Kidney stones and diet
Frederick Williams
stones? The enquirer has Crohn's disease.
--
He is not here; but far away
The noise of life begins again
And ghastly thro' the drizzling rain
On the bald street breaks the blank day.
Ron Peterson
wrote:
> Will any particular diet lessen the risk of getting uric acid kidney
> stones? The enquirer has Crohn's disease.
http://kidneydiseases.about.com/od/stonetypes/a/Overview0013.htm says:
"Preventing Uric Acid Stones
The main method of preventing uric acid kidney stones is similar to
treating them; the key is good fluid intake (more than 2 liters per
day) and raising the urine pH with either potassium bicarbonate or
potassium citrate. If this approach isn’t successful and there is a
significant amount of uric acid in the urine, trying allopurinol to
decrease production can be effective."
--
Ron
Frederick Williams
Thank you.
Matti Narkia
Other tips:
- Drink lemon juice, This raises citrate content of urine, which
may inhibit kidney stone formation.
- Avoid foods with high oxalate content such as rhubarb, spinach,
some roots, wheat germs, soy beans, peanuts, okra, chocolate and
batate (sweet potatoes).
- Use less salt, preferably no more than 1500 mg/d. Using too much
salt raises blood's calcium content, which may increase the risk
of kidney stone formation.
- Reduce red meat consumption. Red meat proteins form uric acids,
which can cause formation of uric acid stones.
- Get plenty of magnesium. Use supplements, if necessary.
- Get enough vitamin B6. Use supplements, if necessary.
Links:
Prevention's Healing with Vitamins Kidney Stones
<http://www.mothernature.com/Library/Bookshelf/Books/10/76.cfm>
Magnesium and vitamin B6 for kidney stone prevention
<http://findarticles.com/p/articles/mi_m0ISW/is_267/ai_n15677755>
Kidney Stones Articles...
<http://www.essense-of-life.com/info/tkidneystones.htm>
--
Matti Narkia
Matti Narkia
Somehow I failed to notice that the first poster only wanted info about
uric acid kidney stones. My message was more general, but I guess no
harm was done :-). Below some information specifically about uric acid
stones prevention:
What foods increase the risk for uric acid stones?
<http://www.medicinenet.com/script/main/art.asp?articlekey=80834&page=2>
"Cut the purines: Purines are found in high concentrations in
anchovies, sardines, herring, mackerel, scallops, gravy, meat,
and meat products. Organ meats such as liver, brain, sweetbread,
and kidney have particularly high levels. Studies have found that
a high intake of purines can increase the amount of uric acid in
the urine, leading to the formation of uric acid stones".
What foods decrease the risk for uric acid stones?
<http://www.medicinenet.com/script/main/art.asp?articlekey=80834&page=3>
"Dairy connection: Research has shown that milk and yogurt
consumption can lower serum uric acid levels. In one study, those
who consumed milk one or more times per day had a lower serum uric
acid level than did those who did not drink milk. Similarly, those
who consumed yogurt at least once every other day had a lower serum
uric acid level than did those who did not consume yogurt."
The Role of Diet in the Prevention of Common Kidney Stones
<http://www.medscape.com/viewarticle/521368>
<http://www.medscape.com/viewarticle/521368_print>
"The effect of excess animal protein (purine) is most obvious for
the uric acid stone former. Uric acid, a byproduct of purine
metabolism, is excreted in large quantities in the urine. Excess
protein creates urine with high total urine uric acid, potentially
high supersaturation of urine uric acid, and a low pH, necessary
for formation of uric acid stones. There is no inhibitor of uric
acid crystal formation (Menon & Resnick, 2002), so dietary
measures focus on reducing uric acid and increasing urine volume.
Reduction of animal protein to 12 ounces per day for adults is
recommended. This is plenty to meet the dietary needs of most
Americans, many of whom typically consume several more ounces of
animal protein daily than is recommended. Protein from plant
sources (beans, legumes, etc.) can be substituted as a dietary
alternative without negative consequences. Calcium oxalate stone
formers reducing their animal protein should note the oxalate
content of substitute proteins."
Ferrari P, Bonny O.
[Diagnosis and prevention of uric acid stones]
Ther Umsch. 2004 Sep;61(9):571-4. German.
PMID: 1549311
<http://www.ncbi.nlm.nih.gov/pubmed/15493118>
jay
> stones? The enquirer has Crohn's disease.
Fructose consumption contributes to plasma uric acid. Besides
sweetened processed foods (ie breakfast cereals) and drinks (ie
colas). Does he have high LDL?
Taka
> LOW CARB diets also do great damage to the kidneys themselves. Many
> people report kidney damage after Low Carb dieting. Many of these
> people have to go on dialysis machines for LIFE after dieting with Low
> Carb.
>
> As for benefits, look no farther then the Dr. of low carb, Robert
> Atkins himself. WHEN HE DIED they did an autopsy on his body. The
> report noted he had VERY clogged arteries and was in overall poor
> health due to eating fatty foods more often than usual.
These are VERY strong words, do you have any references to back it
up? Never heard about Atkins having clogged arteries - perhaps he was
like the Masai, i.e. thickened but dilated and not inflammed? Never
heard about kidney damage/stones from low carb but I have seen reports
about fructose damaging kidneys ...
> What people on Low Carb will HIDE from people asking questions is that
> the Low Carb diet is VERY HIGH IN FATS. So high in fats that no
> cardiologist has ever recommended the Low Carb diet to anyone.
That's the point to be high in mostly saturated fat - have you seen
the translated Kwasnievski's pages from Poland? How could high
saturated fat possibly damage kidneys when the damage is mostly of the
glycation type - the people on low carb and high fat have very low
HbC1a, i.e. gycated hemoglobin or AGEs.
Taka
crisology
wrote:
> Will any particular diet lessen the risk of getting uric acid kidney
> stones? The enquirer has Crohn's disease.
Clin Chim Acta. 2004 Jul;345(1-2):17
kidney stone patients are advised to increase their fluid intake..
fruit intake should be increased.
Arq Bras Endocrinol Metabol. 2006 Aug;50(4):823-31.
Reduction of animal protein and salt intake, higher fluid intake and
potassium consumption should be implemented.
Kidney Int. 2008 Jan;73(2):192-9.
Dietary casein promotes a progressive decline in the glomerular
filtration rate (GFR) of remnant kidneys associated with metabolic
acidosis and an endothelin-mediated increase in renal acidification.
Our study suggests that the casein-induced decline in GFR of the
remnant kidney is mediated by metabolic acidosis through endothelin A
receptors.
