Posts by Deacon

11

Need Advice

by scary_goat2000 in

jw
friends

need some help from you guys.. i am a divorced jw (ex was never baptized) free to remarry.

i have been seeing a wonderfull christian woman and have moved in with her.

we plan to marry in the spring.

rambles in the storm....

by Deacon in

jw
friends

how far down the path is it before the changes take place.

im pretty sure its different for everyone.

the time taken to recognise that things have changed permanently...depends on factors like acceptance, circumstances and willingness to deal with it.. im talking about the realisation regarding the wtbt society.

Deacon

How far down the path is it before the changes take place. Im pretty sure its different for everyone. The time taken to recognise that things have changed permanently...depends on factors like acceptance, circumstances and willingness to deal with it.

Im talking about the realisation regarding the WTBT Society. Im talking about the fundamental issues regarding failed prophecy...but mostly about the realisation regarding how Witnesses treat each other.

We were taught that the anointed were sacred. My experience with all but two, is that they are eccentric buffoons at best....and egocentric maniacs at worst. We were taught that 1914 was Christs return to earth...but that was not the message until 1925..prior to that it was going to be the end.

We were taught that ....you know what..? You all know what we were taught...99% here know the doctrines...

Im sat here in a thunderstorm, with some scared cats running around, trying to put a handle on the whole situation..trying to see where to go, but mainly, what to believe in. I think it would be fair to say that the majority here..have long lost faith in religion and the concept of the bible god....and while I dont want to willingly go down that route...I find my cynicism hardening toward religion in general and JW's in particular.

I still pray..every night..and during the day...sometimes I stop my car and just pray for 20 minutes or so...asking for direction, asking for any help at all...just point me..Ill follow...Im still waiting..

So..the effects of deprogramming are still working the way through...I have given up on ever rejoining the JW's...it made me feel sad and inadequate for 40 years, more than that, at times it made me feel worthless, I cannot take the hypocrisy of the religion or the people in it...and all of them do it without knowing they are hypocrites...

I have no answers for me..just keep on looking, keep on hoping.. but the reality I now accept, is that we are not special people..we will die just like the rest..and what happens then, well...

There are a number of really gentle and sensitive persons on this board..people like Joel..who deserve a little more respect than they have been given. Most of us feel we deserve more respect than we receive, in his case, it is very true..HIs life is far more complicated than most of ours...I am a little dissapointed that people like him, who bore all the personal hatred of some with a lot of dignity...have not been upbuilt in human companionship on This ex JW board...we all have the same history...and yet we have not learned to pick battles with those who can take it, and those who cannot.

I guess when Joel and others have recovered a little strength, they will return for the friends they have on the board..and for their own upbuilding...I hope so..

I learned a lot from people here...Path, 6, Prisca, Mommy, JanH, Farkel, Allan, Englishman...Im not going to mention anymore because it would be half the board...but in the learning was a filtering out..a sifting of information...and now Im really confused! LOL..

Even to those I think are the most pompous and arrogant ***holes....I learn things from...

Its just a journey, but this time we can take it with eyes wide open...and no allegience to false prophets.

I think thats what I meant to say...

22

Victims of Groupthink

by larc in

jw
friends

groupthink,.

before i begin, i want to acknowledge two people who drew out the implications of the findings of social psychology in understanding the dynamics of the culture of the jehovah's witnesses.

jang offered some exellent information on this subject.

Deacon

. http://128.100.159.139/FIS/Courses/LIS2149/Groupthink.html

70

My husband is smoking pot

by jurs in

jw
friends

i know this is not witness related but i just caught my husband smoking pot.

i am so upset !!!

he is an alcoholic and has a terrible temper.

Deacon

Jurs

If alcohol or drugs are involved in any family problems...then they ARE the problem.

Being in the biz (medicine)...Ive listened to all angles of viewpoints re: the matter.

Bottom line is, generally it is not beneficial for anyone to abuse substances, and specifically not for individuals who cannot say no or who have no off switch.

My professional observation over 24 years of practice..there is no minimum or maximum as to what substance usage causes problems...for some it is as little as one drink, to others its 20 pints of beer or a bottle or two of spirits...one hit of pot or a pound of it...

If the reliance is there on anysubstance...then the problem is there too.

