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myDNAhealth launches the only Nutritional Genomics Test available, Optimal Health Pro

myDNAhealth launches Optimal Health Pro, the latest scientifically developed nutritional genomic test to battle future health problems like Type 2 Diabetes.

Following a new partnership with leading laboratory dispensary Regenerus Laboratories, award-winning nutritional genomics experts myDNAhealth is proud to release its Optimal Health Pro to the public.
Optimal Health Pro is specifically designed for nutrition and health practitioners interested in applying nutritional genomics in their practice. The product allows users to optimise their health through personalised nutrition and lifestyle programs in a bid to prevent chronic diseases.

“Optimal Health Pro essentially gives those most at risk a glimpse of the future and therefore a chance to change it.” said Berenice Williams, co-founder of myDNAhealth. “Think of Optimal Health Pro as the gift of hindsight today and ask yourself. If you could see yourself in twenty years and didn’t like the image… would you change?”

myDNAhealth researched and interpreted the complex relationships between nutritional molecules, genetic variants, the biological systems, diet and lifestyle factors impacting gene expression. Optimal Health Pro is the apex of that research and allows practitioners to offer this powerful risk analysis and personalised nutrition tool to their patients/clients.

What is Optimal Health Pro?

myDNAHealth is the only company to analyses data from online questionnaires alongside personal genetic variants.

The test addresses no less than 25 health concerns and in conjunction with a series of lifestyle and nutrition questionnaires, assesses the user’s future risk of a number of long-term health issues, from methylation cycle balance to Type 2 Diabetes.

Nutritional Genomics lies at the heart of the test, this header comprises two fields of science: Nutrigenetics, which investigates genetic variants, and nutrigenomics, which relates to the impact of lifestyle and diet on gene expression.

To accurately predict the risk of specific chronic health conditions requires an understanding of both. Reducing the danger of said diseases requires an appropriate personalised nutrition guide alongside other potentially relevant lifestyle choices. People with long term conditions such as high cholesterol and type 2 diabetes have specific dietary requirements for foods that are lower in fat and refined sugars. There are certain genotypes that increase the risk for these metabolic diseases and knowing this information can encourage a personal nutrition approach to reduce disease risk.

The Optimal Health Pro report, identifies and characterises gene variants associated with differential responses to nutrients and relates these variations to different disease states. For example, the combination of low folate intake and a reduced enzyme due to an MTHFR gene variant, increases susceptibility to disease, even if either of them, on their own, might not.

The reports also show how dietary factors influence gene expression. They also address the effect of lifestyle choices on DNA structure, known as epigenetics, which subsequently impacts protein and metabolite levels. For example, we know that high-fat diets change our gene expression through epigenetic changes.

Who is Optimal Health Pro for?

Optimal Health Pro reports are for anybody who cares about their future health and is ready to make some positive changes. What we do now can have a dramatic effect on our future.

If you are looking for small habits to change, want to know how your body responds to your diet, or to reduce your risk of life-changing health problems, Optimal Health Pro can guide you along your journey to reaching your optimal health.

Where can I get more information?

myDNAhealth, Tel 01603 861 614; practitioner@mydnahealth.co.uk, www.mydnahealth.co.uk

Regenerus Laboratories, www.regeneruslabs.com, info@regeneruslabs.com

The post myDNAhealth launches the latest Nutritional Genomics Test, Optimal Health Pro appeared first on myDNAhealth.

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Consumers still unsure of the importance of whole grain and fibre

While whole grain and higher fibre foods have been gaining traction over the past couple of years, new research by Nestle has revealed that the vast majority of UK adults are still unaware that wholegrain can help to reduce type-2 diabetes and that it is good for heart health.

The Lancet has also recently published a study commissioned by the WHO that found a link between higher intakes of dietary fibre and whole grain foods and a reduction in the risk of several diseases, including heart disease, stroke and diabetes. Risk reduction associated with a range of critical outcomes was greatest when daily intake of dietary fibre was between 25 grams and 29 grams.

These studies are very important as there is increased public confusion over what to base their meal choices on, and the impact dietary choices have on the risk of certain diseases.

How to get more fibre into your diet?

The ideal intake of fibre is not less than 30 grams a day. Provided the right foods are eaten, this level can be easily achieved.

  • Eat wholegrain bread and oats, barley and rye. A cup of oats has 5 grams of fibre, a slice of rye bread has 26 grams and a slice of wholemeal bread 23 grams.
  • Add fruit to your daily diet such as apples, berries, pears, melon and oranges. An apple has 125 grams and an orange 138 grams of fibre.
  • Consume at least five portions of colourful vegetables each day. A large broccoli head has 358 grams of fibre, a cauliflower 475 grams, a carrot 103 grams and a cup of peas 83 grams.
  • Include beans, pulses, nuts and seeds. A cup of cooked lentils contains about 35 grams of fibre.
  • The post Consumers still unsure of the importance of whole grain and fibre appeared first on myDNAhealth.

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    It’s all in the name: some considerations when naming your meat-free recipes and dishes

    Plant-based diets were historically the norm in many cultures. Its industrial societies saw meat-eating grow from being an occasional treat to weekly or even daily making vegetarianism a hard sell. According to NatCen, Britain’s largest independent social research agency, three in ten people in Britain (29%) say they have reduced the amount of meat they ate. (2016 survey)


    The challenge: How to make the plant-based diet the mainstream diet? One strategy is to change the language used to describe plant-rich foods.

    World Resources Institute has researched what works and what doesn’t when it comes describing plant-rich foods in a way that can appeal to consumers and shift them away from meat and animal food choices.

    • Don’t use “Meat-Free”: Meat-free means less of what meat eaters like as it emphasises what is missing from a dish which can trigger a person’s desire to avoid losing out on something.
    • Don’t use “vegan” to describe plant-based dishes: Vegan can mean different from me so avoid the “us-them” mentality. Research has found the word “vegan” to be divisive online and this may prevent people from trying the growing range of plant-based proteins available. The recommendation is to use a symbol on menus or packaging to indicate a dish is suitable for vegans.
    • Don’t use “vegetarian”: Naming a food as vegetarian can invoke a mix of positive and negative perceptions. A study by the London School of Economics found that 56 per cent of meat eaters were less likely to order a plant-rich dish if it was contained within a vegetarian box. Study participants reported they are concerned about a perceived lack of protein and iron and that a vegetarian diet may be nutritionally unbalanced. Many also see vegetarian diets as boring and bland. The recommendation is to use a symbol on menus or packaging to indicate a dish is suitable for vegetarians.
    • Don’t use “healthy restrictive” language: Generally, people just don’t see healthy foods as all that enjoyable. If plant-rich foods are already thought of as boring and bland, highlighting these foods’ health benefits can throw “not tasty” into the mix of potential negative perceptions.
    • Do highlight “the place of origin”: Showcasing the origin of the dish can be more appealing. Highlighting the link between food and the natural environment can have a positive impact. For example, Sainsbury’s name change from “Meat-free Breakfast” to “Field Grown Breakfast” resulted in a 17 per cent increase in sales.

