Rapid Responses to:
|
|
Rapid Responses: Rapid Responses published:
-
![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Deaths from alcoholic liver disease in the midlands
- JK Anand (10 August 2002)
-
Aspartame (Canderal/ NutraSweet, etc.) Triggers Toxicity of Liver
- Betty L. Martini, 9270 River Club Parkway, Duluth, Georgia 30097, USA (11 August 2002)
-
Hepatitis C increases morbidity and mortality in those who abuse alcohol
- Graham R Foster (17 August 2002)
-
Mortality from liver disease is not rising in South Wales
- Neil D Hawkes, Zahra Ahmed, and Shakeel Ahmed (24 September 2002)
-
Author's reply
- Neil C Fisher (30 October 2002)
-
Mortality from liver disease in the West Midlands, 1993-2000: observational study
- Cheryl V Jasper, N C Fisher, J Hanson, A Phillips, J N Rao, and E T Swarbrick (24 February 2003)
|
|
|||
|
JK Anand, Retired public health physician
Send response to journal:
|
Editor-The authors tell us that rates of increase in deaths from alcoholic liver disease were similar for "white men, white women and Asian men". They go on to say that eighty per cent of "Asian men" were judged to be of Sikh religion. To put matters in context, we really need to know what percentage of the "Asian men" in the Midlands are Sikhs. Secondly, if the graph displayed is to be our guide, then alcoholic liver disease mortality reached a plateau in 1995, took off again in 1996, peaked in 1998 and started to fall again. Will it continue to fall? Or will it climb further? We do not know. Surely we do not need more research before taking steps to cut down the availability of alcohol to the swinging Britons swigging beer and whisky. Thirdly, a cautionary note on assigning religions from names. Mostly the method works well. However, there can be difficulties. Take "Amreek Jheeta". We need to know the given middle name to inject a little more certainty in this game. If he is Amreek Singh Jheeta, then he is more likely to be a Sikh. If he is Amreek Masih Jheeta, then he is a Christian convert originating from the subcontinent. Finally, does the label of religion matter? Sikh religion does not approve of intoxicating drinks. You are not permitted to take alcohol (even in a can) in to a Sikh temple (the Gurdwara). Please forgive me my ignorance but I thought wine was an accepted part of Eucharist. We should forget the religion of the forefathers and concentrate on the culture of the Britons of today. And this culture is: the pub and the club. The Britons have yet to learn to enjoy alcohol in moderation. JK Anand |
|||
|
|
|||
|
Betty L. Martini, ? Founder of Worldwide Volunteer Force warning consumers off aspartame Mission Possible International, 9270 River Club Parkway, Duluth, Georgia 30097, USA
Send response to journal:
|
Aspartame is a neurotoxic drug. It is a molecule composed of three components, aspartic acid, a methyl ester which turns into methyl alcohol and phenylalanine. The Trocho Study of l998 has shown that the formaldehyde converted from the methanol accumulates in the cells and damages DNA with most toxicity in the liver. H. J. Roberts, M.D., in Aspartame Disease: An Ignored Epidemic (www.aspartameispoison.com, www.sunsentpress.com or 1 800 814 - 9800 )said on page 480: "In a recent National Health and Nutrition Examination Survey, 2.6 % of the US population surveyed had elevated serum ALT for which no cause of chronic liver disease could be found (James 1999). Even though 70% of the adult population consumes aspartame products, aspartame disease was not suspected as a likely causative contributory cause. It is of historic interest that Dr. Misael Urite (l982) expressed concern that the FDA had not adequately considered the potential toxicity of aspartame in patients with liver disease shortly after its forthcoming release was announced. Persons with cirrhosis of the liver are at increased risk because they may be unable to maetabolize aspartame and its breakdown products adequately (Jagenberg 1977; Heberer 1980; Dhont 1982). The possibility of aspartame toxicity should be entertained in patients diagnosed in having nonalcoholic steato hepatitis. This liver disorder has become a common liver disorder in North America and can progress to cirrhosis (James 1999). Its frequent features