One thing I know for absolute sure. Whether is is drink or drugs...the individual is not reacting under their own mental capacity and rationality...you have no relationship with a bottle or a joint..and that is what you are dealing with.

9

Tick list for establishing whether a cult or not..

by Deacon in

jw
friends

1/.milieu control: control of the group environment and communication .

2/.manipulation: leaders are perceived as being chosen by god, history or some supernatural force.

salvation can only be attained through the cult .

Deacon

1/.Milieu control: control of the group environment and communication

2/.Manipulation: Leaders are perceived as being chosen by God, history or some supernatural force. Salvation can only be attained through the cult

3/.Purity demands: An us vs. them mentality is developed, in which cult members are the only pure and good.

4/.Confession: group confession and self-criticism is used in order to produce personal change

5/.Sacred Science: The cult's doctrines and ideology are considered sacred and must not be doubted or questioned.

6/.Loading the language: Conventional words and phrases are given special, in-group meanings.

7/.Doctrine over person: Members are conditioned to feel guilt if they ever question group doctrine. One must subject one's experience to the "truth," as taught by the group.

8/.Dispensing of Existence: The group contains the elite; outsiders are evil, unsaved, and may not even have the right to exist. Leaving the group will have devastating consequences.

9/.An authoritarian power structure, with authority concentrated at the top

10/.Charismatic or Messianic leader(s) (They define Messianic as meaning that the leaders identify themselves as God or state that they are the only persons capable of interpreting the Bible properly

11/.The use of deceitful methods in recruitment of new members and/or raising of money

12/.Isolation from society; filtering of information

13/.The use of mind control methods on the membership.

70

My husband is smoking pot

by jurs in

jw
friends

i know this is not witness related but i just caught my husband smoking pot.

i am so upset !!!

he is an alcoholic and has a terrible temper.

Deacon

LOL 6...

My professional experience with both alcohol and marijuana, is that while some beers can be of nutrient value..marijuana is not.

It is the personality of the individual here, whether addictive or a self abuser..people dont drink to excess for nutritional value. Drugs for effect are just extensions of that factor.

Alanon will give some very clear rational direction for your life Jurs, it will enable you to focus on what is important and allow your husband to choose what he wants to do.

I would recommend one book to read as well..

its called sober for good by anne Fletcher ISBN 0-395-91201-6

I wish you well and all the love in the world.

70

My husband is smoking pot

by jurs in

jw
friends

i know this is not witness related but i just caught my husband smoking pot.

i am so upset !!!

he is an alcoholic and has a terrible temper.

Deacon

Adverse Effects of Marijuana.
Issue: Dec 1, 1999

Could I become chemically dependent on marijuana?

Yes. When you're chemically dependent on marijuana, it means you crave it and you need to take more and more to get the same effect. You may have withdrawal symptoms when you stop using it. Because marijuana is a lot stronger than it used to be, you're also more likely to abuse it and become dependent on it today than in the past.

Is marijuana use associated with other drug use?

Yes. Usually people use legal drugs like alcohol or cigarettes before they start using marijuana. Marijuana is the most commonly used illegal substance in the United States. It's often the first illegal drug used and sometimes leads to the use of other illegal drugs.

What are the common side effects of marijuana use?

Some of the common side effects of marijuana are:

* Trouble remembering things

* Sleepiness

* Anxiety

* Paranoia

* Altered time perception

Using marijuana for a long time makes some people lose interest in school, work, relationships and other activities. It may cause legal problems and can be dangerous in certain situations, like driving.

How might marijuana affect me physically?

Some of the common physical effects of marijuana include:

* Tremors

* Nausea

* Headache

* Worsening coordination

* Breathing problems

* Increased appetite

* Reduced blood flow to the brain

* Changes in the reproductive organs

Like tobacco, marijuana contains many chemicals that can hurt the lungs and cause cancer. One marijuana cigarette can cause more damage to the lungs than many tobacco cigarettes, because marijuana has more tar in it and is usually smoked without filters. Unpleasant side effects from marijuana occur in about 40 to 60 percent of people who use marijuana.

70

My husband is smoking pot

by jurs in

jw
friends

i know this is not witness related but i just caught my husband smoking pot.

i am so upset !!!

he is an alcoholic and has a terrible temper.

