Newsgroup: it.salute.alimentazione
Titolo: Eccessi di Omega3?

Anche delle cose e buone e utili, si sa, il troppo stroppia.
Allora mi chiedo: qual è il "troppo" di acido eicosapentaenoico (EPA) e di 
acido docosaesaenoico (DHA), di cui è ricco l'olio di pesce, oltre il quale 
l'eccesso di acidi grassi polinsaturi potrebbe esporre al rischio, per 
esempio, di un'eccessiva produzione di radicali liberi?
Inoltre, non è preferibile assumere gli stessi acidi grassi esenziali 
all'interno di un piatto di pesce, che oltre a fornire proteine, vitamine e 
sali minerali dà anche antiossidanti naturali che porteggono gli acidi 
grassi essenziali, prima di ricorrere alle pillole?

 ha scritto nel messaggio
news:1ng1rprp...@news.lillathedog.net...

Secondo gli esperti di omega 3 più di quanto ne sggerisce Sears che parla si
2,4 grammi,
quantità difficilmente raggiungibile anche con una porzione di salmone al
giorno.
C'è da dire che gli esperti di qualsiacosa non hanno sempre una visione
spassionata del qualcosa della quale si occupano.
Ciao
Gianni

 grassi essenziali, prima di ricorrere alle pillole?
Si, bisognerebbe però valutare come agisce la cottura. 

 Si, bisognerebbe però valutare come agisce la cottura.
Sì, ma la cottura incide anche sugli omega 6 e sull'arachidonico.
-- 
Enrico C 

 esempio, di un'eccessiva produzione di radicali liberi?
Secondo le ultime raccomandazioni dell'International   Society  for  the
Study of        Fatty      Acids    and   Lipids, per la prevenzione
cardiovascolare occorrerebbe assumere almeno 500 mg / giorno di EPA + DHA 
Mia riflessione, (non so se rilevante!):
 La raccomandazione si basa, mi pare, soprattutto su studi americani. 
 Se è vero che gli Omega3 dovrebbero essere in rapporto equlibrato con gli
Omega 6, bisogna vedere però qual è il livello di Omega 6 degli americani e
se è comparabile al nostro... 
Per quanto riguarda i livelli max, lo studio scandinavo citato alla fine
parrebbe ridimensionare i timori di perossidazione dei PUFA, mi pare...
=====================================
http://www.issfal.org.uk/pufa%20intakes.htm
RECOMMENDATIONS FOR INTAKE OF
POLYUNSATURATED FATTY ACIDS IN HEALTHY ADULTS
(Revised in accordance with the recommended changes agreed  by the ISSFAL
Board at ISSFAL 2004, June 28, 2004)
    For cardiovascular health, a  minimum intake of eicosapentaenoic acid
and docosahexaenoic acid combined of:  500 mg/day
 This recommendation is based on a review of major epidemiologic studies
conducted in the   US   in which the intakes of w3 PUFA among healthy
adults were estimated and the subsequent risk for death from CHD was
determined. Six such studies were available, and five studies reported
statistically significant inverse trends between CHD risk and EPA+DHA
intake or a significantly reduced risk at the highest (vs the lowest)
quintile of intake. Meta-analysis by intake group of these data showed a
significant relationship between risk for CHD death and EPA+DHA intake
(p=0.03).  The relative risk reduction in the highest vs. the lowest
intake  groups was 37%, and the intake in that quintile averaged 566 mg
EPA+DHA per day.
 
            Based on large prospective population studies and
well-controlled case-control studies, an intake of about 500 mg of EPA+DHA
per day would be expected to significantly reduce risk for death from CHD
in healthy adults.  This intake is both safe and achievable by diet alone,
even for pregnant and lactating women for whom mercury intake can be an
issue.
 
EPA+DHA Intakes in US Epidemiologic Studies : Eight studies have been
reported with the following characteristics : 1) the population was from
the US and was CHD-free at baseline, 2) risk for CHD death, primary cardiac
arrest, and/or sudden cardiac death were reported, 3) risk was assessed
across a range of estimated EPA+DHA intakes, and, 4) multivariate analysis
was used to calculate relative risk or odds ratios. Two studies (Morris et
al 1995, Hu et al 2003) fitting these criteria were not included because
they reported results from either a shorter follow-up (4 yrs  in Morris et
al 1995 vs. 11 yrs in Albert et al 1998, both from the Physicians’ Health
Study;) or a patient subset (only diabetic nurses from the Nurses Health
Study  in Hu et al 2003   vs all participants in Hu et al 2002) from the
other studies already included. Of the six remaining studies, five found
CHD benefit with increasing intakes of EPA+DHA  or at the highest intake
quintile vs the lowest. One study reported no benefit (Ascherio et al
1995). All six studies were included to estimate the EPA+DHA intake
associated with the lowest risk for death from CHD (Table 3).
 
