Immune-boosting Foods: Citrus Fruits

Grapefruit, oranges, tangerines, lemons and limes are all excellent sources of ascorbic acid, the form of vitamin C found in plants. As a component of food, this nutritional superstar has myriad immune functions, including enhancing the movement of phago¬cytes, boosting NK-cell activity and building and maintaining mucous membranes and collagen, a tissue that plays a vital role in wound healing.

Vitamin C is also required for the manufacture of hormones that help the body deal with stress and it helps convert toxins to water-soluble substances that can be excreted by the body. But it's just one of more than 100 phytochemicals that citrus fruits contain. Both oranges and grapefruit are also loaded with naringenin, which is thought to work against HIV infection and tumour formation.

The oil in citrus rinds contains Iimonene, which researchers think helps enzymes to deactivate cancer-causing substances in the body. Iimonene may also encourage tumours to shrink by slowing down the rate at which the cells divide.

The proof: Contrary to popular claims, vitamin C cannot cure the common cold or make cancer patients live longer. Even so, its importance for health can't be disputed. Many studies have found an unmistakable correlation between low levels of vitamin C in the blood and increased risk of cancer, especially cancer of the oesophagus, mouth, pancreas and stomach. Just by adding a small amount of lemon peel to their diets, participants in one US study appear to have lowered their incidence of skin cancer by as much as 34 per cent.

Put citrus fruits to work: Most animals manufacture their own vitamin C, but humans have lost their ability to do so. Since the body doesn't store the vitamin (any excess is eliminated through the urine), try to get a little bit every day. (There is no benefit in taking large doses of supplements.) To benefit from limonene, add a twist of citrus peel to your drink.

Immune-boosting Foods: Garlic

Garlic fans adore the bulb's pungent flavour and so should health seekers. Several of the same chemicals that contribute to garlic's intense flavour also appear to help block cancer by preventing the formation of some carcinogens that damage DNA. Garlic may also stimulate an increase in the production of the immune-system chemicals interleukin-2, tumour necrosis factor and interferon gamma — the same substances that are used by doctors in some cancer dierapies that are based on manipulation of the immune system. 

The proof. Fresh garlic juice can kill various microorganisms. Small studies have hinted at its effectiveness in promoting human health. Some studies even suggest that eating lots of chopped garlic may lower the risk of colon and stomach cancer by up to 35 per cent and 50 per cent respectively. The reduction in stomach cancer among garlic eaters suggests that the tasty bulb contains compounds that stop the growth of ulcer-causing Helicobacter pylori bacteria, since gastric ulcers have been identified as a strong risk factor for stomach cancer. 

Put garlic to work. How much garlic do you need to eat to harness its healing powers? Generally, benefits have been observed in people who eat 5 to 18 g (about two to six cloves) of raw or lighdy cooked garlic a week. (Overcooking can destroy the beneficial enzymes.) Add garlic to stir-fries; toss it in sauces, stews and soups; or opt instead to use its close cousins - shallots, onions, chives or leeks. Be wary of garlic pills; some contain few active ingredients, so fresh garlic is best. Also, although some folk remedies involve applying crushed garlic directly to the skin, don't, as it could be too strong for you and would cause severe irritation.

P/S: After chopping garlic, let it sit on the kitchen bench for about 15 minutes before cooking. This allow ample time for its various health-protective substances to form. Heat stops this important process.

Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease)

--A rapidly progressive, degenerative disease of the upper and lower motor neurons characterized by atrophy of the hands, arms, legs, and, eventually, the entire body. Seventy percent of individuals die within 5 years of diagnosis.
 
Causes and Incidence
The etiology of amyotrophic lateral sclerosis (ALS) is unknown, but proposed explanations include genetics, metabolic disturbances, and external agents. Although the incidence worldwide is 60 to 70 people per 100,000, with large clusters of cases in the western Pacific, the incidence in the United States is only about 5 in 100,000. The disease usually occurs in men between 40 and 70 years of age.
 
Disease Process
Patterns of degeneration occur in the brain and spinal cord. The anterior horn cells deteriorate, resulting in denervation of muscle fibers. Atrophy of the precentral gyrus and loss of Betz's cells occur in the cortex. Motor neurons are lost in the brainstem, although neurons that control the sensory and urinary sphincters are spared. The corticospinal tract and large motor neurons in the spinal cord also atrophy.
 