Deacon

Effects of Marijuana on the Lung and Its Immune Defenses
Donald P. Tashkin, M.D.,
UCLA School of Medicine

Abstract

Habitual marijuana use may lead to the following effects on the lung:

acute and chronic bronchitis;
extensive microscopic abnormalities in the cells lining the bronchial passages (bronchial epithelium), some of which may be premalignant;
overexpression of genetic markers of progression to lung cancer in bronchial tissue;
abnormally increased accumulation of inflammatory cells (alveolar macrophages) in the lung; and
impairment in the function of these immune-effector cells (reduced ability to kill microorganisms and tumor cells) and in their ability to produce protective inflammatory cytokines.
Clinically, the major pulmonary consequences that may ensue from regular marijuana use (approximately one "joint" per day on the average) are pulmonary infections and respiratory cancer. Infections of the lung are more likely in marijuana users due to a combination of smoking-related damage to the ciliated cells in the bronchial passages (the lung's first line of defense against inhaled microorganisms) and marijuana-related impairment in the function of alveolar macrophages (the principal immune cells in the lung responsible for defending it against infection). Patients with preexisting immune deficits due to AIDS or cancer chemotherapy might be expected to be particularly vulnerable to marijuana-related pulmonary infections. Finally, biochemical, cellular, genetic, animal, and human studies all suggest that marijuana is an important risk factor for the development of respiratory cancer. However, proof that habitual use of marijuana does in fact lead to respiratory cancer must await the results of well-designed case-control epidemiologic studies. Such studies should now be feasible after the passage of 30 years since the initiation of widespread marijuana use among young individuals in our society in the mid-1960’s.
Introduction

Marijuana is the second most widely smoked substance in our society after tobacco (Johnston et al. 1995, 1996). Since marijuana is smoked, the lung is exposed to higher concentrations of the inhaled smoke constituents than any other tissue, causing concern about possible harmful effects of marijuana on the lung by analogy with the wellknown detrimental effects of tobacco on the lung (U.S. Department of Health, Education, and Welfare 1979). Pulmonary consequences of regular tobacco smoking include (1) lung cancer; (2) chronic obstructive pulmonary disease (COPD), which consists of chronic bronchitis and emphysema; and (3) an increased incidence of respiratory tract infection due to smoking-related impairment in the lung's host defenses. The importance to public health of these pulmonary consequences of tobacco is underscored by the fact that lung cancer accounts for over 125,000 deaths each year in the United States; COPD causes approximately 90,000 deaths per year and more chronic disability than any other medical illness; and respiratory tract infection (acute bronchitis and pneumonia) is a frequent cause of impairment in activities of daily living, increased utilization of health care resources, and even mortality. In this report, the evidence concerning the potential for habitual use of marijuana to produce adverse effects on the lung comparable to those caused by tobacco will be reviewed.

Smoke Contents of Marijuana and Tobacco

Analysis of the smoke contents of marijuana and tobacco reveals much the same gas phase constituents, including chemicals known to be toxic to respiratory tissue (Hoffmann et al. 1975; Novotny et al. 1982). Moreover, these gas phase components are present in somewhat similar concentrations in the smoke generated from the same quantity of marijuana and tobacco. The particulate phase (tar) constituents of marijuana and tobacco smoke are also generally similar, with the major exception that marijuana contains tekahydrocannabinol (THC) and scores of other llIC-like (cannabinoid) compounds not found in tobacco, while tobacco tar contains nicotine not found in marijuana. With regard to the carcinogenic potential of marijuana, it is noteworthy that the tar phase of marijuana smoke contains many of the same carcinogenic compounds contained in tobacco smoke, including polycyclic aromatic hydrocarbons, such as benz[a]pyrene, which was recently identified as a key factor promoting human lung cancer (Denissenko et al. 1996).

Animal Studies

Animal and human studies provide the biologic evidence that regular exposure of the lung to the noxious components in marijuana smoke is, in fact, injurious to lung tissue. Studies in animals exposed to varying doses of marijuana smoke for from 12 to 30 months have shown extensive damage in dogs (Roy et al.1976) and monkeys (Fligiel et al. 1991) to the smaller airways, which are the major site of injury due to tobacco-related COPD, as well as acute and chronic pneumonia in rats (Fleischman et al. 1979; Rosenkrantz and Pleischman 1979) and monkeys (Fligiel et al. 1991). On the other hand, rats exposed for 1 year to increasing doses of marijuana smoke failed to demonstrate any anatomic or functional evidence of emphysema, whereas such evidence was apparent in tobacco-exposed rats (Huber and Mahajan 1988).