I don't understand why I'm seeing suggestions (including 1 that I
quoted) for "reducing" meat. Unless a person just wants to "reduce"
kidney stones to pebbles, why not ELIMINATE meat?
With fruit,
Chris
crisology
> Never heard about kidney damage/stones from low carb
"CONCLUSION: Consumption of an LCHP diet for 6 weeks delivers a marked
acid load to the kidney, increases the risk for stone formation,
decreases estimated calcium balance, and may increase the risk for
bone loss. Copyright 2002 by the National Kidney Foundation, Inc."
LCHP = low carbohydrate high protein.
J Child Neurol. 2007 Apr;22(4):375-8.
Kidney stones and the ketogenic diet: risk factors and prevention.
Kidney stones continue to occur in approximately 1 in 20 children on
the ketogenic diet"
Arq Bras Endocrinol Metabol. 2006 Aug;50(4):823-31.
Renal stone disease: Causes, evaluation and medical treatment.
The purpose of the present review is to provide an update about the
most common risk factors or medical conditions associated with renal
stone formation..
Reduction of animal protein and salt intake, higher fluid intake and
potassium consumption should be implemented.
Epilepsia. 2003 May;44(5):735;
Kidney stones, carbonic anhydrase inhibitors, and the ketogenic diet.
PURPOSE: Because carbonic anhydrase inhibitors and the ketogenic diet
are each known risk factors for kidney stones, simultaneous use of
these therapies has been discouraged"
Pediatr Nephrol. 2000 Nov;15(1-2):125-8.
Risk factors for urolithiasis in children on the ketogenic diet.
Kidney stones have been associated with use of the ketogenic diet in
children with refractory seizure disorders. We performed a case-
control study examining risk factors for the development of stones on
the ketogenic diet, and prospectively followed children initiating the
ketogenic diet to evaluate the incidence of urolithiasis. Clinical
characteristics of 18 children presenting with stones (8 uric acid
stones, 6 mixed calcium/uric acid stones, 1 calcium oxalate/phosphate
stone, 3 stones not evaluated) were compared with characteristics of
non-stone-forming children initiating the ketogenic diet
Patients maintained on the ketogenic diet often have evidence of
hypercalciuria, acid urine, and low urinary citrate excretion. In
conjunction with low fluid intake, these patients are at high risk for
both uric acid and calcium stone formation"
Long-term use of the ketogenic diet in the treatment of epilepsy
A retrospective chart review of children treated with the ketogenic
diet for more than 6 years at the Johns Hopkins Hospital was
performed.. 28 patients (15 males, 13 females), currently aged 7 to 23
years, were identified…After 6 years or more.. Kidney stones occurred
in seven children and skeletal fractures in six..tolerability for
children are maintained after prolonged use of the ketogenic diet.
However, side effects, such as slowed growth, kidney stones, and
fractures, should be monitored closely.-The Johns Hopkins University
School of Medicine,.November 2006
J Urol. 2000 Aug;164(2):464-6.
Nephrolithiasis associated with the ketogenic diet.
..Nephrolithiasis is a known complication of this diet with a reported
stone rate as high as 10%..
CONCLUSIONS: The ketogenic diet induces several metabolic
abnormalities that increase the propensity for stone formation.
Urologists should be aware of this potential complication"
Epilepsy Res. 1999 Dec;37(3):181-90.
Clinical efficacy of the ketogenic diet.
The ketogenic diet is an effective alternative therapy used to control
intractable seizures. It involves consuming a calorie-restricted diet
in which the fat:carbohydrate + protein ratio ranges from 2:1 to 5:1.
The diet is a radical medical therapy and nutritional well-being is a
constant concern. Renal stones have occurred in 5-8% of children on
the diet; lipids are elevated, but the significance of this is not
known.
> That's the point to be high in mostly saturated fat
Why opt for a high fat diet as opposed to a low fat/no simple sugar
diet? Coconut is the best source for saturated fat.
Chris
Taka
If you restrict fat together with carbohydrates you are left with
excessive protein (unless starving) which could cause the kidney
stones. But if protein intake matches the body needs and you make up
for the calories by adjusting saturated fat intake (coconut is
probably the safest - no dioxins - and easily metabolized) I don't see
how there could be any renal damage. Problems may arise long term if
you supply the fat from PUFAs which are intrinsically unstable and
generate free radicals - this is the problem in most modern studies.
Taka
Matti Narkia
> Problems may arise long term if
> you supply the fat from PUFAs which are intrinsically unstable and
> generate free radicals - this is the problem in most modern studies.
>
>
Although PUFAs are susceptible to lipid peroxidation, when exposed to
air and light, a vast majority of modern studies about long-chain
omega-3 PUFAs and oxidative stress show that these fatty acids do not
generally increase oxidative stress nor lipid peroxidation in humans,
but may instead even reduce them. See the following abstract from
Do We Go Rancid after Eating Fish?
By Rosemary C. Wander
IIFET 2000: Microbehavior and Macroresults July 10-15, 2000 in Corvallis,
Oregon USA
>http://www.orst.edu/dept/IIFET/2000/abstracts/wander.html> :
"Fish off-flavor and odor develops, in part, through oxidation of
the long-chain, highly unsaturated fatty acids, eicosapentaenoic
acid (EPA) and docosahexaenoic acid (DHA), fish contain, a
condition referred to as rancidity. This deterioration proceeds
through a free-radical mediated, chain reaction. Even though
numerous epidemiologic studies have shown that fish consumption
decreases cardiovascular mortality, there is concern that its
consumption could increase in vivo lipid oxidation, contributing to
the development of such diseases as cardiovascular disease, cancer,
and diabetes. In the past, a limitation to measuring in vivo
oxidation was the lack of appropriate tools. Recently, more
sensitive measures have been developed, e.g., the adduct formed by
the reaction of malondialdehyde with thiobarbituric acid using high
pressure liquid chromatography, F2-isoprostanes, malondialdehyde by
gas chromatography/mass spectrometry, and protein oxidation. Using
these techniques, we measured lipid oxidation in plasma of post
menopausal women after they consumed a supplement of fish oil
containing an amount of EPA/DHA equivalent to two servings of
Chinook salmon. In vivo oxidation was either similar to or lower
than that which occurred when the women were not consuming the fish
oil. On the other hand, plasma concentrations of thiobarbituric
acid reactive substances (TBARS), a much older method for
measuring lipid oxidation, consistently increased. Using
low-density lipoprotein (LDL)obtained from the same subjects, we
determined that the ex vivo rate of oxidation of LDL enriched with
EPA and DHA was slower than LDL not enriched. These data suggest
that oxidative stress is not increased but may actually be lowered
by fish consumption."
