Many people know how DHA is now added to some infant formulas, because it is a substance that is important for baby's brain growth.
This means eating omega-3 enriched eggs increased the DHA AND *iron level* in blood but had no effect on cholesterol levels. Am J Clin Nutr. 2002 Jun;75(6):1084-92
Most animals make very little DHA metabolically, however small amounts are manufactured internally through the consumption of α-linolenic acid, an omega-3 fatty acid found in chia, flax, and many other seeds and nuts. DHA is a major fatty acid in sperm and brain phospholipids, especially in the retina.
Dietary DHA can reduce the level of blood triglycerides in humans, which may reduce the risk of heart disease.
Low levels of DHA cause reduction of brain serotonin levels and have been associated with ADHD, Alzheimer's disease, and depression, among other diseases, and there is mounting evidence that DHA supplementation may be effective in combating such diseases.
DHA has been an ingredient in several brands of premium infant formula sold in North America since 2001, after approval by the Food and Drug Administration and Health Canada.
It, together with arachidonic acid (ARA), are permitted in infant formula because both are components of breast milk found around the world. DHA makes infant formula more like human milk than "conventional" formula containing linolenic acid and linoleic acid, which are precursors.
A study published in the April 2005 issue of The Journal of Pediatrics (Clandinin, M.T. The Journal of Pediatrics, April 2005; pp 461-467) found that preterm infants fed baby formulas fortified with DHA derived directly from algae gained weight faster than infants fed formula fortified with DHA from fish oil.
en.wikipedia.org/wiki/Docosahexaenoic_acid
DHA is taken up by the brain in preference to other fatty acids. The turnover of DHA in the brain is very fast, more so than is generally realized.
DHA deficiencies are associated with
foetal alcohol syndrome,
attention deficit hyperactivity disorder, cystic fibrosis, phenylketonuria, unipolar depression, aggressive hostility, and adrenoleukodystrophy. Decreases in DHA in the brain are associated with cognitive decline during aging and with onset of sporadic Alzheimer disease.
Fish oil decreases the proliferation of tumour cells, whereas arachidonic acid, a longchain n-6 fatty acid, increases their proliferation.
These opposite effects are also seen with inflammation, particularly with rheumatoid arthritis, and with asthma. DHA has a positive effect on diseases such as hypertension, arthritis, atherosclerosis, depression, adult-onset diabetes mellitus, myocardial infarction, thrombosis, and some cancers.
� Fish oil capsules (which contain both DHA and EPA [eicosapentaenoic acid], another omega-3 fatty acid)
� DHA extracted from algae (which contains no EPA)
More interestingly, an alternative pathway for DHA biosynthesis-the
anaerobic
polyketide synthase pathway was also reported recently to occur in Schizochytrium, another member of the Thraustochytriidae.
Several aspects of brain PtdSer metabolism and functions seem related to the high polyunsaturated fatty acids content, particularly docosahexaenoic acid (DHA).
The specific fatty acids, eicosapentaenoic acid and docosahexaenoic acid, are homologues of the n-6 fatty acid, arachidonic acid (AA).
(ho�mol�o�gous - Similar in structure and evolutionary origin, though not necessarily in function.)
The depression of delta6 and delta5 desaturases in diabetes is rapidly correlated by lower contents of arachidonic acid and higher contents of linoleic in almost all the tissues except brain.
However, docosahexaenoic n-3 acid enhancement, mainly in liver phospholipids, is not explained yet. In experimental non-insulin dependent diabetes, the effect upon the delta6 and delta5 desaturases is not clear.
"Docosahexaenoic acid abundance in the brain: a biodevice to combat oxidative stress." Nutr Neurosci 5(3): 149-57.
Docosahexaenoic acid (DHA) (22:6) is a polyunsaturated fatty acid of the n - 3 series which is believed to be a molecular target for lipid peroxides (LPO) formation.
Its ubiquitous nature in the nervous tissue renders it particularly vulnerable to oxidative stress, which is high in brain during normal activity because of high oxygen consumption and generation of reactive oxygen species (ROS).
