-mg/d group also had a significant increase in antibody titer to tetanus vaccine. Subjects in the upper tertile of serum alpha-tocopherol (vitamin E) concentration (>48.4 micromol/L [2.08 mg/dL]) after supplementation had higher antibody response to hepatitis B and DTH. Vitamin E supplementation had no effect on antibody titer to diphtheria and did not affect immunoglobulin levels or levels of T and B cells. No significant effect of vitamin E supplementation on autoantibody levels was observed. CONCLUSIONS: Our results indicate that a level of vitamin E greater than currently recommended enhances certain clinically relevant in vivo indexes of T-cell-mediated function in healthy elderly persons. No adverse effects were observed with vitamin E supplementation.

References
1 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52-66.
2 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52.
3 Tabers Cyclopedic Medical Dictionary. 16th ed. Philadelphia:FA Davis Company; 1985. p 120.
4 Wiedermann U, Chen XJ, Enerblack L, Hanson LA, Kahu H, Dahlgren UI. Vitamin A deficiency increases inflammatory responses. Scand J Immunolo 1996 Dec;44(6):58-84.
5 Kosogorova LS, Kovalenko NN, Liubenko VA, Novosad FI. Recovery of immunological responsiveness in patients with bronchial asthma during nicotinamide treatment. Probl Tuberk 1996;(5):41-4.
6 Martin W. On treating allergic disorders. Letter. Townsend Letter for Doctors 1991 Aug/Sep:671-1.
7 Cohen HA, Neuman I, Nahum H. Blocking effect of vitamin C in exercise-induced asthma. Arch Pediatr Adolese Med 1997 Apr;151(4):367-70.
8 Meydani SN, Meydani M, Blumberg JB, Leka LS, Siber G, Loszewski R, Thompson C, Pedrosa MC, Diamind RD, Stollar BD. Vitamin E supplementation and in vivo immune response in healthy elderly subjects. A randomized controlled trial. JAMA 1997 May 7;277(17):1380-6.
9 Kadrabova J, Madaric A, Kovacikova Z, Podivinsky F, Ginter E, Gazdik F. Selenium status is decreased in patients with intrinsic asthma. Biol Trace Elem Res 1996 Jun;52(3):241-8.
10 Ojuawo A, Lindley KJ, Milla PJ. Serum zinc, selenium and copper concentration in children with allergic colitis. East Afr Med J 1996 Apr;73(4):236-8.
11 Greene LS. Asthma and oxidant stress: nutritional, environmental, and genetic risk factors. J Am Coll Nutr 1995 Aug;14(4):317-24.
12 Read MA. Flavonoids: naturally occurring anti-inflammatory agents [comment]. Am J Pathol 1995;147(2):235-7.

Source: USANA Health Sciences

Nutritional health: acne

Description
Acne vulgaris, the most common form of acne, is an inflammatory disease of the sebaceous (oil secreting) glands and hair follicles of the skin. It is characterized by comedones (blackheads) , papules (pimples), and pustules (blisters). (1)

Causes
(a) Many factors can cause acne. Research has centered on hormonal dysfunction and oversecretion of sebum as possible primary causes.(2) A diet high in fat can contribute to acne vulgaris. Acne is associated with oily skin due to an excess of sebum, the fatty secretion of the sebaceous glands. Eating fat increases sebum production.(3,4)

(b) The Western diet has been associated with an increased incidence of acne.(3) A diet low in fiber may be a contributing factor. Far less acne is found among the black population in Zambia eating their traditional diets, than among young blacks in the United States.(4)

(c) One new theory is that a deficiency of pantothenic acid may play a role in some cases.(5)

At Risk
This disease is most common in adolescence. Acne activity is primarily dependent on the genetic sensitivity of the hair follicle and oil gland to androgenic (male) hormones circulating in the blood stream.

Prevention and Management
General:
Most teenage acne will clear as the follicles mature and become less sensitive to the hormone induced changes, however in some, it will persist well into adulthood, especially those with strong genetic tendencies toward acne. The most important method of prevention is to keep the skin clean and free from dirt and oil.(6)

Nutritional Influences:
A low-fat, high-fiber, nutrient-dense diet adequate in vitamins and minerals and low in sugar, refined and convenience foods should be consumed. In one experimental study, patients experienced a rapid clearing of acne following supplementation with one ounce of bran cereal daily.(7) More studies are needed to determine if a high fiber diet is useful in treating acne.
Blood zinc levels are often lower in people who suffer from acne.(8)

Studies have shown that selenium is beneficial for treating acne pustules, possibly because one of the functions of selenium is to help fight infections. Patients with low RBC glutathione peroxidase levels and pustular acne responded best to selenium supplementation.(9)

Vitamin E works closely with selenium. Syndromes caused by selenium deficiency overlap those caused by a vitamin E deficiency; because of the close relationship, vitamin E and selenium are often combined to make treatment more effective.(10)

Vitamin A and its synthetic derivatives appear to be beneficial; high doses are needed, however. Because of the potential for toxicity, vitamin A and vitamin A derivatives should be used only under medical supervision.