    Sources:
    www.wri.org
    http://www.natcen.ac.uk

    The post It’s all in the name appeared first on myDNAhealth.

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    Are cruciferous vegetables a superfood?

    When a new piece of research comes out on a specific food and its health benefits, the first thing that the media will do is to mention the term superfood. But what do they mean by superfood? Do they imply it contains a wide range of essential vitamins and nutrients that can promote a healthy wellbeing?

    myDNAhealth asked Federico Bernuzzi who is currently doing a PhD in Molecular Nutrition at the Quadram institute in Norwich to answer this question. Federico’s research focuses on understanding how broccoli is good for us. Although he says he wouldn’t necessary call cruciferous vegetables superfoods, they are definitively important vegetables that the British population should be consuming more of.

    Cruciferous vegetables include a wide range of vegetables. The most common ones are the following: broccoli, cauliflower, different forms of cabbage, Brussel sprouts, kale, swede, turnip and even rocket. These vegetables are rich in molecules known as glucosinolates; compounds that the plant produces to defend itself against diseases and pests (Traka & Mithen, 2008).

    The special feature of glucosinolate is that they are formed by sulphur atoms. Have you ever stopped and considered what is that awful smell when you are cooking cauliflower, broccoli and cabbage? It is exactly the sulphur molecules in the glucosinolates that are being broken down.

    It turns out the human body is not able to metabolise these glucosinolates. Instead the collection of microorganisms in our gut known as the gut microbiota does that job for us. A specific community of these microorganisms that can produce a specific set of enzymes known as myrosinase, convert these glucosionlates to molecules known as isothiocyanates. These isothiocyanates are the active substances of the plant. In fact, these isothiocyanates play an important role in maintaining our health (Traka & Mithen, 2008).

    Glucoraphanin is the glucosinolate found in broccoli. In our digestive system it is converted to an isothiocyanate called sulforaphane (SF). SF helps to reduce inflammation. One way it does so is by switching on genes involved in fighting inflammation. For example, SF and potentially other isothiocyanates can increase the levels of glutathione in the body. Glutathione has been associated as a “master antioxidant” (ZHANG & CALLAWAY, 2002).

    Additional health benefits of cruciferous vegetables

    Over the past couple of years, the Quadram Institute (formerly known as Institute of Food Research) has been carrying out small-scale human intervention trials in men with an increased risk of developing prostate cancer. In these studies, men were split into two groups: one received a 400g portion of a broccoli soup high in glucoraphanin. The control received a standard broccoli soup. This broccoli high in glucoraphanin have been specifically designed and grown to have 2-3 times higher concentration of glucosinolates compared to the normal broccoli you would find in the supermarket.

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    A review: Blood type dietary approaches

    The myDNAhealth approach is a genetic test of actionable genes and consultation questionnaires in order to assess a person’s lifestyle and hence, any potential for epigenetic changes. We use current scientific evidence to provide actionable advice to help people improve their lifestyle and hence, their wellbeing.

    What else is currently been marketed as a genetic diet? Our PHD intern, Anna Ten Bioscience (Quadram Institute), MPhil in Medical Sciences, BSc (Hons) Medical Biochemistry, investigates the GenoType Diet.

    The GenoType diet book

    The trade marked GenoType diet, created by Dr D’Adamo, promises to “help you live the longest, fullest and healthiest life possible” “without the need for expensive tests, or even a visit to the doctor” (ref book). In the entertaining book, the author explains that there exist six GenoTypes (Genetic Archetypes, based on your genes, determined by your blood type, and your environment before birth – in the womb; not to be confused with the scientific term genotype – your actual genes) the Hunter, the Gatherer, the Teacher, the Explorer, the Warrior and the Nomad.

    The book takes you through a fun set of activities, which, with the aid of tests that you can buy ranging from a blood type home test, SNP test for what looks like one gene, and a taste test) to determine your GenoType and provide you a list of super foods and toxic foods to obtain the ultimate, personalised lifestyle experience.

    Determining the GenoType according to the book

    The book argues that Dr D’Adamo’s GenoType calculator is more accurate at predicting risk factors for genetic diseases than “expensive and time consuming” laboratory testing but how easy and reliable is it to determine your GenoType? Is it as easy as “no effort or expense”?

    Being a semi-regular blood donor, Anna knows her blood type is B+. Without buying the $9.95 home blood test, she can eliminate several GenoTypes.

      The Hunter GenoType is always blood type O.
      The Teacher and the Warrior are blood type A or AB.
      The typical B blood genotypes are the Gatherer and the Nomad.
      The Explorer can be any blood type therefore Anna knows she is either a Gatherer, a Nomad or an Explorer.

    Anna reports that being Rhesus positive, she almost instantly knows she is a Nomad, as this GenoType is almost always Rhesus positive. But can she truly be sure of her GenoType? She finds a tape measure and follows the protocol of the GenoType calculator which includes measuring her standing height, sitting height, upper leg length, lower leg length, index and ring fingers. She also thoroughly examines the patterns of her finger prints. She deduces that she is very symmetrical. According to the book, this means that she had a very happy gestation period and should have a great epigenetic profile. This symmetry excludes the Explorer GenoType, as Explorers are asymmetrical.

    How can she tell if she is a Gatherer or a Nomad? She could take the $119.95 secretor genetic test. The test measures whether you secrete your blood type antigens into your bodily fluids. 85% of the world are secretors, 15% are not, according to the GenoType diet and the unlucky 15% have a lower fat burning rate and higher risk of inflammation (ref book). Conveniently, Anna has the exact item that she needs to differentiate whether she is a Gatherer or Nomad, as the book promised, in her home! She finds a very common item, which most people definitely have in their household, which solves her genetic mystery. What is this common item you need to decipher your genotype? A dental mould of her upper jaw of course! She analyses the cast of her upper teeth, focusing on the front incisors and fifth molars, and deduces that she is a Nomad.