Nurses’ Health Study (NHS) : Beginning in 1976, the NHS enrolled 121,700
registered nurses who completed lifestyle and medical questionnaires (Hu et
al 2002). A food frequency questionnaire (FFQ) was used to estimate w3 PUFA
intake. The daily EPA+DHA intake was calculated and compared to the risk of
CHD death over the ensuing 16 years.
 
US Physicians’ Health Study (PHS) : This prospective cohort study initiated
in 1982 was similar to the NHS, and enrolled a total of 20,551 US male
physicians between the ages of 40 and 84 years who were free of major
illness (Albert et al 1998).  A FFQ similar to that employed in the NHS was
used to assess w3 PUFA intake. The association between the latter and the
11-year risk for sudden cardiac death (and total mortality) was
ascertained.
 
Seattle Primary Cardiac Arrest Study : This was a population-based,
case-control study conducted in the Seattle area (Siscovik et al 1995). All
cases of primary cardiac arrest in subjects between 25-74 years over a
6-year period were identified. Controls were identified from the same
population and matched for age and sex. A total of 295 cases and 398
controls were included in this report. Dietary intake of fish was
ascertained using the Seafood Intake Scale, a quantitative FFQ developed
for this study. Spouses of both cases and controls were interviewed
regarding their partner’s fish intake over the previous month. The odds
ratio for being a case (vs. a control) as a function of EPA+DHA intake were
calculated.
 
Multiple Risk Factor Intervention Trial (MRFIT) : MRFIT was a multi-center,
open-label study in which 12,866 men at high risk for developing CHD (based
on smoking status, serum cholesterol and blood pressure) were randomized to
either usual care or to interventions addressing all three risk factors.
Dietary data were collected at baseline by standardized 24-hr recall. The
present analysis (Dolecek 1992) included health outcomes from those in the
usual care group over 10.5 years.
 
Cardiovascular Health Study (CHS) : The CHS focused on men and women over
the age of 65 at entry (Mozaffarian et al 2003). About 5,200 individuals
were recruited from four communities from Medicare rolls between 1989 and
1990. A picture version of the National Cancer Institute’s FFQ was
administered at baseline and specifically distinguished between
tuna/non-fried fish, and fried fish/fish sandwiches. Outcomes were
collected for a mean of 9.3 years, and the risk for total ischemic heart
disease death was determined in relation to the amount of EPA+DHA consumed.
 
Health Professionals’ Follow-up Study (HPS) : This study, which was
patterned after the NHS and the PHS, began in 1986 and enrolled 51,529 male
health professionals (non-physicians such as dentists, pharmacists, etc.)
between 40 and 75 years of age (Albert et al 2002). The same FFQ as used in
those studies was used here. A total of 44,895 men free of CHD who had
satisfactorily completed the FFQ were followed for CHD events for 6 years.
 
Additional Scandinavian Data : Dietary intake of EPA, DPA and DHA was 1.08
g/d and 0.72 g/d among a national representative sample 1517 men and 1627
women, respectively, (16-79 years of age) in 1993-4 (Johansson et al 1998).
Japanese and Icelandic people have an even higher intake of marine w3 PUFA.
Life expectancy is among the highest in the world in these countries. Brude
et al (1997) challenged the peroxidation fear by giving 5 g/d of w3 PUFA to
male smokers with hyperlipidemia for six weeks and measured all parameters
of lipid peroxidation in LDL from patients with and without antioxidants.
w3 PUFA neither rendered the LDL particles more susceptible to undergo in
vitro oxidation nor influenced mononuclear cells’ ability to oxidize
autologous LDL, whereas moderate amounts of antioxidants protected LDL
against oxidative modification. This represents strong evidence against any
harmful effect of w3 PUFA on peroxidation of LDL in plasma.  
 
