Peat Wrong On DHA

Kvothe

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DHA is the most toxic of all PUFA, It is much worse than 18:2, and one of the main factors contributing to mental impairment and brain damage.

J Biol Chem. 1998 May 29;273(22):13605-12.
Formation of isoprostane-like compounds (neuroprostanes) in vivo from docosahexaenoic acid.
Roberts LJ 2nd, Montine TJ, Markesbery WR, Tapper AR, Hardy P, Chemtob S, Dettbarn WD, Morrow JD.
Abstract
F2-isoprostanes are prostaglandin F2-like compounds that are formed nonenzymatically by free radical-induced oxidation of arachidonic acid. We explored whether oxidation of docosahexaenoic acid (C22:6omega3), which is highly enriched in the brain, led to the formation of F2-isoprostane-like compounds, which we term F4-neuroprostanes. Oxidation of docosahexaenoic acid in vitro yielded a series of compounds that were structurally established to be F4-neuroprostanes using a number of mass spectrometric approaches. The amounts formed exceeded levels of F2-isoprostanes generated from arachidonic acid by 3.4-fold. F4-neuroprostanes were detected esterified in normal whole rat brain and newborn pig cortex at a level of 7.0 +/- 1.4 ng/g and 13.1 +/- 8 ng/g, respectively. Furthermore, F4-neuroprostanes could be detected in normal human cerebrospinal fluid and levels in patients with Alzheimer's disease (110 +/- 12 pg/ml) were significantly higher than age-matched controls (64 +/- 8 pg/ml) (p < 0.05). F4-neuroprostanes may provide a unique marker of oxidative injury to the brain and could potentially exert biological activity. Furthermore, the formation of F4-neuroprostane-containing aminophospholipids might adversely effect neuronal function as a result of alterations they induce in the biophysical properties of neuronal membranes.

2. J Org Chem. 2007 Dec 7;72(25):9698-703. Epub 2007 Nov 10.
Asymmetric synthesis of 14-A4t-neuroprostane: hunting for a suitable biomarker
for neurodegenerative diseases.
Zanoni G(1), Brunoldi EM, Porta A, Vidari G.
(1)Department of Organic Chemistry, University of Pavia, Viale Taramelli,
10-27100 Pavia, Italy. [email protected]
Oxidative stress has long been associated with aging and age-related pathologies,
such as neurodegenerative diseases. One of the direct effects of oxidative stress
in vivo is the formation of prostaglandin-like compounds, named isoprostanes, by
the action of reactive oxygen species on membrane phospholipids. A particular
subclass of isoprostanes, named neuroprostanes, is formed from docosahexaenoic acid (C22:6omega3, DHA) and is considered to be specific for neuronal oxidative stress. Since isoprostanes are considered as golden standards for oxidative stress, and due to the specificity of neuroprostanes for this condition in neurons and their relation with Alzheimer's and Parkinson's diseases, they are envisioned to be suitable biomarkers for these pathologies.
Herein we describe the first total synthesis of 14-A4t-NeuroP in an enantioselective and
stereoselective fashion, by means of a new and rapid approach for the
installation of the omega chain based on a chemoselective Julia-Kocienski
olefination. Furthermore, the construction of the 4,5-cis-disubstituted
cyclopentenone moiety characteristic of class A neuroprostanes is achieved in a
stereospecific fashion, and suitable reaction conditions have been tuned to avoid
epimerization of the labile stereogenic centers

4. Ann Neurol. 2005 Nov;58(5):730-5.
Lipid peroxidation is an early event in the brain in amnestic mild cognitive
impairment.
Markesbery WR(1), Kryscio RJ, Lovell MA, Morrow JD.
(1)Alzheimer's Disease Research Center, Sanders-Brown Center on Aging, University
of Kentucky, Lexington, KY 40536, USA. [email protected]
Multiple studies demonstrate that the brain in Alzheimer's disease (AD) contains
extensive oxidative damage. Most of these studies used advanced-stage AD patients
raising the question of whether oxidative damage is a late effect of
neurodegeneration or precedes and contributes to the pathogenesis of AD. Here we
describe F(2)-isoprostane (F(2)-IsoP) and F(4)-neuroprostane (F(4)-NP) levels in
longitudinally followed, well documented autopsied normal control subjects and
patients with amnestic mild cognitive impairment (MCI), and late-stage AD. Gas
chromatography/negative ion chemical ionization/mass spectrometry was used to
determine F(2)-IsoP and F(4)-NP levels. Significant increases in F(2)-IsoP levels
were found in frontal, parietal and occipital lobes in MCI and late AD compared
to controls but no significant differences were present between MCI and late AD.
A significant increase in F(4)-NPs was present in parietal and occipital lobes in
MCI compared to controls and a significant increase was present in these regions
and hippocampus in late AD compared to controls. The only difference between MCI
and late AD was significantly increased F(4)-NP in hippocampus in late AD. Our
data indicate that lipid peroxidation is present in the brain of MCI patients and
suggest that oxidative damage may play a role in the pathogenesis of AD

Eur J Clin Nutr. 2012 Aug;66(8):885-90.
Serum fatty-acid composition and the risk of Alzheimer's disease: a longitudinal population-based study.
Rönnemaa E, Zethelius B, Vessby B, Lannfelt L, Byberg L, Kilander L.

