Feed your genes: how our genes respond to the food we eat

What should I eat?

‘Have you ever wondered why some people can eat a high fat diet and have no problem with cholesterol, or why others can have an after-dinner espresso and not be kept awake all night?’

Nutrigenomics is an emerging science which investigates how the foods we eat interact with our genes, to affect our health. The human genome project was completed in 2003 and enabled us for the first time, to read nature’s complete genetic blueprint for building a human being.  As humans, we are 99.9% genetically identical to each other, but we vary slightly due to variations in certain genes.1,2 These are sometimes called gene mutations or SNPs (pronounced as ‘snips’ and an abbreviation for single nucleotide polymorphism, meaning that a tiny part of the DNA pattern differs from one variation of a gene to another).   Have you ever wondered why some people can eat a high fat diet and have no problem with cholesterol, or why others can have an after-dinner espresso and not be kept awake all night?  Due to these common variations in genes, we are beginning to understand how individuals respond differently to dietary intake, medication, or lifestyle factors such as stress, toxic exposure and exercise.

How can our genes determine our responses to the food we eat?

The goal of the human genome project was to provide researchers with powerful tools to understand the genetic factors in human disease. The field of nutrigenomics is showing us how nutrients and bioactive components in food can ‘switch on or off’ certain genes, which then impact on important metabolic and physiological processes in the body, such as detoxification and energy production. A significant example is sulforaphane, a compound produced through digestion of cruciferous vegetables, particularly broccoli and broccoli sprouts. Sulforaphane upregulates, or ‘switches on’ a variety of genes that give the body instructions to make proteins which protect cells from damage: in other words, it contributes to switching on our internal defence and ‘spring cleaning’ mechanisms. In this way, sulforaphane has been shown to be involved in inhibiting inflammation, cancer development and the build-up of toxins which can damage cells and lead to disease development. 3-5

How do we send messages to our cells?

Each of our ≃21,000 genes6 provide messages that instruct your body to make a specific protein (these proteins are involved in creating and maintaining your functioning body).  When genes switch on and send a message to cells, it is called ‘gene expression.’ For example, when we digest carbohydrate such as rice, it is converted to glucose and absorbed into our bloodstream.  The INS gene is expressed, or ‘switched on’ and sends a coded message to the pancreas, telling it to produce a certain amount of the protein hormone insulin.  Insulin directs the glucose out of the blood and into body cells, to be turned into energy.  Once blood glucose levels return to normal, the INS gene is switched off and the pancreas stops producing insulin.  Mutations in this gene cause an error in communication with the pancreas and have been linked to diabetes in newborns.7

‘…we need to be cautious of media hype, whereby one day coffee is ‘good’ for us and another day ‘bad,’ because the way that each individual responds to something like caffeine can vary so drastically…’

Certain genes can affect the rate that we break down, use and get rid of almost everything we consume.  Taking caffeine as an example, the gene which instructs how caffeine is broken down in the liver is CYP1A2.  Individuals with what is referred to as a ‘fast’ version of the CYP1A2 gene can metabolise (break down) and excrete caffeine quickly, while those with a slower version cannot.8  It is also interesting that the gene is more active in men than women and that it is inhibited by taking the contraceptive pill.9 This type of information becomes more useful when used as part of larger studies, such as those which show that fast metabolisers of caffeine have a lower risk of heart attack when increasing consumption of caffeinated coffee. This may have nothing to do with the caffeine, but could be that having quickly removed the caffeine from their body, they are able to make better use of the heart-protective compounds in the coffee. 10 Other studies have shown that slow metabolisers of caffeine are more likely to experience high blood pressure, as the caffeine has a prolonged stimulatory effect on their adrenal system. 11 This is where we need to be cautious of media hype, whereby one day coffee is ‘good’ for us and another day ‘bad,’ because the way that each individual responds to something like caffeine can vary so drastically and can be linked back to their individual genetic profile.  Indeed, where many studies show conflicting results, it is worth bearing in mind that they might not have accounted for genetic influence.