Human Studies

Early human studies yielded mixed results: some reported an association between regular marijuana use and chronic bronchitis and emphysema (Chopra 1973; Hall 1975), while others failed to find such a relationship (Boulougouris et al. 1976; Rubin and Comitas 1975). These studies may be criticized because of deficiencies in experimental design, including (1) failure to control for the important confounding variable of tobacco, (2) only small numbers of participants, and (3) probable selection biases.

Chronic respiratory symptoms

Subsequently, Tashkin and colleagues (1987) reported the following findings in a large sample of volunteers recruited from the LosAngeles area, including 144 heavy, habitual smokers of marijuana only (MS) and 135 smokers of marijuana plus tobacco (MTS), as well as 70 smokers of tobacco only (TS) and 97 nonsmokers (NS). Compared to NS, a significantly higher proportion of MS (15-20 percent) acknowledged symptoms of chronic bronchitis (chronic cough and phlegm production). While 20-25 percent of TS also reported symptoms of chronic bronchitis, the proportion of symptomatic TS did not differ significantly from that of symptomatic MS (despite a marked disparity in the amount of each substance smoked per day: 3 joints of marijuana vs. more than 20 cigarettes of tobacco), and no additive effects of marijuana and tobacco were noted. Similar findings were reported by Bloom and coworkers (1987) in a randomly stratified sample of young individuals (15 40 years of age) residing in the Tucson area' with the exception that these investigators noted an additive effect of marijuana and tobacco that was not observed in the Los Angeles study.

Lung function

In the Tucson study (Bloom et al. 1987), regular marijuana use (approximately 1 joint/day on the average) by young persons was associated with significant impairment in measurements that reflect the function of the small airways—the major site of COPD. These changes were even greater than those noted in young regular tobacco smokers, and the effects of both marijuana and tobacco appeared to be additive. The authors concluded that regular marijuana smoking was a risk factor for the development of COPD, which, in its advanced stages, is characterized by disabling shortness of breath. In contrast, the Los Angeles study (Tashkin et al. 1987) failed to find any impairment in small airways function in association with even heavier regular use of marijuana (3 - joints per day), although mild, statistically significant narrowing of large, central airways was noted in the marijuana users. Recently, a longitudinal analysis of the lung function results obtained in Los Angeles (Tashkin et al. 1997) revealed an accelerated rate of decline in lung function with age (as is characteristic of tobacco smokers who are destined to develop symptomatic COPD) in the tobacco-smoking participants but failed to find such an effect in the marijuana smokers. The mixed findings from these two studies leave open the question as to whether habitual smoking of marijuana, in the absence of tobacco, can lead to COPD.

Bronchoscopic findings: visual appearance and microscopic alterations in bronchial wall biopsies

Bronchoscopy was performed in 53 NS, 40 MS, 31 IS, and 44 MTS who participated in the LosAngeles study (Fligiel et al. in press; Gong et al. 1987) to ascertain whether regular smoking of marijuana with or without tobacco might cause damage to the airways and lung that might not be reflected by abnormalities in lung function. Visual inspection of the appearance of the large, central airways showed that a large proportion of smokers of marijuana or tobacco alone (but rarely nonsmokers) showed evidence of increased redness (erythema) and swelling (edema) of the airway tissues and increased mucous secretions, and the findings in the combined smokers of both marijuana and tobacco appeared additive (Roth et al. 1996). These visual findings were correlated with microscopic evidence of increased numbers and size of small blood vessels in the bronchial wall, tissue edema, and replacement of the normal ciliated surface lining cells (ciliated columnar epithelial cells) by mucus-secreting goblet cells. These observations may explain the relatively high proportion of marijuana smokers who complain of chronic cough and phlegm. Overproduction of mucus by the increased numbers of mucus-secreting cells in the face of diminished numbers of ciliated cells (cells with hair-like projections) that normally function to transport the mucus toward the mouth by rapid ciliary motion might leave cough as the only mechanism to remove mucus from the airways.