[Unicode Message / Messaggio Unicode]

 pare...
In questo studio si parla invece delle fonti di omega 6 vegetali (LA, acido 
linoleico). come alcuni oli di semi: girasole, soia, ecc.
Per ri-bilanciare il rapporto omega 3/6, oltre agli omega3 di origine 
animale (pesci), anche quelli di origine vegetali possono essere utile, 
dicono questi studi (acido alfalinoLenico, ALA,  di semi di lino, collza, 
noci, ecc. "{alpha}-linolenic acid , found in green leafy vegetables, 
flaxseed, rapeseed, and walnuts"....), utili soprattutto in assenza di 
omega 3 dei pesci
Mie considerazioni:
(Le noci cmq, hanno anche un discreta proporzione di LA...)
(L'olio di colza poi presenta i noti problemi per la presenza di acido
erucico, quindi l'unica forma utile è semmai la varietà canola, ma solo con
spremitura a freddo per evitare i grassi trans della raffinazione).
http://www.ajcn.org/cgi/content/abstract/70/3/560S
American Journal of Clinical Nutrition, Vol. 70, No. 3, 560S-569S, 
September 1999
© 1999 American Society for Clinical Nutrition
Supplements
Essential fatty acids in health and chronic disease1,2
Artemis P Simopoulos
1 From The Center for Genetics, Nutrition and Health, Washington, DC.
Human beings evolved consuming a diet that contained about equal amounts of 
n-3 and n-6 essential fatty acids. Over the past 100-150 y there has been 
an enormous increase in the consumption of n-6 fatty acids due to the 
increased intake of vegetable oils from corn, sunflower seeds, safflower 
seeds, cottonseed, and soybeans. Today, in Western diets, the ratio of n-6 
to n-3 fatty acids ranges from {approx}20-30:1 instead of the traditional 
range of 1-2:1. Studies indicate that a high intake of n-6 fatty acids 
shifts the physiologic state to one that is prothrombotic and 
proaggregatory, characterized by increases in blood viscosity, vasospasm, 
and vasoconstriction and decreases in bleeding time. n-3 Fatty acids, 
however, have antiinflammatory, antithrombotic, antiarrhythmic, 
hypolipidemic, and vasodilatory properties. These beneficial effects of n-3 
fatty acids have been shown in the secondary prevention of coronary heart 
disease, hypertension, type 2 diabetes, and, in some patients with renal 
disease, rheumatoid arthritis, ulcerative colitis, Crohn disease, and 
chronic obstructive pulmonary disease. Most of the studies were carried out 
with fish oils [eicosapentaenoic acid (EPA) and docosahexaenoic acid 
(DHA)]. However, {alpha}-linolenic acid , found in green leafy vegetables, 
flaxseed, rapeseed, and walnuts, desaturates and elongates in the human 
body to EPA and DHA and by itself may have beneficial effects in health and 
in the control of chronic diseases.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15630029
1: Circulation. 2005 Jan 18;111(2):157-64. Epub 2005 Jan 3. 	Related 
Articles, Links
    Click here to read 
    Interplay between different polyunsaturated fatty acids and risk of 
coronary heart disease in men.
    Mozaffarian D, Ascherio A, Hu FB, Stampfer MJ, Willett WC, Siscovick 
DS, Rimm EB.
    Channing Laboratory, Department of Medicine, Brigham and Women's 
Hospital and Harvard Medical School, Boston, Mass, USA. 
    BACKGROUND: Consumption of polyunsaturated fatty acids (PUFAs) may 
reduce coronary heart disease (CHD) risk, but n-6 PUFAs may compete with 
n-3 PUFA metabolism and attenuate benefits. Additionally, seafood-based, 
long-chain n-3 PUFAs may modify the effects of plant-based, 
intermediate-chain n-3 PUFAs. However, the interactions of these PUFAs in 
relation to CHD risk are not well established. METHODS AND RESULTS: Among 
45,722 men free of known cardiovascular disease in 1986, usual dietary 
intake was assessed at baseline and every 4 years by using validated 
food-frequency questionnaires. CHD incidence was prospectively ascertained. 
Over 14 years of follow-up, participants experienced 218 sudden deaths, 
1521 nonfatal myocardial infarctions (MIs), and 2306 total CHD events 
(combined sudden death, other CHD deaths, and nonfatal MI). In 
multivariate-adjusted analyses, both long-chain and intermediate-chain n-3 
PUFA intakes were associated with lower CHD risk, without modification by 
n-6 PUFA intake. For example, men with > or = median long-chain n-3 PUFA 
intake (> or =250 mg/d) had a reduced risk of sudden death whether n-6 PUFA 
intake was below (<11.2 g/d; hazard ratio [HR]=0.52; 95% confidence 
interval [CI]=0.34 to 0.79) or above (> or =11.2 g/d; HR=0.60; 95% CI=0.39 
to 0.93) the median compared with men with a < median intake of both. In 
similar analyses, > or = median intake of intermediate-chain n-3 PUFAs (> 
or =1080 mg/d) was associated with a reduced total CHD risk whether n-6 
PUFA intake was lower (HR=0.88; 95% CI=0.78 to 0.99) or higher (HR=0.89; 
95% CI=0.79 to 0.99) compared with a < median intake of both. 
Intermediate-chain n-3 PUFAs were particularly associated with CHD risk 
when long-chain n-3 PUFA intake was very low (<100 mg/d); among these men, 
each 1 g/d of intermediate-chain n-3 PUFA intake was associated with an 
approximately 50% lower risk of nonfatal MI (HR=0.42; 95% CI=0.23 to 0.75) 
and total CHD (HR=0.53; 95% CI=0.34 to 0.83). CONCLUSIONS: n-3 PUFAs from 
both seafood and plant sources may reduce CHD risk, with little apparent 
influence from background n-6 PUFA intake. Plant-based n-3 PUFAs may 
particularly reduce CHD risk when seafood-based n-3 PUFA intake is low, 
which has implications for populations with low consumption or availability 
of fatty fish.