How can I apply nutrigenomics to my everyday diet?

Fish oil is a much-confused subject, which receives frequent media attention.  A few studies have now shown that people who have a particular version of the PPARϒ gene respond much better to the blood lipid-lowering effect of fish oils (polyunsaturated fats), with subsequent reduction in risk of heart disease.12 Individuals with other variations of the PPARϒ gene fare better when monounsaturated fats (e.g. olive oil, coconut oil) are consumed in greater quantities.13 We also know that zinc is a vital component of PPARϒ gene expression14 and that alcohol inhibits the gene, so by understanding which version of the gene we inherited, we are able to take a proactive approach to managing the risk of weight gain, type 2 diabetes and alcohol-associated breast cancer, which are linked with certain variations of the PPARϒ gene. For example, we can adjust the ratios of the types of fats we eat, understanding that while oily fish, avocado and sunflower seeds are all generally accepted to be healthy foods, that more of one and less of another may be more beneficial to us as an individual, depending on which variation of the PPARϒ gene we have. We can also monitor our zinc levels, adjusting diet or supplements in a more targeted way and can make more informed decisions about our alcohol intake.


Enabling a more personalised supplementation programme

…the methylation process is critical to overall health…’

Folic acid is a synthetic (chemically man-made) form of vitamin B9, which is used in many supplements and fortified foods including wheat flour and breakfast cereals, while folate is the natural form of vitamin B9, found in green leafy vegetables such as broccoli and spinach. Pregnant women are recommended to supplement 400mcg folic acid daily in their first trimester, to prevent birth defects, however we now know that for some women with a very common genetic mutation, this may not be as beneficial as they would hope. 15,16  Both synthetic folic acid and natural folate need to be converted by the body, through various stages, into an active form of the vitamin B9.  This process requires the MTHFR gene to produce an enzyme called methylenetetrahydrofolate reductase (hence its abbreviation to MTHFR!). It is estimated that 60% of the US population have a mutated variant of this gene, which results in the enzyme activity being less effective i.e. they are less capable of converting folic acid and folate to its active form. This has a knock-on effect on many processes and has been linked to various health issues, including cardiovascular disease; recurrent miscarriage; migraine; mental disorders such as autism, anxiety or depression; and digestive problems such as IBS.

It is important to note that not everyone with the MTHFR mutation will experience associated health issues, but the methylation process is so critical to overall health, that it is very useful to know which variant of the gene you were born with.  Those with mutated variants can be guided towards making better choices of activated B vitamin supplements and to keeping a closer eye on certain blood markers such as vitamin B12, cholesterol and homocysteine, which are affected by inefficient conversion of dietary folate or supplemental folic acid to its active form.

Supporting a targeted exercise and weight management regime

‘…some genetic profiles respond better to aerobic exercise and are able to burn fat efficiently, while others are so predisposed to inflammation, that they may achieve much better results with less intense exercise…’

Do you spend hours at the gym, but can’t seem to shift weight, or do you experience delayed onset muscle soreness after exercise? The reasons may lie in your genes and by knowing which of your genes influence inflammation and fat storage, for example, you can make better choices about the way you exercise.  Studies show that some genetic profiles respond better to aerobic exercise and are able to burn fat efficiently,17 while others are so predisposed to inflammation, that they may achieve much better results with less intense exercise, focusing on resistance training,18 combined with active recovery sessions, such as gentle walking or cycling.  For some people, seeing their genetic profile can be a light bulb moment, as they gain a clearer picture of some of the reasons behind their difficulty to lose weight or regulate appetite and understand their risk of obesity (including childhood obesity) or diabetes. When this information is presented alongside the scientific research to support which measures can be taken to influence specific genes, it provides actionable areas to target, in terms of diet, lifestyle supplements and exercise.

