mysite blog

Plasma Phospholipid Long-Chain ω-3 Fatty Acids and Total and Cause-Specific Mortality in Older Adults: A Cohort Study

Tue, 04 Jun 2013 15:12:00 +1200

Background: Long-chain ω-3 polyunsaturated fatty acids (ω3-PUFAs), including eicosapentaenoic acid (EPA) (20:5ω-3), docosapentaenoic acid (DPA) (22:5ω-3), and docosahexaenoic acid (DHA) (22:6ω-3), have been shown to reduce cardiovascular risk, but effects on cause-specific and total mortality and potential dose-responses remain controversial. Most observational studies have assessed self-reported dietary intake and most randomised trials have tested effects of adding supplements to dietary intake and evaluated secondary prevention, thus limiting inference for dietary ω3-PUFAs or primary prevention.

Objective: To investigate associations of plasma phospholipid EPA, DPA, DHA, and total ω3-PUFA levels with total and cause-specific mortality among healthy older adults not receiving supplements.

Design: Prospective cohort study.

Setting: 4 U.S. communities.

Participants: 2692 U.S. adults aged 74 years (±5 years) without prevalent coronary heart disease (CHD), stroke, or heart failure at baseline.

Measurements: Phospholipid fatty acid levels and cardiovascular risk factors were measured in 1992. Relationships with total and cause-specific mortality and incident fatal or nonfatal CHD and stroke through 2008 were assessed.

Results: During 30,829 person-years, 1625 deaths (including 570 cardiovascular deaths), 359 fatal and 371 nonfatal CHD events, and 130 fatal and 276 nonfatal strokes occurred. After adjustment, higher plasma levels of ω3-PUFA biomarkers were associated with lower total mortality, with extreme-quintile hazard ratios of 0.83 for EPA (95% CI, 0.71 to 0.98; P for trend = 0.005), 0.77 for DPA (CI, 0.66 to 0.90; P for trend = 0.008), 0.80 for DHA (CI, 0.67 to 0.94; P for trend = 0.006), and 0.73 for total ω3-PUFAs (CI, 0.61 to 0.86; P for trend < 0.001). Lower risk was largely attributable to fewer cardiovascular than noncardiovascular deaths. Individuals in the highest quintile of phospholipid ω3-PUFA level lived an average of 2.22 more years (CI, 0.75 to 3.13 years) after age 65 years than did those in the lowest quintile.

Limitation: Temporal changes in fatty acid levels and misclassification of causes of death may have resulted in underestimated associations, and unmeasured or imperfectly measured covariates may have caused residual confounding.

Conclusion: Higher circulating individual and total ω3-PUFA levels are associated with lower total mortality, especially CHD death, in older adults.

Mozaffarian D Lemaitre RN King IB Song X Huang H Sacks FM Rimm EB Wang M and Siscovick DS (2013).
Ann Intern Med 158:515-525

The Missing Element: Compromising Australia's Intelligence

Mon, 03 Jun 2013 16:10:00 +1200

There is an endemic nutritional deficiency likely to be affecting a large proportion of your patients, as well as the next generation of Australian children. Reducing IQs, sapping vitality, expanding waistlines and impeding reproductive health... Can all this be influenced by one nutrient?

Given the average modern diet, lifestyle and environment... You would be forgiven for asking ‘which one?’ But in truth, beyond Vitamin D and Omega 3 essential fatty acids (some of our other most notable nutritional deficiencies), it is Iodine that should be sitting squarely in our sights as one of our primary ‘first port of call’ within any clinical nutritional assessment in Australia.

This becomes increasingly significant when we appreciate that, of all the things to be deficient in, Iodine, Omega 3 and Vitamin D each facilitate some of the most universal and integral functions within the body, impacting multiple hormones (both steroidal and metabolic), the integrity of the nervous system (both cognitive and sensory) and ultimately the metabolism of every cell in the body (both directly and indirectly).

Iodine

Iodine is a large, volatile Halogen that is utilised in the body in BOTH its natural forms (as Iodine and Iodide) and therefore, due to poor biological inter-conversion; we often need to acquire it in both these forms. Iodine/Iodide is concentrated to the highest degree in the tissues that require it the most. Over 30% of our total body store is concentrated within the thyroid gland, which can retain up to 50mg alone (preferring the Iodide form), whilst the rest is distributed throughout the breasts (preferring the Iodine form), skin, gastric mucosa and visceral organs and can equate to a total Iodine/Iodide body store as high as 1,500mg across all tissues in very replete individuals. This incidentally makes it quite difficult to accurately assess overall body Iodine status through current conventional and non-invasive means.

Now, whilst the nervous system is not the primary location of Iodine concentration in the body, the importance of Iodine to healthy cognitive development is perhaps one of Iodine’s greatest significance to our health.

The Deficiency

Due to the age and quality of our agricultural topsoil in Australia, limited seafood/seaweed consumption, increased consumption of processed food (that no longer contains sufficient traces of Iodine from changes to salt fortification and dairy sanitation), Australia now stands as one of the most markedly Iodine deficient nations in the world (and almost exclusively so out of those in the developed world!)

The Effects

Given the factors described above, consideration of Iodine deficiency is particularly relevant to the clinical presentations of Fibrocystic Breast Disease, other female reproductive Cysts/Nodules, Fatigue, resistant Weight Gain, Thyroid Disease of any nature, and Cognitive Impairment - especially during Pregnancy.

With regards to IQ, moderate to severe Iodine deficiency during pregnancy has been shown to result in a reduced average IQ in the newborn during their early childhood. This is related to the fact that during the first two trimesters of pregnancy, the foetus is totally dependent on the mothers T4 production for healthy brain development. Even a small decrease in the serum T4 level during pregnancy, (from either Iodine deficiency or other reasons for thyroid disease), is an important risk factor for impaired psychomotor development in infants.

Iodine & Halides: The Double Whammy

The other half of the Iodine deficiency story is the suppression of what Iodine IS present, by the other Halides (i.e. Fluoride and Bromide). Being Halogens just like Iodine, these Halides can wreak havoc on Iodine utilisation and therefore its retention in the body and also have their own subsequent toxicities associated with them that make them particularly detrimental in situations of autoimmunity (of all descriptions, but especially thyroid related). Thus adequate avoidance of these Halides is clearly equally as important as Iodine replenishment in the resolution of Iodine deficiency and its associated conditions.

Most notably, avoiding Fluoride may be particularly crucial for optimising IQ and neurological function, for reasons beyond simply it’s Iodine displacement, after over 36 multi-age human studies have linked Fluoride to neurological impairments and reductions in IQ itself.

So How DO We Accurately Determine Our Iodine Status?

Whilst ‘Skin Patch Testing’ is quite entrenched in popular wisdom as an appropriate means of determining Iodine status, it has been shown for over 80 years to be more reflective of simply dermal oxidation conditions and ambient humidity. With close to 90% of the Iodine evaporating from the skin within 72 hours and only 1-4% making its way to the blood stream, at no greater or reduced rate between different regions of more or less replete or even healthy skin, skin patch testing for Iodine is completely unreliable as a tool for determining total body Iodine status.

As mentioned, the specificity of Iodine concentration and utilisation throughout the body means a much more functional and in depth sampling method is needed. Namely, urine. Urine affords us not only an insight into metabolic activity (from what was circulating in the blood) and therefore the current background Iodine exposure to the body, but if we administer a ‘loading’ Iodine dose (50mg) beforehand and then collect the urine for the following 24 hours, we can gain an insight into the body’s ability/inclination to ‘take up’ that Iodine and thus infer our overall total body Iodine SUFFICIENCY - not simply the ‘level’ of what is a very unevenly distributed element, making the ‘Iodine Pre & Post Load Urine Test’ the gold standard for clinical Iodine assessment .
There is also the option to assess Halide levels alongside Iodine within this urine test and gain an even more complete assessment of ‘Iodine Sufficiency’ by identifying what level of obstructions to Iodine might be present via the Halides also.

This ‘functional’ assessment of Iodine status, allows us to select appropriate clinical doses of Iodine and determine the efficacy of our replenishment/treatment regimes over time.

Replenishing Iodine

Minimum Recommended Daily Intakes for Iodine is around 150mcg for adults and 220mcg for pregnant women (acknowledging that there is a greater need during this key time). However these numbers are determined from population studies seeking to simply alleviate goitre and by no means reflect total body optimisation doses. It has been determined that women intending to fall pregnant should aim to obtain at least 280mcg of Iodine from combined food and supplement sources in order to maintain the minimum urine levels of Iodine required to see a preventative benefit of cognitive impairment in their child.

So the dose required to achieve true body sufficiency is likely to be somewhat greater than RDI doses for many individuals, especially here in Australia, and can only be determined by appropriate urine testing. How much greater may just surprise you.

Note:

It is recommended to always start slowly on any concentrated nutritional replenishment program (especially for Iodine)
Follow-up testing is always required at moderate intervals (3mo) to ensure efficacy of treatment and monitor for excessive supplementation.
Elimination of the toxic Halides, (Fluoride and Bromide), will enhance and perhaps dictate clinical success.
Thyroid ‘sufficiency’ is determined by testing TSH, T4 and T3 – and for Autoimmunity, via Thyroid Antibodies.
Testing for changes in these is recommended during any Iodine replenishment program.
Those with Iodine sensitivity or severe Graves Disease may not be able to handle high dose supplemental
Iodine, (despite likely being Iodine deficient) and thus specific strategies will need be employed for these individuals.