of persistent fatigue, upper abdominal discomfort, diabetes and hyperglycemia are also encountered in aspartame disease. Obese persons and diabetic patients who consume considerable aspartame appear to be at higher risk fof the development of chronic nonalcoholic steatohepatitis, especially when addicted to such products. The term "nonalcoholic" is misleading in this instance because aspartame contains ten percent methyl alcohol." (end of quote from book) Mission Possible International is a worldwide volunteer force in 50 states and 22 countries warning consumers off aspartame. We are now taking case histories for class action. Because so many aspartame victims are developing hepatitis James Bowen, M.D. gave the following information for the aspartame support groups on line with permission to publish: Date: Mon, 04 Jun 2001 02:22:52 -0400 To: "aspartame@onelist.com" <aspartame@onelist.com> From: Betty Martini <Mission-Possible-USA@altavista.net> Subject: Steato Hepatitis, another extensive NutraSweet Plague, James Bowen, M.D. (for global distribution) Permission to Publish Cc: "AspartameSurvivors@onelist.com" <AspartameSurvivors@onelist.com> For those on aspartame support groups who have had questions about the liver problems from aspartame, and why some physicians question hepatitis in aspartame victims. From James Bowen, M.D. June 4, 2001 Steato Hepatitis, characterized by an accumulation of fat in the hepatocyte (liver cell) resulting from ingestion of aspartame is focused in the mitochondria. Mitochondria are the energy furnaces of the cell and aspartame (APM) metabolism into more toxic derivatives, formaldehyde and formic acid take place in the mitochondria. As in all NutraSweet poisoning the formaldehyde and formic acid immediately attack the tissues they are generated in so we see a new co-existent plague of "anti- mitrochondrial antibody hepatitis" generated right along with the steato hepatitis because the immune system reacts to the degenerated tissues. The breakdown of fats into energy producing chemicals has obligatory metabolism via mitochondrial mechanisms. When mitochondria are rendered defective by aspartame poisoning fat cannot be processed to be used for energy. The formation of fat from dietary calories proceeds because fat is built up directly in the cytosol of cells and accumulation is not dependent on mitochondrial function. So liver cells and fat cells and after fats cells (lipocytes) store fat and cannot get rid of it no matter how badly it is needed to supply energy to the body. Thanks to NutraSweet these victims literally cannot starve the fat off of their bodies or out of their livers because of their compromised mitochondrial functional capacity. To make matters worse the mitochondrial DNA is severely damaged. Methanol/formaldehyde poisoning occurring as the direct result of the obligatory metabolism of methyl radicals is the most common form of genetic damage, caused by formaldehyde cross linkage of DNA strains. The mitochondrial DNA is thousands of times more vulnerable to this than nuclear DNA, and lack the excellent repair mechanisms that protects the integrity of nuclear DNA. The presently understood mitochondria DNA repair mechanisms are merely excisional, that is the DNA rendered abnormal by the aspartame/methanol poisoning is merely excised leaving the mitochondrial function at best insufficient, defective and incomplete. Which in addition to producing inadequate and incomplete energy metabolism spins off highly damaging free radicals. Methanol/formaldehyde poisoning is noted for this. This vicious circle amounts to tremendous degenerative process in the human organism and the unfortunate results too numerous to be repeated here but are well detailed on www.dorway.com and other excellent sites such as www.holisticmed.com/aspartame, as well as Dr. Hyman Roberts text on the subject. (Aspartame Disease: The Ignored Epidemic - 1 800 814 - 9800 or www.sunsentpress.com/ ). This amounts to virtual "genocide", and is further emphasized by the fact this mitochondrial DNA damage is directly transmitted by female NutraSweet users to her children and grandchildren, and to subsequent generations via her female descendents. ___________________________End of article