Rapid Responses to:
|
|
Rapid Responses: Rapid Responses published:
-
![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Single Patient Based Medicine and EBM to avoid bias in our researches.
- Sergio Stagnaro (3 September 2004)
-
Alcohol, mild cognitive impairment and dementia.
- Dr. Naseem A. Qureshi, MD, IMAPA, LMIPS, Dr.Ibrahim Al-Hoqail, Dean, College of Medicine, MOH, Riyadh, Saudi Arabia. (6 September 2004)
-
Woe to me
- Prem K Kunjukrishnan, Lekshmi Premkumar ;Trust grade psychiatrist (7 September 2004)
-
Criteria for frequent consumption of Alcohol
- Padmanabha M Pillai (7 September 2004)
-
Confusing classification of alcohol consumption
- Christopher Bell (21 September 2004)
-
Non-drinkers have higher risk than infrequent drinkers to develop dementia?
- Nilamadhab Kar (4 October 2004)
|
|
|||
|
Sergio Stagnaro, Specialist in Blood, Gastrointestinal, and Metabolic Diseases. Researcher in Biophysical Semeiotics. Via Erasmo Piaggio 23/8 16037 Riva Trigoso (Genova) Italy.
Send response to journal:
|
Sirs, Apart from the large presence of apolipoprotein E, populations of Kuopio and Joensuu, eastern Finland, are apparently strange. In my opinion, on the contrary, overlooking Single Patient Based Medicine (2-4) (See website HONCode 233736, www.semeioticabiofisica.it), the authors of the paper, on the base solely of EBM, state that “Alcohol drinking in middle age showed a U shaped relation with risk of mild cognitive impairment in old age. Risk of dementia increased with increasing alcohol consumption only in those individuals carrying the apolipoprotein e4 allele”. In my 47-year- long “clinical” experience with the aid of Biophysical Semeiotics, cognitive impairment in old age as well as different forms of dementia in old age can be certainly aggravated or precipitated by environmental factors, like too much alcohol, but exclusively in individuals affected since their birth by precise biophysical-semeiotics constitutions, I described in former articles (2-4). As far as early diagnosis of Alzheimer's Disease is concerned, readers can see it described in detail in the above-cited website (5). Finally, I drank no alcohol at midlife; nevertheless I have demonstrated clearly that my cognitive functions are not impaired…until now, at least. 1) Anttila T., Helkala E-L., Viitanen M., et al. Alcohol drinking in middle age and subsequent risk of mild cognitive impairment and dementia in old age: a prospective population based study. BMJ 2004;329:539 (4 September), doi:10.1136/bmj.38181.418958.BE (published 10 August 2004) 2) Stagnaro-Neri Marina, Stagnaro Sergio. Introduzione alla Semeiotica Biofisica. Il Terreno oncologico”. Travel Factory SRL., Roma, 2004. http://www.travelfactory.it/semeiotica_biofisica.htm 3) Stagnaro S., Stagnaro-Neri M., La Melatonina nella Terapia del Terreno Oncologico e del “Reale Rischio” Oncologico. Ediz. Travel Factory, Roma, 2004. 4) Stagnaro S., Stagnaro-Neri M., Le Costituzioni Semeiotico- Biofisiche.Strumento clinico fondamentale per la prevenzione primaria e la definizione della Single Patient Based Medicine. Ediz. Travel Factory, Roma, 2004. 5) Stagnaro S., Stagnaro-Neri M., Alzheimer's Disease Byophysical Semeiotics supports the pathophysiology of Koudinov's theory. Clinical Medicine and Health Research. http://clinmed.netprints.org/cgi/eletters/2001100005v1#9 11 January 2002 and http://forums.nytimes.com/webin/WebX?11@122.SR0aaJDP0CS^413409@.f05ac92Fine modulo Competing interests: None declared |
|||
|
|
|||
|
Dr. Naseem A. Qureshi, MD, IMAPA, LMIPS, Medical Director [A], Director, CME&R Buraidah Mental Health Hospital, Postcode.2292, Saudi Arabia, Dr.Ibrahim Al-Hoqail, Dean, College of Medicine, MOH, Riyadh, Saudi Arabia.