Long-chain polyunsaturated fatty acids (LCPUFA), specifically arachidonic acid and docosahexaenoic acid (DHA), accrue rapidly in the grey matter of the brain during development, and brain fatty acid (FA) composition reflects dietary availability.
two families with opposing effects which are referred to as "essential fatty acids" (EFA): arachidonic acid (AA) and pentaene (eicosapentaenoic acid: EPA) and hexaene (docosahexaenoic acid: DHA) acids.
It is only when omega-3 fatty acids, alpha-linolenic acid (ALA), or eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were added to the diet that sudden cardiac death (ALA, EPA plus DHA) and nonfatal myocardial infarction (only ALA) were significantly lowered.
The protective effect of omega-3 fatty acids occurs rapidly, within weeks. The mechanism for preventing ventricular fibrillation seems to be through a direct effect on myocytes.
One of the hallmarks of cystic fibrosis (CF) lung disease is the presence of intense, neutrophil-dominated airway inflammation, and many researchers have focused on developing therapies to reduce inflammation in CF lung disease.
Other treatments with potential anti-inflammatory effects include pentoxifylline, leukotriene antagonists, docosahexaenoic acid, and azithromycin.
Also, in view of competition between arachidonic and docosahexaenoic acids in a number of functional processes, docosahexaenoic acid or its precursors would be expected to be therapeutic.
Delta-6 Desaturase (D6D) and Delta-5 desaturase (D5D) are the key enzymes for the synthesis of highly unsaturated fatty acids (HUFAs), such as arachidonic acid (20:4, n -6) and docosahexaenoic acid (22:6, n -3), that are incorporated in phospholipids (PLs) and perform essential physiological functions.
The long-chain polyunsaturated fatty acids, docosahexaenoic acid (DHA) and arachidonic acid (AA), are important for optimal visual function and neurodevelopment
cycles of de-esterification/re-esterification of docosahexaenoic acid (22:6n-3) and arachidonic acid (20:4n-6) within brain phospholipids operate independently of each other, and thus that the enzymes regulating each of these cycles are not likely sites of n-3/n-6 competition.
Cell culture and animal feeding studies indicate that oleic, linoleic, conjugated linoleic, gamma-linolenic, dihomo-gamma-linolenic, arachidonic, alpha-linolenic, eicosapentaenoic and docosahexaenoic acids can all influence lymphocyte proliferation, the production of cytokines by lymphocytes, and natural killer cell activity.
The polyunsaturated fatty acid (PUFA) composition of the mammalian central nervous system is almost wholly composed of two long-chain polyunsaturated fatty acids (LC-PUFA), docosahexaenoic acid (DHA) and arachidonic acid (AA).
The main findings are that light sensitivity of retinal rod photoreceptors is significantly reduced in newborns with n-3 fatty acid deficiency, and that docosahexaenoic acid (DHA) significantly enhances visual acuity maturation and cognitive functions.
The brain is more highly enriched than most other tissues in long-chain polyunsaturated fatty acids (PUFA),
particularly docosahexaenoic acid (DHA).
Patients with the Zellweger syndrome and its variants have very low levels of docosahexaenoic acid (DHA) in the brain, retina, and other tissues.
Such a marked DHA deficiency could be related to the pathogenesis of peroxisomal disorders. Therefore, restoring the DHA levels in these patients can probably improve the clinical course of the disease.
PUFAs such as eicosapetaenoic acid (EPA) and docosahexaenoic acid (DHA) competitively inhibit arachidonic acid with a resultant decrease in inflammatory eicosanoids and cytokines.
Lysophosphatidylcholine as a carrier of docosahexaenoic acid to target tissues.
(Not enough phosphorus and choline, then what?)
Impaired arachidonic (20:4n-6) and docosahexaenoic (22:6n-3) acid synthesis by phenylalanine metabolites as etiological factors in the neuropathology of phenylketonuria.
(Above - PKU- is linked to tyrosine!)
accretion of arachidonic acid occurs earlier than docosahexaenoic acid, suggesting earlier development of n6-fatty acid endogenous synthesis.
