ISCHEMIA CEREBRALE

L'azione neuroprotettiva è ben nota per gli acidi grassi omega 3,  tuttavia merita un distinguo sulla loro attività verso l'Ischemia cerebrale. 

Merita di evidenziare come la probabile causa di tale differenza sia la maggiore attività anti-trombotica degli Omega 3 di pesce (EPA e DHA)  che causerebbe l'aumento molto marcato di ictus emorragici.

  Dai più recenti studi si evidenzia come tale effetto si manifesti marcatamente già a soli 0,6-0,8 gr di EPA+DHA: aumento dell'incidenza dell'ictus del +30 e + 76%

Al contrario, un apporto bilanciato di ALA-Omega3/LA-Omega 6 non altera significativamente i parametri coagulativi neppure a dosaggi di 8+8 gr/g (Atherosclerosis 1999 Jan;142(1):159-68 -Comparison of the effects of two low fat diets with different alpha-linolenic:linoleic acid ratios on coagulation and fibrinolysis-Allman-Farinelli MA) 

Si ricorda che VitalOil apporta 3+3 gr di ALA-w3+LA-w6

E' interessante inoltre il risultato di uno studio in Giappone, (con una dieta già ricca di omega-3) che evidenzia un netto beneficio di una dieta bilanciata anche in Omega 6.


ABSTRACTS tratti da      

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J Nutr Health Aging 2001;5(3):167-72
Diet and stroke.

Renaud SC.

INSERM, Unit 330, University Bordeaux 2, 146 Rue Leo Saigant, 33076 Bordeaux Cedex, France. serge.renaud@bordeaux.inserm.fr

In industrialized countries, stroke is the most frequent life-threatening neurological disorder. The mortality trend for stroke appears to be similar to that of coronary heart disease (CHD) in different countries. Thus the dietary changes that protect from CHD, may also protect from stroke. The purpose of the present paper is not to review exhaustively the associations between foodstuffs and stroke. It is rather to emphasize a few important relationships that may be conducive to efficient recommendations in Public Health.  

The intake of saturated fat, considered as the main environmental factor for CHD, does not appear to be also closely related to stroke. It has even been observed in the Framingham prospective study, that saturated fats were associated with a protective effect on stroke.

  The multivariate analysis of the ecological study reported in the present paper suggests that the villain for stroke could be the high intake of linoleic acid, the main polyunsaturated fatty acid prescribed through the world, to most of the CHD patients.

  Observation and intervention studies suggest that the fatty acid with the most efficient protective effect on stroke is alpha-linolenic acid (ALA) as for CHD clinical manifestations.

  Also similarly to CHD, fruit, vegetables and folic acid, may have important protective effect on stroke.

  Finally, at very moderate intake, alcohol may be related to a similar lowering on the risk of stroke as on that of CHD.

Nevertheless alcohol, at high intake for intoxication (binge drinking) has been associated with up to a 10 fold increased in the risk of stroke.

  Finally, the diet recommendations suggested by the present analysis are similar to those used in the Lyon Diet Heart Study and in Finland, in the last 20 years. In both of these intervention studies mortality from CHD, cancer and stroke have been markedly reduced by more than 50 %.


The Lancet -Aug 1999, 447-55

 Gissi-Prevenzione

Tutti gli studi che hanno analizzato le correlazioni fra Ictus o Tia e la presenza degli Omega 3 hanno evidenziato l'effetto protettivo per l'ALA-Omega 3. Nello studio Italiano più importante (GISSI Prevenzione- 1999 Lancet) che ha coinvolto 11324 soggetti post-infartuati il rischio di Ictus aumentava del 30 % assumendo solo 0,8 gr/g di olio di pesce (EPA+DHA).

Dalla tabella sottostante emerge che il rischio di ictus è maggiore del beneficio cardiaco, pertanto  l'impiego degli Omega 3 di pesce (EPA+DHA) può essere consigliato solo in pazienti ad alto rischio di infarto 

 

n=11324 post infarctuated subjects tested for 1260 gg, EPA + DHA 0,8 gr/day Vs placebo

Relative Risk (CI 95%)

Coronary Heart Desease deaths + not fatal Myocardial Infarct 0,75 (-25%)
Fatal and not fatal Stroke  1,30 (+30%)
Tot. Death + not fatal MI + not fatal Stroke 0,85 (-15%)

Diversamente dall'ALA-Omega 3, tale correlazione è stata confermata anche da un'analisi sull'incidenza dell'Ictus in Groenlandia: "n-3 fatty acids as a risk factor for haemorrhagic stroke" Henning Sloth Pedersen, 1999 The Lancet, Vol. 353 (812-3) e dal seguente studio:


Neuroepidemiology 2002 May-Jun;21(3):107-14

Fish consumption and stroke: a community case-control study in Asturias, Spain.
Caicoya M. -Service of Clinical Epidemiology and Preventive Medicine, Monte Naranco Hospital, Oviedo, Spain. 

