Swedish Snus

[Neeranam]

I've been taking Snuss from Sweden for the last 4 or 5 months to try and qquit smoking. I have quit smoking but now addicted to Snuss and it seem pretty hard to come off.

Has anyone succesfully given it up - how?

Any other info about this drug welcome.

Cheers

NN

[tutsiwarrior]

I've been taking Snuss from Sweden for the last 4 or 5 months to try and qquit smoking. I have quit smoking but now addicted to Snuss and it seem pretty hard to come off.

Has anyone succesfully given it up - how?

Any other info about this drug welcome.

Cheers

NN

I've used Copenhagen snuff (pretty much identical to the loose swedish snoose in the yellow can) since 1974 and it is highly addictive. The only times I haven't used snuff is when it hasn't been available then I immediately go back on the red Marlboros to cushion the withdrawal.

Snoose/snuff takers are a small but dedicated bunch. I'd drive to BKK from Suphan to stock up if it were available. I hear that at the swedish church they only got the snoose sachets; no good fer me...I gots ta get me fingers all redolent and sticky...

(de non-initiated cringe and ponder ' ...sounds like...sounds like... ')

[lannarebirth]

I've been taking Snuss from Sweden for the last 4 or 5 months to try and qquit smoking. I have quit smoking but now addicted to Snuss and it seem pretty hard to come off.

Has anyone succesfully given it up - how?

Any other info about this drug welcome.

Cheers

NN

Snuss/ snuff highly addctive. Harder to get off of than cigarettes IMO. Maybe try some Nicorette gum, for the fix and the oral craving and then gradually reducing the dosage or weaning to a Nicorette inhaler. Or you can give it up by eating all the time, but then you have to get the weight off later.

[Neeranam]

I'd drive to BKK from Suphan to stock up if it were available

It is available in Bkk. PM me and I can tell you.

Snuss/ snuff highly addctive. Harder to get off of than cigarettes IMO. Maybe try some Nicorette gum, for the fix and the oral craving and then gradually reducing the dosage or weaning to a Nicorette inhaler. Or you can give it up by eating all the time, but then you have to get the weight off later.

I'll try the eating - it's impossible for me to put on weight.

[taxexile]

snuff , highly carcinogenic and aptly named.

[Neeranam]

3 days done - the worst is over, I hope!

Definately harder than cigarettes.

Final test will be back at work today - wish me luck!

Edited May 8, 2007 by Neeranam

[meadish_sweetball]

snuff , highly carcinogenic and aptly named.

Actually, there is no conclusive hard proof that wet snuff ('snus' in Swedish - just one s) of the type sold in Sweden, significantly raises the risk for cancer. The Board of Social Services responsible for issuing warnings and giving health advice to Swedish citizens, were sued for making such claims, and had to remove the warnings that claimed wet snuff is carcinogenic.

Check it out for yourself if you do not want to take my word for it. The info is out there.

It is, however, conducive to heart disease and circulation problems, and as has been noted, perhaps even more addictive than cigarettes due to the fact that it provides a continuous supply of nicotine as opposed to cigarettes.

[gusG]

3 days done - the worst is over, I hope!

Definately harder than cigarettes.

Final test will be back at work today - wish me luck!

Easy, don't go to work.Good luck anyway.Gus

[Neeranam]

QUOTE(taxexile @ 2007-05-04 19:58:51)

snuff , highly carcinogenic and aptly named.

Actually, there is no conclusive hard proof that wet snuff ('snus' in Swedish - just one s) of the type sold in Sweden, significantly raises the risk for cancer.

mmm, where did taxexile get his information?

[meadish_sweetball]

WHO made claims of carcinogenocity a few years ago, but these were based on animal studies and not human studies.

I will have to back down a little though, as The Lancet as of today publishes a very thorough trial that proves snus-users run double the risk of non snus-users of getting cancer of the pancreas.

It should be noted that this 'twice as large risk' means 8 in 10.000 develop it, as opposed to 4 in 10.000 among non-users.