We suggest that deficiencies of DHA and plasmalogens in peroxisomal disorders, Alzheimer's disease (AD), depression, and attention deficit hyperactivity disorders (ADHD) may be responsible for abnormal signal transduction associated with learning disability, cognitive deficit, and visual dysfunction.
These abnormalities in the signal-transduction process can be partially corrected by supplementation with a diet enriched with DHA.
Women who deliver prematurely have increased pools of n-6 fatty acid and decreased n-3 fatty acids, despite the lower PG production. Supplementation with long chain n-3 fatty acids such as docosahexaenoic acid may be useful in prolonging the duration of gestation in some high-risk pregnancies.
...fatty acid compositions of the yolk lipids are very similar for all the lizard species, irrespective of parity mode; in particular, the proportions of docosahexaenoic acid are consistently low.
(Lizards...hold the phone...true for the Western Fence Lizard?)
"Secondary carnitine deficiency and impaired docosahexaenoic (22:6n-3) acid synthesis: a common denominator in the pathophysiology of diseases of oxidative phosphorylation and beta-oxidation."
The diet of our ancestors was less dense in calories, being higher in fiber, rich in fruits, vegetables, lean meat, and fish. As a result, the diet was lower in total fat and saturated fat, but contained equal amounts of n-6 and n-3 essential fatty acids.
Linoleic acid (LA) is the major n-6 fatty acid, and alpha-linolenic acid (ALA) is the major n-3 fatty acid.
In the body, LA is metabolized to arachidonic acid (AA), and ALA is metabolized to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
The ratio of n-6 to n-3 essential fatty acids was 1 to 2:1 with higher levels of the longer-chain polyunsaturated fatty acids (PUFA), such as EPA, DHA, and AA, than today's diet.
Today this ratio is about 10 to 1:20 to 25 to 1, indicating that Western diets are deficient in n-3 fatty acids compared with the diet on which humans evolved and their genetic patterns were established.
It is pointed out that docosahexaenoic acid appears more effective as regards induction of peroxisomal beta-oxidation.
Similarly, docosahexaenoic appears more powerful in terms of suppression of hepatic delta9-desaturase activity and mRNA-levels.
The potential inhibitory effect of polyunsaturated fatty acids, particularly docosahexaenoic acid, on mitochondrial beta-oxidation is discussed.
Diets enriched in EPA and DHA suppressed antigen-specific delayed hypersensitivity reactions and mitogen-induced proliferation of T cells.
Cocultures of accessory cells and T cells from mice given different diets revealed that purified fatty acid ethyl esters acted directly on the T cell, rather than through the accessory cell.
The loss of proliferative capacity was accompanied by
reductions in interleukin (IL)-2 secretion
and IL-2 receptor alpha chain mRNA transcription, suggesting that dietary EPA and DHA act, in part, by interrupting the autocrine IL-2 activation pathway.
Dietary EPA and DHA blunted the production of intracellular second messengers, including diacylglycerol and ceramide, following mitogen stimulation in vitro. Dietary effects appear to vary with the agonist employed (i.e., anti-CD3 [TcR], anti-CD28, exogenous IL-2, or phorbol myristate acetate and ionomycin).
Feeding flaxseed increases linolenic acid in the egg yolk about 30-fold, and docosahexaenoic acid (DHA) increases nearly fourfold.
When individuals are fed four n-3 PUFA-enriched eggs a day for 4 wk, plasma total cholesterol levels and low-density lipoprotein cholesterol (LDL-C) do not increase significantly.
Plasma triglycerides (TG) are decreased by addition of n-3 PUFA-enriched eggs to the diet. N-3 PUFA may influence LDL particle size, causing a shift toward a less atherogenic particle.
Blood platelet aggregation is significantly decreased in participants consuming n-3 PUFA-enriched eggs.
Overall results of studies to date demonstrate positive effects and no negative effects from consumption of n-3-enriched eggs. Three n-3 PUFA-enriched eggs provide approximately the same amount of n-3 PUFA as one meal with fish.
In the pancreas, lungs, and ileum of CF knock-out mice, membrane-bound arachidonic acid levels have been shown to be increased while docosahexaenoic acid levels are decreased.