Knowledge is power

It is important to understand that we cannot change the genes that we were born with, however, we can influence the way that they express themselves (switch on and off) and impact on our health. Good health is determined by healthy cells.  We constantly replace most of the cells in our body and can choose to optimise cell function by sending messages through the food we eat and lifestyle choices that we make, such as smoking, stress management and physical exercise.

A genetic test and in-depth analysis can help you to understand which foods will benefit you the most, which nutritional supplements could enhance your wellbeing and which type of exercise will have a positive effect on your health. Rather than trying to work out which of the latest scientific research is relevant to you, this can take out some of the guesswork and enable you to optimise your health with a truly personalised plan.  If you eat healthily and exercise regularly, but cannot shift weight, understanding your genetic profile could help to target your diet and exercise regime.  If you have a history of heart disease, cancer, diabetes or other major diseases in your family and would like to better understand your risk and then take a more-informed, proactive approach to your health, this is a test for you.

On a personal note

Having completed a FitGenes profile myself, I am now aware of the health issues to which I am more predisposed.  While I currently enjoy excellent health, I feel empowered knowing which of those potential health issues to focus on and I have already made changes to what I previously believed to be extremely healthy diet and exercise patterns.  I have always known that lack of sleep through my twenties (work hard, play hard decade) and thirties (kittens and babies, plus work hard and much less play hard decade) was in no way beneficial to my health, I now appreciate just what a priority I need to make sleep as I start my forties decade! I have made further tweaks to my diet, changed the supplements I take and altered my exercise routine.  Rather than taking my current state of good health for granted, I am taking proactive steps to monitor and manage my areas of risk, for example, undertaking further diagnostic tests such as a complete hormone profile and keeping a closer eye on markers of inflammation.  My biggest challenge is to improve the quality of my sleep, which like so many people, is all too often pushed down the priority list, in an attempt to gain more hours in the day.

I would encourage you to take a proactive approach to your health – whether you are hoping to conceive a child (yes, you too dads-to-be, it takes two sets of genes to make a baby); determined to optimise your exercise training; attempting to reduce or manage risk of family diseases; or simply wanting to age healthily. Please see here for further details of what a FitGenes test involves and contact me if you have any questions. To quote Dr Paul Beaver, co- founder of FitGenes, ‘your genes are not your destiny!’