 issue.
Notare che dicono "achievable by diet alone". Vale a dire, l'assunzione 
minima raccomandata dall'ISSFAL di 500 mg giorno di EPA+DHA può essere 
ottenuta anche solo dall'alimentazione.

 range of 1-2:1.
Ecco i rapporti Omega6-Omega3 di alcuni oli (da 
http://xoomer.virgilio.it/tatanone/omega3_nelson.htm
 )
Type of Oil - Omega-6:Omega-3 Ratio
Semi di lino - 0.3:1
Colza - 2:1
Noci - 5:1
Soia - 7:1
Mais - 58:1
Cartamo - 365:1
L'altro, più recente, studio, però, sembra ridimensionare l'effetto di 
contrasto degli Omega 6 rispetto agli Omega3, mi pare... Boh! :)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15630029
1: Circulation. 2005 Jan 18;111(2):157-64. Epub 2005 Jan 3. 	
[...]


 On Mon, 04 Jul 2005 09:10:46 GMT, Filippo wrote in

[...]
Sull'evoluzione dei consumi di omega6/ omega 3 nell'alimentazione umana, ho 
trovato questo testo (se capisco bene, viene dal dipartimento ricerche di 
un'azienda farmaceutica: sigma-tau S.p.A. - SCIENTIFIC DEPARTMENT )... 
Interessante notare cmq alcuni dati che riportano: il rapporto 
omega6/omega3 sarebbe stato non molto diverso nella dieta Paleolitica e 
nella dieta Mediterranea della Grecia pre-1960... mentre nella dieta 
occidentale americana o nordeuropea il rapporto omega6/omega3 si impenna...
http://www.st-hs.com/TMA_Forum/PUFA%20-%20Calvani%20Benatti%20-%20Feb%202K3.pdf
 