    What does the GenoType mean?

    Anna learns that as a Nomad she should be sensitive to the elements but will age well, which is nice for anyone to hear (read). She learns that she has the enviable gift of controlling her macrophages – the cells responsible for inflammation – with her mind. However, if she does not regularly visualise her macrophages regulating her Nitric Oxide levels she can be prone to neuromuscular diseases and chronic fatigue.

    According to the book, her optimal GenoType diet is a “herder diet” and for optimal health she must eliminate chicken and bear meat from her diet. She does not regularly consume bear meat so eliminating this toxic food will be an issue, but she is disappointed that following this diet plan will mean no more Nandos.

    Anna further learns that for Nomads some cheeses are super foods while others are toxins to avoid, she wonders how the author of this diet plan made the distinction between these dairy products. She also finds out that she has been poisoning herself with toxic bananas and oranges all these years. She is disappointed that her super drink is beer as she has never been a beer drinker. She discovers that all the six genotypes are poisoning themselves with ketchup and mayonnaise.

    So What Am I (SWAMI)?

    Anna finds that since the GenoType Diet book was published in 2010, So What Am I (SWAMI) packages have evolved. The basic SWAMI package is £350 and the most expensive package is £650. The packages promise to “go one step further into your genes and epigenetics” and all offer “Complete SWAMI testing” although it is unclear what the test is. As she already knows her blood type is B+ and that according to her biometric analysis from the GenoType Diet book she is a Nomad, she wonders how the SWAMI packages can improve health. She fills in the Contact Us form to enquire about the test but never receives a reply.

    Conclusion

    The Blood type diet theory has been widely criticised by the scientific community (Cusack et al 2013, Wang et al 2014). The GenoType Diet book is quite entertaining to read and provides fun activities for the reader, including measuring your leg length and head circumference.

    The reference section of the book refers the reader to various books however it is extremely unclear how the author reached some conclusions in the health risk sections of some GenoTypes. For example, that the Explorer GenoType was at risk of breast cancer “especially if female, type A blood and left handed”! The patient example of the Teacher GenoType was also upsetting to read, as the book’s author claimed to cure a patient of multiple myeloma, an aggressive and incurable blood cancer with GenoType diet and supplementation.

    About the reviewer: Anna Ten, Year 2 PhD in Bioscience (Quadram Institute), MPhil in Medical Sciences (University of Cambridge), BSc (Hons) Medical Biochemistry (University of Leicester)

    Anna has over five years of laboratory experience, in haematology and hepatology research, and is on a Professional Internship for PhD students with myDNAhealth where she is researching genetics and epigenetics for dental health related conditions. She has completed year 1 of her PhD at the Gut microbes and Health department of the Quadram Institute of Biosciences where she is researching immunometabolic changes in liver disease.

    References
    Leila Cusack, Emmy De Buck, Veerle Compernolle, Philippe Vandekerckhove; Blood type diets lack supporting evidence: a systematic review, The American Journal of Clinical Nutrition, Volume 98, Issue 1, 1 July 2013, Pages 99–104, https://doi.org/10.3945/ajcn.113.058693
    Wang J, García-Bailo B, Nielsen DE, El-Sohemy A (2014) ABO Genotype, ‘Blood-Type’ Diet and Cardiometabolic Risk Factors. PLOS ONE 9(1): e84749. https://doi.org/10.1371/journal.pone.0084749

    Disclaimer: The review and comments posted on this page is that of Anna Ten only.

    The post A book review: Blood type dietary approaches appeared first on myDNAhealth.

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    Should we stop calorie counting? The short answer for most of us is yes. Counting calories is increasingly becoming controversial in the weight loss world. While some insist on the simple formula ‘eat less calories than you burn and you will lose weight’, for many this just does not seem to work. Here’s why:

    1. The body is great at adapting. If you give your body less calories it will simply slow down and use less energy for its internal processes. If you are following a low calorie diet you may notice weight loss at first but once the body gets used to the calorie reduction the weight loss tends to plateau.
    2. The quality of calories is important. If you eat nutrient-dense foods it will boosts your metabolism and provide your body with a rich supply of nutrients to maintain and repair tissue, all of which takes energy. Focus on quality natural food and you can still lose excess weight and be healthier.
    3. Calorie counting can result in poor food choices. For example, having a biscuit with your afternoon tea break might mean a calorie counter denies you a proper meal to ‘make up’ for it. Calorie counting may also cause you to avoid healthy snacks like nuts and avocados because they are high in calories, so instead you may opt for nutrient deficient, heavily processed or ‘lite’ foods which the body has little use for.
    4. Science tells us that eating less calories should lead to weight loss, but in reality this only works to a certain extent. If instead you follow the general principles of a healthy balanced diet, then obsessing over the calorie content of foods becomes unnecessary.

    The post Three reasons to stop calorie counting appeared first on myDNAhealth.

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    The term vegetable oil is misleading as individuals have different perception of these type of oils. Vegetable oils include the following:

    ·         Corn

    ·         Soybean

    ·         Canola

    ·         Sunflower

    ·         Peanut

    ·         Cottonseed

    ·         Safflower

    Olive/extra virgin olive oil, avocado and coconut oil these are all fruit oils and are not considered vegetable oils

    One of the main features about vegetable oils is that they are rich in Omeg-6 polyunsaturated acids. Although small amounts of omega-6 are essential for health, the problem is that the Western diet consumes far too much Omega-6. As the Western diet is also deficient in Omega-3 the outcome is an unbalanced ratio of Omega-6 to Omega3 fatty acids. Over the long term this can lead to a formation of a wide range of diseases such as cancer (Perumalla Venkata & Subramanyam, 2016; Wu et al., 2004), heart diseases (DiNicolantonio & O’Keefe, 2018) and diabetes (Okuyama et al., 2016). An optimal omega-6 to omega-3 ratio is 2:1 or even better 1:1. Modern world diet has dramatically shifted this ratio 15:1 up to 50:1 (Kiecolt-Glaser et al., 2013; Simopoulos, 2002).

    These oils are more commonly referred to as industrial oils as they require an industrial process to make them, extracting oil from seed results in a very low yield. Producing these oils requires the use of chemical solvents. Firstly, a solvent such as hexane a volatile hydrocarbon is used to extract the oil from the seed.  The oils are then hydrogenated at a high temperature in the presence of a catalyst. In the final steps the oils are deodorized.

    Vegetable Oils and heart diseases. What is the link?