View List of References

    1. National Human Genome Research Institute Presentation (2008) Human Genetic Variation. [Online] National Human Genome Research Institute (www.genome.gov/pages/education/modules/geneticvariation.pdf)
    2. Bethedsa (2007) Understanding Human Genetic Variation. National Institutes of Health (US) Curriculum Supplement Series. [Online] National Center for Biotechnology Information (www.ncbi.nlm.nih.gov).
    3. Tortorella S M, Royce S G, Licciardi P V, Karagiannis T C (2015) Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition. Antioxidants and Redox Signalling, 22 (16): 1382-1424. [Online] PubMed Central (www.ncbi.nlm.nih.gov/pmc).
    4. Guerrero-Beltran C E, Calderon-Oliver M, Pedraza-Chaverri J, Chirino Y I (2012) Protective effect of sulforaphane against oxidative stress: recent advances. Experimental and Toxicologic Pathology, 64 (5): 503-508. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
    5. Yang L, Palliyaguru D L, Kensler T W (2016) Frugal Chemoprevention: Targeting Nrf2 with Foods Rich in Sulforaphane. Seminars in Oncology, 43 (1): 146-153. [Online] Seminars in Oncology (www.seminoncol.org).
    6. Frazer K A (2012) Decoding the human genome. Genome Research, 22: 1599-1601. [Online] Genome Research (www. genome.cshlp.org).
    7. Edghill E L et al. (2008) Mutations in the INS Gene Are a Common Cause of Neonatal Diabetes but a Rare Cause of Diabetes Diagnosed in Childhood or Adulthood. Diabetes Journals, 57 (4): 1034-1042. [Online] Diabetes Journals (www. diabetes.diabetesjournals.org).
    8. Cornelis M C, El-Sohemy A, Kabagambe E K, Campos A H (2006) Coffee, CYP1A2 Genotype, and Risk of Myocardial Infarction. Journal of the American Medical Association, 295(10): 1135-1141. [Online] The JAMA Network (www.jamanetwork.com).
    9. Rasmussen B B, Brix T H, Kyvik K O, Brosen K (2002) The interindividual differences in the 3-demthylation of caffeine alias CYP1A2 is determined by both genetic and environmental factors. Pharmacogenetics, 12 (6): 473-478. [Online] Pharmacogenetics and Genomics (www.journals.lww.com/jpharmacogenetics).
    10. Butt M S & Sultan M T (2011) Coffee and its Consumption: Benefits and Risks. Critical Reviews In Food Science And Nutrition, 51 (4). [Online] Taylor & Francis Online (www.tandfonline.com).
    11. Palatini P, Ceolotto G, Ragazzo F, Dorigatti F, Saladini F, Papparella I, Mos L, Zanata G, Santonastaso M (2009) CYP1A2 genotype modifies the association between coffee intake and the risk of hypertension. Journal of Hypertension, 27 (8): 1594-1601. [Online] Journal of Hypertension (www.journals.lww.com/jhypertension).
    12. Lindi V, Schwab U, Louheranta A, Laakso M, Vessby B, Hermansen K, Storlien L, Riccardi G, Rivellese A (2003) Impact of the Pro12Ala polymorphism of the PPAR-gamma2 gene on serum triacylglycerol response to n-3 fatty acid supplementation. Molecular Genetics & Metabolism, 79 (1): 52-60. [Online] PubMed (www.ncbi.nlm.nih.gov).
    13. Soriguer F, Morcillo F, Cardona F, Rojo-Martinez G, Almaraz M, Ruiz de Adana M, Olveira G, Tinahones F, Esteva I (2006) The Journal of Nutrition, 136 (9): 2325-2330. [Online] The Journal of Nutrition (www. jn.nutrition.org).
    14. Meerarani P, Reiterer G, Toborek M, Hennig B (2003) Zinc modulates PPARgamma signaling and activation of porcine endothelial cells. Journal of Nutrition 133 (10): 3058-64. [Online] PubMed (www.ncbi.nlm.nih.gov).
    15. Greenberg J A, Bell S J, Guan Y, Yu Y-H (2011) Folic Acid Supplementation and Pregnancy: More Than Just Neural Tube Defect Prevention. Reviews in Obstetrics and Gynaecology, 4 (2): 52-59. [Online] PubMed Central (www.ncbi.nlm.nih.gov/pmc).
    16. Scholl T O & Johnson W G (2000) Folic acid: influence on the outcome of pregnancy. American Journal of Clinical Nutrition, 71 (5): 1295s-1303s. [Online] American Journal of Clinical Nutrition (ajcn.nutrition.org).
    17. Macho-Azcarate T, Calabuig J, Marti A, Martinez J A (2002) A maximal effort trial in obese women carrying the β2-adrenoceptor Gln27Glu polymorphism. Journal of Physiology and Biochemistry, 58 (2): 103-108. [Online] SpringerLink (www.link.springer.com).
    18. Yao, L, Delmonico M J, Roth S M, Hand B D, Johns J, Conway J, Douglass L, Hurley B F (2007) Adrenergic Receptor Genotype Influence on Midthigh Intermuscular Fat Response to Strength Training in Middle-Aged and Older Adults. Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 62 (6): 658-663. [Online] PubMed Central (www.ncbi.nlm.nih.gov/pmc).

