Essential Fatty Acids (EFAs) and Health:

Sydney · 11-14-2006, 09:04 AM

Gosh - I am really trying to understand this. I read all the articles you posted. Since I have FM and RSD I understand that EFA
Omega 3 and 6 are good for inflammation. My diet is very poor for various reasons thus I need the supplements. Now - I am also deficient in Vitamin D (1(18). I have read where a protocal for low D is synthetic 50,000 pils once per week for 4 -6 weeks Or maybe 8. Anyway that does work as I know someone who did it. Her level jumped from 8 to 60 (25-)H) However, my naturopathic dr. says to take the natural D (which contains A also) . I was taking 4,000 natural D a day and then realized I was taking 10,000 A a day. I read where this was the max per day.

Now for the EFA part. The naturopathic dr. also recommended Blue Ice Cod Liver Oil - 1 T a day. The directions on the bottle say one half teaspoon. The ingredients in one half teaspoon are 5,750 A, 575 D , 145-375 EPA and 150-360 DHA. Wow! If I take 1T - I thought I'd really be overdosing on the A. Also, I am taking the D. which contains 1,000 A in every 400 D capsule.
I called to be sure these were the correct directions. He said "yes" I can take 1 T of this CLO because it is natural A not synthetic. I am not overdosing. However, he did say to cut back on some of the natural D and switch to synthetic. Yet , I'm still getting about 36,00 A a day with the CLO.

Questions? Should I just be taking a regular fish liver oil instead of the one with all the A to get the maximum EFA's?
What do you think of the dosage of A in 1T - too high?
I read about the one in the article you posted. which is supposedly recommended. However, it was originated from plants not fish oil. I'm confused. Sorry I can't remember the name now. I read it earlier. Is A important for my condition. Should I take some CLO and some regular fish oil?

So - in light of all this info - can someone - mrsd help me out with this. I Also, because of the FM and RSD and Mer. Per. what would an appropriate dose of these EPA's be? The Blue Ice doesn't have that much in just one half teaspoon. I had previously been taking Icelandic at Icelandic.com and that had a lot more /EPA and less A.
Hope I am not confusing you. Just trying to do this correctly to try to get out of this chronic pain. I figured this is worth a try. The Dr. also said I should try to get my D level up to 80 and I would get some pain relief. He is big on D. Thanks, Sydney

mrsD · 11-14-2006, 10:39 AM

Is retinol, not betacarotene. Your doses are still not that high, unless you are planning on getting pregnant or are pregnant already.
Here is what Dr. Mercola has to say about it:
http://www.mercola.com/forms/carlsons.htm

Vit A retinol has been implicated in birth defects..so it is low or not present
in most prenatals.

Betacarotene is the type of A present in vegetables, and it has to be converted to real A in the body. If someone is hypothyroid, this often fails, and the skin
turns an orange color as the betacarotene builds up there. (this happened to me).

If you want to increase your fatty acids only--it is best to use fish BODY oils, in addition to the cod liver oil you are currently using. The fish oils I have been discussing are fish BODY oils, not CLO. As long as you are being supervised by a doctor, I would defer to him/her.

Extremely high Vit A intake has been linked to pseudotumor cerebri.. but that is very high doses, which you are not yet at.

The doses typically used to treat acne by dermatologists are in the 25,000 IU to 50,000 IU range. You are far below that.
Most prenatals today have had Vit A removed, or drastically lowered, and betacarotene substituted.

Sydney · 11-14-2006, 08:28 PM

Thanks for the clarfication of synthetic vs. natural Vit D. Looks like I am OK with the Cod Liver Oil. However, I think I will also get some regular fish oil. Unfortuantely, I also have high choleserol (388). triglycerides((207) and worst of all my CRP is 5.3. I am afraid to take the statins because of my FM condition. Don't want to risk additional muscle problems.
Due to numerous meds over the past 2 - 3 years and lack of activity I have gained about 70 pounds. It seems no matter what I eat I just gain the weight. It is very frustrating. I went from a petite size to a woman's. Not very good for my conditions or my body.
Thanks for all the links to various web sites. I wish I had your talent. You amaze me. I love research and am determined to find something to get rid of this pain and be able to walkk again. I just keep researching and trying.
Thanks
Sydney

mrsD · 11-15-2006, 06:12 PM

I think you have a typo in that last post... D instead of A?