The Importance of Cofactors

Tyrosine
For proper thyroid (and adrenal) health, Tyrosine is the most important substrate to include with Iodine to ensure its appropriate utilisation. However do note that excessive amounts of Tyrosine (3g+ per day) can suppress the conversion of T4 to more active T3 (which may be useful in Hyperthyroidism but would be counterproductive in Hypothyroidism). So combined baseline levels of Iodine and Tyrosine would provide a powerful supportive supplement in your clinic dispensary.

Selenium
Additionally, whenever Iodine is being supplemented, small amounts of Selenium should always be included to ensure proper utilisation of Iodine and conversion of T4 to T3 (however too much can be just as bad as too little). Zinc also supports the conversion of T4 to T3, however the Australian population is not as universally deficient in Zinc, so it is perhaps advisable to assess both Zinc and Selenium status via more general mineral testing (such as hair or red blood cell analysis) during any thyroid/Iodine based treatment.

Vitamin A
Vitamin A is the often forgotten, but perhaps most crucial nutritional consideration after Iodine sufficiency for proper thyroid hormone function in the body. In fact, whilst zinc is indeed important for the conversion of T4 to T3, supplementation with Zinc has been shown to not be as effective as supplementing with Vitamin A in raising T3 and Free T3 in those with hypothyroid presentation.
This is because the true retinoid forms of Vitamin A (those found in Liver and Cod Liver Oil) are required to support the action of thyroid receptor activity around the body, (through a multitude of shared interactions with retinoid receptors).

This is demonstrated in regions of the world where Iodine sufficiency HAS been confirmed (such as Sudan), yet goitre still remains endemic to that region due to the prevalence of pronounced Vitamin A deficiency.
If we then consider how inefficiently most individuals convert beta-carotene to vitamin A (from sources such as carrots), the importance of preformed Vitamin A supply to maintain optimum thyroid function becomes evident.

Vitamin D & DHA
On the topic of optimising cognitive function, it is important to also note the importance of both Vitamin D and DHA to brain health, particularly during early neurological development, along with the prevalence of their deficiency in Australia.

DHA has been well established as an essential nutrient to both brain structure and function, with increases in newborn brain weight, and subsequently childhood IQ, seen in mothers achieving higher levels of DHA during pregnancy.

Equally, Vitamin D receptors have been shown to appear within a wide variety of brain tissues during early foetal development, increasing nerve growth in the brain when activated. This effect also extends to adulthood where Vitamin D metabolically supports areas of the brain involved in planning, processing of information, and the formation of new memories. The National Institutes of Mental Health has recently concluded that it is vital that mothers get enough vitamin D during pregnancy in order for their baby’s brain to develop properly.
To eliminate any guesswork in this area as a clinician, both Vitamin D and DHA levels can both be easily and accurately tested via blood spot, (using the ZRT Vitamin D test and the Holman Omega-3 test respectively).

Cod Liver Oil & Iodine/Tyrosine: A Powerful Clinical Combination
It is quite interesting to note, that of all the fish oil sources available, Arctic Cod Livers naturally concentrate the highest ratios of DHA to EPA as well as providing significant amounts of preformed Vitamin A and Vitamin D, making Cod Liver Oil one of the most powerful ‘all in one’ food based supplements for supplying our most important fat soluble nutrients.

As a result, combining Arctic Cod Liver Oil with supplemental baseline levels of Iodine and Tyrosine, provides us with one of our most powerful and comprehensive therapeutic platforms with which to base multiple further clinical treatments on, in the optimisation of overall neurological, metabolic and cellular function, at all stages of life, but especially early life and the support of the next generation of Australian mothers and children.

To Your Best,

Please contact us for references

>>Tweet this article

Featured Tests

Urine Iodide (Pre/Post)	Complete Thyroid Profile
Urine Iodide/Halide (Pre/Post)	Vitamin D Test

About the Author

Warren Maginn, BHSc. (Nutr. Med.) Grad. Cert. (Hum. Nutr.) - Practitioner and Educator

Warren Maginn holds a Bachelor Degree in Nutritional Medicine and is Research Nutrition’s National Technical Educator, carrying extensive technical knowledge in the field of Functional Medicine. Warren is also a Nutritional Medicine Practitioner and Lecturer for Endeavour College in Brisbane. He is passionate about assisting practitioners and students to gain greater technical insights from current functional medicine understanding and how to apply this knowledge in clinical practice.

Want to learn more about Functional Testing?

September 2013 Workshop Attendee special: 25% OFF the Introductory DVD modules!

Supplement aids age-related macular degeneration

Mon, 27 May 2013 17:52:00 +1200

A supplement containing a combination of lutein, zeaxanthin, and ω-3 long-chain polyunsaturated fatty acids significantly benefits patients with age-related macular degeneration, according to a study published online March 21 in JAMA Ophthalmology.

ABSTRACT

Importance: It has been shown that the functionality of the macula lutea depends on the nutritional uptake of lutein and zeaxanthin and that it is inversely associated with the risk of age-related macular degeneration (AMD). Additionally, ω-3 long-chain polyunsaturated fatty acids (LC-PUFAs) may also be protective.

Objective: To investigate the effect of a 12-month intervention with macular xanthophylls and ω-3 LC-PUFAs on xanthophylls and fatty acids in plasma, antioxidant capacity, and optical density of the macular pigment of patients with nonexudative AMD.

Design: The LUTEGA study was a randomized, double-blind, placebo-controlled, parallel clinical trial that was conducted for 12 months.

Setting: University Eye Hospital and Institute of Nutrition, Friedrich Schiller University Jena, Germany.

Participants: A total of 172 individuals with nonexudative AMD.

Intervention: Individuals were enrolled and randomly divided as follows: placebo group, group 1 (a capsule containing 10 mg of lutein, 1 mg of zeaxanthin, 100 mg of docosahexaenoic acid, and 30 mg of eicosapentaenoic acid administered each day), and group 2 (same substances but twice the dose used in group 1). One hundred forty-five participants completed the study successfully.

Main Outcome Measures: Plasma xanthophyll concentrations and fatty acid profiles, optical density of the macular pigment, and antioxidant capacity in plasma (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid [Trolox] equivalent antioxidant capacity and photochemiluminescence).

Results: The concentrations of the administered carotenoids in plasma as well as the optical density of the macular pigment increased significantly in the groups randomized to receive supplementary macular xanthophylls and ω-3 LC-PUFAs after 1 month of intervention and remained at this level through the end of the study. Use of the double dose resulted in a beneficial alteration of the fatty acid profile in the plasma of patients with AMD in comparison with the dose in group 1. The lipophilic antioxidant capacity in plasma was significantly elevated with the intervention.

Conclusions and Relevance: A supplement containing a fixed combination of lutein, zeaxanthin, and ω-3 LC-PUFAs during 12 months significantly improved plasma antioxidant capacity, circulating macular xanthophyll levels, and the optical density of the macular pigment.

Reference
Macular Xanthophylls and ω-3 Long-Chain Polyunsaturated Fatty Acids in Age-Related Macular DegenerationA Randomized Trial
Christin Arnold, Dipl-Troph; Lisa Winter, Dipl-Troph; Kati Fröhlich, PhD; Susanne Jentsch, Dipl-Ing; Jens Dawczynski, MD; Gerhard Jahreis, PhD; Volker Böhm, PhD
JAMA Ophthalmol. 2013;131(5):564-572. doi:10.1001/jamaophthalmol.2013.2851.

Tox VS. Detox: Where to Begin?

Mon, 04 Feb 2013 19:54:00 +1300

As many of us have likely begun the year with some form of the ever ubiquitous New Years ‘Detox Program’, (or at least contemplated it with a sincere and earnest vigour), the issues of Toxicity living in our modern world and lifestyle, are likely to be acutely in mind.

Embarking on the new year is also a time of taking stock, both past and future, and apart from the just as obligatory ‘New Year’s Resolutions’ (that may already be losing their fervour for some of us by this point), we may be seeking some further guidance or confirmation on our health direction, to galvanise our resolve in a more concrete and sustainable sense than simply good intentions alone.

As always, the insights we need to gain this level of enlightenment and confidence in life, relies on the quality of information and perception available to us.

This goal of ‘health as a state of balance’ therefore requires both an assessment of excesses (toxicities) as well as deficiencies, to truly assist in arriving somewhere in the middle, and would do well to begin with an assessment as fundamental as body mineral balance and composition.

For this reason Hair Analysis provides one of the best starting points for any functional health investigation, by offering a very affordable and accessible ‘snapshot’ of our overall mineral balance, including an incredibly reliable indication of overall toxic metal exposure over the past few months (the growth of the hair sampled) and is most reliable when a ‘wash process’ IS applied to the hair sample during testing, to ensure minimal contamination to results. This can give some very useful insights into the purity of the current diet and environment, as well as indicate any glaring deficits in mineral nutrition or sometimes even overzealous supplementation (for the more conscientious).