BACKGROUND/OBJECTIVES:
It is unknown if a specific fatty-acid composition influences the development of Alzheimer's disease (AD). Nutrition is a possible target for prevention of dementia and especially omega-3-based fatty acids (n-3 FAs) have previously been suggested to be beneficial for cognition. The objective was to ascertain whether serum FAs predicts the risk of incident AD and dementia in a longitudinal population-based cohort.
SUBJECTS/METHODS:
Uppsala Longitudinal Study of Adult Men started in 1970. The proportions of FAs in serum cholesteryl esters were estimated in men (n=2009) who were 50 years old at baseline. During a 35 year follow-up time, 213 men had developed dementia, out of which 91 AD. The associations were analyzed with Cox proportional hazards and logistic regression; adjusted for age, education and vascular risk factors.
RESULTS:
Subjects with a higher proportion of saturated FAs had a decreased risk of AD in crude and multi-adjusted models (hazard ratio for 1-s.d. increase in palmitic acid 0.72; 95% confidence intervals: 0.59-0.89). These associations persisted even in the group of approximately 85-year-old survivors. n-3 FAs FAs were not associated with decreased risk of AD or dementia.
CONCLUSIONS: In contrast to experimental studies, saturated FAs were inversely associated with risk of AD. No evidence of a protective effect of n-3 FAs against dementia was found. The results remained essentially unchanged if competing risk from mortality was taken into account.
 
Last edited:
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I think the masses use of vegetable oil and fish oil is extreme. If anything hydrogenated coconut oil is the antidote (if it wasn't for the heavy metals as a result of the catalyst).

Do you have information to amounts and types of Metals in CO?Was it Ni?What else and how much?
 

CLASH

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Sep 15, 2017
Messages
1,219
Considering the marginal requirement for DHA and alpha linolenic acid in adults (if said requirement does in fact exist) and considering the benefits of seafood and grass fed beef/ pastured eggs, I think the best course of action would be to eat some quality seafood and some quality grass fed meats. Mussels, oysters, shrimp, and scallops, with some grass fed meat (and pastured eggs if available) a few times a week would most likely meet the needed intake for linolenic acid and DHA (if such a need does in fact exist). If grass fed dairy is tolerated than I think that would be helpful as well. Also avoiding intake of high omega 6 may help to lower the supposed "need" for these omega 3's, so avoiding seed oils, most nuts and seeds and improperly fed animals.

I think fish oil supplements and intake of high amounts of fatty fish with high amounts of highly unsaturated omega 3's (especially cooked; due to the peroxidation potential of these fats) may be a possible detriment in the long run.
 

magnesiumania

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Joined
Jul 17, 2018
Messages
607
DHA is the most toxic of all PUFA, It is much worse than 18:2, and one of the main factors contributing to mental impairment and brain damage.

J Biol Chem. 1998 May 29;273(22):13605-12.
Formation of isoprostane-like compounds (neuroprostanes) in vivo from docosahexaenoic acid.
Roberts LJ 2nd, Montine TJ, Markesbery WR, Tapper AR, Hardy P, Chemtob S, Dettbarn WD, Morrow JD.
Abstract
F2-isoprostanes are prostaglandin F2-like compounds that are formed nonenzymatically by free radical-induced oxidation of arachidonic acid. We explored whether oxidation of docosahexaenoic acid (C22:6omega3), which is highly enriched in the brain, led to the formation of F2-isoprostane-like compounds, which we term F4-neuroprostanes. Oxidation of docosahexaenoic acid in vitro yielded a series of compounds that were structurally established to be F4-neuroprostanes using a number of mass spectrometric approaches. The amounts formed exceeded levels of F2-isoprostanes generated from arachidonic acid by 3.4-fold. F4-neuroprostanes were detected esterified in normal whole rat brain and newborn pig cortex at a level of 7.0 +/- 1.4 ng/g and 13.1 +/- 8 ng/g, respectively. Furthermore, F4-neuroprostanes could be detected in normal human cerebrospinal fluid and levels in patients with Alzheimer's disease (110 +/- 12 pg/ml) were significantly higher than age-matched controls (64 +/- 8 pg/ml) (p < 0.05). F4-neuroprostanes may provide a unique marker of oxidative injury to the brain and could potentially exert biological activity. Furthermore, the formation of F4-neuroprostane-containing aminophospholipids might adversely effect neuronal function as a result of alterations they induce in the biophysical properties of neuronal membranes.