by Dr. James Bowen,POB 177, Walla Walla, Washington 99362, email drjimbowen@hotmail.com For further information on aspartame's effect on the liver see the Trocho Study on www.dorway.com/nomarkle.html Books on the liver by Sandra Cabot, M.D., of Mission Possible Australia also on www.dorway.com and Excitotoxins: The Taste That Kills by neurosurgeon Russell Blaylock, M.D. Also see Detox page on this web page. (Newton Labs), Aspartame: Methanol and the Public Health by Dr. Woodrow Monte, journal article on www.dorway.com/nomarkle.html Betty Martini, Founder, Mission Possible International 770 242-2599 www.dorway.com _______________ References: Trocho C; Pardo R, Raferas I, Virgil J Remesar X, Fernandez-Lopez JA, Alemany M, Life Sci: 1998;63 (g)337-49, PMID; 9714421, UI: 98378223 |
|||
|
|
|||
|
Graham R Foster, Reader in Hepatology at Imperial College Faculty of Medicine St Mary's Hospital, Praed Street, London, W2 1PG
Send response to journal:
|
Dear Editor, I read with interest the article from Fisher and colleagues showing that deaths from liver disease have doubled in recent years (1). Data from death certificates indicates that this is related to alcoholic cirrhosis but figures on total national alcohol consumption suggests that there has been no associated increase in alcohol use that could account for the observed increase in mortality. Chronic hepatitis C infection is common in the UK (2) and exacerbates alcohol induced liver damage leading to an increased prevalence of cirrhosis in infected patients who use alcohol (3). Given that chronic hepatitis C infection is more prevalent in those who abuse alcohol (4) one plausible explanation for the observed increase in deaths from ‘alcoholic cirrhosis’ is that many of those who abuse alcohol are also infected with hepatitis C and it is the presence of two hepatotoxic agents that leads to end stage liver disease and death. Clinical experience in London suggests that many patients with presumed alcoholic cirrhosis are not tested for infection with hepatitis C (GRF – unpublished observations) and it would be interesting to know how many patients in the West Midlands study who died from ‘alcoholic cirrhosis’ were formally tested for hepatitis C. Since combination therapy with a pegylated interferon plus ribavirin cures 50 - 60% of patients with chronic hepatitis C infection (5,6) identification and therapy of those who are infected is an effective intervention that will reduce mortality from liver disease. Graham R Foster PhD FRCP Reader in Hepatology Imperial College Faculty of Medicine St Mary’s Hospital, Praed Street, London W2 1PG Tel 0207 886 6400 Facs 0207 402 2796 1. Fisher NC, Hanson J, Phillips A, Rao JN, Swarbrick ET. Mortality from liver disease in the West Midlands, 1993-2000: observational study. Bmj 2002;325(7359):312-3. 2. Sallie R, King R, Silva E, Tibbs C, Johnson P, Williams R. Community prevalence of hepatitis C viraemia: a polymerase chain reaction study. J Med Virol 1994;43:111-114. 3. Harris DR, Gonin R, Alter HJ, Wright EC, Buskell ZJ, Hollinger FB, et al. The relationship of acute transfusion-associated hepatitis to the development of cirrhosis in the presence of alcohol abuse. Ann Intern Med 2001;134(2):120-4. 4. Rosman AS, Waraich A, Galvin K, Casiano J, Paronetto F, Lieber CS. Alcoholism is associated with hepatitis C but not hepatitis B in an urban population. Am J Gastroenterol 1996;91(3):498-505. 5. Manns MP, McHutchison JG, Gordon SC, Rustgi VK, Shiffman M, Reindollar R, et al. Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial treatment of chronic hepatitis C: a randomised trial. Lancet 2001;358(9286):958-65. 6. Pegylated (40 kDa) Interferon Alfa-2a (PEGASYS*) in Combination With Ribavirin: Efficacy and Safety Results From a Phase III, Randomized, Actively-Controlled, Multicenter Study. DDW; 2001; Atlanta, USA. |
|||
|
|
|||
|
Neil D Hawkes, Consultant Gastroenterologist Prince Charles Hospital, Merthyr Tydfil, North Glamorgan, CF47 9DT, Zahra Ahmed, and Shakeel Ahmed
Send response to journal:
|
Editor- Fisher et al’s observational study showed that death from chronic liver disease has almost doubled between 1993 and 2000, and they attribute this to a 3-fold increase in deaths from alcoholic liver disease1.
