Not everyone affected by these foods is diagnosed with a chronic disease; more than 60 million Americans experience episodes of acid indigestion as often as once each month and some studies suggest that as many as 15 million experience episodes of acid indigestion daily. Many people self-medicate with antacids when they could adjust their diet including reducing coffee and caffeine consumption in order to find relief. These conditions are serious: at least 10 million people are hospitalized each year for gastrointestinal disorders and the annual total of health care costs associated with these exceeds $40 billion. 1

Heartburn Acid Reflux & GERD

Heartburn, or pain behind the breastbone, is a condition in which there is reflux of acid from the stomach into the sensitive esophagus, often caused by a relaxation or weakening of the lower esophageal sphincter, the ring of muscle between the esophagus and the stomach. Foods, including dietary fat, chocolate, mints, coffee, onions, citrus fruit, and tomatoes, have been associated with increased incidence of acid reflux in susceptible persons.2

When symptoms are recurrent or esophageal tissue is damaged, GERD develops. GERD affects 5-7% of the global population.3, 4 When untreated, it can cause complications such as chest pain, bleeding, esophageal stricture (narrowing or obstruction of the esophagus) or Barrett�s esophagus (a pre-malignant condition). Symptoms that indicate damage to the esophagus has occurred include: pain, dysphagia (difficulty swallowing), bleeding and choking. Some risk factors of these more serious conditions are alcohol use, pregnancy, weight gain and coffee consumption.5

Ulcers

Ulcers are another common problem, afflicting approximately 20 million Americans, according to the American College of Gastroenterology. Ulcers can occur in the stomach or duodenum, and are regions where the lining has been destroyed by stomach acids or digestive juices. Even small areas of damage can cause intense pain. The presence of the bacteria Helicobacter pylori is also implicated as a predisposing factor in ulcer development, but not everyone infected with H. pylori develops ulcers. It is unknown why this is the case, although a strong immune system provides protection against the bacters ability to colonize damaged areas of the stomach lining. Increased levels of cortisol and other stress hormones stimulated by caffeine consumption and coffee drinking suppress the activity of the immune system and raise stress levels which are associated with ulcer formation. Other predisposing factors include: being male, family history, prolonged stress, skipping meals, cigarette smoking and coffee ingestion⁶.

Of all the dietary habits that people find difficult to change, coffee drinking is one of the most challenging because it is so entrenched in cultural habits and caffeine addiction.⁷ Withdrawal symptoms can involve painful headaches, nausea, vomiting, and loose stools.⁸ People whose health problems would be ameliorated if they gave up coffee can improve their chance for successfully quitting coffee if they have both a satisfying alternative and a method to slowly decrease their caffeine intake to reduce withdrawal symptoms.

The Following Characteristics of Coffee have an Adverse effect on the upper GI tract:

• Coffee Decreases Pressure in the Lower Esophageal Sphincter
  • Coffee has been shown to decrease pressure in the lower esophageal sphincter, contributing to gastroesophageal reflux. This suggests that coffee can either cause or exacerbate heartburn in susceptible individuals.^{9, 10, 11}
  • The type of coffee bean roasting method used does not reduce the tendency of coffee to produce gastroesophageal reflux. Sensitive individuals, even when consuming coffee produced through different roasting processes, while fasting or after a meal, experienced heartburn, regurgitation and dyspepsia.¹²
  • Coffee consumption has been associated with greater incidence of heartburn than drinking other fluids such as water.¹³
  • Both caffeinated and decaffeinated coffee exacerbate gastroesophaeal reflux, and coffee creates more reflux than caffeine added to water, suggesting that other components of coffee contribute to its aggravating effect.¹⁴

• The Acidity of Coffee Irritates the Stomach
  • Coffee is highly acidic and it can stimulate the hypersecretion of gastric acids. Decaffeinated coffee has been shown to increase acidity to a greater degree than either regular coffee or caffeine alone.¹⁵ Both caffeine and coffee stimulate gastric acid secretion and decaffeinated coffee raises serum gastrin levels.^{16, 17} A study comparing the ability of decaffeinated coffee with that of a high protein meal to increase gastric acid secretion and gastrin levels found that decaffeinated coffee was a more powerful stimulant of acid secretion and gastrin release than the high protein.¹⁸
  • Coffee tends to speed up the process of gastric emptying, which may result in highly acidic stomach contents passing into the small intestine more rapidly than normal. This may lead to injury of the intestinal tissue.¹⁹
  • There is a clear relationship between reduction of stomach acid and heartburn relief.²⁰