I searched and collected without cherry-picking some related studies
from Medline, and in only one of them lipid peroxidation increased
_modestly_. In all the other studies oxitadive stres and/or lipid
peroxidation either was _reduced_ or did not increase. Here are
the studies:
Parra D, Bandarra NM, Kiely M, Thorsdottir I, Martínez JA.
Abstract
Impact of fish intake on oxidative stress when included into a moderate
energy-restricted program to treat obesity.
Eur J Nutr. 2007 Dec;46(8):460-7. Epub 2007 Nov 17.
PMID: 18026868
<http://www.springerlink.com/content/438688530t01m861/>
Taccone-Gallucci M, Manca-di-Villahermosa S, Battistini L, Stuffler RG,
Tedesco M, Maccarrone M.
N-3 PUFAs reduce oxidative stress in ESRD patients on maintenance HD by
inhibiting 5-lipoxygenase activity.
Kidney Int. 2006 Apr;69(8):1450-4.
PMID: 16531984
<http://www.nature.com/ki/journal/v69/n8/abs/5000291a.html;jsessionid=BB303A5D2A1BA88890D0AE886A00798D>
<http://tinyurl.com/6ne8ro>
Kyrylenko OIe, Kukoba TV, Moĭbenko OO, Nikula TD.
[Effect of omega-3 polyunsaturated fatty acids of animal origin on
changes in regulation of lipid peroxidation in patients with ischemic
heart disease]
Lik Sprava. 2004 Oct-Nov;(7):71-3. Ukrainian.
PMID: 15724620
<http://www.ncbi.nlm.nih.gov/pubmed/15724620>
Tholstrup T, Hellgren LI, Petersen M, Basu S, Straarup EM, Schnohr P,
Sandström B.
A solid dietary fat containing fish oil redistributes lipoprotein
subclasses without increasing oxidative stress in men.
J Nutr. 2004 May;134(5):1051-7.
PMID: 15113944
<http://jn.nutrition.org/cgi/content/full/134/5/1051>
Parinyasiri U, Ong-Ajyooth L, Parichatikanond P, Ong-Ajyooth S,
Liammongkolkul S, Kanyog S.
Effect of fish oil on oxidative stress, lipid profile and renal function
in IgA nephropathy.
J Med Assoc Thai. 2004 Feb;87(2):143-9.
PMID: 15061297
<http://www.ncbi.nlm.nih.gov/pubmed/15061297>
Barbosa DS, Cecchini R, El Kadri MZ, Rodríguez MA, Burini RC, Dichi I.
Decreased oxidative stress in patients with ulcerative colitis
supplemented with fish oil omega-3 fatty acids.
Nutrition. 2003 Oct;19(10):837-42.
PMID: 14559317
<http://www.nutritionjrnl.com/article/S0899-9007(03)00162-X/abstract>
Grundt H, Nilsen DW, Mansoor MA, Nordøy A.
Increased lipid peroxidation during long-term intervention with high
doses of n-3 fatty acids (PUFAs) following an acute myocardial infarction.
Eur J Clin Nutr. 2003 Jun;57(6):793-800.
PMID: 12792664
<http://www.nature.com/ejcn/journal/v57/n6/abs/1601730a.html>
Kesavulu MM, Kameswararao B, Apparao Ch, Kumar EG, Harinarayan CV.
Effect of omega-3 fatty acids on lipid peroxidation and antioxidant
enzyme status in type 2 diabetic patients.
Diabetes Metab. 2002 Feb;28(1):20-6.
PMID: 11938024
<http://www.ncbi.nlm.nih.gov/pubmed/11938024>
Higdon JV, Liu J, Du SH, Morrow JD, Ames BN, Wander RC.
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 F(2)-isoprostanes.
Am J Clin Nutr. 2000 Sep;72(3):714-22.
PMID: 10966889
<http://www.ajcn.org/cgi/content/full/72/3/714>
Gapparova KM, Pogozheva AV, Kulakova SN, Tutel'ian VA.
[Effects of omega-3 polyunsaturated fatty acids of vegetable and animal
origin on clinical and metabolic indicators and the intensity of lipid
peroxidation in patients with ischemic heart disease and impaired
carbohydrate tolerance]
Vopr Pitan. 2000;69(1-2):46-9. Russian.
PMID: 10943007
<http://www.ncbi.nlm.nih.gov/pubmed/10943007>
Mori TA, Puddey IB, Burke V, Croft KD, Dunstan DW, Rivera JH, Beilin LJ.
Effect of omega 3 fatty acids on oxidative stress in humans: GC-MS
measurement of urinary F2-isoprostane excretion.
Redox Rep. 2000;5(1):45-6.
PMID: 10905544
<http://www.ingentaconnect.com/content/maney/rer/2000/00000005/00000001/art00011?token=004a17018fdce546e5865462440444255475f2136782a44705e4e26634a492f2530332976>
<http://tinyurl.com/6rpgq2>
Tanaka Y, Mizote H, Inada H, Motohiro T, Kobayashi H, Fukahori S, So H,
Otani M, Nakamizo H, Asagiri K, Akiyoshi K, Tsuru T, Hikida S.
Efficacy of n-3 polyunsaturated fatty acid enriched enteral nutrient
solution in relieving oxidative stress in patients with severe
psychophysiologic disorders.
Kurume Med J. 2004;51(1):83-90.
PMID: 15150903
<http://www.ncbi.nlm.nih.gov/pubmed/15150903>
Taka
> Taka wrote:
> > Problems may arise long term if
> > you supply the fat from PUFAs which are intrinsically unstable and
> > generate free radicals - this is the problem in most modern studies.
>
> Although PUFAs are susceptible to lipid peroxidation, when exposed to
> air and light,
and also when exposed to iron and ROS leaking from the mitochondrial
respiratory chain.
They should also use the "newest" methods of measuring the so called
AGEs such as HbAc1 which may be mediated by PUFA peroxidation. The
arachidonic acid (AA) metabolism activated by stress leads to more
free radicals than the spontaneous oxidation of Omega-3 PUFAs.
Therefore when we supply Omega-3 LC-PUFAs to AA-overloaded subjects
(which the american post menopausal women certainly are) we see a
decrease in oxidative stress because the LC-PUFAs suppress the AA-
induced chronic inflammation. All this is "beneficial" only short
term though ...
> Using
> low-density lipoprotein (LDL)obtained from the same subjects, we
> determined that the ex vivo rate of oxidation of LDL enriched with
> EPA and DHA was slower than LDL not enriched. These data suggest
> that oxidative stress is not increased but may actually be lowered
> by fish consumption."