    Since the banning of saturated fat in the 1970s as it raises cholesterol levels in the blood and high blood cholesterol causes coronary heart diseases, authorities have persuaded people to replace vegetable oils with saturated fats, in the hope to reduce the incidence of heart diseases.

    The Sydney Diet Heat Study a randomized controlled trial (RCT) was designed to assess the effectiveness of omega 6 fats in reducing coronary heart diseases compared to saturated fat. The results showed that the intervention group who consumed Omega-6s had higher overall death rates from the controls and also had higher death rate of cardiovascular diseases  (Ramsden et al., 2013). A second RCT showed that although the individuals who consumed vegetable oils, the polyunsaturated fats did indeed lower serum cholesterol, a 30 mg/dL drop of cholesterol was associated with a 22% increased risk of death (Ramsden et al., 2016).

    Vegetable oils and cancer risk. What is the evidence?

    Animal studies have shown that when mice and rats are fed corn oil they develop cancer. One study stated that mice fed a diet high in corn oil developed colon cancer, as the p53 tumour suppressor gene was suppressed (Wu et al., 2004).

    Vegetable oils and liver diseases:

    Non-alcoholic fatty liver disease (NAFLD),  strongly associated with both obesity and insulin resistance, is on the rise. Currently there is no approved pharmacological treatment for NAFLD. A couple of studies have shown that increasing omega 6 consumption can speed up the rate of developing NAFLD (ARAYA et al., 2004; Patterson, Wall, Fitzgerald, Ross, & Stanton, 2012).

    Conclusion:

    One of the main reasons why these oils are bad for our heath is that as they have many double bonds, under cooking temperatures they are prone to get oxidized and generate lipid peroxides (Prabhu, 2000; Tańska, Roszkowska, Skrajda, & Dąbrowski, 2016).

    Most of these omega-6 oils come from processed food such as salad dressings and various confectionery items such as crips, pastries etc. Therefore, naturally avoiding all these foods and eating whole and unprocessed foods will help to correct the omega 6 to omega 3 ratios. For cooking use olive oil and even butter. For dressing salads use extra-virgin olive oil, one of the main staples of the Mediterranean diet and avoid salad dressings at all costs.

    Written by: Federico Bernuzzi: BSc in Biochemistry, MSc in Epidemiology and Biostatistics, 2nd Year PhD in Molecular Nutrition at the Quadram Institute

    References:

    ARAYA, J., RODRIGO, R., VIDELA, L. A., THIELEMANN, L., ORELLANA, M., PETTINELLI, P., & PONIACHIK, J. (2004). Increase in long-chain polyunsaturated fatty acid n−6/n−3 ratio in relation to hepatic steatosis in patients with non-alcoholic fatty liver disease. Clinical Science, 106(6), 635 LP-643. Retrieved from http://www.clinsci.org/content/106/6/635.abstract

    DiNicolantonio, J. J., & O’Keefe, J. H. (2018). Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis. Open Heart, 5(2). Retrieved from http://openheart.bmj.com/content/5/2/e000898.abstract

    Kiecolt-Glaser, J. K., Epel, E. S., Belury, M. A., Andridge, R., Lin, J., Glaser, R., … Blackburn, E. (2013). Omega-3 fatty acids, oxidative stress, and leukocyte telomere length: A randomized controlled trial. Brain, Behavior, and Immunity, 28, 16–24. https://doi.org/https://doi.org/10.1016/j.bbi.2012.09.004

    Okuyama, H., Langsjoen, P. H., Ohara, N., Hashimoto, Y., Hamazaki, T., Yoshida, S., … Langsjoen, A. M. (2016). Medicines and Vegetable Oils as Hidden Causes of Cardiovascular Disease and Diabetes. Pharmacology, 98(3–4), 134–170. https://doi.org/10.1159/000446704

    Patterson, E., Wall, R., Fitzgerald, G. F., Ross, R. P., & Stanton, C. (2012). Health Implications of High Dietary Omega-6 Polyunsaturated Fatty Acids. Journal of Nutrition and Metabolism, 2012, 539426. https://doi.org/10.1155/2012/539426

    Perumalla Venkata, R., & Subramanyam, R. (2016). Evaluation of the deleterious health effects of consumption of repeatedly heated vegetable oil. Toxicology Reports, 3, 636–643. https://doi.org/https://doi.org/10.1016/j.toxrep.2016.08.003

    Prabhu, H. R. (2000). Lipid peroxidation in culinary oils subjected to thermal stress. Indian Journal of Clinical Biochemistry, 15(1), 1–5. https://doi.org/10.1007/BF02873539

    Ramsden, C. E., Zamora, D., Leelarthaepin, B., Majchrzak-Hong, S. F., Faurot, K. R., Suchindran, C. M., … Hibbeln, J. R. (2013). Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ : British Medical Journal, 346. Retrieved from http://www.bmj.com/content/346/bmj.e8707.abstract

    Ramsden, C. E., Zamora, D., Majchrzak-Hong, S., Faurot, K. R., Broste, S. K., Frantz, R. P., … Hibbeln, J. R. (2016). Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ, 353. Retrieved from http://www.bmj.com/content/353/bmj.i1246.abstract

    Simopoulos, A. P. (2002). The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomedicine & Pharmacotherapy, 56(8), 365–379. https://doi.org/https://doi.org/10.1016/S0753-3322(02)00253-6

    Tańska, M., Roszkowska, B., Skrajda, M., & Dąbrowski, G. (2016). Commercial Cold Pressed Flaxseed Oils Quality and Oxidative Stability at the Beginning and the End of Their Shelf Life. Journal of Oleo Science, 65(2), 111–121. https://doi.org/10.5650/jos.ess15243

    Wu, B., Iwakiri, R., Ootani, A., Tsunada, S., Fujise, T., Sakata, Y., … Fujimoto, K. (2004). Dietary Corn Oil Promotes Colon Cancer by Inhibiting Mitochondria-Dependent Apoptosis in Azoxymethane-Treated Rats. Experimental Biology and Medicine, 229(10), 1017–1025. https://doi.org/10.1177/153537020422901005

    The post Vegetable oils and why they should be avoided! appeared first on myDNAhealth.

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    Within the past 10 years there has been an explosion of studies looking at the role of the gut microbiota and microbiome in health and diseases. The microbiome is the genetic material of the microbiota which is the community of micro-organisms that live on and inside the human body (Valdes, Walter, Segal, & Spector, 2018). The gut is host to approximately 100 trillion of these micro-organisms; the large majority are bacteria, but also fungi, viruses and protozoa are present (Bull & Plummer, 2014). These micro-organisms perform a large range of different functions including producing a diverse set of metabolites which in turn influences the host health (Bull & Plummer, 2014).