Microscopic findings in biopsies of the bronchial mucosa (superficial layer of cells) revealed that a much higher proportion of MS than NS (and a proportion comparable to, if not greater than, that of IS) exhibited a variety of cellular abnormalities. The latter included abnormal proliferation of cells (reserve cells, goblet cells), transformation of normal ciliated cells into abnormal cells resembling skin (squamous metaplasia), accumulation of inflammatory cells, and abnormalities in the cell nuclei (Fligiel et al. in press; Gong et al. 1987). Some of these changes (e.g., nuclear alterations and squamous metaplasia) have been described as precursors to the subsequent development of lung cancer in tobacco smokers (Auerbach et al. 1961) and thus may be considered to be premalignant. Smokers of both marijuana and tobacco exhibited these microscopic cellular abnormalities to the greatest extent, suggesting an additive injurious effect of marijuana and tobacco on airway tissue. These findings in healthy, largely nonsymptomatic, young marijuana smokers confirm and extend previous bronchoscopic observations of Tennant (1980) in symptomatic U.S. servicemen who smoked cannabis (in the form of hashish) heavily.

Genetic markers of precancer progression

A specific combination of genes (oncogenes, tumor suppressor genes) that are responsible for regulating cell growth must be activated and/ or mutated for lung cells to transform into cancerous cells. Bronchoscopic biopsies from 63 participants in the Los Angeles study (12 MS, 9 MTS, 14 TS, and 28 NS), none of whom used crack cocaine, were examined for alterations in some of the genes known to be involved in the development of lung cancer. Immunohistology was used to detect the overexpression of the protein products of these genes by epithelial cells in the bronchial biopsies (Roth et al. 1996). Protein products for two of the three genes examined were markedly overexpressed in the biopsies from MS compared to NS (and even to a greater extent than in the biopsies from TS), and the effects of marijuana and tobacco were additive. Expression of the third gene, the p53 oncogene, which may play a role in as many as 75 percent of all lung cancers, was found only in a smoker of marijuana plus tobacco, as well as in one of 12 combined smokers of marijuana, cocaine, and tobacco who were also examined. These results indicate genetic evidence of extensive growth dysregulation in these relatively young smokers of marijuana alone and, particularly, in the combined smokers of marijuana and tobacco, implying an important role of marijuana use in progression to lung cancer.

Structure and function of alveolar macrophages

Alveolar macrophages are the principal immune-effector (inflammatory) cells in the lung and are primarily responsible for protecting the lung against infectious microorganisms. A saline (salt water) rinse was used in participants in the Los Angeles study at the time of bronchoscopy to harvest cells from the air spaces in the lung (over 90 percent of which are alveolar macrophages). Approximately two and three times as many alveolar macrophages were obtained from the lungs of marijuana or tobacco smokers, respectively, as from nonsmokers, and the effects of smoking both substances were additive (Barbers et al. 1987). These observations indicate that regular marijuana use produces an inflammatory response, i.e., an accumulation of increased numbers of alveolar macrophages, in the lung. Under the electron microscope, alveolar macrophages from marijuana or tobacco smokers showed a striking increase in size and complexity of inclusion bodies in their cytoplasm (probably due to ingestion by these cells of particulate material in the smoke), and macrophages from combined smokers of marijuana and tobacco were nearly completely filled by these inclusions (Bears et al. 1989). It might be expected that the padding of these important cells with large inclusion bodies would interfere with their function.

Various aspects of alveolar macrophage function have been evaluated by contributing researchers in the Los Angeles study. Compared to NS, alveolar macrophages of both MS and IS showed a significantly reduced ability to kill a common fungal organism (Candida albicans) (Sherman et al. 1991). Moreover, alveolar macrophages of MS, but not IS, showed a significant impairment in (1) their ability to ingest and kill an important bacterial pathogen (Staphylococcus aureus); (2) their ability to kill tumor cell targets; and (3) their ability to produce a variety of proinflammatory cytokines, which play a key role in immunologic responses to infection and malignancy (Baldwin et al. 1996).

Role of Marijuana in Cancer

The following lines of evidence suggest that marijuana may play an important role in the development of respiratory cancer.