4. EVOLUTIONARY ASPECTS OF DIET
Studies of hunter-gatherer societies indicates that man evolved on a diet 
that was low in
saturated fat and the amounts of n-3 and n-6 fatty acids was quite equal.
Over the past 10000 years with the development of agriculture, changes 
began to take
place in the food supply, especially during the last 100-150 years, that 
lead to increases in
saturated fat from grain-fed cattle; increases in trans-fatty acids from 
the hydrogenation of
vegetable oils; and enormous increase in n-6 fatty acids (about 30 g/day) 
due to the production of
oils from vegetable seeds such as corn, safflower, and cotton (Fig. 4) (4).
FIGURE 4. SCHEME OF THE RELATIVE PERCENTAGES OF DIFFERENT DIETARY FATTY 
ACIDS AND POSSIBLE
CHANGES SUBSEQUENT TO INDUSTRIAL FOOD PROCESSING, INVOLVING ANIMAL 
HUSBANDRY AND
HYDROGENATION OF FATTY ACIDS.
Increases in meat consumption have lead to increased amounts of arachidonic 
acid (C20:4
n-6, AA), about 0.2-1.0 mg/day (5), whereas the amount of LNA is only 2.92 
g/day (6) and
amounts of EPA, DHA are 48 and 72 mg/day, respectively. Thus a relative and 
absolute decrease
in the amount of n-3 fatty acids has lead to an imbalance and increase in 
the ratio of n-6/n-3.
Intake of n-3 fatty acids is much lower today because of the decrease of 
fish consumption
and the industrial production of animal feeds rich in grains containing n-6 
fatty acids, leading to
production of meat reach in n-6 and poor in n-3 fatty acids. The same is 
true for cultured fish and
eggs (7; 8). Even cultivated vegetables contain fewer n-3 fatty acids than 
do plants in the wild
(9). In today’s diet this ratio is 20-30/1, whereas at the time when the 
human genetic code was
established in response to diet, it was 1-4/1.
The ratio of n-6/n-3 in various populations, is reported in the following 
table (Tab. 1).
TABLE 1. RATIOS OF N-6 TO N-3 FATTY ACIDS IN VARIOUS POULATIONS
POPULATION n-6/n-3 Ref.
Paleolithic 0.79
Greece before 1960 1.00-2.00
Current Greece 1.10-2.10
Current United States 16.74
Current United Kingdom and Northern Europe 15.00
Current Japan 4.00
BIBLIOGRAPHY
[...]
4. Leaf A, Waber PC. A new era for science in nutrition. Am J Clin Nutr 
1987; 45:1048-53.
5. Phinney SD, Odin RS, Johnson SB et al. Reduced arachidonate in serum 
phospholipids and cholesteryl esters
associated with vegetarian diet in humans. Am J Clin Nutr 1990; 51:385-92.
6. Raper NR, Cronin FJ, Exler J. Omega-3 fatty acid content of the US food 
supply. Am J Coll Nutr 1992; 11:304-8.
7. Van Vliet T, Katan MB. Lower ratio of n-3 to n-6 fatty acids in cultured 
than in wild fish. Am J Clin Nutr 1990;
51:1-2.
8. Simopoulos AP, Salem N Jr. n-3 fatty acids in eggs from range-fed Greek 
Chickens. N Engl J Med 1989;
321:1412.
9. Simopoulos AP, Salem N Jr. Purslane: a terrestrial source of omega-3 
fatty acids. N Engl J Med 1986; 315:833.
10. Eaton SB, Eaton SB III, Sinclair Aj et al. Dietary intake of long-chain 
polyunsaturated fatty acids during the
paleolithic World Rev Nutr 1998; 83:12-23.
11. Simopoulos AP. Overview of evolutionary aspects of omega-3 fatty acids 
in the diet. World Rev Nutr 1998;
83:1-11.
12. Simopoulos AP. The Mediterranean diet: what is so special about the 
diet of Greece? The scientific evidence. J
Nutr 2001; 131:3065S-73S.
13. Sanders TAB. Polyunsaturated fatty acids in food chain in Europe. Am J 
Clin Nutr 2000; 71(suppl):S176-S8.
14. Sugano AM, Hirata F. Polyunsaturated fatty acids in food chain in 
Japan. Am J Clin Nutr 2000;
71(suppl):S189-S96.
[...]


10% of total energy is not recommended. Below this ceiling there is little
evidence that high dietary intake of n–6 or n–3 PUFAs implies health risks.
Key Words: Polyunsaturated fatty acids • adverse effects • lipid
peroxidation • cholesterol • blood glucose
	   INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
LIPID PEROXIDATION
EFFECTS ON SERUM CHOLESTEROL
EFFECTS ON GLUCOSE HOMEOSTASIS
EFFECTS ON HEMOSTASIS
IMMUNOSUPPRESSION
CARCINOGENESIS
LIVER FUNCTION
OTHER CONCERNS
CONCLUSION
REFERENCES
 