This lipid abnormality is reversed following oral administration of docosahexaenoic acid (DHA). In addition, DHA therapy reverses the increased neutrophil infiltration in the lungs of CF knock-out mice.
P.S. I have more, but this was already getting too long.
[ 27. September 2006, 11:07 AM: Message edited by: Marnie ]
Posted by mtnwoman (Member # 8385) on :
Hi Marnie,
My googling brought me this info re DHA and immunity:
quote: Supplementation with DHA, but not with EPA, suppresses T lymphocyte activation, as assessed by expression of CD69. EPA alone does not, therefore, influence CD69 expression. No other marker of immune function assessed in this study was significantly affected by either EPA or DHA.
I wouldn't think that suppressing T lymphocyte activation is a good thing.
Anyone?
Posted by Jellybelly (Member # 7142) on :
Interesting stuff. Thought it interesting about preemies being given DHA in their formulas putting on weight better. The DHA makes it closer to breast milk.
My grandaughter was born at 26 1/2 weeks gestation, thats a full 3 months early. She was very tiny at 1 lb 16 oz. My daughter was fortuneately able to give her breast milk all the way through her nearly 3 month stay in the hospital and then breast feed her when she came out. She did REALLY well, and was actually looking quite "pudgy" when she was released from the hospital at just over 5 lbs.
So, I have seen the reality of this compared to other moms who struggled to give their preemies breast milk and the problems with weight gain that they often had with their children.
I have been using a product for many years called Omega Twin. It is Flax and Borage Oil. I have always leaned toward Borage oil, because it seemed to be higher in Omega 3 and 6, not sure if it is true, but concentrations were higher per capsule usually.
Omega Twin used to come only in a liquid form and had to be refridgerated, kind of a pain, but it seemed worth the trouble because it had the highest levels of of 3,6, and 9 I had seen anywhere.
Recently though Omega Twin has come out in a capsule form that doesn't have to be kept cold. Concentrations are very high still. 3 capsules have 1365 mg of omega 3, 570 mg of omega 6, and 525 mg of omega 9, plus 105 mg of gamma-linolic.
I buy it on line, and have found it pretty affordable that way.
Now reading Marnie's stuff, I am not sure if this is the kind of ratios we might need, but very high sourse of Omegas and it, isn't from fish oil.
EPA supplementation increased plasma and platelet phospholipid EPA but reduced DHA.
DHA supplementation increased DHA and EPA in plasma and platelet phospholipids.
Both EPA and DHA increased fasting insulin significantly.
EPA, but not DHA, tended to increase fasting glucose, but not significantly so.
American Journal of Clinical Nutrition, Vol. 71, No. 5, 1085-1094, May 2000
Docosahexaenoic acid [DHA, 22:6(n-3)] prevents cardiovascular disease by decreasing obesity.
It also prevents cancer and other geriatric diseases. We studied the chronic pleiotropic effects of DHA on transcription including that of mRNAs for uncoupling proteins (UCP).
Journal of Nutrition. 2001;131:2636-2642.
However, insulin resistance influenced the myocardial fatty acid composition with decreased n-6 and n-3 PUFA contents and increased monounsaturated fatty acid content.
Only slight alterations were observed in mitochondrial fatty acid composition, and they were corrected by DHA intake. Moreover, insulin resistance decreased the glutamate-supported respiration, and DHA intake did not influence this effect.
In conclusion, the impairment of cardiac mitochondrial function was more pronounced in the insulin-deficient state than in insulin resistance.
The modification of fatty acid composition of cardiac and mitochondrial membranes by DHA partially prevented the mitochondrial alterations induced in the two models.
Am J Physiol Regul Integr Comp Physiol 286: R519-R527, 2004. First published November 6, 2003
Relative to placebo, DHA, but not EPA, enhances vasodilator mechanisms and attenuates constrictor responses in the forearm microcirculation.
Improvements in endothelium-independent mechanisms appear to be predominant and may contribute to the selective blood pressure-lowering effect observed with DHA compared with EPA in humans.