Glutathione: the unsung hero of antioxidants

Glutathione is considered by scientists to be one of most powerful antioxidants, yet remains relatively unknown, compared to other nutrients.  Manufactured in every cell in the body, but produced in large amounts by the liver, glutathione is made from three building blocks of protein, the amino acids cysteine, glycine and glutamine.1,2  At this time of year, when many of us feel more exposed to stress, infection, reduced sleep, alcohol and other toxins, due to end of year events and Christmas parties, it is interesting to understand how nutrients such as glutathione are working away in the background to protect us from the damage these factors can cause.

Glutathione is one of the key nutrients found in many green vegetables, which can help to speed up phase II detoxification in the liver.6

The liver processes a wide variety of potentially harmful substances, including alcohol, steroid hormones, medication and toxic metals, in two stages, known as phase I and phase II detoxification.3 Most chemicals, either produced by the body or to which we are exposed through our diet and environment, first undergo phase I detoxification, which produces highly reactive and carcinogenic by-products.  In other words, the products our body is trying to eliminate, are temporarily converted into substances which are potentially even more harmful than they were originally. These by-products are then further processed in phase II and rendered less harmful, into a state in which they can be removed from the body, excreted in bile and urine.

liverThe timing of these processes in the liver is critical and if phase I reactions happen too fast for phase II to deal with the toxic by-products, they can promote the development of cancer.4 For example, cigarette smoke speeds up phase I, which can lead to a build-up of highly toxic substances waiting to be removed via phase II.  Meanwhile, the beneficial properties of broccoli and other cruciferous vegetables help to speed up phase II detoxification and thereby contribute to cancer prevention.5 Glutathione is one of the key nutrients found in many green vegetables, which can help to speed up phase II detoxification in the liver.6

Our ability to protect our body against major disease such as cancer or heart disease is closely related to the balance between our exposure to harmful free radicals and our intake of protective antioxidant nutrients.3 To explain this in more detail, we need to understand that oxygen underpins all plant and animal life and is required by every human cell to release energy from food, which subsequently drives all our body functions.  However, oxygen is chemically reactive, highly unstable and can oxidise other molecules, meaning that it steals part of other atoms and compounds.  Classic examples are rusty iron and browned fruit, whereby oxygen has stolen an electron, the outer part of the iron or fruit atoms and the resulting oxidation reaction causes the original compounds to be damaged. Now imagine that this is going on inside you!  Free radical is another name for a damaged atom or group of atoms, which has a missing electron and ‘attacks’ neighbouring atoms, in an attempt to steal an electron back.  This in turn damages the neighbouring atom and the cycle continues.

…damage caused to body cells by free radicals triggers inflammation, cancer, arterial damage and ageing.2,8

Free radicals are produced by all combustion processes which involve oxygen, such as smoking, the burning of petrol to create exhaust fumes; frying or barbecuing food; radiation (including sunlight); and even by many normal body processes such as converting food to energy, or exercising.7 Collectively, we refer to these damaging factors as oxidative stress and the damage caused to body cells by free radicals triggers inflammation, cancer, arterial damage and ageing.2,8 The liver is an organ which is particularly susceptible to damage caused by oxidative stress.8

sunburn             bbq-meat      exercise

While we can limit our exposure to some free radicals, it is impossible to avoid them completely and therefore the role of antioxidants is crucial for maintaining the balance which promotes good health.  Antioxidant nutrients such as vitamins A, C and E, beta carotene, zinc, selenium and co-enzyme Q10 work as a team to disarm free radicals, by sharing and donating electrons, which then repair the oxidised or damaged free radical and prevent further damage to cells.  Various warning signs indicate that we don’t have the balance right and that our antioxidant intake is insufficient, compared to our level of free radical exposure.  These include recurrent or difficulty in shaking off infections; slow skin healing; excessive wrinkles for your age; or inability to detoxify after exposure to free radicals, such as feeling groggy or achy after exercise, or being exposed to pollution. Do any of these issues sound familiar?electron-donation