mrsD · 11-15-2006, 06:13 PM

Here is an article from PsychCentral:

http://psychcentral.com/news/2006/11...zheimers-risk/

Sydney · 11-15-2006, 09:58 PM

Sorry about the typo. I did mean to say Vit A - not Vit D. I am so involved with this Vit. D issue as well i just got confused in the post. You certainly pick up on everything Good Job! I appreciate your attention to detail and efficency as well as your knowledge base.
Thanks, Sydney

mrsD · 11-28-2006, 04:26 PM

I found this one linked to the others she just posted here on another thread:

Quote:

J Nutr Health Aging. 2004;8(3):163-74. Links
Roles of unsaturated fatty acids (especially omega-3 fatty acids) in the brain at various ages and during ageing.

* Bourre JM.

INSERM Research Director. Unit U26 Neuro-pharmaco-nutrition. Hopital Fernand Widal, 200 rue du Faubourg Saint Denis. 75745 Paris cedex 10. jean-marie.bourre@fwidal.inserm.fr

Among various organs, in the brain, the fatty acids most extensively studied are omega-3 fatty acids. Alpha-linolenic acid (18:3omega3) deficiency alters the structure and function of membranes and induces minor cerebral dysfunctions, as demonstrated in animal models and subsequently in human infants. Even though the brain is materially an organ like any other, that is to say elaborated from substances present in the diet (sometimes exclusively), for long it was not accepted that food can have an influence on brain structure, and thus on its function.

Lipids, and especially omega-3 fatty acids, provided the first coherent experimental demonstration of the effect of diet (nutrients) on the structure and function of the brain. In fact the brain, after adipose tissue, is the organ richest in lipids, whose only role is to participate in membrane structure. First it was shown that the differentiation and functioning of cultured brain cells requires not only alpha-linolenic acid (the major component of the omega-3, omega3 family), but also the very long omega-3 and omega-6 carbon chains (1). It was then demonstrated that alpha-linolenic acid deficiency alters the course of brain development, perturbs the composition and physicochemical properties of brain cell membranes, neurones, oligodendrocytes, and astrocytes (2).This leads to physicochemical modifications, induces biochemical and physiological perturbations, and results in neurosensory and behavioural upset (3).

Consequently, the nature of polyunsaturated fatty acids (in particular omega-3) present in formula milks for infants (premature and term) conditions the visual and cerebral abilities, including intellectual. Moreover, dietary omega-3 fatty acids are certainly involved in the prevention of some aspects of cardiovascular disease (including at the level of cerebral vascularization), and in some neuropsychiatric disorders, particularly depression, as well as in dementia, notably Alzheimer's disease. Recent results have shown that dietary alpha-linolenic acid deficiency induces more marked abnormalities in certain cerebral structures than in others, as the frontal cortex and pituitary gland are more severely affected. These selective lesions are accompanied by behavioural disorders more particularly affecting certain tests (habituation, adaptation to new situations). Biochemical and behavioural abnormalities are partially reversed by a dietary phospholipid supplement, especially omega-3-rich egg yolk extracts or pig brain. A dose-effect study showed that animal phospholipids are more effective than plant phospholipids to reverse the consequences of alpha-linolenic acid deficiency, partly because they provide very long preformed chains.

Alpha-linolenic acid deficiency decreases the perception of pleasure, by slightly altering the efficacy of sensory organs and by affecting certain cerebral structures. Age-related impairment of hearing, vision and smell is due to both decreased efficacy of the parts of the brain concerned and disorders of sensory receptors, particularly of the inner ear or retina. For example, a given level of perception of a sweet taste requires a larger quantity of sugar in subjects with alpha-linolenic acid deficiency. In view of occidental eating habits, as omega-6 fatty acid deficiency has never been observed, its impact on the brain has not been studied.