    Development of the human microbiota

    The development of the microbiota begins at natural child birth. This then continues through breast feeding along with the surrounding environment which colonises the infant’s gut with beneficial bacteria. In the early stages of development, the microbial diversity of the child is low and is mainly formed by two main species, Actinobacteria and Proteobacteria (Rodríguez et al., 2015). About 2,5 years after birth, the infant’s composition and diversity of their microbiome resembles that of an adults (Rodríguez et al., 2015).

    What do these microbes do?

    The microbiota can digest specific food components that humans are not capable of doing such as dietary fibre. A special set of bacteria utilises the fibre to produce short chain fatty acids (SCFAs) (Wong, de Souza, Kendall, Emam, & Jenkins, 2006). The major SCFAs produced are acetate, propionate and butyrate.

    Acetate

      reaches the peripheral tissue and affects both cholesterol and fatty acid metabolism and can reduce appetite (Frost et al., 2014).

    Propionate

      is transferred to the liver where it regulates both gluconeogenesis, a metabolic pathway that results in the generation of glucose from certain non-carbohydrate carbon substrates. It can also help suppress appetite by interacting with the fatty acid receptor present on the gut (De Vadder et al., 2014).

    Butyrate

      is the main energy source for human colon cells and induces apoptosis of human colon cancer cells (De Vadder et al., 2014).

    Other specific products of the gut microbiota that can impact on human health are Indolpropionic acid and the conversion of glucosinolates found in cruciferous vegetables to isothiocyanates.

    Indolpropionic is a potent antioxidant which may reduce the risk of type 2 diabetes (de Mello et al., 2017).

    Certain isothiocyanates such as Sulforaphane promote detoxification and reduce inflammation (Mithen, Armah, & Traka, 2011).

    Microbiota diversity and health

    Although it is still not clear what a healthy microbiome consists of, greater microbial diversity is often considered to be a healthy gut. Low bacterial diversity has been associated with several different conditions such as inflammatory bowel diseases (Manichanh et al., 2006), psoriatic arthritis (Scher et al., 2014), type 1 diabetes (de Goffau et al., 2013), obesity (Turnbaugh et al., 2008) and type 2 diabetes (Lambeth et al., 2015).

    The transplant of faeces from a lean healthy donor, to the infected patient is now routinely used to treat patients with severe infections such as Clostridium difficle (Schneider et al., 2018). This procedure referred to as faecal microbiota transplantation (FMT) is also currently being explored to treat other pathologies (Kootte et al., 2017).

    How does food and medications modulate the microbiota?

    The biggest factor that has an impact on our microbiota is diet. For example, sweeteners such as sucralose, aspartame and saccharin, common sugar replacements have been shown to alter the gut microbiota (Bian et al., 2017; Nettleton, Reimer, & Shearer, 2016). Food additives such as emulsifiers commonly found in processed food also affect the gut microbiota of animals such as mice. Mice fed a low concentration of two commonly used emulsifiers: carboxymethylcellulose and polysorbate 80 had reduced microbial diversity compared to mice with no emulsifiers (Chassaing et al., 2015).

    Medication also plays a big role. Antibiotics have shown to reduce beneficial species in the gut (Blaser, 2016). Other drugs such as progesterone, TNFα inhibitors and rupatadine also have an impact (Jackson et al., 2015).

    What’s the future …

    Although we have a better understanding that the microbes in our gut influence our health and that consumption of dietary fibre along with prebiotics is associated with better health, a lot of questions remain unanswered. For example, are microbes responsible for the food choices that we make? Can low doses of antibiotics found in animal products affect our microbiome and in turn our health? Finally, what are the effects of pesticides found in food on the microbiome? Should everyone consume organic food instead?

    Having a much better understanding of an individual’s microbiome may lead to personalised nutrition. Given the current limited understanding on how probiotics and/or prebiotics affect the microbiome and whether FMT can ameliorate other diseases such as obesity, more clinical evidence is needed.

    myDNAhealth collaborates with the Quadram Institute, a leading institute understanding how food and the gut microbiota are linked in order to promote health and prevent the onset of non-communicable diseases.

    Written by: Federico Bernuzzi: BSc in Biochemistry, MSc in Epidemiology and Biostatistics, 2nd Year PhD in Molecular Nutrition at the Quadram Institute

    References:

    Bian, X., Chi, L., Gao, B., Tu, P., Ru, H., & Lu, K. (2017). Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice   . Frontiers in Physiology  . Retrieved from https://www.frontiersin.org/article/10.3389/fphys.2017.00487

    Blaser, M. J. (2016). Antibiotic use and its consequences for the normal microbiome. Science (New York, N.Y.), 352(6285), 544–545. https://doi.org/10.1126/science.aad9358

    Bull, M. J., & Plummer, N. T. (2014). Part 1: The Human Gut Microbiome in Health and Disease. Integrative Medicine: A Clinician’s Journal, 13(6), 17–22. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4566439/

    Chassaing, B., Koren, O., Goodrich, J., Poole, A., Srinivasan, S., Ley, R. E., & Gewirtz, A. T. (2015). Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome. Nature, 519(7541), 92–96. https://doi.org/10.1038/nature14232

    de Goffau, M. C., Luopajärvi, K., Knip, M., Ilonen, J., Ruohtula, T., Härkönen, T., … Vaarala, O. (2013). Fecal Microbiota Composition Differs Between Children With β-Cell Autoimmunity and Those Without. Diabetes, 62(4), 1238 LP-1244. Retrieved from http://diabetes.diabetesjournals.org/content/62/4/1238.abstract

    de Mello, V. D., Paananen, J., Lindström, J., Lankinen, M. A., Shi, L., Kuusisto, J., … Uusitupa, M. (2017). Indolepropionic acid and novel lipid metabolites are associated with a lower risk of type 2 diabetes in the Finnish Diabetes Prevention Study. Scientific Reports, 7, 46337. Retrieved from http://dx.doi.org/10.1038/srep46337

    De Vadder, F., Kovatcheva-Datchary, P., Goncalves, D., Vinera, J., Zitoun, C., Duchampt, A., … Mithieux, G. (2014). Microbiota-Generated Metabolites Promote Metabolic Benefits via Gut-Brain Neural Circuits. https://doi.org/10.1016/j.cell.2013.12.016