>
> I searched and collected without cherry-picking some related studies
> from Medline, and in only one of them lipid peroxidation increased
> _modestly_. In all the other studies oxitadive stres and/or lipid
> peroxidation either was _reduced_ or did not increase. Here are
> the studies:
>
> Parra D, Bandarra NM, Kiely M, Thorsdottir I, Martínez JA.
> Abstract
> Impact of fish intake on oxidative stress when included into a moderate
> energy-restricted program to treat obesity.
> Eur J Nutr. 2007 Dec;46(8):460-7. Epub 2007 Nov 17.
> PMID: 18026868
> <http://www.springerlink.com/content/438688530t01m861/>
>
> Taccone-Gallucci M, Manca-di-Villahermosa S, Battistini L, Stuffler RG,
> Tedesco M, Maccarrone M.
> N-3 PUFAs reduce oxidative stress in ESRD patients on maintenance HD by
> inhibiting 5-lipoxygenase activity.
This pinpoints the mechanism why Omega-3 seem beneficial short term -
the 5-lipoxygenase metabolite of AA called LTB4 is one of the worst
things to have in the body!
> Kidney Int. 2006 Apr;69(8):1450-4.
> PMID: 16531984
> <http://www.nature.com/ki/journal/v69/n8/abs/5000291a.html;jsessionid=...>
You see, when it comes to long term the picture is different. It
takes at least 2 years to significantly alter the membrane lipid
composition by dietary fat interventions and for obese people storing
linoleic acid in their adipose tissue it may be significantly longer.
> Eur J Clin Nutr. 2003 Jun;57(6):793-800.
> PMID: 12792664
> <http://www.nature.com/ejcn/journal/v57/n6/abs/1601730a.html>
You get a positive net damage from Omega-3 only if you are not
overloaded with AA or incorporate it in significant amounts into the
cellular/mitochondrial membranes. Also if you are young and healthy
the body can compensate for the lipid peroxidation by endogenous
antioxidants and phase 2 detoxification but again this is a strain
which will exhaust the capacity in the long term.
Taka
> <http://www.ingentaconnect.com/content/maney/rer/2000/00000005/0000000...>
Matti Narkia
>
> They should also use the "newest" methods of measuring the so called
> AGEs such as HbAc1 which may be mediated by PUFA peroxidation. The
> arachidonic acid (AA) metabolism activated by stress leads to more
> free radicals than the spontaneous oxidation of Omega-3 PUFAs.
> Therefore when we supply Omega-3 LC-PUFAs to AA-overloaded subjects
> (which the american post menopausal women certainly are) we see a
> decrease in oxidative stress because the LC-PUFAs suppress the AA-
> induced chronic inflammation. All this is "beneficial" only short
> term though ...
>
speculation without any evidence whatsoever.
The bottom line is that
1) Studies show that fish and fish oil do not increase oxidative
stress nor lipid peroxidation, but may even reduce them.
2) Studies show that benefits of eating fish outweigh risks.
3) Studies show that very high blood levels of marine-derived omega-3
fatty acids are are associated with lower level of atherosclerosis.
4) Studies show that eating fish regularly reduces cardiovascular and
all-cause mortality.
The most important point is that _eating fish regularly reduces
all-cause mortality_. That's a final decider, which you cannot
argue against. Here some evidence about above points:
Turunen AW, Verkasalo PK, Kiviranta H, Pukkala E, Jula A, Männistö S,
Räsänen R, Marniemi J, Vartiainen T.
Mortality in a cohort with high fish consumption.
Int J Epidemiol. 2008 Jun 25. [Epub ahead of print]
PMID: 18579573
<http://ije.oxfordjournals.org/cgi/content/abstract/dyn117>
"Background Our aim was to assess the mortality of fishermen and
fishermen's wives in Finland, presuming that the mortality
reflects their high consumption of contaminated fish.
Methods All Finnish fishermen, registered since 1980, were
identified from the Professional Fishermen Register (N = 6410),
and the fishermen's wives from the national population register
(N = 4260). The cohorts were individually linked with
cause-of-death data until 2005 at Statistics Finland.
The follow-up started in the year after the first registration
as a fisherman and at marriage (if later) for the wives. The
standardized mortality ratios (SMRs) were calculated based
on the national mortality rates. In addition, blood samples
and food frequency questionnaire data were collected from a
volunteer sample.
Results The average fish consumption and serum concentrations
of fish-derived fatty acids and environmental contaminants
were higher among the fishermen and their wives than among the
general population from the same region. The fishermen and their
wives had lower mortality from all causes (SMR 0.78, 95% confidence
interval (CI) 0.73–0.82, and 0.84, 0.76–0.93, respectively), and
ischaemic heart diseases (0.73, 0.65–0.81, and 0.65, 0.50–0.83)
than the general population. Mortality from cerebrovascular
diseases and malignant neoplasms was decreased among the fishermen
(0.67, 0.52–0.85, and 0.90, 0.80–1.01), but not among the wives. In
addition, the fishermen's mortality from water transport accidents
was extremely high (8.31, 5.65–11.79).
Conclusions The fishermen and their wives had lower mortality from
many natural causes. The high intakes of environmental contaminants
in fish were not seen as excess mortality."
Mozaffarian D, Rimm EB.
Fish intake, contaminants, and human health: evaluating the risks and
the benefits.
JAMA. 2006 Oct 18;296(15):1885-99. Review. Erratum in: JAMA. 2007 Feb
14;297(6):590.
PMID: 17047219
<http://jama.ama-assn.org/cgi/content/full/296/15/1885>
"Context Fish (finfish or shellfish) may have health benefits and
also contain contaminants, resulting in confusion over the role of
fish consumption in a healthy diet.
Evidence Acquisition We searched MEDLINE, governmental reports,
and meta-analyses, supplemented by hand reviews of references and
direct investigator contacts, to identify reports published
through April 2006 evaluating (1) intake of fish or fish oil and
cardiovascular risk, (2) effects of methylmercury and fish oil on
early neurodevelopment, (3) risks of methylmercury for
cardiovascular and neurologic outcomes in adults, and (4) health
risks of dioxins and polychlorinated biphenyls in fish. We
concentrated on studies evaluating risk in humans, focusing on
evidence, when available, from randomized trials and large
prospective studies. When possible, meta-analyses were performed
to characterize benefits and risks most precisely.