The tar phase of marijuana smoke, as already noted, contains many of the same carcinogenic compounds contained in tobacco smoke, induding nitrosamines, reactive aldehydes, and up to a 50 percent higher concentration of carcinogenic polycydic hydrocarbons, induding benz[a]pyrene (Hoffmann et al. 1975). Benz[a]pyrene, which has recently been shown to promote mutations in the p53 oncogene (Denissenko et al. 1996), is believed to play an important role in human cancer.
One marijuana cigarette was shown by Wu and colleagues (1988) to deposit four times as much tar in the lung as a single filtered tobacco cigarette of approximately the same weight. The higher content of carcinogenic polycyclic hydrocarbons in marijuana tar and the greater deposition of marijuana tar in the lung act together to amplify exposure of the marijuana smoker to the carcinogens in the tar phase.
Painting tar from marijuana smoke on the skin of mice produced lesions correlated with malignancy (Cottrell et al. 1973).
Marijuana tar induced comparable numbers of mutations to those produced by tar from the same quantity of tobacco in a common bacterial assay for mutagenicity (Wehner et al. 1980).
Exposure of hamster lung cell cultures to marijuana or tobacco smoke over a period of 2 years led to accelerated malignant transformation within 3-6 months of marijuana exposure compared to control (unexposed) cell cultures. Moreover, the changes in the cells exposed to marijuana smoke were more impressive than those in the tobacco-exposed cells (Leuchtenberger and Leuchtenberger 1976).
Biopsies of bronchial lining tissue of habitual marijuana smokers demonstrated extensive cellular alterations, some of which may be considered premalignant. Effects of smoking both marijuana and tobacco on these cellular changes appeared to be additive (Fligiel et al. in press).
Bronchial immunohistology revealed overexpression of genetic markers of lung tumor progression in smokers of marijuana (Roth et al. 1996).
Preliminary findings suggest that marijuana smoke activates cytochrome P4501A1, the enzyme that converts polycyclic hydrocarbons, such as benz[a]pyrene, into active carcinogens (Roth preliminary data).
Alveolar macrophages from marijuana-only smokers have reduced ability to kill tumor cell targets (Baldwin et al. 1996).
Pretreatment of mice with THC for 2 weeks prior to implanting Lewis lung cancer cells (a non-small-cell immunogenic carcinoma) into the animals caused larger, faster-growing tumors, a finding that was correlated with the increased immunosuppressive cytokine produced by the tumor cells, transforming growth factor-beta (Zhu et al. 1997). These findings suggest a THC-related impairment in immune responsiveness to tumor antigens.
Several case-series reports indicate an unexpectedly large proportion of marijuana users among cases of lung cancer (Sridhar et al. 1994; Taylor 1988) and upper aerodigestive tract cancers (cancers of the oral cavity, pharynx, and larynx); (Donald 1991; Endicott et al. 1993; Taylor 1988) that occurred before age 45 years. These case-series reports suggest that marijuana may play a role in the development of human respiratory cancer. Without a control group, however, the effect of marijuana use on cancer risk cannot be estimated, nor can the potentially confounding effect of tobacco and other risk factors be controlled.
Taken together, the observations from a number of biochemical, cellular, genetic, tissue, animal, and clinical studies provide a biologically plausible basis for the hypothesis that marijuana is a risk factor for human cancer. What is lacking is epidemiologic evidence that marijuana indeed increases the risk of developing respiratory cancer. Because of the long period of time (latency period) required for induction of human carcinomas and the infrequent use of marijuana in the general U.S. population prior to 1966, there are currently no published epidemiologic studies that examine the association between marijuana and cancer. However, at the present time, epidemiologic investigation of this association may have become feasible since approximately 30 years have elapsed since the start of widespread marijuana use in the United States among teenagers and young adults, who are currently reaching an age when respiratory cancers are more common.
Effects of Marijuana on the Immune System

In vitro and animal studies

The recent finding of cannabinoid receptors (to which THC binds) on white blood cells (Bouaboula et al.1993) is consistent with observations that THC is capable of influencing immune responses. In vitro and animal studies suggest that THC has a general immunosuppressive effect on a variety of immune cells, induding rnacrophages, natural killer cells, and T cells (Burnette Curley and Cabral 1995; Huber et al. 1975, 1980; Klein et al. 1991; Kusher et al. 1994). Mice exposed to D9THC were unable to develop protective immunity against lung infection by Legionella pneumophilia, an opportunistic pathogen (Newton et al. 1994).