    Frost, G., Sleeth, M. L., Sahuri-Arisoylu, M., Lizarbe, B., Cerdan, S., Brody, L., … Bell, J. D. (2014). The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism. Nature Communications, 5, 3611. Retrieved from http://dx.doi.org/10.1038/ncomms4611

    Jackson, M. A., Goodrich, J. K., Maxan, M.-E., Freedberg, D. E., Abrams, J. A., Poole, A. C., … Steves, C. J. (2015). Proton pump inhibitors alter the composition of the gut microbiota. Gut. Retrieved from http://gut.bmj.com/content/early/2015/12/30/gutjnl-2015-310861.abstract

    Kootte, R. S., Levin, E., Salojärvi, J., Smits, L. P., Hartstra, A. V, Udayappan, S. D., … Nieuwdorp, M. (2017). Improvement of Insulin Sensitivity after Lean Donor Feces in Metabolic Syndrome Is Driven by Baseline Intestinal Microbiota Composition. Cell Metabolism, 26(4), 611–619.e6. https://doi.org/10.1016/j.cmet.2017.09.008

    Lambeth, S. M., Carson, T., Lowe, J., Ramaraj, T., Leff, J. W., Luo, L., … Shah, V. O. (2015). Composition, Diversity and Abundance of Gut Microbiome in Prediabetes and Type 2 Diabetes. Journal of Diabetes and Obesity, 2(3), 1–7. https://doi.org/10.15436/2376-0949.15.031

    Manichanh, C., Rigottier‐Gois, L., Bonnaud, E., Gloux, K., Pelletier, E., Frangeul, L., … Dore, J. (2006). Reduced diversity of faecal microbiota in Crohn’s disease revealed by a metagenomic approach. Gut, 55(2), 205–211. https://doi.org/10.1136/gut.2005.073817

    Mithen, R., Armah, C., & Traka, M. (2011). Cruciferous Vegetables – and Biological Activity of Isothiocyanates and Indoles BT  – Vegetables, Whole Grains, and Their Derivatives in Cancer Prevention. In M. Mutanen & A.-M. Pajari (Eds.) (pp. 1–30). Dordrecht: Springer Netherlands. https://doi.org/10.1007/978-90-481-9800-9_1

    Nettleton, J. E., Reimer, R. A., & Shearer, J. (2016). Reshaping the gut microbiota: Impact of low calorie sweeteners and the link to insulin resistance? Physiology & Behavior, 164, 488–493. https://doi.org/https://doi.org/10.1016/j.physbeh.2016.04.029

    Rodríguez, J. M., Murphy, K., Stanton, C., Ross, R. P., Kober, O. I., Juge, N., … Collado, M. C. (2015). The composition of the gut microbiota throughout life, with an emphasis on early life. Microbial Ecology in Health and Disease, 26, 10.3402/mehd.v26.26050. https://doi.org/10.3402/mehd.v26.26050

    Scher, J. U., Ubeda, C., Artacho, A., Attur, M., Isaac, S., Reddy, S. M., … Abramson, S. B. (2014). Decreased Bacterial Diversity Characterizes the Altered Gut Microbiota in Patients With Psoriatic Arthritis, Resembling Dysbiosis in Inflammatory Bowel Disease. Arthritis & Rheumatology, 67(1), 128–139. https://doi.org/10.1002/art.38892

    Schneider, K. M., Wirtz, T. H., Kroy, D., Albers, S., Neumann, U. P., Strowig, T., … Trautwein, C. (2018). Successful Fecal Microbiota Transplantation in a Patient with Severe Complicated Clostridium difficile Infection after Liver Transplantation. Case Reports in Gastroenterology, 12(1), 76–84. Retrieved from https://www.karger.com/DOI/10.1159/000481937

    Turnbaugh, P. J., Hamady, M., Yatsunenko, T., Cantarel, B. L., Duncan, A., Ley, R. E., … Gordon, J. I. (2008). A core gut microbiome in obese and lean twins. Nature, 457, 480. Retrieved from http://dx.doi.org/10.1038/nature07540

    Valdes, A. M., Walter, J., Segal, E., & Spector, T. D. (2018). Role of the gut microbiota in nutrition and health. BMJ, 361. Retrieved from http://www.bmj.com/content/361/bmj.k2179.abstract

    Wong, J. M. W., de Souza, R., Kendall, C. W. C., Emam, A., & Jenkins, D. J. A. (2006). Colonic Health: Fermentation and Short Chain Fatty Acids. Journal of Clinical Gastroenterology, 40(3). Retrieved from https://journals.lww.com/jcge/Fulltext/2006/03000/Colonic_Health__Fermentation_and_Short_Chain_Fatty.15.aspx

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    Research update: COMT val158Met rs4680

    Catechol-O-methyltransferase (COMT) is an enzyme which degrades catechols such as catecholamines (dopamine, adrenaline) and catecholestrogens (formed by cytochrome P450 in the liver). It catalyses the transfer of a methyl group from a donor compound (S adenosyl methionine, SAM) onto the oxygen of one of the hydroxyl groups, in the presence of Mg2+ (1).

    COMT exist in two isoforms, a soluble and a membrane-bound form (S-COMT and MB-COMT, respectively). However, both are encoded on a single COMT gene, found on chromosome 22. The sequence of the two proteins is the same, with MB-COMT having an additional N-terminal section which tethers it to the membrane (2). Both isoforms catalyse the same reaction and have the same active site.

    While S-COMT is most abundant in the liver, MB-COMT is predominantly expressed in the brain where it plays a role in dopamine inactivation (3). In some areas of the brain, dopamine transporters readily take up dopamine from the synaptic cleft into the pre-synaptic neuron to terminate the dopamine signal. However, in areas with extremely low levels of these transporters, such as the prefrontal cortex (PFC), COMT plays a much more important role in terminating dopaminergic transmission through dopamine degradation (4).

    The rs4680 polymorphism is an extensively studied functional SNP of COMT. A change from G>A results in the conversion of a Valine to Methionine (Val158Met in MB-COMT). The Met allele is associated with a significant reduction in enzyme activity and decreased thermostability (5)(6).

    Because of impaired enzyme activity, the Met allele is associated with higher extracellular dopamine levels in the PFC, as dopamine is not degraded as quickly (3). This presumably results in prolonged stimulation of the post-synaptic neuron and/or allows for greater dopamine availability at the synapse.