Circulation. 2000;102:1264
Docosahexaenoic acid (DHA), an omega-3 fatty acid, belongs to the class of nutrients called essential fatty acids.
DHA has been shown to reduce levels of blood triglycerides.
High triglycerides are linked with heart disease in most, but not all, research.
DHA alone appears to be just as effective as fish oils (which contain both DHA and eicosapentaenoic acid [EPA]) in beneficially lowering triglyceride levels in people at risk for heart disease. 1
In part, this may be because some DHA is converted to EPA in the body. 2 Unlike EPA, however, DHA may not reduce excessive blood clotting. 3
DHA deficiency plays an important role in a group of congenital diseases called peroxisomal disorders, which damage the protective covering (myelin) around nerves.
(Above is for you, James...)
Daily oral supplementation of 100-600 mg of DHA has been shown to increase blood levels of DHA,
to protect myelin,
and to improve the signs and symptoms of these potentially devastating disorders. 10
Certain microalgae contain DHA and are used as a vegetarian source of this nutrient in some supplements.
Whether DHA inhibits thromboxane synthetase or thromboxane A2/prostaglandin H2 receptor function remains unresolved.
Hashimoto et al30 have shown that rats fed DHA intragastrically had reduced plasma norepinephrine levels.
***Increased adenyl purines such as ATP***,
released both spontaneously and in response to norepinephrine from segments of caudal artery, were significantly inversely associated with BP.
ATP causes vasodilation by stimulating the release of NO from endothelial cells,31 via a direct action on vascular smooth muscle cells,32 and by hyperpolarizing smooth muscle cells.33
DHA was postulated to alter membrane fatty acid composition and
accelerate ATP release from vascular endothelial cells, which, in conjunction with reduced plasma norepinephrine, may be responsible for the fall in BP.30
circ.ahajournals.org/cgi/reprint/102/11/1264.pdf
Generalized peroxisomal disorders are severe congenital diseases that involve the central nervous system, leading to severe psychomotor retardation, retinopathy, liver disease, and early death.
In these disorders, peroxisomes are not normally formed and their enzymes are deficient.
Characteristically, plasmalogen synthesis and �-oxidation of very-long-chain fatty acids (VLCFAs) are affected.
We found that patients with generalized peroxisomal disorders have a profound brain deficiency of docosahexaenoic acid (DHA; 22:6n-3) and low DHA concentrations in all tissues and the blood.
Given the fundamental role of DHA in neuronal and retinal membranes, a DHA deficiency of this magnitude might be pathogenic.
Thus, we studied the possible therapeutic effect of normalizing DHA concentrations in patients with peroxisomal disorders. We chose the DHA ethyl ester (DHA-EE) because of its high degree of purity at daily oral doses of 100-500 mg.
This article summarizes the results of treatment of 13 patients with DHA-EE, with some follow-up evidence of clinical improvement.
Supplementation with DHA-EE normalized blood DHA values within a few weeks. Plasmalogen concentrations increased in erythrocytes in most patients and after DHA concentrations were normalized, amounts of VLCFAs decreased in plasma.
Liver enzymes returned almost to normal in most cases.
From a clinical viewpoint, most patients showed improvement in vision, liver function, muscle tone, and social contact.
In 3 patients, normalization of brain myelin was detected by magnetic resonance imaging.
In 3 others, myelination improved. In a seventh patient, myelination is progressing at a normal rate. These results suggest a fundamental role of DHA in the pathogenesis of Zellweger syndrome.
DHA therapy is thus strongly recommended, not only to alleviate symptoms in patients with life-threatening diseases, but also to clarify remaining questions regarding the role of DHA in health and disease.
American Journal of Clinical Nutrition, Vol. 71, No. 1, 376S-385s, January 2000
Few people know that the human brain is comprised of over 60% fat or that its most abundant fat (25%) is called docosahexaenoic acid (DHA).
DHA is an omega-3 long chain polyunsaturated fatty acid (not to be confused with the hormone DHEA).
It is the primary structural fat in both the gray matter of the brain and the retina of the eye. DHA is essential for brain and eye development and function.