So 'highly carcinogenic' is still not quite true.

[taxexile]

sorry neeranam , my comments were related to tobacco chewing plugs rather than snuff.

good luck with your efforts to stop using it.

Department of Oral Surgery and Oral Medicine, Faculty of Odontology, Malmo University, Sweden.

In the year 2002, about 275,000 inhabitants around the world developed oral cancer and over half of them will die of their disease within 5 years. Oral and oropharyngeal squamous cell carcinoma (OOSCC) accounts for about 1% of all cancers in Sweden - which is low compared to the incidence on the Indian subcontinent and in other parts of Asia, where it is one of the most common forms of cancer. The incidence in Sweden is increasing, however. The study comprised 80% (132/165) of all consecutive cases living in the Southern Healthcare Region, born in Sweden and without previous cancer diagnosis (except skin cancer), who were diagnosed with OOSCC during the period September 2000 to January 2004. Using the Swedish Population Register, 396 cancer-free controls were identified and matched by age, gender and county. Of these individuals, 320 (81%) agreed to take part in the study. Cases and controls were subjected to a standardised interview, identical oral examinations including panoramic radiographs, and cell sampling for human papillomavirus (HPV) analysis. In total 128 patients with planned curative treatment were followed for a median time of 22 months (range 0 - 36). The aims were to assess different potential risk factors in OOSCC such as oral hygiene, dental status, oral mucosal lesions, alcohol and tobacco use, virus infection, and some related to lifestyle. A further aim was to assess the influence of these factors on recurrence or occurrence of a new second primary tumour (SPT) of squamous cell carcinoma. In multivariate analysis average oral hygiene (OR 2.0; 95% CI 1.1-3.6) and poor oral hygiene (OR 5.3; 95% CI 2.5-11.3), more than 5 defective teeth (OR 3.1; 95% CI 1.2-8.2) and more than 20 teeth missing (OR 3.4; 95% CI 1.4-8.5), as well as defective or malfunctioning complete dentures (OR 3.8; 95 % CI 1.3-11.4) were identified as significant risk factors for development of OOSCC. Regular dental care reduced the risk of OOSCC (OR 0.4; 95% CI 0.2-0.6). The cases reported a higher consumption of alcohol than the controls. More than 350 g of alcohol per week (OR 2.6; 95% CI 1.3-5.4) and 11-20 cigarettes per day (OR 2.4; 95% CI 1.3-4.1) were dose-dependent risk factors. The results showed a tendency for women to have a greater risk (OR 1.8) than men at any given level of tobacco consumption. There was no increased risk of OOSCC among users of Swedish moist snuff. There was a significant relationship between high-risk human papillomavirus (HPV) infection and OOSCC (OR 63; 95% CI 14-280). Forty-seven of the cases (36%) were high-risk HPV infected and 7 (5.3%) were low-risk HPV infected in the specimens collected from the oral cavity. The corresponding figures for the controls were 3 (0.94%) and 13 (4.1%), respectively. The high-risk HPV types found in the oral cavity were the same types as observed in cervical cancer. Tumour stage was associated with both higher relative rate (RR) of recurrence or second primary tumour (SPT) of squamous cell carcinoma, and death in intercurrent diseases (DICD), defined as death before the occurrence of recurrence or SPT. High-risk HPV infected patients had an almost threefold increased RR of recurrence/SPT, but seemingly a lower RR of DICD compared to high-risk negative cases. Patients with tonsillar carcinoma had a significantly higher cause-specific RR of recurrence/SPT (RR 2.06; CI 0.99 - 4.28) compared to patients with OSCC of other sites. High alcohol consumption was associated with a high RR of recurrence/SPT, but not with DICD. There was no increased RR of recurrence/SPT related to smoking, but an association between smoking and DICD. In conclusion, the results in this study confirm that both smoking tobacco and alcohol consumption are risk factors for OOSCC. The use of Swedish moist snuff had no effect on the risk. Independent risk factors identified are poor oral hygiene, inadequate dental status and malfunctioning complete dentures. Regular dental check-ups are a preventive factor. Among other possible risk factors studied, high-risk HPV infection appears to be the strongest. High-risk HPV infection increases the cause-specific RR of recurrence or SPT. Tumour stage influences the rate of recurrence/SPT.