Urine Porpyhrin testing on the other hand, like Pyrrole testing (Porpyrins are comprised of 4 Pyrroles) that when elevated can indicate an increased demand for B6 and Zinc in certain individuals, also tells us about the potential presence of many chemical as well as metal toxins in the body and to what degree/severity they are obstructing function (namely Heme synthesis in red blood cells). For this reason Porphyrin testing can be a valuable indication of overall toxic interference for an individual (both chemical and metal) and what exposures and cofactors are going to need to be addressed to maximise metabolic harmony for them (regardless of the actual toxin ‘levels’ in some very sensitive patients).

At the end of the day, a healthy and efficient liver is going to provide us one of our greatest assets to achieving the balance and harmony of vibrant health. For this reason a Urine HDP (Hepatic Detox Profile) offers a very tangible and resourceful insight into current Phase I and II liver activity, and therefore to what degree we can excrete whatever toxicity we are currently (and invariably) exposed to, WITHOUT the burden of challenging the liver with toxic pharmaceutical agents (we are NOT normally exposed to), to find out.

Wishing you the very best Happiness, Harmony and start to 2013

by Warren Maginn, BHSc. Nutr. Med. - Practitioner and Educator

ADHD is associated with a ‘Western’ Dietary Pattern in Adolescents- Omega 3’s may provide protection

Mon, 04 Feb 2013 16:09:00 +1300

Researchers from Perth's Telethon Institute for Child Health Research found that a diet high in the Western pattern of foods was associated with more than double the risk of having an ADHD diagnosis compared with a diet low in the Western pattern, after adjusting for numerous other social and family influences.
The study was published in the International Journal of Attention Disorders.

"We looked at the dietary patterns amongst the adolescents and compared the diet information against whether or not the adolescent had received a diagnosis of ADHD by the age of 14 years. In our study, 115 adolescents had been diagnosed with ADHD, 91 boys and 24 girls," Dr Oddy said.

Researchers suggested that a Western dietary pattern may indicate the adolescent has a less optimal fatty acid profile, whereas a diet higher in omega-3 fatty acids is thought to hold benefits for mental health and optimal brain function. It also may be that the Western dietary pattern doesn't provide enough essential micronutrients that are needed for brain function, particularly attention and concentration, or that a Western diet might contain more colours, flavours and additives that have been linked to an increase in ADHD symptoms. It may also be that impulsivity, which is a characteristic of ADHD, leads to poor dietary choices such as quick snacks when hungry.

Dr Oddy said that whilst this study suggests that diet may be implicated in ADHD, more research is needed to determine the nature of the relationship.

Another study from the University of Pittsburgh shows that Fish is really Brain food: It is well established that omega-3 fats boost brain power in later life. Researchers set out to assess omega-3 intake and its affect on cognition during the middle years. Participants were 280 community volunteers between 35 and 55 years of age who were free of major neuropsychiatric disorders, and were not taking fish oil supplements. Dietary biomarkers were blood levels of the omega-3 fats ALA (found in flaxseed and walnuts) and EPA and DHA (found in fatty fish). Five major dimensions of cognitive functioning were assessed with battery of neuropsychological tests. Results showed that higher DHA levels were related to better performance on tests of nonverbal reasoning and mental flexibility, working memory, and vocabulary. As DHA levels increased, so did cognition. Neither EPA nor ALA was notably related to cognitive performance. The researchers conclude that, " ...among the [three omega-3s], only DHA is associated with major aspects of cognitive performance in non-patient adults less than 54-years-old. These findings suggest that DHA is related to brain health throughout the lifespan and may have implications for clinical trials of neuropsychiatric disorders."

References:
Amber L. Howard, Monique Robinson, Grant J. Smith, Gina L. Ambrosini, Jan P. Piek, and Wendy H. Oddy. ADHD Is Associated With a 'Western' Dietary Pattern in Adolescents. Journal of Attention Disorders, 2010; DOI: 10.1177/1087054710365990
Muldoon M, Ryan C, Sheu L, et al: Serum phospholipid docosahexaenoic acid is associated with cognitive functioning during middle adulthood. Journal of Nutrition 2010; 140:848-853
Zhang C, Bazan N: Lipid-mediated cell signalling protects against injury and neurodegeneration. Journal of Nutrition 2010; 140:858-863

Featured Product

DHA Junior

Supports brain and visual function for children ages 3+
Strawberry-flavoured
Contains healthy levels of 100% natural vitamins A and D


Available in 119ml liquid, or 180 soft-gels

Cortisol - Life's Double Edged Sword

Mon, 17 Dec 2012 16:57:00 +1300

We in the modern world, often lead frenetic and unbalanced lifestyles. Day to day life often involves continuous stress, not only from emotional stressors (such as marital, financial, and occupational) but also from physical stressors (such as sleep deprivation, caffeine consumption, pain and extreme exercise) all without adequate recovery.

Further physical stressors exist however and contribute to this overall load also, including the toxic and immune related onslaughts of petrochemical and metal toxins as well as infections (gut/yeast) and allergen exposures (diet/environmental).

Whilst many individuals are able to cope with these demands, the adrenal glands may, over time, start to have an impaired response to stressors, and reduced adrenal hormone output. The resulting adrenal insufficiency, may present with a constellation of symptoms from chronic fatigue to allergies, anxiety to infertility.

Subsequently, some key symptoms of Adrenal Dysfunction include morning or evening fatigue, allergies, increased infections, insomnia, poor recovery from exercise, apathy, chemical sensitivity, decreasing attention span, depressed mood, unstable blood sugar, low sex drive and that “burned out” feeling .

The Adrenal Gland and Cortisol Production

The Zona Fasiculata of the adrenal cortex secretes approximately 15-20 mg of Cortisol per day in a fluctuating pulsatile manner (known as the ‘Diurnal Rhythm’) that includes two primary peaks in the day (one around 8am in the morning and another somewhere around 3-4pm in the afternoon, before subsiding to negligible levels during sleep hours when Melatonin opposes its production (in those maintaining adequate sleep wake cycles).

Note: The Zona Fasiculata is stimulated to produce Cortisol in response to ALL the above mentioned stressors! (The Psychological, Emotional, Physical, Chemical, Toxic, Allergic and Infective).

Cortisol has a wide range of effects on the mind and body and all other hormone systems (especially the Thyroid and Reproductive). As part of the response to stress, it mobilises body resources to accommodate a demand to our system for ‘fight or flight’ responses, and in doing so it can suppress the production of other more ‘rest and digest’ (repair and maintenance) related hormones (including those of the immune system).

This not only temporarily shuts down ‘repair’ processes but also diverts crucial body resources elsewhere, for consumption at a rate often far higher than can be replenished until the demand has subsided. Therefore multiple and complex chronic disease and severe nutrient depletion are often the concomitant result of Adrenal depletion.

So Cortisol production can be considered to reflect our overall body reserve for accommodating stressors in all their forms, and since both high and low Cortisol levels are associated with multiple and often ambiguous symptoms, Cortisol testing is often required, to provide accurate insights into the severity and nature of this important body status/function and provides the holistically minded practitioner with the accurate measurement required to assess such cases objectively, as well as their ongoing response to treatment to replenish this reserve capacity.

Cortisol Testing

Cortisol testing can be carried out via Blood, Urine and Saliva.
Saliva testing often carries with it some limitations with regard to many other steroidal hormones, however Saliva testing for Cortisol production does provide one of the best clinical uses of this technology, assessing the bioavailable Cortisol levels by excluding the Cortisol-binding globulin (CBG)-bound hormone and is a well established method for the diagnosis of Cushing’s Disease (Hypercortisolism).

Importantly, the convenience of saliva collection also allows for the all important multiple (4x) sampling required over the course of a day (at morning, mid morning, mid afternoon and evening) to accurately assess the ‘Diurnal Rhythm’.

Blood spot testing on the other hand is another minimally-invasive testing method, that provides a valuable first morning test to give an excellent snapshot of adrenal function (at its primary peak of the day) without the stress and inconvenience of more complex tests or blood draw collection.

Urine Cortisol readings (within a full 24 hour hormone excretion panel) provide an excellent overall snapshot of Cortisol production throughout the entire Diurnal Rhythm (yet will not necessarily reveal the peaks and troughs of its production during that period) and is most useful when assessing Cortisol’s relationship to all the other steroidal hormones (which are best assessed this way) and in those with disrupted/chaotic sleep cycles (such as shift workers and in those with severe insomnia).

Therefore, the Diurnal (4x) Saliva Cortisol test, provides one of the most accurate and insightful methods for assessing Cortisol’s universally important status to mind and body health.

Please contact us for more information on ZRT's Cortisol Test

Evidence for DHA’s Role in All Aspects of Human Health

Mon, 17 Dec 2012 16:23:00 +1300

A review of literature published last year in the journal Nutrients confirms the scope of evidence supporting DHA's critical role in the evolution and maintenance of human physiology. From the late Paleolithic period, consumption of DHA-rich foods (i.e. seafood) began to correspond with brain development, which surged in the last 200,000 years. Modern science has delved deeply into this relationship, noting the technological and lifestyle changes that have contributed to radical alterations of dietary essential fatty acid ratios, and quite possibly certain negative health effects from inadequate DHA.