In contrast, omega-9 fatty acid deficiency, specifically oleic acid deficiency, induces a reduction of this fatty acid in many tissues, except the brain (but the sciatic nerve is affected). This fatty acid is therefore not synthesized in sufficient quantities, at least during pregnancy-lactation, implying a need for dietary intake. It must be remembered that organization of the neurons is almost complete several weeks before birth, and that these neurons remain for the subject's life time. Consequently, any disturbance of these neurons, an alteration of their connections, and impaired turnover of their constituents at any stage of life, will tend to accelerate ageing. The enzymatic activities of sytivities of synthesis of long-chain polyunsaturated fatty acids from linoleic and alpha-linolenic acids are very limited in the brain: this organ therefore depends on an exogenous supply. Consequently, fatty acids that are essential for the brain are arachidonic acid and cervonic acid, derived from the diet, unless they are synthesized by the liver from linoleic acid and alpha-linolenic acid. The age-related reduction of hepatic desaturase activities (which participate in the synthesis of long chains, together with elongases) can impair turnover of cerebral membranes. In many structures, especially in the frontal cortex, a reduction of cervonic and arachidonic acids is observed during ageing, predominantly associated with a reduction of phosphatidylethanolamines (mainly in the form of plasmalogens). Peroxisomal oxidation of polyunsaturated fatty acids decreases in the brain during ageing, participating in decreased turnover of membrane fatty acids, which are also less effectively protected against peroxidation by free radicals.

PMID: 15129302 [PubMed - indexed for MEDLINE]
Related Links

ALA= alpha linolenic acid as found in flax oil, walnuts and canola oil.
Long chain fatty acids = DHA and EPA

from http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15129302

mrsD · 11-28-2006, 05:38 PM

from the same author. It discusses enriching foods/meat for better health.

Quote:

J Nutr Health Aging. 2005 Jul-Aug;9(4):232-42. Links
Where to find omega-3 fatty acids and how feeding animals with diet enriched in omega-3 fatty acids to increase nutritional value of derived products for human: what is actually useful ?

* Bourre JM.

Membre de l'Academie de Medecine, INSERM Neuro-pharmaco-nutrition, Hopital Fernand Widal, 200 rue du Faubourg Saint Denis, 75745 Paris cedex 10. jean-marie.bourre@fwidal.inserm.fr 43 40.

Omega-3 polyunsaturated fatty acids have two major field of interest. The first lies in their quantitative abundance and their role in the development and maintenance of the brain. The second is their role in the prevention of different pathologies, mainly the cardiovascular diseases, and more lately some psychiatric disorders, from stress to depression and dementia. Thus, dietary omega-3 fatty acids are very important to ensure brain structure and function, more specifically during development and aging. However, concerning essential alpha-linolenic acid (ALA), most occidental diets contain about 50 % of the recommended dietary allowances.

The problem is to know which foods are naturally rich in this fatty acid, and to determine the true impact of the formulations (enriched in omega-3 fatty acids, either ALA or EPA and DHA) in chows used on farms and breeding centres on the nutritional value of the products (meat, butter, milk and dairy products, cheese, and eggs, etc), and thus their effect on the health of consumers, especially to ensure adequate quantities in the diet of the aging people. The consequences (qualitative and quantitative) of modifications in the composition of animal foods on the value of derived products consumed by humans are more marked when single-stomach animals are concerned than multi-stomach animals. Because, for example, hydrogenating intestinal bacteria of the latter group transform a large proportion of polyunsaturated fatty acids in their food into saturated fatty acids, among others, thus depriving them of any biological interest.

Under the best conditions, by feeding animals with extracts of linseed and rapeseed grains for example, the level of ALA acid is increased approximately two-fold in beef and six-fold in pork, ten-fold in chicken, and forty-fold in eggs. By feeding animals with fish extracts or algae (oils) the level of DHA is increased about 2-fold in beef, 7-fold in chicken, 6-fold in eggs, and 20-fold in fish (salmon). To obtain such results, it is sufficient to respect only the physiological needs of the animal, which was generally the case with traditional methods. It is important to stress the role of fish, whose nutritional value for humans in terms of lipids (determined by omega-3 fatty acid levels) can vary considerably according to the type of fats the animals have been fed. The aim of preventing some aspects of cardiovascular disease (and other pathologies) can be achieved, or on the contrary frustrated, depending on the nature of fatty acids present in fish flesh, the direct consequence of the nature of fats with which they have been fed. It is the same for eggs, "omega- 3 eggs" being in fact similar to natural eggs, were used in the formulation of certain formula milks for infants, whose composition was closest to that of breast milk. In fact, the additional cost on the price paid by the consumer is modest compared to the considerable gain in nutritional value in terms of omega-3 fatty acids content. Interestingly, in aged people, ALA recommendations in France are increased (0.8% daily energy intake in adult, 0.9 % in aged) and DHA is multiplied by 2 (0.05 % daily energy intake in adult, 0.1 % in aged; as well as in pregnant and lactating women).