BACKGROUND: The relationship between fish consumption and stroke is controversial. Actually, a low fish consumption may protect against ischemic stroke, while a fish diet is ecologically associated with an increased risk of hemorrhagic stroke. 

OBJECTIVE: This study seeks to examine the relationship between fish consumption and stroke in a population with a high fish consumption and stroke incidence. 

METHODS: A population-based case-control study was performed, lasting from September 1990 to December 1991. The study comprised 440 incident cases of stroke and 473 controls between the ages of 40 and 85. Cases were defined following WHO criteria, and controls were randomly selected from the study base population. Information on fish consumption was obtained with a food frequency questionnaire 

 RESULTS: After controlling for age, energy intake and several stroke risk factors, the risk of stroke increased with the consumption of fish, chi(2) 4.12, p = 0.04. Those in the highest quintile of consumption (46 g of fish/day) had a multivariate adjusted odds ratio (OR) of 1.95 (95% CI: 1.14-3.33) as compared to those in the lowest quintile of fish consumption (11 g/ day). The risk of cerebral infarction also increased with the consumption of fish, showing an OR of 1.98 (95% CI: 1.08-3.47). Those in the highest quintile of n-3 fatty acid consumption (660 mg/day) were at borderline higher risk of stroke, with an OR of 1.76 (95% CI: 0.95-3.26), and also of cerebral infarction (OR: 1.89, 95% CI: 0.95-3.75), as compared to those in the lower quintile of n-3 fatty acids consumption (115 mg/day).  

 CONCLUSION: Although misclassification of exposure and residual confounding by unmeasured factors cannot be ruled out, a high fish consumption was associated with an increased risk of stroke and cerebral infarction in this study. More studies should be done to clarify the effect of fish consumption on stroke and stroke subtype in order to issue recommendations regarding the consumption of fish and the risk of stroke.

 


 

EMBO J 2000 Apr 17;19(8):1784-93
Polyunsaturated fatty acids are potent neuroprotectors.

Lauritzen I, Blondeau N, Heurteaux C, Widmann C, Romey G, Lazdunski M

Institut de Pharmacologie Moleculaire et Cellulaire, CNRS UPR 411, 660 route des Lucioles, Sophia Antipolis, 06560 Valbonne, France.

Results reported in this work suggest a potential therapeutic value of polyunsaturated fatty acids for cerebral pathologies as previously proposed by others for cardiac diseases. 

We show that the polyunsaturated fatty acid linolenic acid prevents neuronal death in an animal model of transient global ischemia even when administered after the insult

Linolenic acid also protects animals treated with kainate against seizures and hippocampal lesions. 

The same effects have been observed in an in vitro model of seizure-like activity using glutamatergic neurons and they have been shown to be associated with blockade of glutamatergic transmission by low concentrations of distinct polyunsaturated fatty acids. 

Our data suggest that the opening of background K(+) channels, like TREK-1 and TRAAK, which are activated by arachidonic acid and other polyunsaturated fatty acids such as docosahexaenoic acid and linolenic acid, is a significant factor in this neuroprotective effect. 

These channels are abundant in the brain where they are located both pre- and post-synaptically, and are insensitive to saturated fatty acids, which offer no neuroprotection.

NOTA: l'acido alfa-linolenico ALA aprendo i canali del K+ (potassio) determina una iperpolarizzazione di membrana, inibendo l'instaurarsi di un potenziale d'azione presinaptico che porterebbe al rilascio del glutammato  e/o rendendo meno sensibile all'azione del glutammato la membrana post-sinaptica.

 

Stroke 1995 May;26(5):778-82 
Serum fatty acids and the risk of stroke.
Simon JA, Fong J, Bernert JT Jr, Browner WS.
General Internal Medicine Section (111A1), Department of Veterans Affairs Medical Center, San Francisco, CA 94121, USA.

BACKGROUND AND PURPOSE: To examine the relationship between serum fatty acids, which reflect dietary intake, and stroke, we conducted a nested case-control study of 96 men with incident stroke and 96 control subjects matched by age, clinical center, treatment group, and date of randomization who were enrolled in the Multiple Risk Factor Intervention Trial. 
METHODS: After confirming the stability of the stored serum samples, we measured serum cholesterol ester and phospholipid fatty acid levels as the percentage of total fatty acids by gas-liquid chromatography and examined their association with incident stroke. Using stepwise conditional logistic regression that controlled for risk factors for stroke, we determined which fatty acids were independent correlates of stroke. 


RESULTS: In univariate models, a standard deviation (SD) increase (1.37%) in phospholipid stearic acid (18:0) was associated with a 37% increase in the risk of stroke, whereas an SD increase (0.06%) in phospholipid omega-3 alpha-linolenic acid (18:3) was associated with a 28% decrease in the risk of stroke (all P < .05).
Only alpha-linolenic acid in the cholesterol ester fraction was associated with the risk of stroke in multivariate models: an SD increase (0.13%) in the serum level of alpha-linolenic acid was associated with a 37% decrease in the risk of stroke (P < .05).
Systolic blood pressure and cigarette smoking were also independently associated with stroke risk. 