Polyunsaturated fatty acids (PUFAs) of the n–6 and n–3 families are
necessary for proper growth and body function (1). They cannot be
synthesized by humans and must be obtained from the diet (1, 2). Deficiency
syndromes resulting from insufficient dietary n–6 and n–3 PUFAs have been
described (3, 4); however, such syndromes can be prevented with low intakes
of n–6 and n–3 PUFAs, which should be achieved in a normal diet (2). The
optimal daily intakes of PUFAs, and the optimal ratio of n–6 to n–3 PUFAs,
remain unknown. When addressing these questions, other dietary constituents
must also be taken into account (2). Very high intakes of PUFAs may carry a
risk of adverse effects; thus, relevant experimental and clinical data on
safety aspects of PUFAs will be reviewed.
LIPID PEROXIDATION
TOP
ABSTRACT
INTRODUCTION
LIPID PEROXIDATION
EFFECTS ON SERUM CHOLESTEROL
EFFECTS ON GLUCOSE HOMEOSTASIS
EFFECTS ON HEMOSTASIS
IMMUNOSUPPRESSION
CARCINOGENESIS
LIVER FUNCTION
OTHER CONCERNS
CONCLUSION
REFERENCES
 
When exposed to oxidant stress, PUFAs can be attacked by free radicals and
oxidized into lipid peroxides (5). The peroxidative breakdown of PUFAs
involves chain reactions that result in a variety of products such as
aldehydes, ketones, and cyclic peroxides (6, 7). These reactions may
propagate and modify lipids and proteins, eg, in cell membranes and
lipoproteins that contain PUFAs (5, 6). Although still not fully
elucidated, lipid peroxidation is thought to be one important mechanism
involved in the pathogenesis of inflammation, cancer, and atherosclerosis
(5–7).
Foods containing lipid peroxides are potentially toxic, and the more PUFAs
are present in the diet, the more likely is peroxidation (5, 7). However,
the rancid and unpleasant taste of foods rich in peroxidation products (5)
usually prevents the intake of large amounts of lipid peroxides. It is
unresolved whether chronic intake of smaller amounts of peroxidation
products in food or supplements containing PUFAs stored or processed under
conditions allowing oxidation presents a health hazard (5, 7).
Oxidative modification of LDL is the best-substantiated example of in vivo
lipid peroxidation. Oxidatively modified LDL (ox-LDL) is assumed to play an
important role in atherosclerosis (8, 9). Compared with native LDL, ox-LDL
has been shown to have several properties thought to promote the
development of atherosclerosis, including uptake by the macrophage
scavenger receptor, leading to the formation of foam cells (8, 9). There is
evidence that LDL is oxidatively modified in vivo (8, 9), although it has
been difficult to develop reliable methods to quantify such modification
(5, 10).
The susceptibility of LDL to oxidative modification under conditions of
artificial oxidative stress can be measured in vitro (11). Although the
clinical relevance of such tests can be questioned (10), an association
between the susceptibility of LDLs to oxidation in vitro and estimates of
coronary atherosclerosis has been described (12). The situation in vivo,
however, is much more complex than that under controlled in vitro
conditions. In the organism, various defense mechanisms including enzymes,
other proteins, and water- and lipid-soluble antioxidants act protectively
against lipid peroxidation in the circulation and in tissues, ie, artery
wall (7). The ideal test for ox-LDL formation should reflect the presence
and amounts of ox-LDL in the arterial intima, but so far this is possible
only in specimens obtained from animal studies or in pathoanatomical
samples. Several methods based on analyses of plasma have been used to
assess ox-LDL formation, but none is considered ideal (5, 10). Measurement
of thiobarbituric acid–reactive substances (TBARS), thought to reflect the
formation of malondialdehyde, is applied commonly in clinical settings.
This test is sensitive and suitable for application in large study
populations; however, it is rather nonspecific and has other limitations as
well (5, 10). The general lack of reliable methods for assessing