• Coffee Is a Risk Factor Associated with Ulcer Susceptibility
  • Coffee is linked to ulcer susceptibility. Both caffeinated and decaffeinated coffees have an acid-stimulating effect, and therefore it is recommended that people with ulcers restrict not only caffeinated but also decaffeinated coffee intake.²¹

• Coffee Elevates Stress Hormones
  • Caffeine in coffee elevates the stress hormones cortisol, epinephrine (also known as adrenaline) and norepinephrine.^{22, 23, 24, 25} These hormones are responsible for increased heart rate, increased blood pressure, and a sense of “emergency alert”. Blood is diverted from the digestive system which can cause indigestion. The circulation of oxygen to the brain and extremities is decreased and the immune system is suppressed.
  • The purpose of the body’s “fight or flight” response initiated by the release of cortisol, epinephrine and norepinephrine is to provide the body with a temporary energy boost for intense physical activity. With today’s sedentary lifestyle, the continual state of increased stress resulting from caffeine consumption may affect symptoms of heartburn and GERD. Although the relationship between stress and symptoms of gastroesophageal reflux is still unclear, evidence suggests that anxiety, along with exhaustion resulting from sustained stress, are both associated with exacerbation of heartburn and esophageal reflux.²⁹

• Coffee Supresses Immune System Function
  • Immune system suppression caused by chronic increased levels of stress hormones induced by caffeine intake can create a situation in which the bacteria Helicobacter pylori can thrive in the stomach. Infection by H. pylori is implicated in ulcers.

• Caffeine Interferes with GABA Metabolism
  • GABA (Gamma-aminobutyric acid) is a neurotransmitter that is naturally produced in the brain and nervous system as well as the GI tract. It plays an important role in mood and stress management and it exerts a calming effect on the GI tract.
  • Caffeine has been found to interfere with binding of GABA to GABA receptors, preventing it from performing its calming function.²⁶ Studies suggest that stimulation of GABA receptors may be beneficial for people with reflux arising from low lower oesophageal sphincter pressure.^{27, 28} In addition to its direct effect on the GI tract, GABA�s role in stress management is also compromised in the presence of caffeine. This is significant as psychological stress has been shown to be an exacerbating factor in heartburn and ulcers.²⁹

Recommendation:

Individuals who suffer from or are susceptible to problems with the upper gastrointestinal tract, would do well to avoid coffee as it has been demonstrated to be a contributing factor associated with increased incidence of gastritis, ulcers, acid reflux and GERD. Dietary changes that include weaning off of coffee and all other sources of caffeine can help relieve symptoms of these disorders.30 Nutrition professionals can support gastrointestinal patients by guiding them through the process of substituting a non-caffeinated, alkaline herbal coffee that brews and tastes just like coffee.

Kicking the Caffeine Habit:

The social prevalence of coffee drinking and the addictive side effects of caffeine can cause problems with patient compliance. Caffeine-free herbal coffee marketed under the brand name of Teeccinoi helps coffee drinkers replace their regular or decaf coffee with a satisfying alternative. Coffee drinkers need a dark, full-bodied, robust brew to help satisfy their coffee craving. Teeccino satisfies the 4 needs coffee drinkers require in a coffee alternative:

1. Teeccino brews just like coffee, allowing coffee drinkers to keep their same brewing ritual.
2. It has a delicious, deep roasted flavor that is very coffee-like.
3. It wafts an enticing aroma.
4. People experience a natural energy boost from nutritious Teeccino.

Teeccino offers the following health benefits to people suffering from upper GI tract disorders:

The Pain-free Way to Wean off of Coffee

Start by mixing normal coffee 3/4 to 1/4 Teeccino Herbal Coffee. Gradually reduce the percentage of coffee over a two to three week period until only 100% Teeccino Herbal Coffee is brewed. Gradual reduction of caffeine is recommended.31 Side effects such as headaches, fatigue, and brain fogginess can be avoided as the body gradually adjusts to less reliance on stimulants.