Send response to journal:
|
Sir: The results of this study by Anttila and colleagues [1] are interesting and have the following serious implications, 1) people must drink alcohol at midlife infrequently to prevent the development of mild cognitive impairment, 2) people must not drink alcohol at midlife frequently (and probably in binge pattern)in order not to develop again mild cognitive impairment, 3) as reported elsewhere and supported by many empirical studies that the mild cognitive impairment is harbinger of dementia, a devastating neurodegenrative disorder coupled with both huge costs in terms of treatment intervention and considerable stress to caretakers, 4) as the carriers of apolipoprotein e4 are known to have an increased risk of dementia with increasing alcohol consumption as compared to non-carriers teetotallers, there should be some biological means to identify such vulnerable populations and probably correction of this genetic defect by gene therapy (if there is one available) that would prevent the development of dementia, multi-infarct/vascular or Alzheimer type. Finally, the implications/results of this prospective study will not be applicable to general world population because of cultural notions, especially in those cultures where alcohol consumption is strictly prohibited. In this context one tends to beg a question, "is incidence of mild cognitive impairment and dementia most common among such cultures? By implication, the answer may or may not be yes but it needs transcultural studies to support or refute this tentative finding. Reference: 1. Tiia Anttila, Eeva-Liisa Helkala, Matti Viitanen, Ingemar Kåreholt, Laura Fratiglioni, Bengt Winblad, Hilkka Soininen, Jaakko Tuomilehto, Aulikki Nissinen, and Miia Kivipelto.Alcohol drinking in middle age and subsequent risk of mild cognitive impairment and dementia in old age: a prospective population based study.BMJ 2004; 329: 539-0 Competing interests: None declared |
|||
|
|
|||
|
Prem K Kunjukrishnan, SpR in Old Age Psychiatry Dewsbury & District Hospital, Lekshmi Premkumar ;Trust grade psychiatrist
Send response to journal:
|
Editor, Woe to me , I am a teetotaler I ne'er did drink spirits All in the hope of a good life. But what is this good life If all I am left with, in my advanced years are A failing mind and heart. I look around me But draw little comfort That those who indulge in bacchanalian excess Will be my companions in sickness and illhealth Green with envy I shall be Of those who moderated themselves And who will,indeed, be living the good life As I fade away. Competing interests: None declared |
|||
|
|
|||
|
Padmanabha M Pillai, Retrired GP South Tyneside, NE 32 5SE
Send response to journal:
|
I find it very difficult to accept the criteria for consumption of Alcohol in this article. To say that among the 30% who drank frequently, 68 % drank once or twice a month and 24% once a week, seems an exaggeration, to say the least. Competing interests: None declared |
|||
|
|
|||
|
Christopher Bell, Professor of Physiology Trinity College Dublin
Send response to journal:
|
Editor By assessing the effect of alcohol consumption in middle-age on cognitive capacity in old age, Anttila et al's study aims to build on data from a number of previous studies that suggest a protective effect on cognitive function during ageing of light-moderate alcohol intake. Reliable data on this relationship would be of considerable potential value in understanding the proceses of age-related neurodegeneration. Unfortunately it is impossible to make any meaningful interpretation of the results, since the authors appear to have selected a study population with a unique consumption profile. The 'light-moderate' alcohol intakes found to have apparently beneficial effects in previous studies (including one from the same Karolinska group) were of the order of 1 unit/day, similar levels to those for which there is evidence for a beneficial effect of alcohol on cardiovascular morbidity. By contrast, Anttila et al equate 'moderate' or 'infrequent' intake with less than one drink per month and pool all intakes greater than this as 'frequent'. Given that 68% of the latter population claimed to take only 1-2 drinks/month, it is difficult to credit that the significant differences found between total abstainers, 'infrequent' drinkers and 'frequent' drinkers actually reflected alcohol-related effects. Competing interests: None declared |