Immune deficits in marijuana smokers

As noted above, alveolar macrophages from the lungs of healthy, habitual marijuana smokers were suppressed in their ability to kill fungaland bacterial organisms, as well as tumor cells. Moreover, the same cells were suppressed in their ability to release proinflarnmatory cytokines. These findings suggest that marijuana is an immunosuppressant with clinically significant effects on host defense, which could have potentially serious health consequences in patients with preexisting immune deficits due to AIDS, organ transplantation (receiving immunosuppressive therapy to prevent rejection of the transplant), or cancer (receiving immunosuppressive chemotherapy). The latter possibility is supported by reports of fungal and bacterial pneumonias in patients with AIDS or organ transplantation who used marijuana (Caiaffa et al. 1994; Denning et al. 1991). Moreover, among HIV-positive individuals, active marijuana use has been found to be a significant risk factor for rapid progression from HIV infection toAIDS and acquisition of opportunistic infections and/or Kaposi's sarcoma (Tindall et al. 1988).

Summary

The evidence for the harmful consequences of marijuana smoking is preliminary and requires lon~term study. In the interim, prudent advice must serve where substantial clinical evidence is lacking. Habitual marijuana use, as often as one joint per day, may result in serious pulmonary consequences. In the short term, breathing may be restricted, coughing may be increased, and resistance may be lowered to opportunistic infections of the lungs such as pneumonia. Respiratory cancer is a likely result in the long term. Heavier use of marijuana is likely to have more potent, adverse health consequences.

References

Auerbach, O.; Stout, A.P.; Hammond, E.D.; and Garfinkel, A. (1961). Changes in bronchial epithelium in relation to cigarette smoking and in relation to lung cancer. New England Journal of Medicine 265:253-267.

Baldwin, G.C.; Buckley, D.M.; Roth, M.D.; Dubinett, S.M.; and Tashkin D.P. (1996). Alveolar macrophages derived from the lungs of tobacco, marijuana and cocaine users are functionally compromised. In: Harris, L.S., ed. Problems of Drug Dependence. Proceedings of the 57th Annual Scientific Meeting of the College on Problems of Drug Dependence. NIDA Research Monograph Series 162. Rockville, MD: U.S. Department of Health and Human Services, p. 192.

Barbers, R.G.; Gong, H., Jr.; Tashkin, D.P.; Oishi, J.; and Wallace, J.M. (1987). Differential examination of bronchoalveolar lavage cells in tobacco cigarette and marijuana smokers. American Review of Respiratory Diseases 135:1271-1275.

Beals, T.F.; Fligiel, S.E.G.; Stuth, S.; and Tashkin, D.P. (1989). Morphological alterations of alveolar macrophages from marijuana smokers. American Review of Respiratory Diseases 139 (part 2):A336.

Bloom, J.W.; Kaltenborn, W.T.; Paoletti, P.; Camilli, A.; and Lebowitz, M.S. (1987). Respiratory effects of non-tobacco cigarettes. British Medical Journal 295:1516-1518.

Bouaboula, M.; Rinaldi M.; Carayon, P.; Carillon, C.; Delpech, B.; Shire, D.; LeFur, G.; and Casellas, P. (1993). Cannabinoid-receptor expression in human leukocytes. European Journal Biochemistry 214:173-180.

Boulougouris, J.C.; Panayiotopoulos, C.P.;Antypas, E.; Liakos, E.; and Stefanis, C. (1976). Effects of chronic hashish use on medical status in 44 users compared with 38 controls. Annals of the New York Academy of Sciences 282:168-172.

Burnette-Curley, D., and Cabral, G.A. (1995). Differential inhibition of RAW264.7 macrophage tumoricidal activity by delta-9-tetrahydrocannabinol. Proceedings of the Society for Expirmental Biology and Medicine 210:64-76.

Caiaffa, W.T.; Vlahov, D.; Graham, N.M.; Astemborski, J.; Solomon, L.; Nelson, K.E.; and Munoz, A. (1994). Drug smoking, Pneumocystis carinii pneumonia, and immunosuppression increase risk of bacterial pneumonia in human immunodeficiency virus-seropositive infection drug users. American Journal of Respiratory and Critical Care Medicine 150(6 part 1):1493-1498.

Chopra, G.S. (1973). Studies on psycho-clinical aspects of long-term marihuana use in 124 cases. International Journal of the Addictions 8:1015-1026.