Symptoms 
 
Early
Weakness, cramps in the hands and forearms
 
Midcourse     
Fatigue; dyspnea; slurred speech; dysphagia; asymmetric spread of muscle weakness to the rest of the body; spasticity; fasciculations; hyperactive deep tendon and extensor plantar reflexes
 
Late 
Paralysis of vocal cords; paralysis of chest muscles, necessitating ventilatory support
 
Potential Complications 

The end stage of ALS can be complicated by disuse syndrome, contractures, skin breakdown, and aspiration pneumonia.
 

Diagnostic Tests 
 
Clinical evaluation  
Any of the above manifestations; motor involvement unaccompanied by sensory abnormalities
 
Electromyography
Fibrillation, positive waves, fasciculations, giant motor units
 
Blood
Possible elevation in creatinine phosphokinase
 
Spinal tap
Elevated total protein; normal cell and IgG concentrations
 
Computed tomography scan
Normal until cerebral atrophy  late in disease
 
Myelogram
Normal; spinal cord atrophy late in disease
 

Treatments 
 
Surgery  
Cricopharyngeal myotomy to alleviate dysphagia; tracheostomy; esophagostomy/ gastrostomy
 
Drugs   
Muscle relaxants (e.g., baclofen) to control spasticity; tricyclic antidepressants to control saliva; phenytoin to reduce cramping
 
General            
Physical therapy to maintain muscle strength; occupational therapy for activity of daily living support; speech therapy to aid communication; splints for neutral joint alignment; leg braces, canes, walkers to aid ambulation; nutritional support/tube feedings; cardiac monitoring; mechanical ventilation; counseling for individual and family; respite care or placement if family is unable to provide care.

Alzheimer's Disease

--A chronic, progressive, neurologic disorder characterized by degeneration of the neurons in the cerebral cortex and subcortical structures, resulting in irreversible impairment of intellect and memory.
 
Causes and Incidence
The cause is unknown, although theories involving genetic links, neurotransmitter deficiencies, viruses, aluminum poisoning, autoimmune disease, and viruses have been advanced. Alzheimer's disease is the fourth leading cause of death among the elderly in the United States. Approximately 3% of individuals over 65 years of age show signs of the disease; the proportion climbs to 20% in those over 80 years of age. The incidence is higher in women.
 
Disease Process
Selective neuronal cells, primarily those involved in the transmission and reception of acetylcholine, degenerate in the cerebral cortex and basal forebrain, resulting in cerebral atrophy of the frontal and temporal lobes, with wide sulci and dilated ventricles. Senile plaques and neurofibrillary tangles are present. The basic pathophysiologic processes accompanying the brain damage are unknown.
 

Symptoms 
 
Early     
Short-term memory loss, impaired insight/judgment, momentary disorientation, emotional lability, anxiety, depression, decline in ability to perform activities of daily living (ADLS)
 
Midcourse         
Apraxia, ataxia, alexia, astereognosis, auditory agnosia, agraphia, prolonged disorientation, progressive memory loss (longand shortterm), aphasia, lack of comprehension, decline in care abilities, insomnia, loss of appetite, repetitive behavior, socially unacceptable behavior, hallucinations, delusions, paranoia
 
Late    
Total dependence in ADLs, bowel and bladder incontinence, loss of speech, loss of individuation, myoclonic jerking, seizure activity, loss of consciousness
 

Potential Complications
The end stage of Alzheimer's disease invites complications commonly associated with comatose conditions (e.g., skin breakdown, joint contractures, fractures, emaciation, aspiration pneumonia, infections).
 
Diagnostic Tests
Definitive diagnosis can be made only through autopsy. 
 
Clinical evaluation     
Any of the above manifestations  after depression, delirium, and other dementia disorders (e.g., head injury, brain tumor, alcoholism, drug toxicity, arteriosclerosis) have been ruled out; family history
 
Mental status  examination  
Decreased orientation, impaired  memory, impaired insight/ judgment, loss of abstraction/ calculation abilities, altered mood
 
Computed tomography/magnetic  resonance imaging
Brain atrophy; symmetric, bilateral, ventricular enlargement
 
Electroencephalogram
Slowed brain wave activity,   reduced voltage
 

Treatments 
 
Surgery
None
 
Drugs        
Medications for treating specific symptoms or behavioral manifestations (i.e., antidepressants, stimulants, antipsychotics, sedatives); experimental drugs include cholinergic, dopamine, and serotonin precursors; neuropeptides; and transcerebral dilators
 
General      
Structured, supportive, familiar environment; orientation and cueing program for daily tasks; safety program; family support and counseling; respite care; institutionalization when home care is no longer possible.