Example: Use the following proportions if you make a 10-cup pot of coffee daily:

References

1. American College of Gastroenterology. Copyright 2004.
2. Terry P, Lagergren J, Wolk A, Nyren O. 2000. Reflux-inducing dietary factors and risk of adenocarcinoma of the esophagus and gastric cardia. Nutrition and Cancer. 38(2): 186-91.
3. International Foundation for Functional Gastrointestinal Disorders. Copyright 2004.
4. Richter JE, Katz PO, Waring JP. Gastroesophageal Reflux Disease. IFFGD, 2000.
5. Wang, J.H., Luo, J.Y., Dong, L., Gong, J. and Tong, M. 2004. Epidemiology of gastroesophageal reflux disease: a general population-based study in Xi’an of Northwest China. World Journal of Gastroenterology. 10(11):1647-51.
6. Abu Farsakh, N.A. 2002.Risk factors for duodenal ulcer disease. Saudi Medical Journal. 23(2):168-72.
7. Braun, S. Buzz: The Science and Lore of Alcohol and Caffeine. Copyright 1996.
8. Strain, E.C., G.K. Mumford, K. Silverman, and R.R. Griffiths. 1994. Caffeine dependence syndrome. Journal of the American Medical Association, 272:1043-1048.
9. Thomas, F.B., Steinbaugh, J.T., Fromkes, J.J., Mekhjian, H.S., and Caldwell, J.H. 1980. Inhibitory effect of coffee on lower esophageal sphincter pressure. Gastroenterology, Dec; 79(6): 1262-6.
10. Boekema, P.J., Samsom, M., van Berge Henegouwen, G.P. and Smout, A.J. 1999. Coffee and Gastrointestinal function: facts and fiction. A Review. Scandinavian Journal of Gastroenterology Supplement. 230: 35-9.
11. Cohen, S. 1980. Pathogenesis of coffee-induced gastrointestinal symptoms. New England Journal of Medicine. 303(3):122-4.
12. DiBaise, JK. 2003. A randomized, double-blind comparison of two different coffee-roasting processes on development of heartburn and dyspepsia in coffee-sensitive individuals.Digestive Diseases and Sciences. 48(4):652-6.
13. Feldman, M. and Barnett, C. 1995. Relationships between the acidity and osmolality of Popular Beverages and reported Postprandial Heartburn. Gastroenterology. 108(1): 125-31.
14. Wendl, B., Pfeiffer, A., Pehl, C., Schmidt, T. and Kaess, H. 1994. Effect of decaffeination of coffee or tea on gastro-oesophageal reflux. Alimentary pharmacology & therapeutics. 8(3):283-7.
15. Cohen, S. and Booth, G.H. Jr. 1975. Gastric acid secretion and lower-esophageal-sphincter pressure in response to coffee and caffeine. New England Journal of Medicine. 293(18):897-9.
16. Coffey, R.J., Go, V.L., Zinsmeister, A.R. and DiMagno, E.P. 1986. The acute effects of coffee and caffeine on human interdigestive exocrine pancreatic secretion. Pancreas. 1(1):55-61.
17. Borger HW, Schafmayer A, Arnold R, Becker HD, Creutzfeldt W. 1976. The influence of coffee and caffeine on gastrin and acid secretion in man. Deutsche medizinische Wochenschrift. 101(12):455-7.
18. Feldman EJ, Isenberg JI, Grossman MI. 1981. Gastric acid and gastrin response to decaffeinated coffee and a peptone meal. JAMA. 246(3):248-50.
19. H. Glatzel and K. Hackenberg, Effects of Caffeine Containing and Decaffeinated Coffee on the Digestive Functions: X-ray Studies of the Secretion and Peristalsis of Stomach, Intestines and Gallbladder, Medizinische Klinik, April 21, 1967;62(16):625-28.
20. Huang, J.Q., Hunt, R.H. 1999. pH, healing rate, and symptom relief in patients with GERD. Yale Journal of Biology and Medicine. 72(2-3): 181-94.
21. Marotta, R.B. and Floch, M.H. 1991. Diet and nutrition in ulcer disease. The Medical Clinics of North America. 75(4): 967-79.
22. Robertson, D., Frolich, J.C., Carr, R.K., Watson, J.T., Hollifield, J.W., Shand, D.G. and J.A. Oates. 1978. Effects of caffeine on plasma renin activity, catecholamines and blood pressure. New England Journal of Medicine. 298(4):181-6.
23. Lane, J.D., Adcock, R.A., Williams, R.B. and C.M. Kuhn. 1990. Caffeine effects on cardiovascular and neuroendocrine responses to acute psychosocial stress and their relationship to level of habitual caffeine consumption. Psychosomatic Medicine. 52(3):320-36.
24. Lane, J.D. 1994. Neuroendrocine Responses to Caffeine in the Work Environment. Psychosomatic Medicine. 546:267-70.
25. Kerr, D., Sherwin, R.S., Pavalkis, F., Fayad, P.B., Sikorski, L., Rife, F., Tamborlane, W.V. and During, M.J. 1993. Effect of caffeine on the recognition of and responses to hypoglycemia in humans. Annals of Internal Medicine. 119(8):799-804.
26. Roca, D.J., G.D. Schiller, and D.H. Farb. 1988. Chronic Caffeine or Theophylline Exposure Reduces Gamma-aminobutyric Acid/Benzodiazepine Receptor Site Interactions. Molecular Pharmacology, May;33(5):481-85.
27. Cantu, P., Carmagnola, S., Savojardo, D., Allocca, M. and Penagini, R. 2003. Effect of non-selective gamma-aminobutyric acid receptor stimulation on motor function of the lower oesophageal sphincter and gastro-oesophageal reflux in healthy human subjects. Alimentary pharmacology & therapeutics. 18(7):699-704.
28. Koek GH, Sifrim D, Lerut T, Janssens J, Tack J. 2003. Effect of the GABA(B) agonist baclofen in patients with symptoms and duodeno-gastro-oesophageal reflux refractory to proton pump inhibitors. Gut. 52(10): 1397-402.
29. Naliboff BD, Mayer M, Fass R, Fitzgerald LZ, Chang L, Bolus R, Mayer EA. 2004. The effect of life stress on symptoms of heartburn. Psychosomatic Medicine. 66(3):426-34.
30. Roberfroid MB. 1997. Health benefits of non-digestible oligosaccharides. Advances in experimental medicine and biology. 427: 211-9.
31. Silverman, K., Evans, S.M., Strain, E.C. and Griffiths, R.R. 1992 Withdrawl Syndrome after the Double-Blind Cessation of Caffeine Consumption. The New England Journal of Medicine. 16(327): 1109-14.
32. Cherniske, S. Caffeine Blues: Wake Up to the Hidden Dangers of America�s #1 Drug. Copyright 1998.
33. Fetrow, C.W. and J.R. Avila. Professional�s Handbook of Complementary and Alternative Medicines. Second Edition. Copyright 2001.
34. Murray, M., and J. Pizzorno. Encyclopedia of Natural Medicine, Revised Second Edition. Copyright 1998.
35. Physicians Desk Reference for Herbal Medicines. Second Edition. Copyright 2000.
36. Roehl, E. Whole Foods Facts: The Complete Reference Guide. Copyright 1996.
37. Biddle, W. 2003. Gastroesophageal reflux disease: current treatment approaches. The Official Journal of the Society of Gastroenterology Nurses and Associates 26(6): 228-36.