Cottrell, J.C.; Sohn, S.S.; and Vogel, W.H. (1973). Toxic effects of marihuana tar on mouse skin. Archives of Environmental Health 26(5):277-278.

Denning, D.W.; Follansbee, S.E.; Scolaro, M.; Norris, S.; Edelstein, H.; and Stevens, D.A. (1991). Pulmonary aspergillosis in the acquired immunodeficiency syndrome. New England Journal of Medicine 324:654-662.

Denissenko, M.F.; Pao, A.; Tang, M-S.; and Pfeifer, G.P. (1996). Preferential formation of benz[a]pyrene adducts at lung cancer mutational hotspots in p53. Science 274:430~32.

Donald, P.J. (1991). Advanced malignancy in the young marijuana smoker. Advances in Experimental Medicine and Biology 288:33-56.

Endicott, J.N.; Skipper, P.; and Hernandez, L. (1993). Marijuana and head and neck cancer. Advances in Experimental Medicine and Biology 335:107-113.

Fleisclunan, RW.; Baker, J.R.; and Rosenkrantz, H. (1979). Pulmonary pathologic changes in rats exposed to marijuana smoke for one year. Toxicology and Applied Pharmacology 47:557-566.

Fligiel, S.E.G.; Beals, T.F.; Tashkin, D.P.; Paule, M.G.; Scallet, A.C.; Ali, S.F.; Bailey, J.R.; and Slikker, W. Jr. (1991). Marijuana exposure and pulmonary alterations in primates. Pharmacology, Biochemistry and Behavior 40:637-642.

Fligiel, S.E.G; Roth, M.D.; Kleerup, E.C.; Barsky, S.H.; Simmons, M.S.; and Tashkin, D.P. (in press). Tracheobronchial histopathology in habitual smokers of cocaine, marijuana and/or tobacco. Chest.

Gong, H., Jr.; Fligiel, S.; Tashkin, D.P.; and Barbers, R.G. (1987). Tracheobronchial changes in habitual, heavy smokers of marijuana with and without tobacco. American Review of Respiratory Diseases 136:142-149.

Hall, J.A.S. (1975). Testimony in marijuana-hashish epidemic and its impact on United States security. In: Hearings of the Committee on the Judiciary, United States Senate. Washington, DC: U.S. Government Printing Office, pp. 147-154.

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About the Author
Donald P. Tashkin, M.D., is a professor Medicine in the division of pulmonary and critical care medicine at the UCLA School of Medicine.

70

My husband is smoking pot

by jurs in

jw
friends

i know this is not witness related but i just caught my husband smoking pot.

i am so upset !!!

he is an alcoholic and has a terrible temper.

Deacon

jurs
Im sorry. Right now just take a deep breath, and try and breathe easy.
This is a problem that you have had experience of, and you know the nature of addictions.

You will need to make a few decisions. Whether to stay or go, what to do about the children...and you will need to talk with a professional in your area. AA or SMART for the alcohol, and drug counselors for the other.

Living with an addict is not easy..it fills every moment of your time ...just wondering...but..you know this was there and its not something new.

Sort your decisions out first..take all the time you need...Then talk with him, talk with your family..his family...and go from there..

So sorry Jurs..

20

HIT with a Hammer

by Amazing in

jw
friends

in conjunction with my appeal for calm, i might add that when we are working on a construction project and hit our thumb with the hammer, we might scream, cuss, and throw the hammer at something out of a sense of anger with the event and with ourselevs.. if my co-wroker hits me with the hammer, then i might turn and take a swing at him out of an immediate reactive sense to defend myself.

likely, i might cuss him out, scream, and threaten.. as the pain subsides, i might then start to calm, and look at what happened and determine needs to take place.

i could accept an apology and move on, or if i thought it was deliberate action on his part, i might take it to the boss and get some sense of justice.. our nation, and really all good nations, were hit with a hard hammer tuesday.

Deacon

hi waiting
I dont recall doing the rounds with you...
but thats not to say I didnt...actually...I only recall posting once about a year ago on one of your threads...spoke to you once in chat..moons ago re: abuse, and I recall I was very respectful...
Well, Im full of shit and arrogant...but hey, I got a smart vote from you..thankyou!!
lol