Conn's Syndrome

A hypertensive disorder resulting from excess production of aldosterone by the adrenal gland.

Causes and Incidence 

Most cases are caused by an adenoma of the adrenal gland. Other causes are adrenal nodular hyperplasia and adrenal carcinoma. Only 0.5% to 2% of those with hypertension are affected. The condition is three times more likely to affect women; the typical age ranges from 30 to 50 years.

Disease Process 

Excess production of aldosterone leads to hypernatremia, hypervolemia, and hypokalemic alkalosis. Mild to severe arterial hypertension occurs because of the increased volume and arteriolar sodium levels. Hypokalemia results from increased renal excretion of potassium, and metabolic alkalosis occurs because of an increase in hydrogen ion secretion. Over time this leads to transient paralysis and tetany.

Symptoms 

In many cases the only manifestation is a mild to moderate hypertension. Other signs and symptoms include episodic weakness, fatigue, paresthesia, polyuria, polydipsia, and nocturia. Glycosuria, hyperglycemia, and personality disturbances are occasionally manifested.

Potential Complications 

Marked alkalosis with transient paralysis, tetany, and positive Chvostek's and Trousseau's signs.
 

Diagnostic Tests 

Plasma renin activity 
Decreased (measured after restricted sodium/diuretic therapy)

Aldosterone levels
Increased (measured after  sodium loading)

Blood chemistry
Normal/increased sodium, decreased potassium

Computed tomography scan
To detect presence of adenoma

Blood pressure
Elevated

Edema
Absent
 

Treatments 

Surgery
Adrenalectomy

Drugs
Spironolactone (Aldactone)

General 
Low-sodium diet; instruction about medication, diet, and surgery.

Adult Respiratory Distress Syndrome (ARDS)

Acute respiratory failure associated with pulmonary injury and characterized by noncardiogenic pulmonary edema, hypoxemia, and severe respiratory distress.

Causes and Incidence 

Adult respiratory distress syndrome (ARDS) is precipitated by a variety of acute processes that injure the lung. Trauma is the most common cause; others are anaphylaxis, aspiration of gastric reflux, pneumonia, inhalation burns from fire or chemicals, drug reactions, drug overdose, near-drowning, and oxygen toxicity. The condition may also develop as the result of an underlying disease process (e.g., leukemia, tuberculosis, pancreatitis, uremia, thrombocytopenic purpura) or as a byproduct of a medical procedure (e.g., coronary artery bypass, multiple blood transfusions, mechanical ventilation, hemodialysis). 

The incidence and mortality are elusive, because ARDS is often misdiagnosed. Other names for ARDS include such names as shock lung, wet lung, stiff lung, white lung, Da Nang lung, or adult hyaline membrane disease. Recent studies place the survival rate at about 50% with treatment.

Disease Process 

The initial injury to the lung is poorly understood. It is hypothesized that activated WBCs and platelets accumulate in the capillaries, interstitium, and air spaces and release prostaglandins, oxygen radicals, proteolytic enzymes, and other products. These injure the cells, increase fibrosis, and reduce bronchomotor tone, leading to capillary leakage of blood and plasma into the interstitial and alveolar spaces. This results in alveolar flooding and reduced surfactant activity, producing atelectasis. Bronchial inflammation and proliferation of epithelial and interstitial cells follow. Collagen accumulates, resulting in severe interstitial fibrosis (stiff lung) with low lung compliance, reduced functional residual capacity (FRC), pulmonary hypertension, perfusion maldistribution, and hypoxemia.
 

Symptoms  

Early   
Dyspnea, particularly on exertion, followed by rapid, shallow respirations, inspirational chest retractions, and wheezing

Late   
Bloody, sticky sputum; racing heart rate; clammy, mottled, cyanotic skin; severe difficulty breathing; confusion; coma

Potential Complications 

Complications include secondary bacterial superinfections, tension pneumothorax, multiple-system organ failure, metabolic and respiratory acidosis, and cardiac arrest.
 