lipoprotein oxidation in the circulation and in artery walls may help
explain conflicting results of in vitro testing and clinical data from PUFA
dietary studies.
In several clinical dietary trials it was shown that when PUFA intake is
increased, the PUFA content of the LDL particles increases concordantly
(13–15). The in vitro susceptibility of LDLs to undergo oxidative
modification was reported to increase when the diet is rich in n–6 PUFAs
compared with monounsaturated fats (13, 14, 16–18). Also, an increase in
plasma TBARS concentrations during an n–6 PUFA–enriched dietary period was
reported (19). In some but not all studies, supplementation with
antioxidants increased the resistance of the LDL particles to oxidation
(14, 15, 20). At present, whether a diet high in n–3 PUFAs increases the
oxidative modification of LDLs is controversial (21). In the large Shunt
Occlusion Trial, patients were supplemented with 4 g n–3 PUFA concentrate
(which also supplied {approx}15 mg vitamin E) daily; compared with the
nonsupplemented control group, no significant differences in serum TBARS
concentrations were seen after 9 mo (22).
Thus, on the basis of in vitro assessments and best substantiated in vivo
for n–6 PUFAs, increased dietary intake of PUFAs may enhance the
susceptibility of LDLs to undergo oxidative modification. However, when it
comes to clinical endpoints there is little evidence to suggest that a high
PUFA intake increases the risk of an adverse outcome. On the contrary, data
from intervention trials show that when saturated fats are replaced by n–6
PUFAs, subjects are less prone to develop atherothrombotic complications
(23–25). Epidemiologic data on large intakes of n–6 PUFAs are lacking.
Traditional Mediterranean diets, to which health-promoting effects are
attributed, are rich in monounsaturated fatty acids (26). Only recently has
the use of plant-derived n–6 PUFAs increased in various populations, and
the long-term effects of such dietary changes are unknown (26). The results
of epidemiologic studies suggest that high n–3 PUFA intake reduces the risk
for cardiovascular disease (27–30), and in intervention trials an increased
n–3 PUFA intake was reported to act favorably on the incidence of
atherothrombotic endpoints (31, 32). The Shunt Occlusion Trial showed a
significant linear trend toward fewer aortocoronary vein graft occlusions
with increasing positive changes in serum phospholipid n–3 PUFA
concentrations (33).
Thus, regardless of the influence on LDL oxidation, there seems to be a net
beneficial effect on clinical outcomes by enrichment with dietary PUFAs.
Several factors may account for these observations. First, serum
LDL-cholesterol concentrations tend to decline when saturated fatty acids
are replaced with PUFAs in the diet (1). Second, PUFAs—in particular n–3
PUFAs—may have antiatherothrombotic effects on growth factors, cytokines,
and signal molecules (34–37). Third, PUFA-rich food sources are often rich
in antioxidants. Fourth, the microenvironment of the artery wall is
different from that of the circulation and, evidently, widely different
from in vitro conditions. Finally, as mentioned previously, the assessment
methods for lipid oxidation in vivo have inherent limitations in reflecting
the processes in the arterial intima.
The dietary requirement of antioxidants with a diet rich in PUFAs has not
been defined. However, along with a PUFA-rich diet, it seems reasonable to
encourage a high intake of antioxidants, preferably incorporated in the
habitual diet.
[...]
CONCLUSION
Evidence suggests that dietary PUFAs, when substituted for saturated fatty
acids, will confer net health gains, most notably in cardiovascular
disease. An upper limit of 10% of energy for n–6 PUFAs is presently
recommended by experts, but a palatable and practicable diet will usually
not exceed this limit. It also seems wise to ensure a high dietary intake
of antioxidants. The risk of adverse effects of dietary PUFAs, whether on
cholesterol or glucose metabolism or hemostatic function (except for large
doses of n–3 PUFAs), seems small.