Among the most noteworthy observation from recent years is the recognition that preformed dietary DHA far surpasses its molecular predecessor ALA (alpha-linolenic acid) when it comes to maintaining tissue DHA. Current research shows conversion rates of ALA to DHA range considerably, but fall well below 1% in some adult populations. Along with other omega-3s, the availability of DHA within cell membranes matters significantly for membrane fluidity, cell signaling, and other functions critical to optimal cell functioning. The sum of evidence "may provide a biochemical basis for a beneficial role for DHA in metabolic syndrome and neurodegenerative disease processes," writes the author.

Specifically, DHA's role in the synthesis of the docosanoid neuroprotectin (and brainderived neurotrophic factor) suggests that its anti-inflammatory effects may mitigate normal cognitive decline associated with aging, as well as the effects of more debilitating disorders such as Alzheimer's, and possibly Parkinson's Disease. Perhaps the strongest evidence for DHA's importance comes from studies with infants. This line of research finds evidence for superior visual acuity, emotional regulation, social behavior, communication, and neurodevelopment among children with higher levels of DHA consumption.

Despite the evidence supporting the importance of DHA, the modern Western diet is now largely deficient in this essential fat. However, as the cost of treating brain disorders continues to mount, research on DHA, along with improved EFA nutrition, takes on new relevance.

The Foods You Eat May Be The Cause Of Your Health Problems

Mon, 17 Dec 2012 13:40:00 +1300

Have you ever thought that perhaps you may have a food allergy? Perchance you thought, "I've eaten these foods before, sometimes every day, and I've never had a problem. Why should I consider being tested for food allergies?"

References to food allergies date back almost 100 years to 1905. Dr. Frances Hare, a British psychiatrist who practiced environmental medicine, linked certain ailments, such as Gout and Eczema, with food. He also found that when eliminating problematic foods, symptoms eventually resolve! Many pioneers have followed Dr. Hare's path. In fact, food allergies continue to be an area of great interest today.

Foods are known to cause a variety of disturbances within the body. These disturbances arise due to different mechanisms. For example, you have most likely known someone who is unable to digest milk products. This is called lactose intolerance and occurs when the body has a deficiency or absence of the enzyme lactase. Other foods, like chocolate, have chemical substances that possess the ability to alters one's mood. You have probably heard of chocoholics; you may even be one yourself. These are not food allergies. Food allergies are the only food-induced disturbance directly related to the immune system.

Let us speak briefly of the immune system, a marvelous and intricately complex component of the human body. Begin by envisioning your immune system as if it were a sentinel standing guard, protecting your body from foreign invaders. With allergies, the foreign invaders are called allergens. Allergens are so called because they induce an allergic reaction, or an exaggerated immune response. The sentinel has a variety of attack methods, including antibodies. Antibodies function to neutralise toxic materials and commence reactions that lead to removal of the allergens. The symptoms you experience are your body's way of telling you about these reactions that are occurring.

The body has five different antibodies. The two most often associated with food allergies are called IgE and IgG. IgE is the antibody that binds to cells of the immune system, specifically mast cells and basophils, and consequently causes a release of histamine. Histamine then causes the capillary dilation and smooth muscle contraction that eventually result in your individualised symptom picture. IgE is fast acting and quickly leads to symptoms such as a runny nose, difficulty breathing, or hives. IgG, on the other hand, is slow acting. Symptoms can take up to three weeks to develop and are therefore sometimes referred to as delayed reactions. Furthermore, IgG can bind directly to the allergen. These antigen-antibody complexes subsequently deposit within tissues of the body and cause a myriad of symptoms, such as knee pain. Recent studies have even suggested that IgG can, at times, act in a similar fashion to IgE.

Food allergies are of great concern because most people, and many practitioners, still do not attribute symptoms of poor or degenerating health to food. Without knowing the cause of the illness, the body continues to suffer.

The incidence of food allergies is widely disputed. Almost ten years ago, 10% of the United States population was estimated to be affected by immune-modulated food sensitivities. The number of food allergens continues to flourish. With this growth, clinical indications are evolving into more complex symptoms. Unfortunately, food allergies are difficult to approximate due to the fluctuation of symptoms from person to person, dissimilar settings between cross samples, and different testing procedures leading to varied test results. For those of us plagued with a single symptom, a multitude of symptoms, or beleaguered with suffering, it matters not the prevalence, but instead the resolution.

The symptoms of any food allergy can be so diverse and so multi-dimensional that they almost boggle and confound the mind. Each individual, being individuals unto themselves, may exhibit symptoms far different from any other individual with the same food allergy. The following are lists of symptoms designed to assist you in your new awareness of the possibility that your symptoms may be a result of an allergic reaction to food. However, it is important to remember that these symptoms can also be associated with other medical maladies and only careful clinical history, exam, and laboratory testing can differentiate between the two.

Digestive System:

Abdominal cramping, abdominal pain, bad breath, belching, bloating after meals, flatulence, gagging, itching on the roof of the mouth, vomiting

Nervous System:

Anxiety, confusion, depression, hyperactivity, inability to concentrate, aggressive behavior, irritability, restlessness

Musculoskeletal System:

Joint inflammation, joint pain, muscle pain, weakness

Genitourinary System:

Bed wetting, urinary frequency, urinary urgency, vaginal, itching, vaginal discharge, premenstrual syndrome

Respiratory System:

Asthma, chest congestion, chronic cough, sore throat, runny nose, postnasal drip, chronic sinus inflammation

Cardiovascular System:

Chest pain, irregular heart beat, high blood pressure, increased heart rate

Integumentary System:

Acne, brittle nails and hair, dandruff, hives, eczema, dry skin, paleness of skin, dark circles under eyes

Miscellaneous:

abnormal cravings, chronic fatigue, dizziness, headaches, difficulty sleeping, nausea, water retention, nightmares, rapid weight fluctuation, obesity, teeth grinding

As you can clearly see, nearly all symptoms can be related to a food allergy. These lists are even abbreviated and do not include every conceivable possibility. So, if your symptoms do not appear here, by no means does this indicate that your symptoms are not due to food allergies.

Now you may begin wondering how you would know if your symptoms are actually the result of food allergies. As stated previously, clinical exam and history taking, as well as laboratory testing, are all very important. Your practitioner's role is integral for understanding, prioritising diagnoses, ruling-out possible underlying causes, interpreting test results, and filtering information. Your practitioner can then help direct treatment that will prevent further outbreaks.

You will be happy to know that most food allergies can be evaluated by drawing a small sample of your blood. This is a near painless test, involving just a needle prick. The blood is than processed and sent to a lab for evaluation.

ELISA is a common lab analysis used when evaluating food allergies due to one or both of the antibodies IgE and IgG. ELISA stands for enzyme-linked immunosorbent assay. This is an impressive sounding test, but actually simple and quite definitive. ELISA is referred to as a quantitative test, meaning that the number of IgE and IgG antibodies in your blood can in fact be counted. After the blood is drawn, the tube is set aside to clot and then spun with a centrifuge. The clear portion (or serum) containing the antibodies is removed from the tube and sent to the lab. At the lab, the serum is added to numerous vials, each containing a single food to be tested. After a period of incubation, an enzyme is added to each vial. This enzyme identifies any antibodies that have reacted with the food. Enzymes that have not identified the antibody-food reactions will be washed away. Last, a colour agent is added to each vial. This colour agent will bind with any enzyme that is left in the vial. The degree of colour in each vial, measured with an optical density reader, determines the degree of antibody activity. The darker the vial, the more antibodies. The more antibodies, the stronger the possibility of that food causing an allergic reaction in your body.

Once you have been tested and the offending foods discovered, your practitioner will assist you with the next stages, elimination and challenge of allergenic foods. The elimination phase is the actual elimination of all foods to which you have reacted. The challenge phase occurs after elimination. It is the period of time when you reintroduce foods back into your diet.

Elimination is at the least, difficult. Careful decision-making with an open-mind is rudimentary to success. You will undoubtedly require patience of yourself. The process can be tedious and time-consuming. Lifestyle and dietary changes will be necessary. It is not simply eliminating a specific food, or foods, but learning to read labels and choosing your dining out meals with deliberate care. When cooking, you many need to learn to prepare your meals differently or even devise new menus and recipes. Moreover, working with family members who do not want to participate could become wearisome. Importantly, no matter what the difficulty, the end result will ultimately be worth the process. Soon, the tasks will become second nature and you will look forward to the end in sight. In fact, in a few months, your entire life will be changed. You will be a new person: healthier, stronger, happier. The struggle, the investigation, the diet, the blood draw, and the waiting time will all have been worth the effort.

The best method of elimination utilised by most practitioners is the quick and immediate elimination of all foods in question. Some refer to this as going, "cold turkey". Beginning the changes in your diet at a slow pace will only prolong the whole process. Discipline is the most aspect in this early stage of altering one's habits. One must be accustomed to reading labels. Problematic foods are oftentimes hidden within the multitude of ingredients of processed foods. An obvious example of this is milk. Milk is the key ingredient in ice cream. Therefore, logical reason says that if one is allergic to milk, then ice cream should also be avoided! Always be mindful that allergenic foods are hidden everywhere. Carrying snacks or nibbles with you always may also behoove you, just in case, and for those times when you simply cannot determine if a food item is safe.