(Reviewed by Meri Rafetto, RD, Theresa Grumet, RD, and Gerri French, RD, MS, CDE)

TCM practitioners agree that auricular acupuncture helps clients develop a balance in mind and body, and helps them to substitute healthy self-nurturing behavior for addictions or habits that are destructive–a process of healing that can be a source of strength with a renewal of the flow of vital forces, or qi.

Auricular acupuncture has been headline celebrity news for some years. Celebrities such as Kate Moss have publicly commended the use of auricular acupuncture. Today, addiction is not just a matter of substance abuse. Shopping, gambling, sex, the internet, food and even the use of Blackberries and other mobile internet devices – can be addictive. The common thread is that all of these are compulsive, emotional disorders, which even Western medical practitioners admit – can be curbed by the use of Auricular Acupuncture.

TCM looks at addiction as a two-part problem. The first part is mental and emotional obsession for something or to do something. Afterwards, there is a physical and emotional craving. TCM practitioners find ear acupuncture treatment helps to deal with that mental obsession. Auricular acupuncture then works to restore this balance.

For more information on herbs and health please contact Pacific College of Oriental Medicine at (800) 729-0941, or visit http://www.PacificCollege.edu

The following information is provided for information purposes. In most cases, the procedures described below should be reserved for individuals subject to court order drug testing, or those individuals in drug rehabilitation programs. For routine drug monitoring, follow the instructions provided with the sample collection container.

Preparation of Restroom

In the event collection protocols preclude direct observation such as those mandated by the Federal regulations, the restroom facility should be prepared in such a manner as to strictly limit the possibility of specimen adulterations. A facility prepared as below has come to be known as a “Dry Room”.