|||
|
|
|||
|
Nilamadhab Kar, Consultant Psychiatrist Wolverhampton PCT, Corner House, 300 Dunstall Road, Wolverhampton, WV6 0NZ
Send response to journal:
|
It is well known that too much drinking, alcohol dependence increase the risk of cognitive impairment and dementia. Saunders et al [1] found that men with a history of heavy drinking (>17.5 units of alcohol per week) for greater than 5 years were found to have a greater than a 5 fold risk of suffering from dementia. Anttila et al [2] reported that persons who drank no alcohol at midlife and those who drank alcohol frequently (several times a month) were both twice likely to have mild cognitive impairment in old age as those persons who drank alcohol infrequently (less than once a month). The authors have found some other interesting findings. They reported that compared to persons who never drank and did not carry the apolipoprotein e4 allele, e4 carriers who drank infrequently were 2.3 times more likely to develop dementia, and carriers who drank frequently were 3.6 times more likely. So at one hand when they are finding that the risk of developing dementia in infrequent drinkers increases 2.3 times in comparison to non- drinkers in presence of apolipoprotein e4; at the other hand they report that infrequent drinking is twice less likely to produce cognitive impairment than no-drinking. This inconsistency is confusing. While both alcohol and presence of apolipoprotein e4 are known risk factors individually it is understandable that the risk increases when both are present. But no- drinking increasing the risk 2 times more than infrequent drinking of less than once per month is difficult to understand. The authors also reported that the risk of dementia for e4 carriers who never drank was not different from that of non-carriers who never drank. This means in their sample having apolipoprotein e4 did not influence the risk of developing dementia. This is contrary to what is known that apolipoprotein e4 is the genetic risk factor for dementia with an established risk for general population [3]. In addition, the authors found among the non-carriers, there was no association between alcohol drinking and the risk of dementia. Whether or not it has taken into question of severity of drinking, this again negates the view of alcohol as a risk for dementia. Results of Anttila et al [2] appear to suggest that infrequent drinking may be protective against developing dementia at least in absence of apolipoprotein e4 allele. But with many controversial findings the study raises more questions than it solves. The reason for this inconsistency could be some of the limitations already mentioned by the authors regarding the reliability of alcohol consumption data, selection bias, non-participation, selective survival related to apolipoprotein E polymorphism, and vascular morbidity associated with heavy drinkers. Besides these, while it is easier to identify and categorise no drinking and heavy (pathological) drinking, categorising infrequent drinkers may be most difficult. In addition, there should be strong reason for doing so on the criterion of less than one drink a month. It is understandable that the interaction of these factors is complex; and with various known and unknown factors as confounding variables influencing it, it will be preferable to assume that the issue of infrequent drinking having less risk of mild cognitive impairment in old age compared to no-drinking is unsettled as yet. References 1. Saunders PA, Copeland JR, Dewey ME, Davidson IA, McWilliam C, Sharma V, Sullivan C. (1991) Heavy drinking as a risk factor for depression and dementia in elderly men. Findings from the Liverpool longitudinal community study. British Journal of Psychiatry, 159: 213-6. 2. Anttila T, Eeva-Liisa H, Viitanen M, Kareholt I, Fratiglioni L, Winbald B, Soininen H, Tuomilehto J, Nissinen A, Kivipelto M. (2004) Alcohol drinking in middle age and subsequent risk of mild cognitive impairment and dementia in old age: a prospective population based study. British Medical Journal, 329: 539-542. 3. Ruitenberg A, van Swieten JC, Wittemann JCM, Mehta KM, van Duijn CM, Hofman A, et al (2002) Alcohol consumption and risk of dementia: the Rotterdam study. Lancet, 359, 281-286 Competing interests: None declared |
|||