This brings us back to glutathione, which works very closely with other antioxidant nutrients such as vitamins A, C and E and in turn is used to produce the body’s most powerful antioxidant enzyme, glutathione peroxidase.  It is this enzyme which enables the liver to protect us from oxidative stress in the form of car exhaust fumes, cigarette smoke, radiation and other carcinogens, infections, excessive alcohol and toxic metals.9  Although it is made in every cell in the body, the liver has the greatest capacity to produce and store glutathione and levels of this important antioxidant are seen to increase significantly when a cell is exposed to oxidative stress.10  So what can we do to assist the production of glutathione? Production requires the amino acids cysteine, glycine and glutamine and therefore ensuring adequate intake of these precursors, or building blocks, along with nutrients to support liver function, is the best approach to promoting adequate glutathione.

Foods to eat:

Sulphur-containing foods which are high in the sulphurous amino acids cysteine and methionine.  Diets low in sulphur-containing amino acids are shown to have a negative impact on glutathione levels.10 Broccoli, kale, cabbage, Brussels sprouts, cauliflower, bok choy, watercress, radish, turnip, onion, garlic, leek, eggs, fish.

Selenium-rich foods. Selenium helps the body to produce and recycle glutathione 4 and is required to make the important antioxidant enzyme glutathione peroxidase.  Brazil nuts, fresh tuna, beef, poultry, egg, spinach, mushrooms, brown rice, chia, flax and sesame seeds.

Brightly coloured fruit and vegetables, plus nuts and seeds which contain vitamins A, C and E.  These work as a team with other antioxidants, to recycle glutathione and prevent cell damage by free radicals. Tomatoes, peppers, melon, pumpkin, butternut squash, sweet potato, spinach, carrots, berries, oranges, kiwi fruit, avocado, almonds, sunflower seeds.

Bone broth is rich in the amino acids glycine and glutamine, which are both required for glutathione production (as well as providing the building blocks to repair damaged cells which line the digestive tract).

Vitamins B6, B12 and folic acid for methylation.  Methylation is a process which occurs more than a billion times per second in every cell of the human body and determines how the cell develops, as well as influencing our overall health.11 Among many other functions, the process of methylation regulates the use of sulphur-containing substances in the body, which includes glutathione.  The specific B vitamins needed for methylation are found in beans, chickpeas, lentils, black eyed peas, asparagus, spinach, broccoli, avocado, nuts, nutritional yeast, poultry and organ meat such as beef liver.

Supplement silymarin, which is extracted from seeds of the milk thistle plant.  Silymarin has been shown to regulate the availability of sulphur-containing amino acids such as cysteine in the liver, thus ensuring that adequate levels are accessible for the liver to produce glutathione. 4, 8


Aside from its antioxidant mechanisms, glutathione plays other roles in the body, as it supports our immune system in various ways; links together with drugs to aid their removal from the body; assists with the creation of new proteins12; protects us from environmental toxins; and is involved in the process of apoptosis, or programmed cell death, of cancer cells.13

Some scientists speculate that glutathione status is one of the most important indicators of health, having studied how levels decline as we age and drop significantly in patients with various diseases.14 The good news is that it is simple to help our body maintain production of this vital but unacclaimed antioxidant, by eating the foods outlined above and by supporting our precious liver, which bears the load of glutathione production.  So give a little love to your liver:  go easy on the alcohol over the festive season; load your plate with brightly coloured vegetables; sip on bone broth, or use it in soups and gravies; and consider taking a liver support supplement which contains milk thistle, B vitamins and sulphur-containing amino acids such as N-acetyl cysteine or methionine.