The time frame for elimination differs with each individual. Times range from three weeks to six months, or until symptoms have regressed or ceased. No matter how long the time frame, be sure to replace any nutrients you would usually get through your eliminated foods with other sources. Be ever vigilant. Remember this is your well-being and you are at the helm.

The challenge phase is next. Choosing foods for the challenge, or reintroduction phase, should be done carefully and methodically. Gradually these foods will be reintroduced into your diet one-by-one. First bring back foods of greater nutritional value, and believed to be unlikely candidates for allergy. Only after introducing those foods should more allergenic foods be tested. This is important because with each new allergic uprising a period of time is lost while your system returns to normalcy. Moreover, challenging foods should be done in their most simplistic whole forms. For example, if you are challenging cow's milk, drink a cup of cow's milk; do not have hot chocolate. If challenging corn, eat corn on the cob without butter, salt, or pepper; do not have chips and salsa. Reactions can be delayed, as mentioned earlier, due to the differing reaction times of IgE and IgG, so waiting a few days between foods is recommended. No foods should be reintroduced while in the throes of the reaction, otherwise the reaction to that food will be masked. Instead, wait until you symptoms subside, and then reintroduce the next food. When symptoms do arise after ingesting a certain food, do not continue to eat that food through the remaining challenges. Again, this will mask your results! One important thought, if you have a known adverse reaction to a specific food, such as shrimp causing hives or anaphylaxis, do not challenge the food, unless supervised within a clinical or hospital setting!

The process of challenge is fun and exciting. As an added bonus, you will learn more about food, your body, and your health. Now, rewards are actually within reach.

Once you have identified your food allergies through the process of testing, elimination, and challenge, the next step for you and your practitioner is to choose a treatment protocol that best suits your symptom picture and is directed at alleviating the underlying cause of your allergies. Your specific treatment may involve diet changes, supplementation, and even allergy shots. Although, injection therapy is rarely prescribed for food allergies.

The search for the underlying cause can be a lengthy process and sometimes bewildering. Often, a direct association with the onset of allergies is not identified or remembered. This is when a thorough investigation may be required by you and your practitioner. You will need to be on high alert, listening carefully to your body and its symptoms. Much akin to an espionage novel, you may find yourself investigating and thinking of where you were, what you were doing, and under what conditions you ate a particular food item. Optimising digestive and immune functions are oftentimes the perfect places to start treatment. With treatment, you may be able to once again eat the foods for which you were found to be allergic. Searching for the underlying cause of your allergies is the key to long-term health.

As you have undoubtedly come to realise, food allergies are not well known, not well investigated, and are therefore, oftentimes overlooked as a possible causative factor to illness. Fortunately, laboratory testing is available and lends to easier identification. Feeling as well and as strong as one can be is the best reward. Ultimately, you will be the victor and you can take total satisfaction and delight that you have accomplished a great deed. Your health and well-being will be in your hands.

Takahashi T, Kitani S, Nagase M, Mochizuki M, Nishimura R, Morita Y, Sasaki N. IgG=mediated histamine release from canine mastocytoma-derived cells. Int Arch Allergy Immunol. 2001 Jul;125 (3):228-35.

Okayama Y, Kirshenbaum AS, Metcalfe DD. Expression of a functional high=affinity IgG receptor, Fc gamma RI, on human mast cells: Up-regulation by IFN-gamma. J Immunol. 2000 Apr 15;164(8):4332-9.

Awazuhara H, Kawai H, Maruchi N. Major allergens in soybean and clinical significance of IgG4 antibodies investigated by IgE- and IgG4-immunoblotting with sera from soybean-sensitive patients. Clin Exp Allergy. 1997 Mar;27(3):325-32.

Opper FH, Burakoff R. Food allergy and intolerance. Gastroenterologist. 1993;1(3)211-220.

Rance R, Kanny G, Dutau G, Moneret Vautrin DA. Food allergens in children. Arch Pediatr. 1999;6(Supp11):61S-66S.

Nutrigenomics Study Shows Dietary Anti-inflammatories Also Decrease Oxidation and Metabolic Stress in Overweight Men

Tue, 09 Aug 2011 14:15:00 +1200

Nutrigenomicsis the study of the relationships between dietary factors and individual genes. New nutrigenomic research was reported from the Netherlands in which a combination product of fish oil, green tea extract, resveratrol, vitamins C and E, and a tomato juice extract produced changes to genes associated with inflammation, blood vessel health, and oxidation of fat in the liver, according to findings published in the American Journal of Clinical Nutrition.

The researchers used a nutrigenomics approach, including proteomics, metabolomics, and transcriptomics, to assess 120 plasma proteins, 274 metabolites, and the transcriptomes of blood cells and fat tissue. The intervention proved beneficial in healthy but overweight men with mildly increased CRP, as shown by large-scale profiling of genes, proteins, and metabolites in plasma, urine, and adipose tissue. Though CRP levels were unchanged, the supplement was associated with a 7% increase in levels if adiponectin, an anti-inflammatory protein hormone linked to various metabolic processes where levels are also inversely related to body fat levels.

In addition to the improvements in adiponectin levels, PI Gertruud Bakker and her team noticed a "multitude of subtle changes...which indicated modulated inflammation of adipose tissue, improved endothelial function, affected oxidative stress, and increased liver fatty acid oxidation." The study was a double-blind, placebo-controlled, crossover trial that utilized 5-week periods for 36 subjects who consumed a supplement containing resveratrol (6.3mg), green tea extract (94.5 mg containing 40% EGCG), alpha-tocopherol (90.7 mg), vitamin C (125 mg), omega-3 fatty acids (1200 mg, of which 380 mg is EPA and 260 mg is DHA), and tomato extract (3.75 mg of lycopene).

The research team noted that the compounds were chosen in order to reproduce real life situations, and that levels were determined by data for their individual anti-inflammatory action. "A more optimal combination many exist," they noted.

Omega-3 Fatty Acids and the Body's Response to Pain and Orthopaedic Injury

Tue, 09 Aug 2011 13:28:00 +1200

Musculoskeletal symptoms and orthopaedic conditions are a common cause of concern for many patients. Concentrated fish oil, providing the omega-3s EPA and DHA, is emerging as a cost effective tool with a favourable safety profile for optimising outcome from traditional treatment strategies. Scientific and clinical evidence shows that EPA and DHA may address all three of the major components of pain and injury: inflammatory response, cellular/tissue structural integrity, and nervous system signalling.

Inflammatory Response
EPA and DHA may significantly modify the class of prostaglandins and leukotrienes produced via COX- and LOX-mediated pathways to encourage a flux away from the 2- and 4- series and towards the 3- and 5- series. In addition, specialised downstream lipid mediators—end products of metabolism from EPA and DHA known as resolvins, protectins, and maresins—are now touted as critical to signalling the termination of acute inflammation toward homeostasis and away from a chronic inflammatory state. Hence, suboptimal EPA and DHA leads to poor tissue repair as a result of insufficient signalling of granulocytes, multi-potent stem cells, macrophages, and fibroblasts.

Cellular / Tissue Structural Integrity
EPA and DHA provide plasma membrane structural support for repairing injured tissue, and provide necessary chemical building blocks for restoring normal function to cell membranes across all tissue types and organ systems. Additionally, by enhancing the novel fibroblast collagen formation, musculoskeletal tissue may undergo structural repair to address a persistent pain generator.

Peripheral and Central Nervous System Signalling
Finally, fish oil may stabilise nerve thresholds and neuroendocrine axes for managing central and peripheral neural pain signalling processes. There is preliminary evidence and rationale for neural pain fiber membrane stabilisation as a result of sufficient EPA and DHA.

Thus, there is powerful construct validity for administering concentrated fish oil to address the biochemical and metabolic processes of musculoskeletal pain and injury.

Fish Oil Enhances Efficacy of Chemotherapy and Improved Response Rate

Tue, 09 Aug 2011 13:07:00 +1200

Fish oil, when combined with chemotherapy for non-small cell lung cancer, significantly enhanced the efficacy of the chemotherapy and improved response rate when compared to those simply receiving the standard therapy, according to research published in ‘Cancer 2011'.

Palliative chemotherapy is aimed at increasing survival and palliating symptoms. However, the response rate to first-line chemotherapy in patients with non-small cell lung cancer (NSCLC) is less than 30%. Experimental studies have shown that supplementation with fish oil (FO) can increase chemotherapy efficacy without negatively affecting non-target tissue. This study evaluated whether the combination of FO and chemotherapy (carboplatin with vinorelbine or gemcitabine) provided a benefit over standard of care (SOC) on response rate and clinical benefit from chemotherapy in patients with advanced NSCLC.

METHODS:
Forty-six patients completed the study, n = 31 in the SOC group and n = 15 in the FO group. Patients in the FO group received 2.5 g EPA + DHA/day.
Response to chemotherapy was determined by clinical examination and imaging. Response rate was defined as the sum of complete response plus partial response, and clinical benefit was defined as the sum of complete response, partial response, and stable disease divided by the number of patients.
Toxicities were graded by a nurse before each chemotherapy cycle. Survival was calculated 1 year after study enrollment.