PMID: 16335030 [PubMed - indexed for MEDLINE]

[Neeranam]

sorry neeranam , my comments were related to tobacco chewing plugs rather than snuff.

good luck with your efforts to stop using it.

Thank you sir.

Actually I heard the same as you about this stuff. I think there was something called Skol bandits in the UK a few years back and they were banned.

The thought was in my mind about the cancer and that helped me get the willingness to try to quit.

6th day now and it's ok - can't sleep well but that won't kill me.

[taxexile]

dont you just love google !

BRITISH JOURNAL OF UROLOGY (London), Volume 75, Number 3: Pages 375-377,

March 1995.

The role of tobacco in penile carcinoma

K. HARISH and R. RAVI

Department of Genito-urinary Surgery, Cancer Institute (WIA), Adyar, Madras, India

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Objective: To study the role of tobacco in squamous cell carcinoma of the penis.

Subjects and methods The use of tobacco in the form of cigarettes, chewing tobacco and snuff was studied in a total of 503 patients and age-matched controls.

Results By multivariate analysis, a significant association was found between smoking (P = 0.002) or chewing tobacco (P < 0.001) and the use of snuff (P = 0.004) in patients with penile carcinoma as compared with controls. A dose-response relationship was observed for both smoking and chewing.

Conclusions The use of tobacco is a significant risk factor for penile carcinoma, and the use of more than one form of tobacco increases this risk.

Keywords squamous cell carcinomas, squamous cell carcinoma, tobacco, chewing, smoking, snuff

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Introduction

Penile cancer has a world-wide distribution, with a low incidence among Muslims and infrequent occurrence among Jews due to religious circumcision. It incidence varies in different parts of the world and is reported to be 0.5 to 1.5 per 100 000 population in the western world [1]. In Southern India, the average annual rate is 2.9 per 100 000 population (Madras Metropolitan Tumour Registry, Cancer Institute. Madras, India).

Phimosis has been shown to be a significant factor in the aetiology of penile cancer [2]. Sexually transmitted diseases have been proposed as aetiological factors, but with no definite proof [3]. Tobacco has been shown to affect many organ systems in the body. Although only the upper aerodigestive and respiratory tracts come in direct contact with carcinogens, smoking has also been shown to increase the risk of distant tumours such as cancer of the uterine cervix [4]. There are a few reports relating smoking to genito-urinary and penile cancers [1,5-7]. In India, apart from smoking, tobacco is used on other forms such as chewing tobacco and snuff.

The aim of the present study was to determine the role of tobacco in the causation of penile carcinoma.

Subjects and methods

A total of 505 patients with squamous cell carcinoma of the penis, who were registered at the Cancer Institute (WIA), Madras, between 1960 and 1990, and 600 controls selected at random from amongst the partners of patients with breast cancer, were included in the study. Data collected included subject age, presence or absence of phimosis, and the use of tobacco in the form of cigarettes, chewing tobacco or snuff. The number of cigarettes smoked and length of smoking were noted, as were the use of areca nut, tobacco or both and the duration of use. Each patient was age-matched with a control. The matching was done on a computer using only the patient index number and age. Any unmatched patients and controls were excluded from the study. The final data were analysed for 503 patients and 503 age-matched controls.

Initial signifance tests were carried out for each factor separately and then a multivariate analysis was performed with the Conditional Logistic Regression Model for matched data.

Results

The results of the study are given in Table 1.

Phimosis was an important risk factor for penile carcinoma, with 30.6% of patients having phimosis as against 5.2% of controls (odds ratio [OR] 7.4 [P<0.001]).