View List of References

    1. Shang, Y, Siow Y L, Isaak C K, Karmin O (2016) Downregulation of Glutathione Biosynthesis Contributes to Oxidative Stress and Liver Dysfunction in Acute Kidney Injury. Oxidative Medicine and Cellular Longevity, 2013. [Online] PubMed Central (www.ncbi.nlm.nih.gov/pmc).
    2. Traverso N, Ricciarelli R, Nitti M, Marengo B, Furfaro A L, Pronzato M A, Marinari U M, Domenicotti C (2013) Role of glutathione in cancer progression and chemoresistance. Oxidative Medicine and Cellular Longevity, 2013. [Online] Hindawi Publishing Corporation (www.hindawi.com/journals).
    3. Jamison J (2003) Clinical Guide to Nutrition & Dietary Supplements in Disease Management. Churchill Livingstone, London.
    4. Hodges R E, Minich D M (2015) Modulation of Metabolic Detoxification Pathways Using Foods and Food-Derived Components: A Scientific Review with Clinical Application. Journal of Nutrition and Metabolism, 2015. [Online] Hindawi Publishing Corporation (www.hindawi.com/journals).
    5. Walters D G, Young P J, Agus C, Knize M G, Boobis A R, Gooderham N J, Lake B G (2004) Cruciferous vegetable consumption alters the metabolism of the dietary carcinogen 2-amino-1-methyl-6-phenylimidazol pyridine (PhIP) in humans. Carcinogenesis, 25 (9): 1659–1669. [Online] Carcinogenesis (www.carcin.oxfordjournals.org).
    6. Lampe J W, Chen C, Li S, Prunty J, Grate M T, Meehan D E, Barale K V, Dightman D A, Feng Z, Potter J D (2000) Modulation of Human Glutathione S-Transferases by Botanically Defined Vegetable Diets. Cancer Epidemiology, Biomarkers & Prevention, 9 (8). [Online] American Association for Cancer Research Journals (www.cebp.accrjournals.org).
    7. Lobo V, Patil A, Phatak A, Chandra N (2010) Free radicals, antioxidants and functional foods: Impact on human health. Pharmacognosy review, 4 (8): 118-126. [Online] PubMed Central (www.ncbi.nlm.nih.gov/pmc).
    8. Kim S H, Oh D S, Oh J Y, Son T G, Yuk D Y, Jung Y S (2016) Silymarin Prevents Restraint Stress-Induced Acute Liver Injury by Ameliorating Oxidative Stress and Reducing Inflammatory Response. Molecules, 21 (4): 443. [Online] Multidisciplinary Digital Publishing Institute (www.mdpi.com).
    9. Lubos E, Loscalzo J, Handy D E (2011) Glutathione Peroxidase-1 in Health and Disease: From Molecular Mechanisms to Therapeutic Opportunities. Antioxidants & Redox Signaling, 15 (7): 1957-1997. [Online] PubMed Central (www.ncbi.nlm.nih.gov/pmc).
    10. Taniguchi M, Mori N, Iramina C, Yasutake A (2016) Elevation of Glucose 6-Phosphate Dehydrogenase Activity Induced by Amplified Insulin Response in Low Glutathione Levels in Rat Liver. Scientific World Journal, 2016. [Online] PubMed Central (www.ncbi.nlm.nih.gov/pmc).
    11. Crider K S, Yang T P, Berry R J, Bailey L B (2012) Folate and DNA Methylation: A Review of Molecular Mechanisms and the Evidence for Folate’s Role. Advances in Nutrition, 3: 21-38. [Online] Advances in Nutrition (www. advances.nutrition.org).
    12. Glutathione compound. Open chemistry database. [Online] (https://pubchem.ncbi.nlm.nih.gov/compound/124886?from=summary#section=Top)
    13. Franco R, Cidlowski J A (2009) Apoptosis and glutathione: beyond an antioxidant. Cell Death and Differentiation, 16: 1303–1314. [Online] Cell Death and Differentiation (http://www.nature.com/cdd/journal).
    14. Kharb S, Singh V, Ghalaut P S, Sharma A, Singh G P (2000) Glutathione levels in health and sickness. Indian Journal of Medical Science, 54 (2): 52-54. [Online] PubMed Central (www.ncbi.nlm.nih.gov/pmc).