    Memory

    This affects influences prefrontal cognitive function, as the prefrontal cortex is an area important for working memory. The association between Val158Met and working memory seemed weak at first, as studies connecting V158Met and working memory have shown mixed results (7–10). However further research focusing on different types of working memory function showed that the SNP has no effect on cognitive processes that only require maintenance of information, but does affect processes demanding active manipulation or updating of information. The Met allele has found to be advantageous here, as it is associated with enhanced cognitive performance (11–15). Thus, Met allele carriers may hold an advantage in memory and attention tasks (16).

    It is believed that there is an optimal intermediate level of dopamine at which prefrontal functioning is most efficient. Too much or too little dopamine seems to have negative effects on working memory. This can be thought of as an inverted-U shaped relationship between prefrontal dopamine levels and PFC performance. As the Met allele is related to higher PFC dopamine levels, Met homozygotes are thought to be closer to the optimum dopamine level on the inverted U curve than Val carriers (Fig 3).

    Stress

    In contrast, Met allele carriers tend to be more sensitive to biological stressors. Along with demonstrating a greater biological response to stressors (greater hypothalamic-pituitary-adrenal function, greater stress hormone response (17)), Met hetero- and homozygotes have been shown to subjectively experience greater stress in response to a task, compared to Val-homozygotes (18).

    Val/val individuals have been shown to respond better to situations of acute and daily stress (19,20).

    While Met homozygotes perform better on working memory tasks under no-stress conditions, working memory performance and cognitive function under acute stress is better for val homozygotes (21). It is believed that stress leads to increased release of dopamine and noradrenaline. This can be thought of as a shift to the right along the x-axis in figure 3. Under such conditions, individuals with Val alleles would benefit, having improved dopaminergic transmission and performance. Those with Met alleles would be at a detriment, as they would reach higher than optimal PFC dopamine levels.

    There seems to be a trade-off between working memory performance and resiliency to stress. The function of COMT may make Met-carriers more sensitive to stress while improving cognitive performance.

    Methylation

    The rs4680 SNP is a G>A transition also abolishes a CpG site, where the cytosines are methylation sites. Each Val allele has one CpG methylation site and the Met allele has none. Val/val subjects with greater stress scores have reduced methylation at this site, and better working memory performance. This is most likely because methylation reduces COMT expression. Therefore, silencing of the COMT gene via methylation partially compensates for its negative effect on working memory. In Val/Met subjects, there was no relationship found between methylation, stress, prefrontal cognition, and COMT expression. (22)

    Suggested dietary and lifestyle intervention

  • Reduce stress.
  • COMT requires magnesium in order to function properly. Consider increasing magnesium intake to maximise the COMT variant enzyme function.
  • COMT’s substrate is SAMe, the primary methyl donor for most methylation reactions. SAMe is a metabolite in the homocysteine-methionine cycle. It has been shown that an increase in dietary folate was associated with an increase (normalisation) of SAMe levels in those with previously low SAMe levels (23). Therefore, increasing folate intake could also help in optimising COMT activity.
  • Aside from metabolism by COMT, a second mechanism of dopamine clearance in the prefrontal cortex is the norepinephrine transporter. However, attempting to upregulate its function could have other negative consequences, since norepinephrine transporter inhibitors are drugs used to treat ADHD (24).

  • Further consideration

    The manifestation of a COMT allele as an observable phenotype is sometimes influenced by other genes. Deficits in multiple mechanisms produce more pronounced and reliable differences in stress response patterns than functional changes of a single component. These include 5-HTT and MAOA (25,26).