Table 1 Relationship between the use of different forms of tobacco and penile carcinoma

Tobacco in the form of cigarettes was a risk factor for penile carcinoma (OR=1.44, P=0.005). No significant association was observed in those who smoked <10 cigarettes per day or those who had smoked for <5 years, whereas a significant amount of risk was seen for those who smoked >10 cigarettes a day and those who had smoked for >5 years. A significant association was noted with a lifetime exposure to >30 pack years.

Chewing tobacco was a significant risk factor for penile carcinoma, with 34.0% of patients in the habit of chewing tobacco as against 15.5% of controls (OR = 3.114, P<0.001). A total of 159 of 171 patients (93.0) chewed both areca nut and tobacco. Therefore it was not possible to adjust for confounding of one of the factors.

Of the patients, 5.4% took snuff as against 1.6% of controls. (OR = 3.396, P = 0.003).

The effect of tobacco was analysed by considering smoking and chewing. A total of 59.4% of patients either smoked or chewed tobacco and 12.3% of patients used both. Either habit was a risk factor (OR = 2.298, P<0.001), and a combination of both habits carried a higher risk (OR = 3.396, P<0.001).

A multivariate analysis was carried out by the Conditional Logistic Regression Model to adjust for the confounding effects of each of the factors analysed. The results are shown in Table 2. All factors were found to be significant.

As the effects of areca nut and tobacco could not be differentiated, a similar analysis was carried out as in Table 2 but with tobacco chewing as a factor instead of chewing. Tobacco chewing was found to have a significant association with penile carcinoma (Table 3).

Discussion

In this study, the association between the three commonly used forms of tobacco (cigarettes, chewing tobacco and snuff) and squamous cell carcinoma of the penis has been analysed. Earlier studies have reported that smoking is a risk factor for squamous cell carcinoma of the penis [1,5-7], but the overall impact of tobacco on penile cancers has thus far not been analysed in detail.

All forms of use of tobacco were found to be significant risk factors for penile carcinoma, even after adjusting for their confounding. A clear dose-relationship response for smoking and chewing was observed, although it was not possible to differentiate between the effect of areca nut and tobacco. In view of tobacco being a proven carcinogen, and also because similar results were obtained in the multivariate analysis when tobacco chewing was analysed as a factor instead of chewing, we believe that tobacco was the important agent and areca nut may at best be a potentiating agent. Data on the frequency of chewing and duration of retention of quid in the oral cavity were not available for analysis. The effect of all three forms of tobacco used together could not be studied as only three patients used all three forms of tobacco. Use of more than one form of tobacco carried a higher risk, as evidenced by an OR of 2.298 for patients with one habit and an OR of 3.396 for patients who both smoked and chewed tobacco.

It has been hypothesized that tumours of the anogenital region, such as those of the utererine cervix, vulva, vagina, anus, and penis, have common and similar aetiological factors [8]. Smoking has been shown to increase the risk of cancers of the uterine cervix, urinary bladder and penis. Chemical analysis of smokeless tobacco indicates that three types of known carcinogens -- N-nitrosamine, polycylic aromatic hydrocarbons and Polonium-210 -- are present. The nitrosamines are metabolized in vivo to products shown to produce genetic changes in cells and also to produce tumours [9]. A higher availability of tobacco-specific nitrosamine to a snuff dipper has been suggested [10,11]. A role for nicotine as an inhibitor of apoptosis and subsequent tumor promotion has been proposed [12]. It has been claimed that cigarette smoke exposure may increase the extent of DNA damage per mutagenic event in bladder cancer [13]. A similar event may apply to other cancers as well. A tobacco-specific nitrosamine 4-(methylnitrosamiol-1-(3-pyridyl)-1-butanone (NNK) was found in the urine of smokers [14]. NNK metabolism takes place in a few tissues and is eventually excreted largely in the urine and to a smaller extent in saliva, faeces and secretions from preputial glands [15]. Accumulation of carcinogens in smegma may be an important factor. Another support for a remote mode of action of smoking is its role as in immunosuppressant by reducing the number of Langerhans' in a linear fashion. Langerhans' cells are dendritic epithelial cells which play an important role in immune surveillance and in the response to neoplastic transformation [16].