RESULTS:
Patients in the FO group had an increased response rate and greater clinical benefit compared with the SOC group (60.0% vs 25.8%, P = .008; 80.0% vs 41.9%, P = .02, respectively). The incidence of dose-limiting toxicity did not differ between groups (P = .46). One-year survival tended to be greater in the FO group (60.0% vs 38.7%; P = .15).

CONCLUSIONS:
Compared with the SOC group, supplementation of FO results in increased chemotherapy efficacy without affecting the toxicity profile and may contribute to increased survival.

Source: Cancer, Feb 15, 2011. PMID: 21328326, by Murphy RA, Mourtzakis M, Chu QS, Baracos VE, Reiman T, Mazurak VC. Division of Human Nutrition, Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada

Mothers Nutrition during Pregnancy can Influence her Child's Risk of Obesity

Tue, 03 May 2011 09:24:00 +1200

Scientists have discovered that a mother's nutrition during pregnancy can strongly influence her child's risk of obesity many years later.

An international study, led by University of Southampton researchers and including teams from New Zealand and Singapore, has shown for the first time that during pregnancy, a mother's diet can alter the function of her child's DNA. The process, called epigenetic change, can lead to her child tending to lay down more fat. Importantly, the study shows that this effect acts independently of how fat or thin the mother is and of child's weight at birth.

Keith Godfrey, Professor of Epidemiology and Human Development at the University of Southampton, who led the study, says:

"We have shown for the first time that susceptibility to obesity cannot simply be attributed to the combination of our genes and our lifestyle, but can be triggered by influences on a baby's development in the womb, including what the mother ate. A mother's nutrition while pregnant can cause important epigenetic changes that contribute to her offspring's risk of obesity during childhood."

Researchers measured epigenetic changes in nearly 300 children at birth and showed that these strongly predicted the degree of obesity at six or nine years of age. What was surprising to the researchers was the size of the effect - children vary in how fat they are, but measurement of the epigenetic change at birth allowed the researchers to predict 25 per cent of this variation.

The epigenetic changes, which alter the function of our DNA without changing the actual DNA sequence inherited from the mother and father, can also influence how a person responds to lifestyle factors such as diet or exercise for many years to come.

"This study indicates that measures to prevent childhood obesity should be targeted on improving a mother's nutrition and her baby's development in the womb. These powerful new epigenetic measurements might prove useful in monitoring the health of the child," adds Professor Godfrey.

"This study provides compelling evidence that epigenetic changes, at least in part, explain the link between a poor start to life and later disease risk. It strengthens the case for all women of reproductive age having greater access to nutritional, education and lifestyle support to improve the health of the next generation, and to reduce the risk of the conditions such as diabetes and heart disease which often follow obesity"

states Mark Hanson one of the research team.

"This study provides the most compelling evidence yet that just focusing on interventions in adult life will not reverse the epidemic of chronic diseases, not only in developed societies but in low socio-economic populations too" says Sir Peter Gluckman FRS research team member of the Liggins Institute at the University of Auckland.

The study team are part of an international consortium involving the Universities of Southampton and Singapore, the Singapore Institute for Clinical Sciences, the Liggins Institute of the University of Auckland, AgResearch New Zealand and the Medical Research Council Lifecourse Epidemiology Unit, University of Southampton.

Professor Cyrus Cooper, who directs the MRC Lifecourse Epidemiology Unit, says: "MRC population-based studies have shown that early life factors influence risk of disease many years later. Now we can begin to see the mechanisms by which this happens, opening up new avenues for medical research and interventions."

Their findings have been published (26 April 2011) in the printed journal Diabetes.

Nutrigenomics Shows Benefit of Magnesium’s Metabolic Actions

Mon, 02 May 2011 12:40:00 +1200

Magnesium may up and down-regulate a number of genes linked to metabolism: Magnesium's favourable effects on certain metabolic pathways is associated with changes in gene expression, says a new study that adds to our knowledge of nutrigenomics.

Four weeks of magnesium supplementation were associated with a decrease in levels of C-peptide, a marker of improved insulin sensitivity. The mineral was also linked to down-regulation of certain "genes related to metabolic and inflammatory pathways", according to findings published in the American Journal of Clinical Nutrition.

"These findings lend support to the hypothesis that dietary magnesium plays a beneficial role in the regulation of insulin and glucose homeostasis,"

wrote researchers led by Simin Liu, MD, ScD, Professor of Epidemiology and Medicine at the University of California, Los Angeles (UCLA).

Study details
The new study adds to a growing body of science supporting the potential health benefits of magnesium and employed a raft of techniques, including biochemical assays of blood samples, RNA extraction, and urine proteomic profiling.

Professor Liu and his co-workers recruited 14 overweight but otherwise healthy people, and randomly assigned them to receive 500 mg per day of elemental magnesium in the citrate form, or a placebo for four weeks. After the intervention, participants underwent a one month ‘washout' period before crossing over to the other intervention.

Results showed that magnesium supplementation was linked to significantly decreased levels of C-peptide,

"which suggested a reduction in pancreatic insulin secretion that may have resulted from an improvement in insulin sensitivity and a subsequent lowered demand on the pancreas",

said the researchers.

In addition, a reduction in the concentrations of fasting insulin was measured by Prof Liu and his team.

No changes in inflammatory biomarkers were recorded, added the researchers.

In terms of gene expression, 24 genes were up-regulated, and 36 genes were down-regulated in response to magnesium supplementation, they said. Amongst the down-regulated genes were ones linked to metabolic and inflammatory pathways, explained the researchers.

"Although a number of the other genes identified as differentially expressed in this trial are unknown," said the researchers, "Our exploratory findings indicated a systemic effect of magnesium supplementation at the level of gene expression.
"This is consistent with our findings that showed a distinct protein profile in urine collected after treatment with magnesium compared with after treatment with the placebo.
"Our findings were suggestive of measurable physiologic changes in the urinary proteome after treatment with magnesium for four weeks, which warrants further investigation into these changes and identification of the proteins involved," they added.

Nutrigenomics is seen by many as the future of nutrition. Nutrigenomics is defined as how food and ingested nutrients influence the genome (personalized nutrition). Nutrigenetics is defined as how a person's genetic make-up affects a response to diet (individual nutrition). The difference between the two is important.

Source: American Journal of Clinical Nutrition
Published online ahead of print, doi: 10.3945/ajcn.110.002949.
"Magnesium supplementation, metabolic and inflammatory markers, and global genomic and proteomic profiling: a randomized, double-blind, controlled, crossover trial in overweight individuals"
Authors: S.A. Chacko, J. Sul, Y. Song, X. Li, J. LeBlanc, Y. You, A. Butch, S. Liu

Omega-3 Fatty Acids May Reduce Gum Disease

Mon, 17 Jan 2011 13:06:00 +1300

Omega-3 fatty acid intake is inversely associated with periodontitis in the US population, according to research published in the Journal of the American Dietic Association.

The new study found that that a moderate dietary intake of the omega-3 polyunsaturated fatty acids DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) were associated with a decreased prevalence of periodontitis of up to 20 percent.

"To date, the treatment of periodontitis has primarily involved mechanical cleaning and local antibiotic application. Thus, a dietary therapy, if effective, might be a less expensive and safer method for the prevention and treatment of periodontitis," wrote the researchers, led by Dr Asghar Naqvi from Harvard Medical School.

"Our results also suggest that DHA ([in] doses recommended by the American Heart Association ...) may be as or more potent in influencing periodontitis," they added.

The study was said to be the first to demonstrate an antibacterial activity of omega-3 fatty acids and their esters against oral pathogens.

Source: natural ingredients.com

Fish Oil Limits Brain Damage

Mon, 17 Jan 2011 13:02:00 +1300

Research led by Dr. Nicolas Bazan, Boyd Professor, Villere Chair, and Director of the Neuroscience Center of Excellence at Louisiana State University Health Sciences Center, has shown that Docosahexaenoic acid (DHA), a component of fish oil, is a powerful therapeutic agent that can protect brain tissue and promote recovery in an experimental model of acute ischemic stroke, even when treatment is delayed by up to five hours.

These findings not only target a new stroke treatment approach, but also provide vital information about the length of the therapeutic window. The NIH-funded research is published in the journal, Translational Stroke Research.

DHA has potent anti-inflammatory effects. Since inflammation is at the root of many chronic diseases, DHA treatment has been widely demonstrated to have beneficial effects in patients with coronary heart disease, asthma, rheumatoid arthritis, osteoporosis, sepsis, cancer, dry eye disease, and age-related macular degeneration, but its potential benefit in stroke was not known.

"We are just now beginning to understand the significant impact of omega-3 essential fatty acids on stroke," notes Dr. Bazan.

To determine how DHA might be effective in stroke treatment and recovery, the LSUHSC research team administered either DHA or saline intravenously at 3, 4, 5, and 6 hours after the onset of stroke. MRIs showed that neurological deficits were reduced by the administration of DHA. DHA treatment reduced swelling and facilitated neurobehavioral recovery.

The volume of the area of destroyed tissue was reduced by an average of 40% when DHA was administered at 3 hours, 66% at 4 hours, and 59% at 5 hours. Further analysis showed it triggered production of Neuroprotectin D1 (NPD1), a naturally occurring neuroprotective molecule in the brain derived from DHA and discovered by Dr. Bazan. Not only did DHA treatment salvage brain tissue that would have died, its repair mechanisms rendered some areas indistinguishable from normal tissue by 7 days.