Evidence Synthesis Modest consumption of fish (eg, 1-2
servings/wk), especially species higher in the n-3 fatty acids
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), reduces
risk of coronary death by 36% (95% confidence interval, 20%-50%;
P<.001) and total mortality by 17% (95% confidence interval,
0%-32%; P = .046) and may favorably affect other clinical
outcomes. Intake of 250 mg/d of EPA and DHA appears sufficient for
primary prevention. DHA appears beneficial for, and low-level
methylmercury may adversely affect, early neurodevelopment. Women
of childbearing age and nursing mothers should consume 2 seafood
servings/wk, limiting intake of selected species. Health effects
of low-level methylmercury in adults are not clearly established;
methylmercury may modestly decrease the cardiovascular benefits of
fish intake. A variety of seafood should be consumed; individuals '
with very high consumption (≥5 servings/wk) should limit intake of
species highest in mercury levels. Levels of dioxins and
polychlorinated biphenyls in fish are low, and potential
carcinogenic and other effects are outweighed by potential benefits
of fish intake and should have little impact on choices or
consumption of seafood (women of childbearing age should consult
regional advisories for locally caught freshwater fish).
Conclusions For major health outcomes among adults, based on both
the strength of the evidence and the potential magnitudes of
effect, the benefits of fish intake exceed the potential risks. For
women of childbearing age, benefits of modest fish intake,
excepting a few selected species, also outweigh risks."
Benefits of fish 'outweigh risks'
<http://news.bbc.co.uk/2/hi/health/6057732.stm>
Sekikawa A et al.
Marine-Derived n-3 Fatty Acids and Atherosclerosis in Japanese,
Japanese-American, and White Men.
J Am Coll Cardiol, August 5, 2008; 52:417-424,
doi:10.1016/j.jacc.2008.03.047
<http://content.onlinejacc.org/cgi/content/short/52/6/417>
"Objectives: We sought to examine whether marine-derived n-3 fatty
acids are associated with less atherosclerosis in Japanese versus
white populations in the U.S.
Background: Marine-derived n-3 fatty acids at low levels are
cardioprotective through their antiarrhythmic effect.
Methods: A population-based cross-sectional study in 281 Japanese
(defined as born and living in Japan), 306 white (defined as white
men born and living in the U.S.), and 281 Japanese-American men
(defined as Japanese men born and living in the U.S.) ages 40 to 49
years was conducted to assess intima-media thickness (IMT) of the
carotid artery, coronary artery calcification (CAC), and serum
fatty acids.
Results: Japanese men had the lowest levels of atherosclerosis,
whereas whites and Japanese Americans had similar levels. Japanese
had 2-fold higher levels of marine-derived n-3 fatty acids than
whites and Japanese Americans in the U.S. Japanese had significant
and nonsignificant inverse associations of marine-derived n-3 fatty
acids with IMT and CAC prevalence, respectively. The significant
inverse association with IMT remained after adjusting for
traditional cardiovascular risk factors. Neither whites nor
Japanese Americans had such associations. Significant differences
between Japanese and whites in multivariable-adjusted IMT (mean
difference 39 µm, 95% confidence interval [CI]: 21 to 57µm, p <
0.001) and CAC prevalence (mean difference 10.7%, 95% CI: 2.9% to
18.4%, p = 0.007) became nonsignificant after we adjusted further
for marine-derived n-3 fatty acids (22 µm, 95% CI: –1 to 46 µm, p =
0.065 and 5.0%, 95% CI: –5.3% to 15.4%, p = 0.341, respectively).
Conclusions: Very high levels of marine-derived n-3 fatty acids
have antiatherogenic properties that are independent of
traditional cardiovascular risk factors and may contribute to
lower the burden of atherosclerosis in Japanese, a lower burden
that is unlikely the result of genetic factors."
The Heart Scan Blog: ERA JUMP: Omega-3 fatty acids and plaque
<http://heartscanblog.blogspot.com/2008/07/era-jump-omega-3-fatty-acids-and-plaque.html>
<http://tinyurl.com/6cyw43>
Japanese diet rich in fish may hold secret to healthy heart
<http://www.eurekalert.org/pub_releases/2008-07/acoc-jdr072208.php>
Omega-3 rather than genetics is key to lack of CHD in Japanese?
<http://www.theheart.org/article/884341.do>
Omega-3 Rather Than Genetics Is Key to Lack of CHD in Japanese?
<http://www.medscape.com/viewarticle/578221>
Matti Narkia
Here a couple of other japanese studies:
Iso H, Kobayashi M, Ishihara J, Sasaki S, Okada K, Kita Y, Kokubo Y,
Tsugane S; JPHC Study Group.
Intake of fish and n3 fatty acids and risk of coronary heart disease
among Japanese: the Japan Public Health Center-Based (JPHC) Study Cohort
I. Circulation. 2006 Jan 17;113(2):195-202. Epub 2006 Jan 9 . '
PMID: 16401768
doi: 10.1161/CIRCULATIONAHA.105.581355
<http://circ.ahajournals.org/cgi/content/full/113/2/195>
"Background— Once- or twice-weekly consumption of fish (or a small
amount of fish intake) reduces the risk of coronary heart disease
and sudden cardiac death in Western countries. It is uncertain
whether a high frequency or large amount of fish intake, as is
the case in Japan, further reduces the risk.
Methods and Results— To examine an association between high intake
of fish and n3 polyunsaturated fatty acids and the risk of coronary
heart disease, a total of 41 578 Japanese men and women aged 40 to
59 years who were free of prior diagnosis of cardiovascular disease
and cancer and who completed a food frequency questionnaire were
followed up from 1990–1992 to 2001. After 477 325 person-years of
follow-up, 258 incident cases of coronary heart disease (198
definite and 23 probable myocardial infarctions and 37 sudden
cardiac deaths) were documented, comprising 196 nonfatal and 62
fatal coronary events. The multivariable hazard ratios (HRs) and
95% confidence intervals in the highest (8 times per week, or
median intake=180 g/d) versus lowest (once a week, or median
intake=23 g/d) quintiles of fish intake were 0.63 (0.38 to 1.04)
for total coronary heart disease, 0.44 (0.24 to 0.81) for definite
myocardial infarction, and 1.14 (0.36 to 3.63) for sudden cardiac
death. The reduced risk was primarily observed for nonfatal
coronary events (HR=0.43 [0.23 to 0.81]) but not for fatal coronary
events (HR=1.08 [0.42 to 2.76]). Strong inverse associations
existed between dietary intake of n3 fatty acids and risk of
definite myocardial infarction (HR=0.35 [0.18 to 0.66]) and
nonfatal coronary events (HR=0.33 [0.17 to 0.63]).
Conclusions— Compared with a modest fish intake of once a week or
&20 g/d, a higher intake was associated with substantially reduced
risk of coronary heart disease, primarily nonfatal cardiac events,
among middle-aged persons."
Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, Ishikawa Y,
Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya
N, Sakata T, Shimada K, Shirato K; Japan EPA lipid intervention study
(JELIS) Investigators.
