The Holman Omega 3 Test™ is the quick and easy way to measure your omega 3 health. The Holman kit includes an at-home method for obtaining a blood spot sample, which is then supplied to Lipid Technologies, LLC for analysis by our precision proprietary method for high sensitivity blood-spot omega 3 analysis. This test identifies your complete fatty acid profile, specifically focusing on your omega 3 and omega 6 fatty acid levels.
Your total omega 3 score is generated from the measured amount of omega 3 in your bloodstream, described as a percentage figure. For example, if your omega 3 score is 5%, it means that 5% of the total fatty acids in your blood are made up of omega 3 fatty acids (a group of fatty acids which includes EPA, DPA, DHA and more).
In certain populations such as the Japanese, who consume large amounts of marine based foods, the total omega 3 score is typically over 15%. Dr. Ralph T. Holman, the grandfather of omega 3 research, pioneer of this test and inventor of the term ‘Omega 3’, has a total omega 3 score of 25% – a direct reflection of his daily intake of fish and fish oils and his avoidance of omega 6 rich oils, which inhibit the metabolism of omega 3.
This report also includes indicators of heart health. Two common tests describe our omega 3 levels as they relate to cardiovascular health. The first is known as the Lands’ Test, named after Dr. Bill Lands who invented this test and terminology. Its technical name is the Omega 3 HUFA test – the term HUFA being an abbreviation of ‘highly unsaturated fatty acids’. These fatty acids generally form the basis for our inflammatory response system. Armed with the knowledge that the inflammatory response produced from omega 6 fatty acids is remarkably powerful (and leads to disease), and that the same response from omega 3 HUFA is less potent in terms of its anti-inflammatory effect, Dr. Lands has established that a lower Omega 6 HUFA score with a higher Omega 3 HUFA score is the ideal condition. Dr. Lands has modeled several populations, their Omega 3 HUFA score and their mortality rate from cardiovascular disease, displayed in graphic form on your personalized Omega 3 report.
Typical Americans have an Omega 3 HUFA score of 20%, which directly correlates to a high incidence of mortality from heart disease. Increasing this score to 50% results in an approximate 50% reduction in mortality, while further increasing the Omega 3 HUFA score to 70% nearly eliminates premature mortality altogether.
The final indicator of heart health as it relates to blood-based omega 3 fatty acids is the Omega 3 Index. The Omega 3 Index is the combined value of two omega 3 fatty acids (EPA and DHA) thought responsible for the main physiological effects of omega 3 in a diet. The science behind the Omega 3 Index resulted from the work of Siscovick and Albert, who examined omega 3 levels in populations and then assessed their risk of sudden death. According to Albert’s data, increasing omega 3 blood values from 3.58% to 6.76% was correlated with a 90% reduction in risk of sudden death (a type of heart attack). Data from Siscovick’s work reported similar outcomes, further confirming the benefits of elevated levels blood omega 3. An American and German scientist later coined the Omega 3 Index in 2004 as a blood-based risk factor framework for projecting cardiovascular disease risks. The recommended Omega 3 Index is 8% or greater, meaning a combined percentage total of EPA and DHA greater than 8%.
If your Omega 3 numbers are low, don’t feel disappointed or alone – the vast majority of Americans have low omega 3 levels. The good news is that you can easily improve your omega 3 score by increasing your dietary intake of oily omega 3 rich fish like salmon, omega 3 eggs and other omega 3 enriched foods. Another effective way of increasing your omega 3 levels is to consume a high quality omega 3 supplement. Ideally you should strive for a daily intake of 1000mg of EPA and DHA, which equates to about 3-4 standard fish oil capsules a day. Best of luck on your quest for complete Omega 3 Health!
Omega-3 Fats – A Clinical Perspective
Stephen Phinney MD, PhD, and Douglas Bibus PhD
Lipid Technologies LLC, Austin, MN
The flow of information from an initial discovery into clinical practice is characterized by the slow accumulation of data that eventually prompts a change in clinical behavior. We are at that point now in managing omega-3 fatty acids to prevent chronic disease and cardiac sudden death. This document provides a brief synopsis of the rationale for testing red cell fatty acids to guide dietary and supplement optimization of individual omega-3 status.
The first documented case of human omega-3 fatty acid deficiency was published by Holman in 1982. But well before that in 1971, Bang and Dyerberg posited that the Inuit could eat prodigious quantities of fat without risk of heart disease because they were protected by the fish oil in their diet. Early studies with fish oil focused on its effect on serum cholesterol and its distribution among lipoproteins, but it soon became apparent that most of the benefits of dietary omega-3 were due to a different mechanism.
During this same time period, the discovery of prostaglandins was followed with a broad range of products called eicosanoids, all made from long-chain fatty acid precursors. These compounds have myriad effects on vascular tone, immune function, and inflammation. The principal precursor for this class of compounds is arachidonic acid, a 20-carbon fatty acid in the omega-6 class. Holman pointed out the inherent competition between the omega-6 and omega-3 fatty acids, both in their precursor/product metabolism, as well as in their incorporation into and release from membranes antecedent to eicosanoid production. This set the stage for our current understanding of a need for balance between these two classes of essential fatty acids to achieve proper functioning of vascular, immune, and inflammatory systems.