PMID: 15980924 [PubMed - indexed for MEDLINE]

from http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15980924

Tessa · 11-12-2007, 10:00 AM

I came across a brief description of this article and searched down the abstract (below). I thought it was fascinating and maybe some are interested.

Vol. 298 No. 12, September 26, 2007 JAMA

Omega-3 Polyunsaturated Fatty Acid Intake and Islet Autoimmunity in Children at Increased Risk for Type 1 Diabetes
Jill M. Norris, MPH, PhD; Xiang Yin, MD, MS; Molly M. Lamb, BA; Katherine Barriga, MSPH; Jennifer Seifert, BS; Michelle Hoffman, RN; Heather D. Orton, MS; Anna E. Barón, PhD; Michael Clare-Salzler, MD; H. Peter Chase, MD; Nancy J. Szabo, PhD; Henry Erlich, MD, PhD; George S. Eisenbarth, MD, PhD; Marian Rewers, MD, PhD

JAMA. 2007;298:1420-1428.

Context Cod liver oil supplements in infancy have been associated with a decreased risk of type 1 diabetes mellitus in a retrospective study.

Objective To examine whether intakes of omega-3 and omega-6 fatty acids are associated with the development of islet autoimmunity (IA) in children.

Design, Setting, and Participants A longitudinal, observational study, the Diabetes Autoimmunity Study in the Young (DAISY), conducted in Denver, Colorado, between January 1994 and November 2006, of 1770 children at increased risk for type 1 diabetes, defined as either possession of a high diabetes risk HLA genotype or having a sibling or parent with type 1 diabetes. The mean age at follow-up was 6.2 years. Islet autoimmunity was assessed in association with reported dietary intake of polyunsaturated fatty acids starting at age 1 year. A case-cohort study (N = 244) was also conducted in which risk of IA by polyunsaturated fatty acid content of erythrocyte membranes (as a percentage of total lipids) was examined.

Main Outcome Measure Risk of IA, defined as being positive for insulin, glutamic acid decarboxylase, or insulinoma-associated antigen-2 autoantibodies on 2 consecutive visits and still autoantibody positive or having diabetes at last follow-up visit.

Results Fifty-eight children developed IA. Adjusting for HLA genotype, family history of type 1 diabetes, caloric intake, and omega-6 fatty acid intake, omega-3 fatty acid intake was inversely associated with risk of IA (hazard ratio [HR], 0.45; 95% confidence interval [CI], 0.21-0.96; P = .04). The association was strengthened when the definition of the outcome was limited to those positive for 2 or more autoantibodies (HR, 0.23; 95% CI, 0.09-0.58; P = .002). In the case-cohort study, omega-3 fatty acid content of erythrocyte membranes was also inversely associated with IA risk (HR, 0.63; 95% CI, 0.41-0.96; P = .03).

Conclusion Dietary intake of omega-3 fatty acids is associated with reduced risk of IA in children at increased genetic risk for type 1 diabetes.

Author Affiliations: Department of Preventive Medicine and Biometrics, University of Colorado at Denver and Health Sciences Center, Denver (Drs Norris, Yin, and Barón, and Mss Lamb, Seifert, and Orton); The Barbara Davis Center for Childhood Diabetes, University of Colorado at Denver and Health Sciences Center, Aurora (Drs Chase, Eisenbarth, and Rewers, and Mss Barriga and Hoffman); Department of Pathology, Immunology, and Laboratory Medicine (Dr Clare-Salzler) and Analytical Toxicology Core Laboratory (Dr Szabo), University of Florida, Gainesville; and Department of Human Genetics, Roche Molecular Systems, Alameda, California (Dr Erlich).

rose · 11-13-2007, 02:13 PM

My apologies if this has already been posted here. Just received this in a newsletter from NOW:

Quote:

Intake of Omega-3 Fatty Acids May Delay Onset of Type I Diabetes

Abstracted by Susan Sweeny Johnson, PhD, Biochem, October 11, 2007, from Jill M. Norris, MPH, PhD; Xiang Yin, MD, MS; Molly M. Lamb, BA; Katherine Barriga, MSPH; Jennifer Seifert, BS; Michelle Hoffman, RN; Heather D. Orton, MS; Anna E. Barón, PhD; Michael Clare-Salzler, MD; H. Peter Chase, MD; Nancy J. Szabo, PhD; Henry Erlich, MD, PhD; George S. Eisenbarth, MD, PhD; Marian Rewers, MD, PhD , “Omega-3 Polyunsaturated Fatty Acid Intake and Islet Autoimmunity in Children at Increased Risk for Type 1 Diabetes”, JAMA. 2007;298:1420-1428.

Type I diabetes mellitus (also know as juvenile diabetes) is an autoimmune disease in which the body’s immune system attacks and destroys islet cells in the pancreas which produce insulin. Although there is a genetic predisposition for the disease, environmental factors also appear to play a role in determining how early in life the autoimmune process begins and how much time passes between the onset of the first autoimmune response and the diagnosis of Type I diabetes when the islet cells are no longer producing insulin.

Studies suggest that early in the progress of the disease, inflammation and the activation of scavenger cells called macrophages by compounds that also induce inflammation may be important1. Since omega-3 fatty acids have been shown to have an anti-inflammatory effect(2, 3, 4, 5) while omega-6 fatty acids have a pro-inflammatory effect5, this study looked at the intake of omega-3 and omega-6 fatty acids in children one to six years old who were genetically at risk for diabetes type I.

In this study, 1770 children were assessed using a food questionnaire given to their parents to determine their average intake of different fatty acids and vitamin D. In addition, the fatty acid composition of their red blood cell membranes was assessed which reflects the actual intake of omega-3 and omega-6 fatty acids. In order to determine onset of the autoimmune component of diabetes type I, blood samples were taken initially and then yearly to detect the presence any of three types of autoantibodies typically present in pre-diabetes type I. If any of the antibodies were detected, the patient’s blood was tested every 3 to 6 months after that. Patients were considered positive for islet autoimmunity (IA), pre-diabetes type I, if the presence of autoantibodies occurred for two tests in a row or if the patient was diagnosed with diabetes type I.

Out of the 1770 patients, 58 developed IA. Statistical analysis showed that the risk of IA was significantly lower in children with higher intakes of omega-3 fatty acids (hazard ratio = 0.45, p=0.04). Also, in support of this result, higher omega-3 fatty acid content of patient red blood cell membranes correlated with lower risk of IA (hazard ratio = 0.63, p=0.03). Neither total omega-6 fatty acid intake nor vitamin D lntake correlated significantly with IA risk.

The average daily intake of omega-3’s during this study was 1.2 g per day, omega-6 was 10.8 g per day, and vitamin D was 400 IU per day. No numbers were given for the highest intake of omega-3.

About 7% of the US population has some form of diabetes. Type I comprises 5-10% of all diagnosed cases(6, 7). Direct medical costs from all types total $92 billion annually8. Using natural products to delay onset of Type I diabetes would save significant governmental and private dollars.

REFERENCES:

1 Chase HP, Cooper S, Osberg I, et al. Elevated C-reactive protein levels in the development of type 1 diabetes. Diabetes. 2004;53(10):2569-2573.

2 Calder PC. Polyunsaturated fatty acids, inflammation, and immunity. Lipids. 2001;36(9):1007-1024.

3 De Caterina R, Madonna R, Massaro M. Effects of omega-3 fatty acids on cytokines and adhesion molecules. Curr Atheroscler Rep. 2004;6(6):485-491.

4 Serhan CN. Resolution phase of inflammation: novel endogenous anti-inflammatory and proresolving lipid mediators and pathways. Annu Rev Immunol. 2007;25:101-137.

5 http://www.ncbi.nlm.nih.gov/sites/en...t=AbstractPlus

6 http://en.wikipedia.org/wiki/Diabetes_mellitus

7 http://diabetes.niddk.nih.gov/dm/pub...cs/index.htm#7

8 http://diabetes.niddk.nih.gov/dm/pub...s/index.htm#14

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