The decline of coal mining and manufacturing industries have led to increased levels of unemployment and economic hardship in the South Wales valley communities. Official statistics report the highest levels of smoking and alcohol use in Wales. Between 1990-1996, in the Merthyr, Rhondda-Cynon-Taf boroughs 23% of persons over 18 years were drinking >21 units per week – this compares with figures of 19% and 18% for Wales2,3 as a whole and England respectively4. Year Crude mortality per 100,000 1993 9.37 1994 7.37 1995 11.38 1996 7.03 1997 7.04 1998 10.76 1999 10.78 2000 10.48Our experience concurs with Fisher et al that the vast majority of chronic liver disease and related deaths are alcohol-related. It is therefore interesting that despite the reported high levels of alcohol consumption in our community, total mortality rates for primary liver disease (ICD codes 570-573) have not increased more than 1.1-fold and are broadly similar to those reported in the West Midlands for 1997-2000. This is in contrast to observations of rising mortality in other parts of the United Kingdom. It is difficult to determine whether the stable rates in our region represent a plateau in mortality, the result of a longer history of high alcohol consumption in the local community, or whether the answer is to be found in the broad sweeping conclusion of Fisher et al, that the relationship between alcohol consumption and liver mortality is not a simple one, implicating the role of genetic and environmental factors within local populations. Doll and Peto’s study of the mortality related to smoking5 is the paradigm of a well designed, long-term, prospective cohort study to examine such relationships, though no parallel study exists for alcohol-related diseases. There is a staggering paucity of detailed historical data relating to alcohol consumption and information available from the Census and National Health Survey is non-specific, allowing only limited conclusions to be drawn when assessing health trends. Given the possible role of population-specific factors, the prescient need for a reliable database on alcohol consumption may need to be tackled at a regional level. The systematic identification of at-risk groups by both general practitioners, hospital physicians and community-based teams, in whom a more detailed alcohol history is obtained, may be the first step to reducing the problem of alcohol-related admissions, and associated morbidity and mortality. The collection and compilation of such data into a central registry would undoubtedly require additional resources, but given the annual cost to the NHS surely this must be both a socio-economic and political priority. |
|||
|
|
|||
|
Neil C Fisher, Consultant Physician & Gastroenterologist Dudley Group of Hospitals, West Midlands DY1 2HQ
Send response to journal:
|
We are very grateful to the correspondents, all of whom made valid comments, for their interest in this study. In response to Dr Anand, we are unable to give the exact proportion of Sikhs amongst people of Asian origin in the Midlands, as this information is not available from the 1991 census. However, of the 835,000 study population, around 55,700 are Indian, 11,800 Pakistani and 2,600 Bangladeshi according to the census. The Indian population will presumably include most or all of the Hindu and Sikh religions. We feel it likely that Sikhs are over-represented in the liver deaths in this study, but the truth may not emerge until data on religious background emerges from the 2001 census. Regarding the issue of assigning religion according to names, we agree that in theory this practice is potentially flawed, but anecdotally having looked after many Asian patients with liver disease I do not ever recollect any ambiguity in the ethnic origin of such a patient as judged by their name. Slightly more likely to confound in practice is the occurence of a white female marrying an Asian male, thus adopting an 'Asian' surname with a 'Christian' forename. However no such examples were found in our study cohort. The comments from Ms Martini are noted with interest. In response to Dr Foster, we agree that it is regrettable that testing for Hepatitis C appears to be incomplete or not documented in many cases of 'alcoholic' liver disease and we would encourage wider usage of such serological testing. Our study did not include casenote analysis for patients with designated alcoholic liver disease and so we did not systematically exclude hepatitis C in such patients. However, among 66 case note reviews in patients with 'unspecified' liver disease, around 50% had documented exclusion of hepatitis C whilst one case tested positive (this was not a patient considered to have alcoholic liver disease by the supervising clinician). Hepatitis C is probably around twofold more prevalent in London compared with the provinces ( Balogun MA et al, Epidemiol Infect 2000;125:705-12) and we do not feel that occult hepatitis C is making any significant contribution to the increasing mortality from alcoholic liver disease in the West Midlands. In practice we would argue that the two do not co-exist very often although we concede that we cannot exclude incorrect designation of cause of death in some cases. Finally, we are grateful to Dr Hawkes & colleagues for sharing their data for South Wales. These do not show the doubling of overall liver mortality that occurred in the West Midlands, but as the authors state, the death rates at the start of their study in 1993 were already at a level that was considerably higher than the national average (see www.medicouncilalcol.demon.co.uk). There are reasonable quality data on alcohol consumption for the UK (eg Statistical Bulletins issued by the dept. of health) and there are also data showing correlation between per capita alcohol (ie distilled spirits) consumption and death rates elsewhere (Roizen et al, BMJ 1999;319:666-70). However we hope that the consultation document on the National Alcohol Strategy for England will provide the platform on which to collate data more accurately for the UK and prevent morbidity from alcohol-related disease in the future. yours sincerely,
Competing interests: None declared |
|||
|
|
|||
|
Cheryl V Jasper, Stress Manager/Analysis West Midlands DY8 2DE, N C Fisher, J Hanson, A Phillips, J N Rao, and E T Swarbrick
Send response to journal:
|
Could not more liver disease situations also come by the overload of IRON? Haemochromatosis can also cause this, however so little is known, or people aware of the situation. www.has-ironoverload.co.uk Competing interests: None declared |
|||