Effects of eicosapentaenoic acid on major coronary events in
hypercholesterolaemic patients (JELIS): a randomised open-label, blinded
endpoint analysis.
Lancet. 2007 Mar 31;369(9567):1090-8.
PMID: 17398308
DOI:10.1016/S0140-6736(07)60527-3
<http://www.thelancet.com/journals/lancet/article/PIIS0140673607605273/abstract>
"Summary
Background
Epidemiological and clinical evidence suggests that an increased
intake of long-chain n-3 fatty acids protects against mortality
from coronary artery disease. We aimed to test the hypothesis that
long-term use of eicosapentaenoic acid (EPA) is effective for
prevention of major coronary events in hypercholesterolaemic
patients in Japan who consume a large amount of fish.
Methods
18 645 patients with a total cholesterol of 6.5 mmol/L or greater
were recruited from local physicians throughout Japan between 1996
and 1999. Patients were randomly assigned to receive either 1800 mg
of EPA daily with statin (EPA group; n=9326) or statin only
(controls; n=9319) with a 5-year follow-up. The primary endpoint
was any major coronary event, including sudden cardiac death, fatal
and non-fatal myocardial infarction, and other non-fatal events
including unstable angina pectoris, angioplasty, stenting, or
coronary artery bypass grafting. Analysis was by
intention-to-treat. The study was registered at
ClinicalTrials.gov, number NCT00231738.
Findings
At mean follow-up of 4.6 years, we detected the primary endpoint in
262 (2·8%) patients in the EPA group and 324 (3.5%) in controls - a
19% relative reduction in major coronary events (p=0.011).
Post-treatment LDL cholesterol concentrations decreased 25%, from
4.7 mmol/L in both groups. Serum LDL cholesterol was not a
significant factor in a reduction of risk for major coronary
events. Unstable angina and non-fatal coronary events were also
significantly reduced in the EPA group. Sudden cardiac death and
coronary death did not differ between groups. In patients with a
history of coronary artery disease who were given EPA treatment,
major coronary events were reduced by 19% (secondary prevention
subgroup: 158 [8.7%] in the EPA group vs 197 [10.7%] in the control
group; p=0.048). In patients with no history of coronary artery
disease, EPA treatment reduced major coronary events by 18%, but
this finding was not significant (104 [1.4%] in the EPA group '
vs 127 [1.7%] in the control group; p=0.132).
Interpretation
EPA is a promising treatment for prevention of major coronary
events, and especially non-fatal coronary events, in Japanese
hypercholesterolaemic patients."
The famous GISSI-study:
Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin
E after myocardial infarction: results of the GISSI-Prevenzione trial.
Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico.
Lancet. 1999 Aug 7;354(9177):447-55. Erratum in: Lancet 2001 Feb
24;357(9256):642. Lancet. 2007 Jan 13;369(9556):106.
PMID: 10465168
DOI:10.1016/S0140-6736(99)07072-5
<http://www.thelancet.com/journals/lancet/article/PIIS0140673699070725/abstract>
"Summary
Background
There is conflicting evidence on the benefits of foods rich in
vitamin E (alpha-tocopherol), n-3 polyunsaturated fatty acids
(PUFA), and their pharmacological substitutes. We investigated
the effects of these substances as supplements in patients who
had myocardial infarction.
Methods
From October, 1993, to September, 1995, 11 324 patients surviving
recent (≤3 months) myocardial infarction were randomly assigned
supplements of n-3 PUFA (1 g daily, n=2836), vitamin E (300 mg
daily, n=2830), both (n=2830), or none (control, n=2828) for 3.5
years. The primary combined efficacy endpoint was death, non-fatal
myocardial infarction, and stroke. Intention-to-treat analyses were
done according to a factorial design (two-way) and by treatment
group (four-way).
Findings
Treatment with n-3 PUFA, but not vitamin E, significantly lowered
the risk of the primary endpoint (relative risk decrease 10% [95%
CI 1–18] by two-way analysis, 15% [2–26] by four-way analysis).
Benefit was attributable to a decrease in the risk of death (14%
[3–24] two-way, 20% [6–33] four-way) and cardiovascular death (17%
[3–29] two-way, 30% [13–44] four-way). The effect of the combined
treatment was similar to that for n-3 PUFA for the primary endpoint
(14% [1–26]) and for fatal events (20% [5–33]).
Interpretation
Dietary supplementation with n-3 PUFA led to a clinically important
and satistically significant benefit. Vitamin E had no benefit. Its
effects on fatal cardiovascular events require further exploration."
Matti Narkia
> Taka wrote:
>>
>> They should also use the "newest" methods of measuring the so called
>> AGEs such as HbAc1 which may be mediated by PUFA peroxidation. The
>> arachidonic acid (AA) metabolism activated by stress leads to more
>> free radicals than the spontaneous oxidation of Omega-3 PUFAs.
>> Therefore when we supply Omega-3 LC-PUFAs to AA-overloaded subjects
>> (which the american post menopausal women certainly are) we see a
>> decrease in oxidative stress because the LC-PUFAs suppress the AA-
>> induced chronic inflammation. All this is "beneficial" only short
>> term though ...
>>
> Because you say so? I don't think so. That is just empty and futile
> speculation without any evidence whatsoever.
>
> The bottom line is that
>
> 1) Studies show that fish and fish oil do not increase oxidative
> stress nor lipid peroxidation, but may even reduce them.
>
> 2) Studies show that benefits of eating fish outweigh risks.
>
> 3) Studies show that very high blood levels of marine-derived omega-3
> fatty acids are are associated with lower level of atherosclerosis.
>
> 4) Studies show that eating fish regularly reduces cardiovascular and
> all-cause mortality.
>
> The most important point is that _eating fish regularly reduces
> all-cause mortality_. That's a final decider, which you cannot
> argue against.
What about, fish, omega-3 PUFAs and brain? Here some studies:
J. K. Virtanen, PhD, RD, D. S. Siscovick, MD, MPH, W. T. Longstreth, Jr,
MD, MPH, L. H. Kuller, MD, DrPH and D. Mozaffarian, MD, DrPH
Fish consumption and risk of subclinical brain abnormalities on MRI in
older adults.
NEUROLOGY August 5 2008;71:439-446
<http://www.neurology.org/cgi/content/abstract/71/6/439>
"Conclusions: Among older adults, modest consumption of tuna/other
fish, but not fried fish, was associated with lower prevalence of
subclinical infarcts and white matter abnormalities on MRI
examinations. Our results add to prior evidence that suggest that
dietary intake of fish with higher eicosapentaenoic acid and
docosahexaenoic acid content, and not fried fish intake, may have
clinically important health benefits."