Diagnostic Tests 

Pulmonary function  
Decreased FRC and compliance;  low/normal pulmonary capillary web pressure; increased shunt fraction

Arterial blood gases
Decreased PaO2; low/normal PaCO2; elevated pH

Lactic acid
Elevated

Radiology 
Blurred margins and alveolar infiltrates on early chest x-rays; normal cardiac silhouette
 

Treatments 

Mechanical ventilation with positive end-expiratory pressure and continuous positive airway pressure is generally required until the underlying problem has been identified and treated. 

Surgery
None

Drugs     
No specific drugs; morphine and pancuronium bromide (Pavulon) are used in the management of mechanical ventilation; antiinfective drugs may be used for underlying infections

General                 
Correction of underlying cause of injury; hyperalimentation to prevent nutritional depletion; blood gas monitoring to prevent oxygen toxicity; careful aseptic technique and monitoring of secretions to prevent superinfection; intubation and ventilation; tracheobronchial suctioning to clear secretions; cardiac monitoring; bed rest; fluid volume replacement; regulation of activity to reduce hypoxia; instruction in communicating with intubated patient; communication tools (e.g., alphabet or picture boards, response switches).

Addison's Disease

Addison's disease is a progressive, chronic disease process resulting from a decline in the production of adrenocortical steroids as the adrenal cortex is destroyed.

Causes and Incidence 

Most cases are the result of idiopathic atrophy of the adrenal cortex; the rest are due to destruction of the entire gland. Clinical signs often are manifested during periods of metabolic stress. About 4 in 100,000 individuals, across all age groups, are affected.

Disease Process 

A decline in cortisol and corticosterone production by the adrenal cortex results in multiple disturbances in fat, protein, and carbohydrate metabolism, which in turn give rise to diminished production of liver glycogen and increased production of insulin. This leads to hypoglycemia and muscle weakness. Electrolyte imbalances and dehydration are caused by an increase in sodium (Na) secretion and a decrease in potassium (K) secretion, leading to low serum concentrations of sodium and chloride and high serum concentrations of potassium. The decrease in cortisol also leads to an increase in adrenocorticotropic hormone (ACTH) and beta-lipotropin, which stimulates melanin production and causes hyperpigmentation. Over time, resistance to infection and stress diminishes. Dehydration may lead to reduced cardiac output and, ultimately, circulatory collapse.
 

Symptoms 

Early
Weakness, fatigue, orthostatic 

hypotension, tanning, freckles, vitiligo, darkened mucosal areas

Midcourse  
Nausea, vomiting, diarrhea, abdominal pain, headaches, dizziness, fainting, intolerance to cold

Late  
Weight loss, dehydration, hypotension, confusion, restlessness, emotional lability, small heart size
 

Potential Complications 

Acute stress or trauma in which the body's store of glucocorticoids is exhausted may trigger an adrenal crisis, which is characterized by generalized muscular debility; severe abdominal, back, and leg cramps; peripheral vascular collapse; and acute renal failure.
 

Diagnostic Tests 

ACTH stimulation test
No increase in cortisol

Blood chemistry  
Elevated potassium and blood  urea nitrogen (BUN); decreased sodium, bicarbonate, and fasting glucose

Complete blood count 
Na:K ratio less than 30:1; elevated hematocrit, eosinophils, and lymphocytes; decreased WBCs

Radiology 
Small heart; small adrenal size, calcifications; renal or pulmonary tuberculosis
 

Treatments 

Surgery
None

Drugs       
IV hydrocortisone, sodium chloride replacement; vasopressors to elevate blood pressure; hydrocortisone/fludrocortisone PO maintenance for life; antibiotics with evidence of infection; antitubercular drugs with evidence of tuberculosis

General      
Fluid replacement IV and PO; high-calorie diet; cardiac monitoring for peaked T waves; rest; monitoring for signs of infection; monitoring of urine output; instruction about the disease and maintenance medications.

Acquired Immune Deficiency Syndrome (AIDS)

Acquired Immune Deficiency Syndrome or better known as AIDS, is a terminal, secondary immunodeficiency syndrome characterized by dysfunction of cell-mediated immunity and manifested by opportunistic infections and malignancies.