In summary, the use of tobacco in any form is a risk factor for penile carcinoma. Tobacco may exert its action through its metabolites, or directly after systemic absorption. Use of more than one form of tobacco multiplies the risk of development of penile carcinoma.

References

1 Dailing JR, Sherman KJ, Hislop TG et al. Cigarette smoking and the risk of anogenital cancer. Am J Epidemiol 1992;135:180-9

2 Muir CS, Nectoux J. Epidemiology of cancer of the testis and penis. Natl Cancer Inst Monogr 1979; 53: 157-64

3 Schrek R, Lenowitz H. Aetiologic factors in carcinoma of the penis. Cancer Res 1947: 7: 180

4 Winkelstien W. Smoking and cervical cancer-current status: a review. Am J Epidemiol 1990; 131: 945-57

5 Harris RE, Hebert JR, Wynder EL. Cancer risk in male veterans utilising the Veterans Administration Medical System. Cancer 1989; 64: 1160-8

6 Bosch FX. Cardis E. Cancer incidence correlations: genital, urinary and some tobacco-related concerns. Int J Cancer 1990; 46: 178-84

7 Hellberg D, Valentin J, Eklund T, Nilsson S. Penile cancer: is there an epidemiological risk for smoking and sexual behaviour? Br Med J 1987; 295: 1306-8

8 Peters RK, Mack TM, Bernstien L. Parallels in the epidemiology of selected anogenital carcinomas. Natl Cancer Inst 1984; 72: 609-15 [PubMed]

9 Mattson ME, Winn DM. Smokeless tobacco association with increased cancer risk. Natl Cancer Inst Mongr 1989; 8: 13-16 [PubMed]

10 Protokoczyk B, Wu M, Cox JE, Hoffman D. In vitro studies on biological availability of tobacco-specific N-nitrosamines to the smokeless tobacco user. Proc Annu Meet Am Ass Cancer Res 1992: 33: A867 (meeting abstract)

11 Prokopczyk B, Wu M, Cox JE, Hoffman D. Bioavailability of tobacco specific N-nitrosamines to the snuff dipper. Carcinogenesis 1992: 13: 863-6 [Abstract]

12 Wright SC, Zhong J, Zheng H, Larrick JW. Nicotine inhibition of apoptosis suggest a role in tumor promotion. FASEB J 1993; 7: 1045-51

13 Spruck CH, Rideout WM, Olumi AF et al. Distinct pattern of p53 mutations in bladder cancer: relationship to tobacco usage. Cancer Res 1993: 53: 1162-6 [PubMed]

14 Hect SS, Akerkar S, Carmnella SG. Metabolites of tobacco specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in smokers urine. Proc Ann Meet Am Ass Cancer Res 1993: 34: A909 (meeting abstract)

15 Castonguay A, Tjalve H, Hecht SS. Tissue distribution of tobacco specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and its metabolites in F244 rats. Cancer Res 1983: 43: 630-8

16 Muller HK, Halliday GM, Knight KA. Carcinogen-induced depletion of cutaneous Langerhans cells. Br J Cancer 1985; 52: 81-5 [PubMed]

Authors

K. Harish, MS, DNB, Postgraduate

R. Ravi, MS, MCh (Urology), Associate Professor.

Correspondence: Dr R. Ravi, Department of Urology, St Bartholomew's Hospital, London EC1A 7BE, UK

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[Neeranam]

lol - definately staying off it then!

[Fred Sanford]

I'm a skoal man. Copenhagen is ok too but that swedish stuff is nasty. Quitting is a bitch, everytime I try, I get sick. I need my skoal and please no bandits