1. Remove all powders, liquids, or any substances that could be introduced into the specimen. Check under the sink and any wall mounted dispensers. Be sure the trash pail is empty or preferably outside the dry room. Prepackaged towelettes for hand-washing may be given to the patient after transfer of the specimen to the collection agent.

2. Blue the toilet water with any variety of dark blue disinfectant/cleaners.

3. Turn off all other water sources. Some facilities find it difficult to dedicate a restroom entirely as a “Dry Room”, but this inconvenience can be made bearable. Under the sink, there are usually two accessible hot and cold water valves whose center screws can be removed, still permitting the handles to properly operate the valves, and be easily removed before the collection procedure. The handles may be replaced after collection and the water turned on to permit normal use.

A restroom prepared in this manner and inspected before each use will permit the collection of urine specimens with a high specimen integrity confidence.

Collection Procedures

When the patient arrives for the preplacement physical examination, positive identification by picture I.D. or other suitable identification should be provided. The patient should then be gowned for the physical. A patient in a hospital gown is much less likely to successfully hide a substitute urine during the physical and bring it into the dry room later. After the physical is complete, the urine specimen collection procedure should commence as follows.

1. Inspect the drug room for proper condition.

2. Have the patient complete any disclosures, releases, or waivers necessary (see Exhibits A-C). Do not allow the patient to bring any coats, purses, backpacks, etc. into the bathroom.

3. Allow the patient to select a container/cap and seal from several available. If a split specimen is to be taken (i.e. one for standard urinalysis and another for drug screening), a large volume container may be selected. All transfers of urine from one container to the next must be done in full view of both the patient and the collection agent.

4. Instruct the patient to fill the container, and close the door to permit privacy.

When the patient has voided, the specimen should be handed to the collection agent who then caps and seals the specimen in full view of the patient.

Phencyclidine (PCP, Angel Dust) is a cheap and popular drug often concentrated in selected socioeconomic groups. PCP may be characterized as a hallucinogenic drug due to the wide range of bizarre behaviors associated with individuals under the influence. It was originally used as a veterinary tranquilizer and has had some human experimentation, but the bizarre recovery room effects made it useless. PCP has been illicitly used since the 1960’s, but not a widely abused drug until the 1980’s when it was placed on cigarettes (Sherms), and smoked. Smoking allows the user to rapidly and accurately titrate their dose. The effects of a drug ingested by smoking are quickly felt since it is rapidly absorbed by the lungs into the bloodstream and circulated to the site of action in the brain. Thus, smoking allows the user a rapid feedback on how “high” they are getting. Phencyclidine is easily manufactured from relatively common chemical precursors, is relatively potent, and long lasting. These factors combined make it a frequently abused illicit drug.

Pharmacological Effects

Phencyclidine is rapidly absorbed from the lung and easily crosses the blood/brain barrier. In an average size (150 lb.) individual, each absorbed milligram (mg) will produce approximately 10 ng/ml concentration in the blood. Symptomatic blood concentrations range from about 4 ng/ml to 100 ng/ml. Symptoms progress from barely observable/perceptible at the lower end to comatose/catatonic at 100 ng/ml. Higher concentrations have been recorded. Observable symptoms include “ether” breath (or “solvent” breath), nystagmus (vertical and horizontal) movements of the eye, “moon walk”, and a diverse variety of behavior including hallucinations, catatonic rigidity, “superhuman” strength, lack of stimulus to pain, time distortions, and lack of memory and events while “stoned”.

Laboratory Methods

Phencyclidine has several analogues and precursors. Most are illegal. Some labratories screen for phencyclidine by immunoassay and confirms by gas chromatography/mass spectrometry (GC/MS).

Cutoff and Detection Post Dose

The immunoassay technique used to detect PCP in urine has a cutoff level of 25 ng/ml. PCP is cleared from the bloodstream with a relatively long half life of 7-11 hours. Because it is a lipid (fat) soluble drug, detection in the urine is possible up to 48 hours or longer post dose. Blood levels correspond much better than urine to behavioral effects, i.e. being under the influence, but urine is a better screening fluid since drugs are concentrated for elimination. Confirmation levels on GC/MS is 25 ng/ml.