Source: sciencedaily.com

Science Validates Triglyceride form of Fish Oil to have up to 70% higher absorption than the Ethyl Ester form which is widely available

Mon, 29 Nov 2010 14:44:00 +1300

Dr. Dryberg and his Danish co-workers report that the availability of omega -3's in the Triglyceride form was significantly higher than omega-3's in the Ethyl ester form, according to new findings published in the form of Prostaglandins, Leukotrienes and Essential Fatty Acids. The blinded, placebo controlled study involved 72 people aged between 21 and 26.

Participants received a daily supplement of one form of omega 3 - daily doses of EPA plus DHA between 3.1 gm and 3.6gm for two weeks. At the end of the intervention, the researchers report that "the mean relative bioavailability of EPA plus DHA from Ethyl ester was 73% v. 124% for Triglyceride which demonstrates a 70% increased absorption for the triglyceride form over the ethyl ester form.

"Our results demonstrate that bioavailability may differ between the commonly used types of concentrated fish oil preparations. Re-esterified triglycerides have superior bioavailability, whereas ethyl esters may have a lower bioavailability."

Wrote researchers from the University of Copenhagen and Aalborg Hospital.

In fish, the omega-3 fatty acids, EPA and DHA, occur naturally in triglyceride form. To make a quality fish oil concentrate, the individual fatty acids must first be removed from the glycerol backbone. To stabilize these delicate fatty acids, they are bound to an ethyl alcohol molecule before they undergo molecular distillation to both purify and to increase the amounts of EPA and DHA.

Once the desired concentration is achieved, a manufacturer chooses from two distinctly different options. The first is to reattach the fatty acids to the glycerol backbone in a process known as "re-esterification" to recreate the natural triglyceride structure. The second, far less costly option is to leave the fish oil as an ethyl ester, a "new to nature" form of fatty acid.

According to Nordic Naturals CEO Joar Opheim,

"It is great to see science proving what we at Nordic Naturals have always believed. Our understanding of the body's utilization of ingested omega-3s has always supported our commitment to re-esterified triglycerides as the best form for our concentrated fish oils".

CLINICAL STUDIES ON BIOAVAILABILITY
Previous to the recent study, six human trials have compared the absorption of ethyl ester (EE) and Triglyceride (TG) fish oil supplements. Of the six studies, four concluded that the TG form absorbs better, and the other two studies did not find a significant difference in absorption.

Dietary fish oil is digested in the small intestine by the emulsifying action of bile salts and the hydrolytic activity of pancreatic lipase. The hydrolysis of a triglyceride (TG) molecule produces two free fatty acids (FFA) and a monoglyceride (one fatty acid combined to glycerol). These metabolic products are then absorbed by intestinal enterocytes and reassembled again as TGs. Carrier molecules called chylomicrons then transport the TGs into the lymphatic channel and finally into the blood.

The digestion of EE fish oils is slightly different due to the lack of a glycerol backbone. In the small intestine it is again the pancreatic lipase that hydrolyzes the fatty acids from the ethanol backbone however the fatty acid-ethanol bond is up to 50x more resistant to pancreatic lipase as compared to hydrolysis of TGs. The EEs that get hydrolyzed produce free fatty acids plus ethanol. The FFA's are taken up by the enterocytes and must be reconverted to TGs to be transported in the blood. The TG form of fish oil contains its own monoglyceride substrate, where as EE fish oils, coupled to ethanol, do not. EE must therefore obtain a monoglyceride substrate from another source. Without a glycerol or monoglyceride substrate TG re-synthesis is delayed, suggesting that transport to the blood is more efficient in natural TG fish oils in comparison to EEs. Furthermore, this delay of TG re-synthesis in EE fish oils could cause an increase in free fatty acids and subsequent oxidation of those free fatty acids.

STABILITY OF ETHYL ESTERS V. TRIGLYCERIDES
EPA and DHA are long-chain polyunsaturated fats (PUFA's) which means they contain several double bonds within their carbon-hydrogen chain. In each location of a double bond, there is vulnerability for free radical attack, which results in an oxidised and rancid oil. The inherent structure of three fatty acids attached to one glycerol backbone in the TG form provides protection to the double bonds in the long-chain PUFA's from being exposed to free radicals. An ethyl ester fatty acid, on the other hand, exists as a single strand, and is exposed on all sides to free radicals. This basic biochemistry suggests the superior stability of TG fish oils both inside a capsule or liquid as well as within the body. Ethyl ester fish oils are less stable, and readily oxidize. Resistance to oxidative damage is a critical quality of a fish oil supplement as a fish oil that has been subject to oxidative damage may do more harm than good.

COMPARISION SUMMARY
Although the majority of concentrated fish oil products on the market contain the ethyl ester form of EPA and DHA, current research points toward the triglyceride form for better absorption and assimilation.

Featured Product:

ProOmega

ProOmega is a double-strength EPA+DHA formula for more omega-3 benefits in fewer servings. This formula is ideal for high-intensity, therapeutic support for body and mind. ProOmega contains 35% EPA / 25% DHA.

650 mg EPA / 450 mg DHA per 2 soft gels
1626 mg EPA / 1126 mg DHA per 1 teaspoon

Omega-3 DHA Protects Against Alzheimer's

Mon, 18 Oct 2010 14:37:00 +1300

Researchers at the University of California, LA conducted a research to address the potential of Omega-3 fatty acid docosahexaenoic acid (DHA) to slow the pathogenesis of Alzheimer's disease (AD) and possibly vascular dementia.

The risk for dementia, a major contributor to incapacitation and institutionalization, rises rapidly as people age, doubling every 5 years after age 65. Tens of millions of new Alzheimer's disease (AD) and other dementia cases are projected as elderly populations increase around the world, creating a projected dementia epidemic for which most nations are not prepared.

Researchers believed that "there is an urgent need for prevention approaches that are safe, effective, and affordable. This review addresses the potential of one promising candidate, the omega 3 fatty acid docosahexaenoic acid (DHA), which appears to slow pathogenesis of AD and possibly vascular dementia."

DHA is pleiotropic, acting at multiple steps to reduce the production of the beta-amyloid peptide, widely believed to initiate AD. DHA moderates some of the kinases that hyperphosphorylate the tau-protein, a component of the neurofibrillary tangle. DHA may help suppress insulin/neurotrophic factor signaling deficits, neuroinflammation, and oxidative damage that contribute to synaptic loss and neuronal dysfunction in dementia.
Researchers conclude that DHA increases brain levels of neuroprotective brain-derived neurotrophic factor and reduces the omega 6 fatty acid arachidonate and its prostaglandin metabolites that have been implicated in promoting AD. Clinical trials suggest that DHA or fish oil alone can slow early stages of progression, but these effects may be apolipoprotein E genotype specific, and larger trials with very early stages are required to prove efficacy. "We advocate early intervention in a prodromal period with nutrigenomically defined subjects with an appropriately designed nutritional supplement, including DHA and antioxidants" reasearchers state.

Numerous studies support role of DHA on cognition and synaptic integrity.

In another recent study researchers at the University of Lorraine in France conclude from a review of the research that the omega-3 fat DHA is one of the "..most valuable diet ingredients whose neuroprotective properties could be crucial for designing nutrition-based strategies able to prevent Alzheimer's disease." DHA (docosahexaenoic acid) makes up a critical component of nerve cell membranes, allowing them more fluidity and enhancing nerve cell communication, as well as increasing their survival, thus reducing risk for degeneration associated with dementia.

References:
Oster T, Pillot T: Docosahexaenoic acid and synaptic protection in Alzheimer's disease mice. Biochimica et Biophysica Acta 2010; March 6th.
Cole G, Frautschy S: DHA may prevent age-related dementia. Journal of Nutrition 2010; 140:869-874.