 Jan Eritsland
[...]
Qui si parla dello stesso studio
http://www.oilofpisces.com/vitamine.html
[....]
Polyunsaturated fatty acids are safe
OSLO, NORWAY. Polyunsaturated fatty acids (PUFAs) of the n-6 and n-3
configurations cannot be synthesized by humans and must be obtained from
the diet. The most common PUFAs are linoleic acid, linolenic acid, and
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found in fish
oils. Linoleic acid is an n-6 configuration while linolenic acid, EPA and
DHA are of the n-3 configuration. Because of the unsaturated nature
(multiple double bonds) of PUFAs they are prone to oxidation which makes
them rancid and potential initiators of chain reactions which can lead to
oxidation of fat and cholesterol molecules in the body. This so-called
lipid peroxidation reaction is believed to be implicated in
atherosclerosis, cancer and inflammation.
Dr. Jan Eritsland, a cardiologist at the Ulleval University Hospital, has
just released a major study dealing with the safety of n-3 and n-6 PUFAs.
Based on numerous reports published in the medical literature Dr. Eritsland
concludes that a high intake of n-3 PUFAs reduces the risk for
cardiovascular disease and heart attack and is entirely safe at least up to
a level corresponding to 10% of the daily calorie intake. He does caution
though that the intake of dietary antioxidants (especially vitamin E) needs
to be increased if the PUFA intake is increased. Supplementation with 4
grams/day of highly concentrated fish oil (containing 3.4 g of EPA and DHA)
was found to lower triglyceride levels, but had no effect on cholesterol
levels or glycemic control (plasma glucose and insulin levels). Although
fish oils are known to reduce the tendency of blood to aggregate (clot) a
recent major trial showed no difference in bleeding episodes among heart
disease patients supplementing with 2 to 5 grams/day of fish oils and the
controls. This held true even if the patients were also taking warfarin or
aspirin. PUFAs of the n-3 family may help prevent cancer and there is no
evidence at all that they promote it. There is, however, some limited
evidence that n-6 PUFAs (linoleic acid) may indeed be involved in the
initiation or promotion of cancer. Most experts recommend that the intake
of linoleic acid not exceed 10% of daily calorie intake. [73 references]
Eritsland, Jan. Safety considerations of polyunsaturated fatty acids.
American Journal of Clinical Nutrition, Vol. 71 (suppl), January 2000, pp.
197S-201S
============================
Altri studi però non hanno riscontrato effetti avversi significativi
neanche da alti dosaggi di omega3 (anche in assenza di supplementazione di
vitamina E antiossidante).
http://www.oilofpisces.com/vitamine.html
[...]
Fish oils do not promote harmful peroxidation
CORVALLIS, OREGON. There is ample evidence that fish consumption and fish
oil supplementation help protect against heart disease. However, the main
components of fish oils, eicosapentaenoic acid (EPA) and docosahexaenoic
acid (DHA) are highly unsaturated and would therefore be prone to
oxidation. This has prompted some researchers to express concern that fish
oils might contribute to the lipid peroxidation involved in the development
of atherosclerosis.
Researchers at the Oregon State University have just released two major
studies designed to further explore this concern. The first study involved
15 postmenopausal women who were randomized to supplement with 15 grams/day
of sunflower oil, 15 grams/day of safflower oil or 15 grams/day of fish oil
(providing 2.0 grams of EPA and 1.4 grams of DHA per day) in a 3-treatment
crossover trial. The researchers conclude that there is no evidence that
fish oil supplementation increases lipid peroxidation when assessed by
measuring the levels of blood plasma malondialdehyde (MDA) and
F2-isoprostanes. However, a slight increase in thiobarbituric acid reactive
substances (TBARS) was noted in the fish oil supplemented group. The
researchers believe this to be insignificant and point out that the TBARS
test is somewhat unreliable.
The second study involved 46 postmenopausal women who were randomly
assigned to receive a daily fish oil supplement (providing 2.5 grams of EPA
and 1.8 grams of DHA) combined with 0, 100, 200 or 400 mg of synthetic
vitamin E (RRR-alpha-tocopherol acetate). Each of the 5-week treatment
periods was followed by a 4-week washout interval in a 4-treatment,
4-period crossover design.
The researchers noted substantial increases in blood plasma levels of EPA
(from 0.110 to 0.734 mmol/L) and DHA (from 0.283 to 0.515 mmol/L). They
also observed an average drop in triglyceride concentrations of almost 30%.
Vitamin E (alpha-tocopherol) levels rose by about 50% after supplementation
with 100 mg/day (50 IU) of alpha-tocopherol-acetate and by about 69% after
supplementation with 400 mg/day (200 IU). The increase in alpha-tocopherol
level was accompanied by a significant decrease in gamma-tocopherol level.
The researchers evaluated the effect of supplementation on lipid oxidation
(TBARS) and protein oxidation (carbonyl groups). They did not observe any
increased protein oxidation, but did find a small but statistically
significant increase in TBARS concentration after fish oil supplementation;
they dismiss this finding as being likely to be clinically irrelevant. The
size of the increase did not change with increased vitamin E intake. The
researchers conclude, “If fish oil consumption does not cause an increase
in oxidation as measured by protein carbonyls, then an increased intake of
vitamin E [during fish oil supplementation] is not necessary.”
Higdon, Jane V., et al. Supplementation of postmenopausal women with fish
oil rich in eicosapentaenoic acid and docosahexaenoic acid is not
associated with greater in vivo lipid peroxidation compared with oils rich
in oleate and linoleate as assessed by plasma malondialdehyde and
F2-isoprostanes. American Journal of Clinical Nutrition, Vol. 72, September
2000, pp. 714-22
Wander, Rosemary C. and Du, Shi-Hua. Oxidation of plasma proteins is not
increased after supplementation with eicosapentaenoic and docosahexaenoic
acids. American Journal of Clinical Nutrition, Vol. 72, September 2000, pp.
731-37
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