Barbiturates have been known since 1864 when Dr. A. von Bayer synthesized barbituric acid. In 1903, barbital was introduced as a hypnotic for routine medicinal use. They were reclassified as Schedule 2 drugs in 1979 requiring a triplicate prescription to reduce the abuse of barbiturates. The benzodiazepines (Valium, Librium, Xanax) are generally safer in overdose and have largely replaced the use of barbiturates in medicinal pharmacology. Barbiturates are numerous, chemically derived from a common 2,4,6 trioxohexahydropyrimidine (barbituric acid) nucleus. Some of the common names are: phenobarbital (Luminol®), secobarbital (Seconal®), pentobarbital (Nembutal®), butalbital (Fiorinal®), amobarbital (Amytal®), and many others.

Pharmacological Effects

Barbiturates reversibly depress the activity of all excitable tissues. The use of phenobarbital in epilepsy, one of the few major remaining useful areas of barbiturate pharmacology, is due to its selective anticonvulsant activity depressing low frequency electrical activity in the cortex. Tolerance to barbiturates occurs with continued use. At first, a generalized sedative effect gives way to tolerance, especially toward effects on mood, sedation, and hypnosis. Like other central nervous system depressant drugs, barbiturates are abused and some individuals develop a dependence on them. Dependence upon and tolerance to barbiturates are closely related. The former, generating the drug seeking behavior that leads to increased usage and consequent higher levels of tolerance and hence the extent, duration, and continuity of abuse prior to withdrawal.

Laboratory Methods

Some labratories utilize immunoassay (EIA) for detecting barbiturates in urine. The immunoassays provide a cost effective, sensitive method for detection and reacts with a number of barbiturates. Gas chromatography/mass spectrometry (GC/MS) is used to further identify and confirm the presence of a particular barbiturate in the sample.

Cutoff and Detection Post Dose

The 200 ng/ml cutoff for the screening immunoassay allows detection of barbiturate use for up to 72 hours post dose. The cutoff level for GC/MS is 200 ng/ml for all barbiturate metabolites (amobarbital, butabarbital, butalbital, pentobarbital, phenobarbital, secobarbital). Various barbiturates have differing half lives of clearance post dose. For instance, the short acting barbiturate, secobarbital, has a half life of 29-34 hours, while phenobarbital, a long acting barbiturate, has a half life of 24-140 hours. Thus, use of phenobarbital may be detected much longer than secobarbital.

Volatile substances include the most frequently abused drug – ethanol. Ethanol (ethyl alcohol, drinking alcohol) is the most widely used intoxicant, legal unless it impairs one’s performance to operate a motor vehicle or other machinery. Some labratories includes this common drug on all Industrial Drug Screens along with other common volatiles detected simultaneously. These include acetone, occasionally found in diabetics, methanol (grain alcohol), and isopropanol (rubbing alcohol). Ethanol is occasionally found in preplacement screens and frequently found in the large Coma Screens, especially in trauma patients (automobile accidents).

Pharmacological Effects

Ethanol in low doses, generally less than 0.04% blood equivalent, is a slight stimulant to humans. It has been demonstrated that a small quantity of alcohol increases the acetylcholine neuroreceptor activity. In larger doses, it has generalized effects graduating from euphoria through stupor. Death generally occurs from unconsciousness and cessation of breathing. This may be complicated by aspiration of vomitus into the lung due to absent gag response. Patients with very high levels may be placed on a respirator or assisted breathing.

Ethanol and Other Drugs

In overdose, ethanol is often found in combination with other drugs – polydrug abuse. Evidence is gathering in scientific literature that the use of marijuana and alcohol together may be more than additive in its effects, i.e. synergistic. This has important consequences for driving under the influence or operation of other machinery. Barbiturates and alcohol are the classic synergistic combination (the interaction of the two drugs so that the sum of the impairment is greater than the individual contributions).

Urine Concentration and Blood Equivalents

Urine concentrations of ethanol, as reported by some labratories, are convertible to blood levels by the following formula: divide the urine concentration by 1.3. For instance, the urine concentration of 0.20% is equivalent to a blood concentration of 0.154%. There is, however, some individual variation in this ratio. Urine levels reflect the average blood concentration over the period of time the urine is produced. To better correlate with current blood levels, a second void may be taken to reflect the blood concentration during the time period between voids.