There are very few sources of DHA in the diet. It can be made from the omega-3 oil alpha-linolenic acid (ALA) found in large quantities in flax oil, in moderate amounts in canola oil and walnuts or in small amounts in green leafy vegetables.
Only about 3-5% of the alpha-linolenic acid consumed becomes either DHA or EPA in healthy individuals.
Some medical authorities incorrectly state that neither DHA or EPA can be converted to the other in the body.
In fact, DHA is made from EPA and there is even a 10% retroconversion back into EPA.
[Conquer JA, Holub BJ. Supplementation with an algae source of docosahexaenoic acid increases (n-3) fatty acid status and alters selected risk factors for heart disease in vegetarian subjects.
J Nutr. 1996 Dec;126(12): pp.3032-9]
The process of converting ALA to either DHA or EPA is hindered in various disease states and requires that some people receive DHA from their diet or supplementally.
Healthy individuals who consume little DHA or EPA in their diet are creating what they need from ALA if their intake of ALA is adequate.
Fish oils, a source of DHA, can be high in vitamin A and vitamin D. Taking more than 25000 IU of vitamin A per day, or 800 IU of vitamin D per day is not recommended
Olive oil may decrease the ability of DHA to decrease inflammation (pain swelling, redness)
If you have diabetes (blood sugar disease), you should not take DHA without first asking your health care professional
PTP-1β (protein tyrosine phosphatase 1β, non-receptor type 1) is a tyrosine phosphatase which: interacts with EGF and PDGF receptors; regulates insulin and leptin signaling; and has affects on LDL-cholesterol and obesity in humans [31]. FUNG decreased ptpn1, which could affect cell proliferation.
In the present study and previous works, we fed mice diets enriched with fungal oil
enriched in AA (FUNG),
fish oil (FISH), or a combination of the two (COMB).
Using enrichment analysis (Table 2), FUNG affected numerous P450 transcripts, including por (P450 cytochrome oxidoreductase), cyp2a4, -2b9, -3a11, -3a16, -3a41, and -4a10 (up regulation of 4a10 confirmed with RTPCR; [1]).
Cytokine-induced expression of cell adhesion molecules (CAMs) was assessed by Western blot. The effect of DHA22:6n3 on cytokine-induced nuclear factor (NF)- B signaling was analyzed by Western blot analysis and electrophoretic mobility shift assay (EMSA).
RESULTS. Stimulation of hRVECs with VEGF165, TNF , or IL-1� for 6 to 24 hours caused significant induction of intracellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 expression.
Pretreatment of the cells with 100 �M of BSA-bound DHA22:6n3 for 24 hours remarkably inhibited cytokine-induced CAM expression. IL-1�, TNF , and VEGF165 induced nuclear translocation and binding of p65 and p50 NF- B isoforms to the VCAM-1 promoter.
DHA22:6n3 pretreatment inhibited cytokine-induced NF- B binding by 25% to 40%. Moreover, DHA22:6n3 diminished IL-1� induced phosphorylation of the inhibitor of nuclear factor (NF)- B (I- B ), thus preventing its degradation.
ONCLUSIONS. IL-1�, TNF , and VEGF165 induced CAM expression in hRVECs through activation of the NF- B pathway.
DHA22:6n3 inhibited cytokine induced CAM expression through suppression of NF- B nuclear translocation and upstream I- B phosphorylation and degradation. DHA22:6n3 could be an important anti-inflammatory agent in the face of increased cytokine production and CAM expression in the diabetic retina.
Investigative Ophthalmology and Visual Science. 2005;46:4342-4347.
Too much AA, not enough DHA.
Let me see if I can simplify...
T-lymphocytes originate from the thymus gland which is why they are called "T" cells. There are many kinds of T cells.
When produced in overabundance, this is thought to cause autoimmune. The system doesn't shut down.
"Hormonal substances (thymosin, interferon γ, interleukins, colony stimulating factors, thymopoetin, etc.) secreted by epithelial cells within the thymic (Hassal's) corpuscles promote the process of thymic "education".
Not only is the differentiation of T cells regulated by thymic epithelial cells, but T cells influence the architecture of the thymus itself."