Causes and Incidence
The cause is thought to be one of several related retroviruses (human immunodeficiency virus, or HIV) that convert viral RNA into a proviral DNA copy, which is incorporated into the DNA of the host cell. The proviral copy then is duplicated with normal cellular genes during each cellular division. HIV is a blood-borne virus and commonly is transmitted through exchange of body fluids during sexual contact, through parenteral exposure or fetal exposure to blood, and through select body fluids from an individual infected with HIV. Infants are at risk of acquiring the HIV during fetal development, delivery, or breast-feeding from an HIV-positive mother.

High-risk behavior for HIV exposure includes unprotected sexual activity and IV drug use with shared needles. Occupational transmission to health care workers is possible through needle sticks or other exposure to HIV-infected blood. Individuals infected with HIV who are asymptomatic are in a carrier state and may transmit the disease without displaying any of the characteristic signs of AIDS.
 

AIDS is a global pandemic, and it is predicted that more than 110 million people worldwide will be infected with HIV by the end of the century. As of 1991 more than 1.1 million people worldwide had died.
 

In the United States the incidence of AIDS has steadily increased from 3.46 per 100,000 population in 1985 to 40.20 per 100,000 population in 1993. Although it is far too early to interpret the reasons, in 1994 the incidence of reported AIDS cases dropped slightly, to 30.07 per 100,000 population. All races and ethnic groups are affected. Currently men far outnumber women as victims of the disease. However, the fastest rise in cases is occurring among minority women. The median age range for all individuals with AIDS is 30 to 39 years.

Disease Process
The current theory holds that as HIV is reproduced, it affects the immune system by infecting the T-helper cell lymphocytes, which usually coexist in a 2:1 ratio with T-suppressor cells. As the viruses replicate, masquerading as helper cells, the number of real helper cells declines, and the T-suppressor cells eventually dominate, leading to immunosuppression and a lowering of the body's prime defense mechanism against intracellular pathogens and the formation of malignant tumors.

Symptoms
AIDS is a chronic, progressive, terminal illness that can be divided into four stages, as defined by the federal Centers for Disease Control and Prevention (CDC): 

Stage I  
An acute, flulike syndrome that develops at the time of initial infection and lasts from days to weeks

Stage II 
An asymptomatic, HIV-positive carrier state that may persist for years

Stage III
Generalized, persistent lymphadenopathy

Stage IV                 
The development of other disease processes, including (1) constitutional disease (weight loss greater than 10% of body weight, persistent diarrhea, fever, malaise, oral thrush); (2) neurologic disease (peripheral neuropathies, paresthesia, myelopathy, dementia); (3) opportunistic infections (bacterial, viral, fungal, or protozoal) and their accompanying clinical features; (4) secondary neoplasms; and (5) other conditions (e.g., endocarditis, interstitial pneumonitis, immune thrombocytopenic purpura)

Potential Complications
The complications are numerous and are associated with the various opportunistic infections or neoplasms, as well as the repetitive nature of the infections. These infections eventually overwhelm the body's compromised immune system, leading to massive infectious invasions in every body system and, eventually, death.

Diagnostic Tests 

Clinical evaluation 
Any of the above manifestations; history of high-risk behavior

Enzyme-linked immunosorbent assay (ELISA)
Screening test for HIV antibody  (may be positive from 0 to 12 months after exposure)

Western blot/ immunofluorescent assay
To confirm reactive seropositive  results obtained by ELISA test 

WBCs/lymphocytes
Depressed

T-cell studies  
Reduced reactivity and function  of T cells; reduced number of T-helper cells, increased number of T-suppressor cells

B-cell studies
Numbers and function normal or  increased

Natural killer (NK) cells
Reduced activity

Complement
Normal or increased

Treatments 

Surgery
Tumor excision of some related neoplasms

Drugs                     
Experimental treatment with various retroviral drugs such as zidovudine (Retrovir; formerly azidothymidine [AZT]); didanosine (Videx; formerly dideoxyinosine [ddI]; and zalcitabine (Hivid; formerly dideoxycytidine [ddC]), using CD4 lymphocyte counts as a treatment guide; prophylaxis with trimethoprim-sulfamethoxazole tablets to prevent Pneumocystis carinii pneumonia (PCP); rifabutin prophylaxis for Mycobacterium avium infection; drugs specific for various opportunistic infections; chemotherapy for carcinomas; prophylactic use of zidovudine following exposure through penetrating injuries is controversial