Laboratory Methods

Ethanol is screened in urine using an automated ethanol dehydrogenase enzymatic assay, and confirmed by quantitative gas chromatography via direct injection with an internal standard on a Carbowax column approved by the FDA for use in clinical laboratories. This gas chromatographic method allows the separation and quantitation by many volatile substances, especially ethanol, but is also useful in quantitation of other abused inhalants such as gasoline or glue (toluene). Positives are repeated with a new sample for confirmations and quantitation. Industrial drug screens are only occasionally positive, but volatiles are frequently found in “for cause” requests. Occasionally, fermentation of urine containing high concentrations of glucose (especially diabetics), is a source of exogenous alcohol. In the event of an alcohol positive in urine, some labratories check for the presence of glucose, and reports it if found.

Cutoff and Detection Post Dose

Using enzyme immunoassay for initial screening and gas chromatography confirmation, volatiles in urine are detected at a cutoff level of 0.04%. Since ethanol metabolizes at 0.02% blood level per hour, detection post dose varies directly with the amount ingested. When an individual no longer feels any effect, ethanol is generally non detectable (less than .02%).

Benzodiazepines are generally classified as minor tranquilizers useful in the management of anxiety. Benzodiazepines include drugs such as diazepam (Valium®), chlordiazepoxide (Librium®), oxazepam (Serax®), lorazepam (Ativan®), alprazolam (Xanax®), clonazepam (Clonopin®), and others. Some, such as flurazepam (Dalmane®), alprazolam (Xanax®) and triazolam (Halcion®), are used as sleeping aids. They have generally replaced barbiturates in the induction of sleep and sedation. Clonazepam (Clonopin®) is useful in the treatment of epilepsy. Many common benzodiazepines are detected in urine by their metabolites oxazepam and nordiazepam. Benzodiazepines are prescription drugs and occasionally sold on the illicit market. They are widely prescribed and relatively free of dangerous acute toxic overdose effects. Some illicit fake methaqualone (Quaalude) from Mexico actually contains large doses of diazepam.

Pharmacological Effects

Benzodiazepines have varied effects and as many as 2,000 have been synthesized. They act selectively on the polysynaptic pathways throughout the central nervous system. Benzodiazepine receptor sites have been identified in the brain. The mechanism of action may be related to the metabolism of gamma aminobutyric acid (GABA). Benzodiazepines undergo extensive biotransformation (metabolism) and identification of the particular benzodiazepine is best performed on blood following a positive urine screening.

Laboratory Methods

The immunoassays (EIA) are utilized to detect benzodiazepines in urine. All positives are confirmed by GC/MS.

Cutoff and Detection Post Dose

Cutoff by immunoassay is 200 ng/ml for benzodiazepine metabolites. This level is sufficient to detect the most common benzodiazepines for 48-72 hours post single dose and as long as a week post dose under some circumstances. GC/MS cutoff levels for the various benzodiazepine metabolites is 100 ng/ml.

Opiates are a very old class of drugs derived from the exudate of the opium poppy and used for centuries for pain relief. Morphine is the principal alkaloid in opium and the name morphine was derived from the Greek god of dreams – Morpheus. The psychological effects of opium were known to the ancient Sumerians, but the first undisputed reference to the opium poppy dates from the third century B.C. Like so many drugs, modern chemistry has extensively experimented with the drug’s chemistry, resulting in more useful, potent, and addictive opioid derivatives. The invention of the hypodermic needle increased the abuse of morphine. The smoking of opium by the Chinese workers in the late 1800’s, use of morphine for Civil War casualties, and lack of regulation until the first part of the 20th century all contributed to the rise of opioid abuse. Heroin, a very potent opioid, was synthesized for use during the Civil War resulting in the addiction of many Civil War soldiers.

Pharmacological Properties

Opioids are the preferred term referring to the large chemistry of exogenous substances binding to opioid receptor sites producing agonistic effects. Opioids share some of the properties of naturally present peptides called endorphins and enkephalins. Opioids have specific receptor sites causing the effects which may be specifically blocked by opioid antagonists such as naloxone or naltrexone, related chemical structures that will bind to the receptor displacing opioids. This drug is used as an antidote to opioid overdose.