(comment in
Eating fish may thwart silent brain damage | Health | Reuters
<http://www.reuters.com/article/healthNews/idUSKRA47341620080804?feedType=RSS&feedName=healthNews&sp=true>
Nurk E, Drevon CA, Refsum H, Solvoll K, Vollset SE, Nygård O, Nygaard
HA, Engedal K, Tell GS, Smith AD.
Cognitive performance among the elderly and dietary fish intake: the
Hordaland Health Study.
Am J Clin Nutr. 2007 Nov;86(5):1470-8.
PMID: 17991661
<http://www.ajcn.org/cgi/content/abstract/86/5/1470>
"Conclusions: In the elderly, a diet high in fish and fish products
is associated with better cognitive performance in a dose-dependent
manner."
Dullemeijer C, Durga J, Brouwer IA, van de Rest O, Kok FJ, Brummer RJ,
van Boxtel MP, Verhoef P.
n 3 fatty acid proportions in plasma and cognitive performance in older
adults. Am J Clin Nutr. 2007 Nov;86(5):1479-85.
PMID: 17991662
<http://www.ajcn.org/cgi/content/abstract/86/5/1479>
"Conclusions: In this population, plasma n–3 PUFA proportions were
associated with less decline in the speed-related cognitive domains
over 3 y. These results need to be confirmed in randomized
controlled trials."
A. Cherubini, C. Andres-Lacueva, A. Martin, F. Lauretani, A. D. Iorio,
B. Bartali, A. Corsi, S. Bandinelli, M. P. Mattson, and L. Ferrucci
Low Plasma N-3 Fatty Acids and Dementia in Older Persons: The InCHIANTI
Study
J. Gerontol. A Biol. Sci. Med. Sci., October 1, 2007; 62(10): 1120 -
1126.
<http://biomed.gerontologyjournals.org/cgi/content/abstract/62/10/1120>
"Conclusions. Dementia is associated with low plasma n-3 FA relative
concentrations. The possibility that higher n-3 FA intake is
associated with a lower risk of cognitive impairment should be
further investigated in prospective studies."
van Gelder BM, Tijhuis M, Kalmijn S, Kromhout D.
Fish consumption, n-3 fatty acids, and subsequent 5-y cognitive decline
in elderly men: the Zutphen Elderly Study.
Am J Clin Nutr. 2007 Apr;85(4):1142-7.
PMID: 17413117
<http://www.ajcn.org/cgi/content/full/85/4/1142>
"Conclusions: A moderate intake of EPA+DHA may postpone cognitive
decline in elderly men. Results from other studies are needed before
definite conclusions about this association can be drawn."
Beydoun MA, Kaufman JS, Satia JA, Rosamond W, Folsom AR.
Plasma n-3 fatty acids and the risk of cognitive decline in older
adults: the Atherosclerosis Risk in Communities Study.
Am J Clin Nutr. 2007 Apr;85(4):1103-11.
PMID: 17413112
<http://www.ajcn.org/cgi/content/full/85/4/1103>
"Conclusions:Promoting higher intakes of n–3 HUFAs in the diet of
hypertensive and dyslipidemic persons may have substantial benefits
in reducing their risk of cognitive decline in the area of verbal
fluency. However, clinical trials are needed to confirm this
finding."
Green KN, Martinez-Coria H, Khashwji H, Hall EB, Yurko-Mauro KA, Ellis
L, LaFerla FM.
Dietary docosahexaenoic acid and docosapentaenoic acid ameliorate
amyloid-beta and tau pathology via a mechanism involving presenilin 1
levels.
J Neurosci. 2007 Apr 18;27(16):4385-95.
PMID: 17442823
<http://www.jneurosci.org/cgi/content/full/27/16/4385>
"Collectively, these results suggest that DHA and DPAn-6
supplementations could be a beneficial natural therapy for AD."
Schaefer EJ, Bongard V, Beiser AS, Lamon-Fava S, Robins SJ, Au R, Tucker
KL, Kyle DJ, Wilson PW, Wolf PA.
Plasma phosphatidylcholine docosahexaenoic acid content and risk of
dementia and Alzheimer disease: the Framingham Heart Study.
Arch Neurol. 2006 Nov;63(11):1545-50.
PMID: 17101822
<http://archneur.ama-assn.org/cgi/content/full/63/11/1545>
"Conclusion The top quartile of plasma PC DHA level was associated
with a significant 47% reduction in the risk of developing
all-cause dementia in the Framingham Heart Study."
Morris MC, Evans DA, Tangney CC, Bienias JL, Wilson RS.
Fish consumption and cognitive decline with age in a large community study.
Arch Neurol. 2005 Dec;62(12):1849-53. Epub 2005 Oct 10.
PMID: 16216930
<http://archneur.ama-assn.org/cgi/content/full/62/12/1849>
"Conclusions Fish consumption may be associated with slower
cognitive decline with age. Further study is needed to determine
whether fat composition is the relevant dietary constituent."
Zhang J, Hebert JR, Muldoon MF.
Dietary fat intake is associated with psychosocial and cognitive
functioning of school-aged children in the United States.
J Nutr. 2005 Aug;135(8):1967-73.
PMID: 1604672
<http://jn.nutrition.org/cgi/content/full/135/8/1967>
"We conclude that high intake of PUFAs may contribute to an
improved performance on the digit span test. In contrast,
increased intake of cholesterol may be associated with a poorer
performance."
Kalmijn S, van Boxtel MP, Ocké M, Verschuren WM, Kromhout D, Launer LJ.
Dietary intake of fatty acids and fish in relation to cognitive
performance at middle age.
Neurology. 2004 Jan 27;62(2):275-80.
PMID: 14745067
<http://www.neurology.org/cgi/content/abstract/62/2/275>
"CONCLUSIONS: Fatty fish and marine omega-3 PUFA consumption was
associated with a reduced risk and intake of cholesterol and
saturated fat with an increased risk of impaired cognitive function
in this middle-aged population."
Kalmijn S, Launer LJ, Ott A, Witteman JC, Hofman A, Breteler MM.
Dietary fat intake and the risk of incident dementia in the Rotterdam Study.
Ann Neurol. 1997 Nov;42(5):776-82.
PMID: 9392577
<http://www.ncbi.nlm.nih.gov/pubmed/9392577>
"Fish consumption, an important source of n-3 polyunsaturated fatty
acids, was inversely related to incident dementia (RR = 0.4
[0.2-0.91), and in particular to Alzheimer's disease (RR = 0.3
[0.1-0.9]). This study suggests that a high saturated fat and
cholesterol intake increases the risk of dementia, whereas fish
consumption may decrease this risk."