    REFERENCES
    1. Nissinen E, Männistö PT. Biochemistry and Pharmacology of Catechol-O-Methyltransferase Inhibitors. International review of neurobiology. [Online] 2010. p. 73–118. Available from: doi:10.1016/B978-0-12-381326-8.00005-3 [Accessed: 23rd August 2018]
    2. Yager JD. Catechol-O-methyltransferase: characteristics, polymorphisms and role in breast cancer. Drug Discovery Today: Disease Mechanisms. [Online] Elsevier; 2012;9(1–2): e41–e46. Available from: doi:10.1016/J.DDMEC.2012.10.002 [Accessed: 23rd August 2018]
    3. Chen J, Lipska BK, Halim N, Ma QD, Matsumoto M, Melhem S, et al. Functional analysis of genetic variation in catechol-O-methyltransferase (COMT): effects on mRNA, protein, and enzyme activity in postmortem human brain. American journal of human genetics. [Online] Elsevier; 2004;75(5): 807–821. Available from: doi:10.1086/425589 [Accessed: 23rd August 2018]
    4. Käenmäki M, Tammimäki A, Myöhänen T, Pakarinen K, Amberg C, Karayiorgou M, et al. Quantitative role of COMT in dopamine clearance in the prefrontal cortex of freely moving mice. Journal of Neurochemistry. [Online] Wiley/Blackwell (10.1111); 2010;114(6): 1745–1755. Available from: doi:10.1111/j.1471-4159.2010.06889.x [Accessed: 23rd August 2018]
    5. Lachman HM, Papolos DF, Saito T, Yu YM, Szumlanski CL, Weinshilboum RM. Human catechol-O-methyltransferase pharmacogenetics: description of a functional polymorphism and its potential application to neuropsychiatric disorders. Pharmacogenetics. [Online] 1996;6(3): 243–250. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8807664 [Accessed: 23rd August 2018]
    6. Dawling S, Roodi N, Mernaugh RL, Wang X, Parl FF. Catechol-O-methyltransferase (COMT)-mediated metabolism of catechol estrogens: comparison of wild-type and variant COMT isoforms. Cancer research. [Online] 2001;61(18): 6716–6722. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11559542 [Accessed: 23rd August 2018]
    7. Rosa A, Peralta V, Cuesta MJ, Zarzuela A, Serrano F, Martínez-Larrea A, et al. New Evidence of Association Between COMT Gene and Prefrontal Neurocognitive Function in Healthy Individuals From Sibling Pairs Discordant for Psychosis. American Journal of Psychiatry. [Online] American Psychiatric Publishing; 2004;161(6): 1110–1112. Available from: doi:10.1176/appi.ajp.161.6.1110 [Accessed: 23rd August 2018]
    8. Joober R, Gauthier J, Lal S, Bloom D, Lalonde P, Rouleau G, et al. Catechol-O-methyltransferase Val-108/158-Met gene variants associated with performance on the Wisconsin Card Sorting Test. Archives of general psychiatry. [Online] 2002;59(7): 662–663. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12090821 [Accessed: 24th August 2018]
    9. Malhotra AK, Kestler LJ, Mazzanti C, Bates JA, Goldberg T, Goldman D. A Functional Polymorphism in the COMT Gene and Performance on a Test of Prefrontal Cognition. American Journal of Psychiatry. [Online] American Psychiatric Publishing; 2002;159(4): 652–654. Available from: doi:10.1176/appi.ajp.159.4.652 [Accessed: 24th August 2018]
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    11. Goldberg TE, Egan MF, Gscheidle T, Coppola R, Weickert T, Kolachana BS, et al. Executive Subprocesses in Working Memory. Archives of General Psychiatry. [Online] 2003;60(9): 889. Available from: doi:10.1001/archpsyc.60.9.889 [Accessed: 24th August 2018]
    12. Bruder GE, Keilp JG, Xu H, Shikhman M, Schori E, Gorman JM, et al. Catechol-O-Methyltransferase (COMT) Genotypes and Working Memory: Associations with Differing Cognitive Operations. Biological Psychiatry. [Online] 2005;58(11): 901–907. Available from: doi:10.1016/j.biopsych.2005.05.010 [Accessed: 24th August 2018]
    13. Aguilera M, Barrantes-Vidal N, Arias B, Moya J, Villa H, Ibáñez MI, et al. Putative role of the COMT gene polymorphism (Val158Met) on verbal working memory functioning in a healthy population. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. [Online] 2008;147B(6): 898–902. Available from: doi:10.1002/ajmg.b.30705 [Accessed: 24th August 2018]
    14. Costa D de S, de Paula JJ, Alvim-Soares AM, Pereira PA, Malloy-Diniz LF, Rodrigues LOC, et al. COMT Val(158)Met Polymorphism Is Associated with Verbal Working Memory in Neurofibromatosis Type 1. Frontiers in human neuroscience. [Online] Frontiers Media SA; 2016;10: 334. Available from: doi:10.3389/fnhum.2016.00334 [Accessed: 24th August 2018]
    15. Egan MF, Goldberg TE, Kolachana BS, Callicott JH, Mazzanti CM, Straub RE, et al. Effect of COMT Val 108/158 Met genotype on frontal lobe function and risk for schizophrenia. [Online] 2001 [Accessed: 30th August 2018]. Available from: www.pnas.orgcgidoi10.1073pnas.111134598 [Accessed: 30th August 2018]
    16. Stein DJ, Newman TK, Savitz J, Ramesar R. Warriors versus worriers: the role of COMT gene variants. CNS spectrums. [Online] 2006;11(10): 745–748. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17008817 [Accessed: 29th August 2018]
    17. Oswald LM, McCaul M, Choi L, Yang X, Wand GS. Catechol-O-methyltransferase polymorphism alters hypothalamic-pituitary-adrenal axis responses to naloxone: a preliminary report. Biological Psychiatry. [Online] Elsevier; 2004;55(1): 102–105. Available from: doi:10.1016/j.biopsych.2003.07.003 [Accessed: 30th August 2018]
    18. Hernaus D, Collip D, Lataster J, Ceccarini J, Kenis G, Booij L, et al. COMT Val158Met Genotype Selectively Alters Prefrontal [18F]Fallypride Displacement and Subjective Feelings of Stress in Response to a Psychosocial Stress Challenge. Le Foll B (ed.) PLoS ONE. [Online] Public Library of Science; 2013;8(6): e65662. Available from: doi:10.1371/journal.pone.0065662 [Accessed: 30th August 2018]
    19. Collip D, van Winkel R, Peerbooms O, Lataster T, Thewissen V, Lardinois M, et al. COMT Val158Met-Stress Interaction in Psychosis: Role of Background Psychosis Risk. CNS Neuroscience & Therapeutics. [Online] Wiley/Blackwell (10.1111); 2011;17(6): 612–619. Available from: doi:10.1111/j.1755-5949.2010.00213.x [Accessed: 30th August 2018]
    20. Walder DJ, Trotman HD, Cubells JF, Brasfield J, Tang Y-L, Walker EF. Catechol-O-methyltransferase modulation of cortisol secretion in psychiatrically at-risk and healthy adolescents. Psychiatric Genetics. [Online] 2010;20(4): 166–170. Available from: doi:10.1097/YPG.0b013e32833a1ff3 [Accessed: 30th August 2018]
    21. Buckert M, Kudielka BM, Reuter M, Fiebacj CJ. The COMT Val158Met polymorphism modulates working memory performance under acute stress. Psychoneuroendocrinology. [Online] Pergamon; 2012;37(11): 1810–1821. Available from: doi:10.1016/J.PSYNEUEN.2012.03.014 [Accessed: 30th August 2018]
    22. Ursini G, Bollati V, Fazio L, Porcelli A, Iacovelli L, Catalani A, et al. Stress-related methylation of the catechol-O-methyltransferase Val 158 allele predicts human prefrontal cognition and activity. The Journal of neuroscience : the official journal of the Society for Neuroscience. [Online] Society for Neuroscience; 2011;31(18): 6692–6698. Available from: doi:10.1523/JNEUROSCI.6631-10.2011 [Accessed: 30th August 2018]
    23. James SJ, Cutler P, Melnyk S, Jernigan S, Janak L, Gaylor DW, et al. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism 1 , 2. The American Journal of Clinical Nutrition. 2004;80(1): 1611–1617.
    24. Zhou J. Norepinephrine transporter inhibitors and their therapeutic potential. Drugs of the Future. [Online] 2004;29(12): 1235–1244. Available from: doi:10.1358/dof.2004.029.12.855246
    25. Jabbi M, Korf J, Kema IP, Hartman C, van der Pompe G, Minderaa RB, et al. Convergent genetic modulation of the endocrine stress response involves polymorphic variations of 5-HTT, COMT and MAOA. Molecular Psychiatry. [Online] Nature Publishing Group; 2007;12(5): 483–490. Available from: doi:10.1038/sj.mp.4001975 [Accessed: 29th August 2018]
    26. Zannas AS, McQuoid DR, Steffens DC, Chrousos GP, Taylor WD. Stressful life events, perceived stress, and 12-month course of geriatric depression: Direct effects and moderation by the 5-HTTLPR and COMT Val158Met polymorphisms. Stress. [Online] Taylor & Francis; 2012;15(4): 425–434. Available from: doi:10.3109/10253890.2011.634263 [Accessed: 30th August 2018]

    The post Research update: COMT val158Met rs4680 appeared first on myDNAhealth.

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