Morphine, heroin, codeine, and many related synthetic opioid analogues produce their major effects on the central nervous system (CNS) and the bowel. Effects are diverse including analgesia, drowsiness (nodding), changes in mood, respiratory depression, and decreased gastrointestinal motility. Pupils are constricted and not responsive to light stimulus. Heroin, the most abused and addictive opioid, is synthesized from morphine by acetylation to diacetylmorphine. After intravenous injection, it is rapidly diacetylated to morphine and further metabolized by the liver to other urinary metabolites including codeine. Codeine is also a popular oral medication. For an opioid addict, heroin is preferable but they will use any available opioid. Methadone is a synthetic opioid which has agonistic actions, but has relatively weak effects on mood and is used to “maintain” opioid addicts. Naltrexone (Trexan) is also useful as a long term antagonistic.

Laboratory Methods

Laboratory detection of morphine and codeine is performed by immunoassay. Confirmation is by gas chromatography/mass spectrometry (GC/MS).

Cutoff and Detection Post Dose

The detection limit of the initial screen is 300 ng/ml, with a sensitivity of 20 ng/ml. This is sufficient to detect heroin use for approximately 24-48 hours post dose and codeine for somewhat longer. Positives are confirmed on GC/MS at a cutoff level of 300 ng/ml.

Cocaine is one of the most abused drugs in the United States. Isolated in 1859 and brought to attention through a series of papers by Dr. Sigmund Freud, cocaine was subsequently adopted as a useful topical anesthetic. Its non prescriptive use was illegalized by the Harrison Act of 1914.

Pharmacological Effects

Generally, 50-100 mg of cocaine is necessary for intranasal “snorting” associated with a “high”. Cocaine injected intravenously is often mixed with heroin, referred to as “speed balling”. Cocaine, in the form of a very pure free base, “crack” is smoked in a pipe. The more direct and concentrated the route of administration, the faster habituation occurs. Euphoric feelings produced by cocaine eventually give way to depression, paranoia, habituation, and other dysfunctions. Primates (monkeys), given the choice between cocaine and food, have died while continuously choosing cocaine. Clearly a dangerous drug, cocaine is not a cheap or easy high, has serious addictive properties, and societal consequences.

Laboratory Methods

Cocaine and its primary metabolite benzoylecgonine are routinely detected by a variety of laboratory techniques. Some Laboratories utilize the immunoassays for initial screening with confirmation of positives by gas chromatography/mass spectrometry (GC/MS).

Cutoff and Detection Post Dose

The initial screening cutoff level is 300 ng/ml for cocaine and its metabolite benzoylecgonine. Use of cocaine for euphoria may result in positive urines above this level for 48-72 hours post dose. Longer times will be observed in the habituated person using large quantities. The GC/MS cutoff level is 150 ng/ml.

Pharmacological Effects

Smoked doses of 20 mg (two potent cigarettes) of delta-9-THC will produce increases of 20 to 50 beats per minute in heart rate, impairment of short term memory and concentration, possibly mood changes such as euphoria, altered perception of time, hunger, and other effects. At higher doses, marijuana interferes with motor coordination and complex task functioning. Activities requiring a high degree of alertness such as operating machinery, driving or working in dangerous environments are contraindicated. Pharmacological effects from inhaled drugs begins almost immediately. Delta-9-THC plasma levels peak 10 to 20 minutes post inhalation and begin to decline. Effects last for two to three hours.

Studies indicate that marijuana and alcohol potentate one another more than either drug alone. Thus, smaller amounts of ethanol and marijuana may increase toxic effects. Peak levels of marijuana metabolites in the urine occur about five hours post dose and thus are not useful in predicting the degree of intoxication. Urinary presence only indicates recent exposure. Note marijuana metabolite testing is available only in urine, not hair.

Laboratory Methods

Immunoassays are used to initially screen specimens for cannabinoids (THC). Confirmation of positives is by GC/MS.

Cutoff and Detection Post Dose

The initial screening cutoff level is 50 ng/ml. The GC/MS cutoff level is 15 ng/ml. The elimination half-life of marijuana ranges from 14-38 hours. At the initial cutoff of 50 ng/ml, the daily user will remain positive for perhaps 7 to 30 days after cessation. At the confirmation level of 15 ng/ml, the frequent user will be positive for perhaps as long as 15 weeks. Marijuana metabolites’ storage and slow release from lipid tissues is the reason for this long detection period.

Passive Inhalation

Urine levels of 5 ng/ml have been reported from passive inhalation. One recent survey indicated that one subject in a passive inhalation experiment achieved a level of 23 ng/ml. This is unusual, but points out the usefulness of higher cutoff levels such as 50 ng/ml. The higher 50 ng/ml level eliminates the possibility of passive inhalation, is a level of very high reliability, and indicates more recent use.