"Regulatory T cells (Treg cells),
formerly known as suppressor T cells,
are crucial for the maintenance of immunological tolerance.
Their major role is to shut down T-cell mediated immunity towards the end of an immune reaction.
These cells can be distinguished from other T-cells by the presence of an intracellular molecule called FOXP3.
Mutations of the FOXP3 gene can prevent regulatory T cell development, causing the fatal autoimmune disease"
"In contrast, the low-fat, high-fish diet significantly decreased the percentage of helper T cells whereas the percentage of
These results indicate that DHA's vasorelaxant actions in SHR aorta are independent of endothelium-derived nitric oxide; however, at DHA concentrations* 30 mol/l, vasodilatory prostanoids that activate AT Psensitive K+ channels (KATP) may be involved.
At lower concentrations, DHA-induced relaxation appears to be attributed to modulation of intracellular Ca2+release and L-type Ca2+channels in vascular smooth muscle cells.
The vasorelaxant properties of DHA may contribute, in part, to the blood pressure-lowering effect of dietary fish oil in this hypertensive model.
[ 27. September 2006, 12:53 PM: Message edited by: Marnie ]
Posted by Marnie (Member # 773) on :
Up for Bea.
Posted by treepatrol (Member # 4117) on :
So are you saying DHA and no AHA??
And where can you buy that?? Or should I use tell me wich combination is right?
1: DHA AHA
2: DHA EPA
Posted by northstar (Member # 7911) on :
This was a great posting, Marnie.....I am still having trouble finding a large block of time to dive into it deeply.
Quickly, though, in response to Treepatrol. I did a quick google for DHA, and found at least one, by Kirkman Labs.
Also, Klutzo posted about his response to Krill Oil and postive effects with hyperlipidemia, so I did a quick google on Krill this a.m., and found that it looks like it may be better than regular fish oil, including phosphtydal choline (sp?) or something like that.. Thank you klutzo ! There are several sources for krill, one of which is Mercola.
My next goal is to add up all the omegas and proportions I need, (1:1),for omega 3 and 6, and find the source. There is something about evening primrose being a source of gamma linolenic, which sounds like a cousing to alpha linolenic, which is the ALA in the fish oil.
It will be this weekend before I can get to it, though, but just wanted to get this to you. I think I want to do a base of krill, add dha, and whatever else, to get the ratios I need.
Northstar
Posted by humanbeing (Member # 8572) on :
Can I just use tons of flax oil on my salads and veggies, and ground flax seeds in everything or do I have to take fish pills/flax pills.
I slowed down on the olive oil and increased the flax oil... (I'm not good with supplements)
Posted by Marnie (Member # 773) on :
Yes...just DHA and it is available. My Supervalue Nutrition store carries it.
It is a small part of the Omega 3's.
Another imbalance...too much Omega 6, not enough of the RIGHT Omega 3, it appears.
This looks to protect the myelin sheath...for those who have been "labeled" MS...
Posted by GiGi (Member # 259) on :
Krill Oil
Krill are tiny crustaceans found in the sea. They are the world's largest biomass and feed the largest animal, the blue whale.
Krill oil extracted from krill is a unique source of phosphatidyl choline. It delivers a superior form of EPA and DHA inside a phospholipid as opposed to a regular triglyceride. This combination confers a faster and more effective delivery of EPA and EHA in the body and specifically to the brain through better absorption and transport.
The phospholipids are also bound to a powerful antioxidant, astaxanthin, known to cross the blood brain barrier. Krill oil also naturally contains several other antioxidants including canthaxanthin, beta carotene, Vitamin E and all trans-retinol Vitamin A. These antioxidants protect this nutrient dense oil of oxidation.
We use the Designs for Health Krill Oil - it was made using a unique cold-extraction process that converts it into a stable oil. This process protects the lipids from alteration and avoids peroxidation. It is free of heavy metals and organohalide pollutants. It is extremely pure. It does not cause reflux or regurgitation seen with common fish oil supplements.
Fish Oil is an essential in today's world even for a vegetarian. I myself would not fool with Mother Nature.