Our appreciation of the potential impact of dietary omega-3 intake on coronary disease risk came first from epidemiology. In 1985, Kromhout first noted the negative correlation between fish intake and coronary disease risk in the Zutphen Study, and this finding has subsequently been corroborated in multiple populations. In large groups without prior heart disease followed for decades, the full benefit of fish intake is achieved with 3 fish meals per week, and the benefits appear to accrue mostly from cold-water ocean fish. Three large intervention studies which increased dietary fish or fish oil, the DART study (Burr, 1989), the GISSI study (GISSI, 1999), and the JELIS study (Yokoyama 2007) have demonstrated significant reductions in coronary death and overall mortality in the supplemented groups.
Given its limited positive effects on serum lipoproteins, considerable attention has been given to other potential mechanisms of action of fish oil. Leaf has demonstrated that the omega-3 fatty acids EPA and DHA are incorporated into heart muscle membranes, where they have an inherently anti-arrhythmic effect. This may explain why the principal benefit seen in human intervention studies is reduction in sudden death and dysrhythmia. Another mechanism for fish oil’s benefit against coronary disease, particularly in the long term, is through the anti-inflammatory effects of omega-3 fats. Inflammation is now recognized as an important driver of atherogenesis independent of cholesterol, and the recently published Jupiter Study (Ridker, 2008) demonstrated a significant reduction in coronary and overall mortality when elevated serum c-reactive protein (CRP) was targeted with rosuvastatin. The mechanistic bridge from statin drug for fish oil is provided by Lopez-Garcia, who has reported an inverse relationship between fish intake and CRP in the Nurses Health Study, implying that variations in the level of fish oil intake from the diet can significantly alter inflammatory status.
Because both the omega-3 and omega-6 families of fatty acids are “essential” (ie, they cannot be produced de novo by endogenous metabolism), and because the enzymes that process the 18-carbon essential precursors into 20- and 22-carbon products are not active in infants, there are defined levels of intake for infant formulas that ensure normal growth and neurological development.
In contrast to the situation for infants, there is as yet no federal recommended intake for omega-3 fats in general, or fish fats in particular, for the adult population. However, the AHA recommends fish twice per week for prevention and 1 g/d of EPA+DHA in patients with ASCVD. ISSFAL recommends a minimum of 440 mg/d of EPA+DHA for the general adult population.
For adults, there are many variables that influence an individual’s daily requirement (examples: the ratio of omega-3 to omega-6 in the background diet, oxidative stress levels, pre-existing diseases such as diabetes or atherosclerosis). In addition, Kunesova has demonstrated that genotype is an important variable that influences membrane omega-3 level independent of diet. Age is also a factor, as the EFA processing enzymes that become active after infancy begin to lose activity with aging.
As a result of these diverse influences, a uniform minimum recommended dose would leave a significant fraction of the population undertreated, and in particular that underserved fraction would tend to be the most vulnerable. Therefore, given a reliable test of an individual’s omega-3 fatty status, it is clinically appropriate to initially evaluate individuals, supplement where appropriate, and monitor the adequacy of omega-3 fatty acid supplementation.
There is a great deal of heterogeneity in fatty composition across different lipid pools within an individual, and omega-3 fatty acids in particular are bio-concentrated in membranes. Since the goal of supplementation is to optimize the individual’s membrane omega-3 content, a membrane fraction is therefore the appropriate analyte for testing. This is most effectively obtained in red blood cells (RBC), which reflect other fixed tissue membranes and are buffered against short term dietary variation (unlike whole blood or serum extracts dominated by triglycerides).
Considerable debate continues as to the relative effectiveness of the omega-3 precursor (alpha-linolenic acid – ALA) compared to the products of its metabolism (EPA and DHA) which are found in fish oil and other marine lipids. However against the background of the high omega-6 intake of the current US diet, ALA is at a competitive disadvantage. Unlike fish, most human tissues contain much more DHA than EPA, but EPA is currently favored for supplement use due to its greater effectiveness in balancing eicosanoid production.
All of this leads us to the following clinical management recommendations.
1. Determine RBC membrane composition, and evaluate EPA+DHA as follows:
a. > 8.0 – excellent
b. 5.0-7.0 – marginal (change diet or add supplement)
c. <5.0 – low (change diet and add supplement
2. Minimum re-test interval is 3-4 months, as this is the life-span of RBC’s
3. The supplement range for omega-3 fats (EPA+DHA) is from 500 mg to 5 grams daily. A typical one gram generic enriched fish oil capsule provides ~300 mg of EPA+DHA. More enriched preparations are available to keep the required number of daily capsules under control at higher dosages.
4. For people who are vegetarians, and for those with fish allergy, DHA produced from cultured algae is available.
Cited References
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The Lancet. 1971 1:1143-5
Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART).
Lancet. 1989; 2:757-61.
Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial.
Lancet. 1999; 354: 447–455.
Holman RT, Johnson SB, Hatch TF. A case of human linolenic acid deficiency involving neurological abnormalities.
Am J Clin Nutr. 1982; 35:617-23.
Ridker PM, et al. Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein NEJM 2008; 359:2195-2207
Kromhout D, Bosschieter EB, de Lezenne Coulander C.
The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med. 1985; 312:1205-9.
Kunesová M, Hainer V, Tvrzicka E, et al. Assessment of dietary and genetic factors influencing serum and adipose fatty acid composition in obese female identical twins.
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Lopez-Garcia E, Schulze MB, Manson JE, et al. Consumption of (n-3) fatty acids is related to plasma biomarkers of inflammation and endothelial activation in women. J Nutr. 2004; 134:1806-11.
M. Yokoyama, H. Origasa, M. Matsuzaki, Y, et al.
Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. The Lancet. 2007. 369:1090-1098