2. J Org Chem. 2007 Dec 7;72(25):9698-703. Epub 2007 Nov 10.
Asymmetric synthesis of 14-A4t-neuroprostane: hunting for a suitable biomarker
for neurodegenerative diseases.
Zanoni G(1), Brunoldi EM, Porta A, Vidari G.
(1)Department of Organic Chemistry, University of Pavia, Viale Taramelli,
10-27100 Pavia, Italy. [email protected]
Oxidative stress has long been associated with aging and age-related pathologies,
such as neurodegenerative diseases. One of the direct effects of oxidative stress
in vivo is the formation of prostaglandin-like compounds, named isoprostanes, by
the action of reactive oxygen species on membrane phospholipids. A particular
subclass of isoprostanes, named neuroprostanes, is formed from docosahexaenoic acid (C22:6omega3, DHA) and is considered to be specific for neuronal oxidative stress. Since isoprostanes are considered as golden standards for oxidative stress, and due to the specificity of neuroprostanes for this condition in neurons and their relation with Alzheimer's and Parkinson's diseases, they are envisioned to be suitable biomarkers for these pathologies.
Herein we describe the first total synthesis of 14-A4t-NeuroP in an enantioselective and
stereoselective fashion, by means of a new and rapid approach for the
installation of the omega chain based on a chemoselective Julia-Kocienski
olefination. Furthermore, the construction of the 4,5-cis-disubstituted
cyclopentenone moiety characteristic of class A neuroprostanes is achieved in a
stereospecific fashion, and suitable reaction conditions have been tuned to avoid
epimerization of the labile stereogenic centers

4. Ann Neurol. 2005 Nov;58(5):730-5.
Lipid peroxidation is an early event in the brain in amnestic mild cognitive
impairment.
Markesbery WR(1), Kryscio RJ, Lovell MA, Morrow JD.
(1)Alzheimer's Disease Research Center, Sanders-Brown Center on Aging, University
of Kentucky, Lexington, KY 40536, USA. [email protected]
Multiple studies demonstrate that the brain in Alzheimer's disease (AD) contains
extensive oxidative damage. Most of these studies used advanced-stage AD patients
raising the question of whether oxidative damage is a late effect of
neurodegeneration or precedes and contributes to the pathogenesis of AD. Here we
describe F(2)-isoprostane (F(2)-IsoP) and F(4)-neuroprostane (F(4)-NP) levels in
longitudinally followed, well documented autopsied normal control subjects and
patients with amnestic mild cognitive impairment (MCI), and late-stage AD. Gas
chromatography/negative ion chemical ionization/mass spectrometry was used to
determine F(2)-IsoP and F(4)-NP levels. Significant increases in F(2)-IsoP levels
were found in frontal, parietal and occipital lobes in MCI and late AD compared
to controls but no significant differences were present between MCI and late AD.
A significant increase in F(4)-NPs was present in parietal and occipital lobes in
MCI compared to controls and a significant increase was present in these regions
and hippocampus in late AD compared to controls. The only difference between MCI
and late AD was significantly increased F(4)-NP in hippocampus in late AD. Our
data indicate that lipid peroxidation is present in the brain of MCI patients and
suggest that oxidative damage may play a role in the pathogenesis of AD

Eur J Clin Nutr. 2012 Aug;66(8):885-90.
Serum fatty-acid composition and the risk of Alzheimer's disease: a longitudinal population-based study.
Rönnemaa E, Zethelius B, Vessby B, Lannfelt L, Byberg L, Kilander L.

BACKGROUND/OBJECTIVES:
It is unknown if a specific fatty-acid composition influences the development of Alzheimer's disease (AD). Nutrition is a possible target for prevention of dementia and especially omega-3-based fatty acids (n-3 FAs) have previously been suggested to be beneficial for cognition. The objective was to ascertain whether serum FAs predicts the risk of incident AD and dementia in a longitudinal population-based cohort.
SUBJECTS/METHODS:
Uppsala Longitudinal Study of Adult Men started in 1970. The proportions of FAs in serum cholesteryl esters were estimated in men (n=2009) who were 50 years old at baseline. During a 35 year follow-up time, 213 men had developed dementia, out of which 91 AD. The associations were analyzed with Cox proportional hazards and logistic regression; adjusted for age, education and vascular risk factors.
RESULTS:
Subjects with a higher proportion of saturated FAs had a decreased risk of AD in crude and multi-adjusted models (hazard ratio for 1-s.d. increase in palmitic acid 0.72; 95% confidence intervals: 0.59-0.89). These associations persisted even in the group of approximately 85-year-old survivors. n-3 FAs FAs were not associated with decreased risk of AD or dementia.
CONCLUSIONS: In contrast to experimental studies, saturated FAs were inversely associated with risk of AD. No evidence of a protective effect of n-3 FAs against dementia was found. The results remained essentially unchanged if competing risk from mortality was taken into account.
«No DHA is toxic because look how many words i posted» omg. Have you considered that this study may have been performed under blue light? Or that the DHA was from a supplement? Have you?
 