Take care.
Posted by northstar (Member # 7911) on :
lyndon, No, it is not a "killer". The omegas and dha are about repairing damage to the body's nervous system, and about helping the body to be strong, so it can also function. It may aid in reducing some symptoms. It is good for the brain, too.
Indirectly, this will help the immune system, which is the other "big guns" needed the get rid of infection.
Northstar
Posted by northstar (Member # 7911) on :
very good summary, interactions, dose/condition, etc.
2. Neuromins is a registered trademark for a form of it.
I will do more searching, and add info here as I find it.
Northstar
Posted by Sojourner (Member # 9424) on :
I'm confused, is EPA a bad thing? My husband has been taking 2400 mgs of EPA and 1200 mgs of DHA per day for about a year. He thought he felt a little less fatigued about a month after he started taking this.
Is there anything wrong with taking the EPA as long as one is gettng enough DHA?
Posted by northstar (Member # 7911) on :
Hi Sojourner My opinion only:
It seems that many things need to be taken with a base. For example, if you are supplementing b12, b6, I have read it is to be done with a "background" of a full B spectrum, including folic acid, biotin, etc. The same prinicple applies to with minerals. I just use a singular multi vit, and multi min supplement as this "background" for any special thing I want to use.
I am going to operate on that same rationale.....the form in nature is the epa/dha combo, as in the fish oil, etc.. I am just going to boost the dha, against a "background" of krill full spectrum.
I also read that if you do just krill, then there is no Vit D in it, so I will have to go to the beach !.....
From what I have read, the krill is considered better than fish oil, for some reason. That may be an advertising gimmick, but I think I saw some comparative studies.
I may also throw in a few fish oil, too. I thought the info about the triglycerides and LDL (low density...lousy lipoproteins) in the cholesterol counts improved, i.e. decreased, with the use of krill.
Northstar
Posted by lesley1954 (Member # 7626) on :
I, too, am interested in this thread, but am having a difficult time absorbing the technical info you posted, Marnie.
My 15-year-old daughter has primarily visual and neuro symptoms. I have been giving her DHA for several months and actually when I think about it, it corresponds with the period during which she has seen the most improvement. Of course, she is on many other things so who can say whether any one thing was more responsible for this improvement.
Her LLMD just recommended adding ALA because her pulse remains high (over 100 most of the time). She also has been dx with POTS, probably a sequelae of Lyme infection. He thinks ALA might help lower her heart rate, hopefully without lowering her BP, which is already low.
Here's my question: Any problem in taking DHA and ALA together? Thanks for your thoughts on this.
Posted by treepatrol (Member # 4117) on :
quote:Originally posted by Marnie: Yes...just DHA and it is available. My Supervalue Nutrition store carries it.
It is a small part of the Omega 3's.
Another imbalance...too much Omega 6, not enough of the RIGHT Omega 3, it appears.
This looks to protect the myelin sheath...for those who have been "labeled" MS...
Thanks
Posted by Charlie D. (Member # 10236) on :
Barry Sears' Zone diet has been on top of this since the early 1990's.
It's a nutrition strategy, not a weight-loss plan, based on the paleolithic research of S. Boyd Eaton et al, published in the mid 80's.
The main issue is to get fish oil that has been independently certified to be toxin-free.
The EPA and DHA are found in higher concentrations in wild salmon, venison, free range cattle, all of which have less fat and less arachidonic acid.
The EPA (and DHA) in fish oil promotes anti-inflammatory action in the immune system, while AA (arachidonic acid) is pro-inflammatory. AA is predominant in the American food supply.
The Japanese and Okinawans, with their fish consumption have the best balance of EPA/AA. Biochemist Barry Sears indicates that test as the gold standard for measuring inflammation in the body.
I have submitted questions about the role of high dose fish oil relative to helping Lyme disease, but don't have the info back yet.
Hope this fills in some blanks. Check it out. I think I've got it mostly right.
Charlie
Posted by AliG (Member # 9734) on :
I just went out & bought Country Life Omega 3 Mood. It has 1000mg EPA & 150mg DHA
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