D-ficient Kids Review

Fri, 02 Jul 2010 17:06:00 +1200

A study from Harvard Medical School found that more than six million children in the United States are vitamin D deficient. The researchers analyzed blood samples for vitamin D using data on about 5,000 children under age 12 years from the National Health and Nutrition Examination Survey (2001-2006). Results showed that one in five children had blood vitamin D levels below acceptable levels. According to the data, two-thirds of children (24million) have blood levels below 75nmol/L, a level considered closer to optimal. (1)

BACKGROUND
Vitamin D, a steroid hormone produced in the skin, has specific regulatory or functional effects on other parts of the body. Vitamin D is hydroxylated in the liver to 25-hydroxyvitamin D (25[OH]D) and further hydroxylated in the kidney to 1,25-dihydroxyvitamin D. Hydroxylation in the kidney is regulated closely by parathyroid hormone (PTH), hypocalcemia, and hypophosphatemia and is inhibited by 1,25- dihydroxyvitamin D. As well, 1,25- dihydroxyvitamin D (produced locally within
cells) regulates gene transcription through nuclear high-affinity VTD receptors. These receptors are found in the classic target organs: gut, bone, kidney, and parathyroid and many other tissues as well, such as brain, breast, colon, heart, pancreas, prostate, skin, and immune system. Vitamin D regulates cell growth and maturation, inhibits renin production, stimulates insulin secretion, and modulates the function of activated T- and B-lymphocytes and macrophages. (2)

Many individual and environmental factors interfere with the ability to have sufficient sun exposure to produce vitamin D endogenously. Over the past 4 decades, increasing scientific evidence has linked vitamin D deficiency to many chronic diseases including hypertension, immune dysfunction, cancer, diabetes, and cardiovascular disease. In adolescents, these relationships have only begun to be explored. It is reasonable to infer that because many of the potential consequences of vitamin D deficiency develop over time, prevention should begin in childhood. (3)

WHY ARE OUR KIDS D-FICIENT?
Newborn infants have a unique source of vitamin D: the mother; cholecalciferol (the parent compound of vitamin D) does cross the placenta, maternal and fetal cholecalciferol blood concentrations are low and placental transfer contributes minimally to the vitamin D status of the fetus or newborn infant because 1,25-Dihydroxyvitamin D [1,25(OH)2D], the physiologically active metabolite, does not cross the placenta. However, the placenta can synthesize 1,25(OH)2D directly, and this might contribute to the infant's circulating level of 1,25(OH)2D. (4) The prenatal nutritional status of the mother directly affects the nutritional status of the fetus and neonate. Prenatal vitamin D deficiency may increase maternal risk of preeclampsia and gestational diabetes and may be associated with reduced bone mineralization in the offspring. (3)

The skin naturally produces vitamin D from the reaction of sunlight (ultraviolet B irradiation) with 7-dehydrocholesterol; however because of the relation of sun exposure to skin cancer, the Centers for Disease Control and Prevention, with the support of many organizations (including the AAP, the American Academy of Dermatology, and the American Cancer Society), recommend that infants younger than 6 months not be exposed to the sun and that all children and adolescents use sunscreens and clothing to protect them from ultraviolet B radiation exposure and to prevent skin cancer. (4)

Good evidence exists that many breastfed infants not supplemented with vitamin D during the first 6 months of life have serum vitamin D concentrations <50 nmol/L and are therefore at increased risk of rickets. This is especially true for infants who have high skin pigmentation and little sun exposure. (4)

RECCOMMENDED INTAKE
The new recommended daily intake of vitamin D is 400 IU/day for all infants, children, and adolescents beginning in the first few days of life - by the American Academy of Pediatrics (AAP): (5)

AAP recommends that exclusively and partially breastfed infants receive supplements of 400 IU/day of vitamin D shortly after birth and continue to receive these supplements until they are weaned and consume >1,000 mL/day of vitamin D-fortified formula or whole milk.
All non-breastfed infants ingesting <1,000 mL/day of vitamin D-fortified formula or milk should receive a vitamin D supplement of 400 IU/day.
AAP also recommends that older children and adolescents who do not obtain 400 IU/day through vitamin D-fortified milk and foods should take a 400 IU vitamin D supplement daily. (6)

CONCLUSION
Because numerous factors contribute to deficiency, routine supplementation should be considered along with monitoring of serum levels to document the attainment of adequate vitamin D. These measures can determine future dosing and dietary guidelines. (3)

Along with adequate vitamin D intake, dietary calcium intake to achieve optimal bone formation and modelling must be ensured. A dietary history is essential in assessing the adequacy of dietary intake for various vitamins, minerals, and nutrients, including vitamin D and calcium. (5)

Additional Facts to consider:

Good evidence also shows that supplements of 400 IU vitamin D/d keep 25(OH)D concentrations higher than 70 nmol/L prevent rickets in white infants. (4)

Rickets is an example of extreme vitamin D deficiency, with a peak incidence between 3 and 18 months of age.

A state of deficiency occurs months before rickets is obvious on physical examination, and the deficiency state may also present with hypocalcemic seizures, growth failure, lethargy, irritability, and a predisposition to respiratory infections during infancy. (5)

References: 1 Mansbach J, Ginde A, Camargo C: Serum 25-hydroxyvitamin D levels among US children aged 1 to 11 years. Pediatrics 2009;124:1404-1410
2 Schwalfenberg G: Not enough vitamin D- Health Consequences for Canadians-Clinical Review. Canadian Family Physician 2007;53:841-854
3 Saintonge S, Bang H and Gerber L: Implications of a New Definition of Vitamin D Deficiency in a Multiracial US Adolescent Population: The National Health and Nutrition Examination Survey III. Pediatrics 2009;123;797-803
4 Greer F: 25-Hidroxyvitamin D: functional outcomes in infants and young children. American Journal of Clinical Nutrition 2008:88
5 Wagner C, Greer F and the Section on Breastfeeding and Committee on Nutrition: Prevention of Rickets and Vitamin D Deficiency in Infants, Children, and Adolescents. Pediatrics 2008;122;1142-1152
6 National Institute of Health- Office of Dietary Supplements -Dietary Supplement Fact Sheet: Vitamin D Health Professional Fact Sheet

Study Examines Association Between Omega-3 Fatty Acid Levels and Chromosome Marker of Biological Ageing in Patients in Coronary Heart Disease

Thu, 01 Jul 2010 17:05:00 +1200

Patients with coronary heart disease who had higher omega-3 fatty acid blood levels had an associated lower rate of shortening of telomere length, a chromosome marker of biological aging, raising the possibility that these fatty acids may protect against cellular aging, according to a study published in the Journal of the American Medical Association.

Several studies have shown increased survival rates among individuals with high dietary intake of marine omega-3 fatty acids and established cardiovascular disease. The mechanisms underlying this protective effect are not well understood, according to background information in the article.

Telomeres are a structure at the end of a chromosome involved in the replication and stability of the chromosome. Genetic factors and environmental stressors can shorten the length of the telomere, with telomere length becoming an emerging marker of biological age.

Ramin Farzaneh-Far, M.D., of the University of California, San Francisco, and colleagues conducted a study to determine whether omega-3 fatty acid blood levels were associated with changes in leukocyte (a type of blood cell) telomere length in a study of 608 outpatients with stable coronary artery disease. The patients were recruited between September 2000 and December 2002 for the Heart and Soul Study, and followed up to January 2009 (median [midpoint], 6.0 years). The researchers measured leukocyte telomere length at the beginning of the study and again after 5 years of follow-up. Multivariable models were used to examine the association of baseline levels of omega-3 fatty acids (docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA]) with subsequent change in telomere length.

The researchers found that individuals in the lowest quartile of DHA+EPA experienced the most rapid rate of telomere shortening, whereas those in the highest quartile experienced the slowest rate of telomere shortening. "Levels of DHA+EPA were associated with less telomere shortening before and after sequential adjustment for established risk factors and potential confounders. Each 1-standard deviation increase in DHA+EPA levels was associated with a 32 percent reduction in the odds of telomere shortening," the authors write.

The researchers concluded that among patients with stable coronary artery disease, there was an inverse relationship between baseline blood levels of marine omega-3 fatty acids and the rate of telomere shortening over 5 years. "These findings raise the possibility that omega-3 fatty acids may protect against cellular aging in patients with coronary heart disease," the researchers write.

Featured Product:

ProOmega

650 mg EPA / 450 mg DHA per 2 soft gels
1626 mg EPA / 1126 mg DHA per 1 teaspoon

Concentrated Essential Fatty Acids (EFAs) and Inflammation

Thu, 29 Apr 2010 15:20:00 +1200

In the past studies have revealed that supplementation of human diets with gamma-linolenic acid (GLA) reduced the generation of lipid mediators and clinical symptoms of chronic inflammatory disorders. However it has also been shown that supplementation with GLA alone may cause a marked increase in serum arachidonic levels (AA), as a potentially harmful side effect.

Arachidonic acid (AA), present in immune cell phospholipids, is the precursor of eicosanoids (PGE2) that promote neutrophil accumulation which leads to tissue injury and inflammation.
In order to increase levels of beneficial PGE1 in the body, GLA is elongated to DGLA, which is the direct precursor of PGE1. However, in some cells, there is the precursor for DGLA to be further metabolized, via delta-5 desaturase, to AA leading to more PGE2 and thus more inflammation.

It is now understood that when EPA and GLA are given together, the human body is able to maximize the production of anti-inflammatory PGE1 and PGE 3, while maximizing the reduction in AA-derived PGE2. Providing EPA with GLA has demonstrated the ability to inhibit delta-5 desaturase enzyme activity, the terminal enzyme responsible for the production of AA and the precursor of PGE2.

To test the in vivo effects of a GLA and EPA combination in humans, healthy adult volunteers consumed a controlled diet supplemented with 3 g/day of GLA and EPA. This supplementation strategy significantly increased serum levels of EPA, but did not increase AA levels. EPA and DGLA levels in neutrophil glycerolipids increased significantly during the 3-week supplementation period.

Most notably, a study in the American Journal of Clinical Nutrition demonstrated that fish oil, in conjunction with GLA, improved lipid and fatty acid profiles in women that measurably reduced their heart attack risk. A mixture of 4 g EPA+DHA and 2 g GLA favorably altered blood lipid and fatty acid profiles in healthy women. The group was estimated to have a 43% reduction in the 10-year risk of myocardial infarction.

Featured Product: ProEFA