CONCLUSIONS: Our findings suggest that higher serum levels of the essential fatty acid alpha-linolenic acid are independently associated with a lower risk of stroke in middle-aged men at high risk for cardiovascular disease.

NOTA: la concentrazione plasmatica dell'ALA è usualmente 0,6-0,7 %, il che significa che innalzandola di un 0,13 % si porta la concentrazione plasmatica dell'ALA a c.a. 0,75 %

VitalOil è in grado di elevare il livello plasmatico dell'ALA a c.a. 1,2-1-4%


Vasc Med 1999;4(4):219-226 
Essential fatty acids and cardiovascular disease: the Edinburgh Artery Study.
Leng GC, Taylor GS, Lee AJ, Fowkes FG, Horrobin D.
Department of Public Health Sciences, Edinburgh University, Scotland, UK.

The aim of this study was to determine whether plasma and red cell fatty acid levels were associated with cardiovascular disease, and whether any association was independent of other major risk factors.
Over 1100 subjects were examined in a random sample survey of the general population (the Edinburgh Artery Study). 
Fatty acids were measured in three plasma fractions (triglyceride, cholesteryl ester and phospholipid) and in red cell phospholipids. 
Fatty acid levels in groups with cardiovascular disease (myocardial infarction (MI), angina and lower limb disease) were compared with a no disease group. 
- In the cholesteryl ester and phospholipid fractions there were significantly lower levels of eicosapentaenoic acid in the MI group on univariate analysis (p<0.05), but not when adjusted for age, sex, smoking and systolic blood pressure using logistic regression.

 
- In the red cell fraction, alpha-linolenic acid 18:3 n 3 (ALA) was significantly lower in those with stroke (p<0.01) and lower limb disease (p<0.05).


Linoleic 18:2 n 6 acid was significantly raised in the triglyceride fraction in those with MI, probably reflecting recent dietary changes. 
- There were significant increases in dihomo-gamma-linolenic acid in the phospholipid and red cell fractions in those with MI, and in the phospholipid fraction in the stroke group.


These results do not support the hypothesis that n-6 fatty acids are protective against cardiovascular disease, although there may be some beneficial effects of the n-3 fatty acid, alpha-linolenic acid. Results from cross-sectional surveys must, however, be interpreted with caution because the presence of disease may affect dietary intake.


Stroke. 2002 Aug;33(8):2086-93.
Linoleic acid, other fatty acids, and the risk of stroke.

Iso H, Sato S, Umemura U, Kudo M, Koike K, Kitamura A, Imano H, Okamura T, Naito Y, Shimamoto T.

Department of Public Health Medicine, Institute of Community Medicine, University of Tsukuba, Ibaraki-ken, Japan. fvgh5640@mb.infoweb.ne.jp

BACKGROUND AND PURPOSE: The role of serum fatty acids as a risk factor for stroke and stroke subtypes is largely unknown. METHODS: A prospective nested case-control study of Japanese 40 to 85 years of age was conducted through the use of frozen serum samples from 7450 participants in cardiovascular risk surveys collected from 1984 to 1989 for 1 community and 1989 to 1992 for the other 2 communities. By the end of 1998, we identified 197 incident strokes whose subtypes were confirmed by imaging studies. Three controls per case were selected by matching for sex, age, community, year of serum storage, and fasting status.

 

 RESULTS: Compared with controls, total (n=197), hemorrhagic (n=75), and ischemic (n=122) strokes had similar proportions of n3 polyunsaturated fatty acids, lower proportions of linoleic and arachidonic acids, and higher proportions of saturated and monosaturated acids, determined by gas chromatography. The multivariate odds ratios associated with a 1-SD increase in linoleic acid (5%) after adjustment for hypertension, diabetes, serum total cholesterol, and other cardiovascular risk factors were 0.72 [95% confidence interval (CI), 0.59 to 0.89] for total stroke, 0.66 (95% CI, 0.49 to 0.88) for ischemic stroke, 0.63 (95% CI, 0.46 to 0.88) for lacunar infarction, and 0.81 (95% CI, 0.59 to 1.12) for hemorrhagic stroke. The respective odds ratios for saturated fatty acids (4%) were 1.13 (95% CI, 1.05 to 1.65), 1.35 (95% CI, 1.01 to 1.79), 1.44 (95% CI, 1.03 to 2.01), and 1.21 (95% CI, 0.82 to 1.80). Further adjustment for other fatty acids attenuated these relations, but the relation between linoleic acid and risk of ischemic stroke remained statistically significant.

 

CONCLUSIONS: A higher intake of linoleic acid may protect against ischemic stroke, possibly through potential mechanisms of decreased blood pressure, reduced platelet aggregation, and enhanced deformability of erythrocyte cells.