Alpha

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I supplement with 400-600mg of DHA almost everyday, especially on the days where I eat some n-6 PUFAs. There's no reason to avoid fish or omega 3 FAs from the research I do, even though RP diets seem to disagree.
 

Kvothe

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«No DHA is toxic because look how many words i posted» omg. Have you considered that this study may have been performed under blue light? Or that the DHA was from a supplement? Have you?

Of course it was a supplement. How can a single fatty acid in isolation not be a supplement?
 

mrchibbs

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Considering the marginal requirement for DHA and alpha linolenic acid in adults (if said requirement does in fact exist) and considering the benefits of seafood and grass fed beef/ pastured eggs, I think the best course of action would be to eat some quality seafood and some quality grass fed meats. Mussels, oysters, shrimp, and scallops, with some grass fed meat (and pastured eggs if available) a few times a week would most likely meet the needed intake for linolenic acid and DHA (if such a need does in fact exist). If grass fed dairy is tolerated than I think that would be helpful as well. Also avoiding intake of high omega 6 may help to lower the supposed "need" for these omega 3's, so avoiding seed oils, most nuts and seeds and improperly fed animals.

I think fish oil supplements and intake of high amounts of fatty fish with high amounts of highly unsaturated omega 3's (especially cooked; due to the peroxidation potential of these fats) may be a possible detriment in the long run.

I agree, eat nutritious foods and any potential requirement is covered
 

Atman

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How did people obtain their precious, essential DHA before cold water seafood became available to the general population?
Why do cold water fish have the ability to synthesize this important fatty acid but mammals do not?
 

mrchibbs

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How did people obtain their precious, essential DHA before cold water seafood became available to the general population?
Why do cold water fish have the ability to synthesize this important fatty acid but mammals do not?

I think it has to do with the ability to survive in a cold environment, which saturated fats are not geared to do. My personal perspective is that much of the benefits attributed to seafood are not from the fatty acids but rather the trace minerals and iodine.
 
J

jb116

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I think it has to do with the ability to survive in a cold environment, which saturated fats are not geared to do. My personal perspective is that much of the benefits attributed to seafood are not from the fatty acids but rather the trace minerals and iodine.
And amino acids!
 

mrchibbs

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And amino acids!

You're totally right, seafood and shellfish in particular have a great amino acid balance, with loads of taurine and glycine etc.
 
Joined
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How did people obtain their precious, essential DHA before cold water seafood became available to the general population?
Why do cold water fish have the ability to synthesize this important fatty acid but mammals do not?

If mammals are properly fed, they do have EPA and DHA in high quantities. The contemporary grain Feed is highly O6-dominant though.
 

magnesiumania

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How did people obtain their precious, essential DHA before cold water seafood became available to the general population?
Why do cold water fish have the ability to synthesize this important fatty acid but mammals do not?
Read Kruses blog on DHA.
 

Tarmander

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I was reading this website today

Ben’s story about trying to prevent diabetes

Kid has antibodies for islet cells and is on his way to getting type 1 diabetes.

He uses higher dose DHA (3g per dayish) along with aspirin, vit D, and some other supplements to suppress those antibodies and stay free of T1D

DHA may have some downsides but it has got to be better than T1D
 

Kvothe

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I was reading this website today

Ben’s story about trying to prevent diabetes

Kid has antibodies for islet cells and is on his way to getting type 1 diabetes.

He uses higher dose DHA (3g per dayish) along with aspirin, vit D, and some other supplements to suppress those antibodies and stay free of T1D

DHA may have some downsides but it has got to be better than T1D

Aspirin seems to be more than capable of doing all the things sometimes attributed to DHA. Unlike DHA, aspirin has a long track record of significantly improving diabetic conditions in humans, whereas the results for the former are inconclusive, at best. Immunosuppression might not be preferable to diabetes, in the long run. The guy says himself that auto-antibodies reappear as soon as you get of the fish oil. I wish some of the studies showing DHA to pe protective against diabetes in rodent studies would display the survival rates for their groups.
 

schultz

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Why do cold water fish have the ability to synthesize this important fatty acid but mammals do not?

Do they even have that ability? I thought all n-3 in fish ultimately comes from algae and/or plant life?
 
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