Vitamin E affects the biologic utilization of vitamin A. The absorption of vitamin A is markedly impaired in vitamin E deficient animals.(11,12)

Excess supplementation of iodine may cause or exacerbate acneiform eruptions.(13) Kelp as a dietary supplement (14) or fast foods (15) may contain sufficient iodine for this adverse effect.
A deficiency of omega-6 essential fatty acids in the pilosebaceous epithelium might account for follicular hyperkeratosis in acne.(16)

Abstracts
Kremer JM, Bigaouette J. Nutrient intake of patients with rheumatoid arthritis is deficient in pyridoxine, zinc, copper, and magnesium. J Rheumatol 1996 Jun;23(6):990-4. OBJECTIVE: To determine nutrient intake of patients with active rheumatoid arthritis and compare it with the typical American diet (TAD) and the recommended dietary allowance (RDA). METHODS: 41 patients with active RA recorded a detailed dietary history. Information collected was analyzed for nutrient intake of energy, fats, protein, carbohydrate, vitamins and minerals, which were then statistically compared with the TAD and the RDA. RESULTS: Both men and women ingested significantly less energy from carbohydrates [women 47.4% (6.4) vs 55% RDA. p = 0.0001: men = 48.9% (7.4). p = 0.025] and more energy from fat [women = 36.8% (4.5) vs 30% RDA. p = 0.001 and men = 35.2% (5.9) p = 0.02]. Women ingested significantly more saturated and mono-unsaturated fat than the RDA (p = 0.02 and p = 0.04 respectively) while men ingested significantly less polyunsaturated fat (PUFA) (p = 0.0001). Both groups took in less fiber (p = 0.0001). Deficient dietary intake of pyridoxine was observed vs the RDA for both sexes (men and women p = 0.0001). Deficient folate intake was seen vs the TAD for men (p = 0.02) with a deficient trend in women (p = 0.06). Zinc and magnesium intake was deficient vs the RDA in both sexes (p values < or =" 0.001)" p =" 0.004" p =" 0.02">Leung LH. Pantothenic acid deficiency as the pathogenesis of acne vulgaris. Med Hypotheses 1995 Jun;44(6):490-2. For years, the pathogenesis of acne vulgaris has been known to be strongly influenced by hormonal factors. However, the exact role of and the interrelationship among the various hormones in question have not been well elucidated. Here, I wish to suggest a radically different theory for its pathogenesis and relate its basic pathology to a deficiency in pantothenic acid, a vitamin hitherto not known to cause any deficiency syndrome in humans. Hence, the effect of hormonal factors in this disease entity becomes secondary to that of the availability of pantothenic acid. A complete cure of this condition is effected by a very liberal replacement therapy with the vitamin.

References
(1) Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation. 1997. p 1173.
(2) Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation. 1997. p 1173.
(3) Rosenberg EW, Kirk BS. Acne diet reconsidered. Arch Dermatol 1981;117:193-95.
(4) Klurfeld DM. The Diet and Acne. Archives of Dermatology 1983;119(4):276.
(5) Leung LH. Pantothenic acid deficiency as the pathogenesis of acne vulgaris. Med Hypotheses 1995 Jun;44(6):490-2
(6) Somer E. The Essential Guide to Vitamins and Minerals. New York:HarperPerennial. 1992.
(7) Putzier E. Dermatomycoses and an antifungal diet. Wiener Medizinische Wochenschrift 1989 Aug 31;139(15-16): 379-80.
(8) Pohit J et al. Zinc status of acne vulgaris patients. J Appl Nutr 1985;37(1):18-25.
(9) Michaelsson G, Edqvist L. Erythrocyte glutathione peroxidase activity in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol (Stockh) 1984;64(1):9-14.
(10) Michaelsson G, Edqvist L. Erythrocyte glutathione peroxidase activity. in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol (Stockh) 1984;64(1):9-14.
(11) Ames SR. Factors affecting absorption, transport and storage of vitamin A. Am J Clin Nutr 1969;22:934.
(12) Ayers S Jr, Mihan R. Acne vulgaris and lipid peroxidation: New concepts in pathogenesis and treatment. Int J Dermatol 1978;17:305.
(13) Hitch JM. Acneiform eruptions induced by drugs and chemicals. JAMA 1967;200:879-80.
(14) Fischer AA. Contact Dermatitis. 3rd ed. Philadelphia:Lea and Febiger;1986. p 593.
(15) How nutritious are fast-foods? Consum Rep 1975;40:278-81.
(16) Downing DT et al. Essential fatty acids and acne vulgaris. J Am Acad Dermatol 1986;14:221-25.

Source

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