General               
Measures to improve overall health (e.g., no smoking, balanced nutrition, drug rehabilitation, flu vaccine, pneumococcal vaccine, hepatitis B vaccine); supportive measures for coping with and adapting to the effects of the disease (e.g., counseling, support groups); instruction in how the disease is spread in order to promote prevention, particularly among high-risk groups; use of universal precautions by health care workers and family members to prevent transmission.

Abruptio Placentae

A premature separation of a normally implanted placenta from the uterine wall, usually occurring in the third trimester of pregnancy.

Causes and Incidence The etiology is unknown but is believed to be related to hypertensive and cardiovascular disease processes or use of cocaine. Abruptio placentae occurs in 0.5% to 3.5% of all deliveries.

Disease Process The placenta releases from the wall of the uterus, and retroplacental bleeding occurs. The degree of release may vary from a few millimeters to complete detachment. Blood can accumulate under the placenta (concealed hemorrhage) or can be passed behind the membranes and out the cervix (external hemorrhage).

Symptoms The signs and symptoms vary with the degree of separation and the resultant amount of hemorrhage. Severe cases involve slight to profuse vaginal bleeding; maternal shock (hypotension, dizziness, rapid pulse, dyspnea, pallor); sudden, severe pain; tender, tightly contracted uterus; and fetal distress or fetal death.

Potential Complications Hypofibrinogenemia with disseminated intravascular coagulation (DIC), uteroplacental apoplexy (Couvelaire uterus), and renal failure are possible, particularly if the woman has preexisting toxemia.
 

Diagnostic Tests 

Abdominal ultrasound
To rule out placenta previa
 

Treatments 
 
Surgery 
Cesarean section (unless vaginal delivery is imminent) when bleeding cannot be controlled
 
Drugs
None
 
General      
Bed rest until bleeding stops; fluid and volume replacement by intravenous administration; blood replacement if necessary to prevent shock; rupture of membranes if delivery is imminent to reduce the possibility of DIC

Immune-boosting Foods: Broccoli

Cancer institutes around the world value broccoli as the number-one anticancer food, and with good reasons. As well as being rich in disease-fighting vitamin C, it also contains sulforaphane, a phyto-chemical that occurs naturally in broccoli and other vegetables of the cruciferous family — kale, cabbage, cauliflower, bok choy, brussels sprouts and many salad greens. Sulforaphane stimulates the body's production of substances called Phase II detoxification enzymes. These enzymes destroy carcinogens (cancer-causing substances) and free radicals before they can attack healthy cells. Second, cruciferous vegetables are loaded with indole-3-carbinol (I3C), a phytochemical shown to inhibit the growth of the type of cancer cells in the breast that are responsive to estrogen. In fact, researchers are now examining the feasibility of putting I3C in a pill to combat breast cancer.

The proof: When scientists fed rats hearty servings of broccoli for a few days, then exposed them to a potent compound that induces breast cancer, the broccoli eaters were half as likely to develop tumors as animals on the standard feed. And the broccoli eaters that did develop cancer ended up with fewer and smaller tumors.

Put broccoli to work: Regardless of how you prepare cruciferous vegetables, eating them is good for you. But if you want to rev up your body's disease-fighting abilities fast, look a little further down the family tree to broccoli sprouts. Scientists at Johns Hopkins University have found that, gram for gram, these tender shoots can contain up to 20 times more sulforaphane than mature broccoli. In other words, 30 g of sprouts yields as much protective power as about 625 g of cooked broccoli!

Ask for broccoli sprouts at your local greengrocer or supermarket, but if you can't find them, why not grow your own? Sprouts of all kinds are powerhouses of health and are very quick and easy to grow. Health food shops will supply you with special sprouting seeds that have not been treated with pesticides and recommend a sprouter that suits the size of your household. Simply follow the manufacturer's instructions. Refrigerate your fat-free, low-kilojoule broccoli sprouts and rinse in fresh, clean water before using. Serve generously in sandwiches and salads before the use-by date.