Kalmijn S, Feskens EJ, Launer LJ, Kromhout D.
Polyunsaturated fatty acids, antioxidants, and cognitive function in
very old men.
Am J Epidemiol. 1997 Jan 1;145(1):33-41.
PMID: 8982020
<http://aje.oxfordjournals.org/cgi/content/abstract/145/1/3>
<http://aje.oxfordjournals.org/cgi/reprint/145/1/33> (free full text
PDF)
"This study raises the possibility that high linoleic acid intake
is positively associated with cognitive impairment and high fish
consumption inversely associated with cognitive impairment."
Taka
OK, I am not interested in the countless statistical association
studies but rather in the molecular mechanism which you don't cite.
They all use the word "may" which means nothing for sure. I agree
it's possible that the combination of Omega-3 with Omega-6 has lower
mortality than the Omega-6 only even in the long term but there is
absolutely no comparison with Omega-6 restricted group which I would
expect to score the best.
Taka
Matti Narkia
>> http://ma.gnolia.com/groups/Nutrition
>
> OK, I am not interested in the countless statistical association
> studies but rather in the molecular mechanism which you don't cite.
Your ideas about molecular mechanisms are pure speculation, you don't
provide any evidence for them. Mechanisms are nice to find out, but
potential mechanisms are not evidence about benefits or harms.
Epidemiological studies and especially clinical trials are.
> They all use the word "may" which means nothing for sure.
That's a common practice in scientific language. And yes, many things
I've quoted cannot regarded absolutely sure yet, but that does not mean
that there is no evidence. It's better to base one's decisions on the
available evidence, although there is not absolute certainty (there
rarely is), than on empty speculation about potential mechanisms.
> I agree
> it's possible that the combination of Omega-3 with Omega-6 has lower
> mortality than the Omega-6 only even in the long term but there is
> absolutely no comparison with Omega-6 restricted group which I would
> expect to score the best.
>
It is important to restrict omega-6s, but it's at least equally and
probably more important to get enough omega-3s. Low enough
omega-6/omega-3 ratio is important in the prevention of many chronic
diseases, but according to current evidence for example in the
prevention of cardiovascular disease increasing omega-3 intake seems
to be much more important than omega-6/omega-3 ratio, which does not
seem to be useful concept in the prevention of CVD:
Griffin BA.
How relevant is the ratio of dietary n-6 to n-3 polyunsaturated fatty
acids to cardiovascular disease risk? Evidence from the OPTILIP study.
Curr Opin Lipidol. 2008 Feb;19(1):57-62. Review.
PMID: 18196988
<http://www.ncbi.nlm.nih.gov/pubmed/18196988>
SUMMARY: This review should help to settle any outstanding
controversy over the dietary ratio of n-6/n-3 polyunsaturated fatty
acids. It reinforces current recommendations to increase the
consumption of preformed eicosapentaenoic acid/docosahexaenoic acid
in fish, and supports dietary measures to increase and decrease
intakes alpha-linolenic acid and linoleic acid, respectively, to
promote the endogenous synthesis of these longer chain n-3
polyunsaturated fatty acids.
Stanley JC, Elsom RL, Calder PC, Griffin BA, Harris WS, Jebb SA,
Lovegrove JA, Moore CS, Riemersma RA, Sanders TA.
UK Food Standards Agency Workshop Report: the effects of the dietary
n-6:n-3 fatty acid ratio on cardiovascular health.
Br J Nutr. 2007 Dec;98(6):1305-10.
PMID: 18039412
<http://journals.cambridge.org/action/displayAbstract?aid=1451932>
"On the basis of this review of the experimental evidence and on
theoretical grounds, it was concluded that the n-6:n-3 fatty acid
ratio is not a useful concept and that it distracts attention away '
from increasing absolute intakes of long-chain n-3 fatty acids
which have been shown to have beneficial effects on cardiovascular
health. Other markers of fatty acid intake, that more closely
relate to physiological function, may be more useful."
Harris WS, Poston WC, Haddock CK.
Tissue n-3 and n-6 fatty acids and risk for coronary heart disease events.
Atherosclerosis. 2007 Jul;193(1):1-10. Epub 2007 May 15. Review.
PMID: 17507020
<http://www.atherosclerosis-journal.com/article/S0021-9150(07)00186-4/abstract>
"The long-chain n−3 FA, especially DHA, were consistently and
significantly reduced in patients experiencing CHD events. These
findings add further support to the view that long-chain n−3 FA are
cardioprotective."
Harris WS.
The omega-6/omega-3 ratio and cardiovascular disease risk: uses and abuses.
Curr Atheroscler Rep. 2006 Nov;8(6):453-9. Review.
PMID:
<http://www.ncbi.nlm.nih.gov/pubmed/17045070>
"This paper reviews a variety of studies that, in the aggregate,
suggest that the ratio is, both on theoretical and evidential
grounds, of little value. Metrics that include the n-3 FAs alone,
especially eicosapentaenoic and docosahexaenoic acids, appear to
hold the greatest promise."
Harris WS, Assaad B, Poston WC.
Tissue omega-6/omega-3 fatty acid ratio and risk for coronary artery
disease.
Am J Cardiol. 2006 Aug 21;98(4A):19i-26i. Epub 2006 May 30. Review.
PMID: 16919513
doi:10.1016/j.amjcard.2005.12.023
<http://www.ajconline.org/article/S0002-9149(05)02186-7/abstract>
"Fatty acid ratios generally failed to distinguish cases from
controls, and any discriminatory power they had derived from the
omega-3 fatty acid component. Tissue EPA + DHA appears to be the
best fatty acid metric for evaluating for CAD risk."
Frederick Williams
>
> Will any particular diet lessen the risk of getting uric acid kidney
> stones? The enquirer has Crohn's disease.
Thank you for all replies.
Matti Narkia
>
> OK, I am not interested in the countless statistical association
> studies but rather in the molecular mechanism which you don't cite.
> They all use the word "may" which means nothing for sure. I agree
> it's possible that the combination of Omega-3 with Omega-6 has lower
> mortality than the Omega-6 only even in the long term but there is
> absolutely no comparison with Omega-6 restricted group which I would
> expect to score the best.
>
aricle should interest you:
Larsson SC, Kumlin M, Ingelman-Sundberg M, Wolk A.
Dietary long-chain n-3 fatty acids for the prevention of cancer: a
review of potential mechanisms.
Am J Clin Nutr. 2004 Jun;79(6):935-45. Review.
PMID: 15159222
<http://www.ajcn.org/cgi/content/full/79/6/935>