Cholesterol: friend or foe?

Cholesterol plays a variety of essential roles in the body, yet receives a very bad press for contributing to heart disease, while cholesterol-lowering statin medications continue to be heavily prescribed worldwide.  Our body produces much more cholesterol than we consume through our diet, so what else is causing the problem?

Types of cholesterol-containing ‘vehicles’

Cholesterol is a waxy, fatty substance produced primarily by the liver and just as oil and water do not mix, neither do waxy cholesterol and watery blood, so cholesterol needs a protective vehicle to surround it and carry it around the body.  One of the most important vehicles is low-density lipoprotein (LDL) which transports cholesterol to various cells in the body.  Here, cholesterol contributes to the function of cell membranes, including brain cell communication and is also converted to vitamin D and steroid hormones such as cortisol and testosterone.  High-density lipoprotein (HDL), another type of transport carrier, removes cholesterol from the blood and takes it back to the liver, to be broken down and excreted in bile.

The liver and digestive system work together to achieve cholesterol balance. 1   If too much or too little cholesterol is built into the membrane of cells, they are unable to function properly and there is an ongoing requirement for cholesterol to be added or removed accordingly.  Only the liver can break down cholesterol, therefore it is always important to nutritionally support liver function in individuals with elevated cholesterol.

Cholesterol and heart disease

clogged-artery-with-platelets-and-cholesterol-plaqueHDL and LDL cholesterol are commonly classified as ‘good’ and ‘bad’ respectively and analysis of blood test results tends to focus around this theme.  However, we also need to consider the sub- types of cholesterol, as the size of lipoprotein carrier particle is important and when it comes to LDL or HDL, bigger is better.  Small, dense LDL cholesterol particles are more likely to attach to the lining of blood vessels, where they can become damaged (oxidised) and contribute to the build up of plaque, which hardens and narrows the arteries which lead to the heart. 2

The risk of developing coronary artery disease is three times greater if levels of small, dense LDL are elevated, 2  while larger, more buoyant HDL particles are associated with reduced risk of cardiovascular disease. 3   Just as we need to consider the size and number of LDL particles, more recent research is highlighting the need to understand that HDL is an important vehicle for carrying various types of cargo around the body, not just cholesterol and in fact, it might be that these other functions are more relevant to our health. 4  For example, HDL vehicles carry fat-soluble vitamins A, D, E and K around the body, of which vitamin E is a potent anti-oxidant and heart-protective vitamin. It also transports coq10coenzyme Q10 (CoQ10), a hormone-like nutrient which is essential for energy production in cells;  particularly important for the function of heart cells;  and is involved in managing blood pressure. 4   CoQ10 is widely overlooked, but should always be considered in relation to the prescription of statin medications, because by blocking production of cholesterol, statins also block production of this very important nutrient and it is advisable to take CoQ10 in supplement form alongside these drugs. Common symptoms of CoQ10 depletion are muscle pain and weakness, which by no coincidence, are two of the most commonly reported side effects of statin medication.

How can we influence our balance of LDL and HDL cholesterol?

Dietary cholesterol intake

Cholesterol is produced by the body at a rate of up to 1.4g per day, while dietary intake (from cholesterol-containing foods such as offal, meat, seafood, egg yolks and dairy products) makes up around 0.4g per day. 1  Therefore, while we should of course be careful of the type of food we are eating, we need to think about it in the wider context of how the food we eat affects our digestive and liver function, because it is these organs that have a much greater influence on our cholesterol levels than dietary intake of cholesterol.  It is increasingly understood that individuals respond differently to dietary cholesterol, with around 25% of the population being classfied as ‘over-responders’ and for whom blood cholesterol levels spike disproportionately in response to dietary cholesterol. 3  However, there are many other factors which affect both the quantity and quality of cholesterol in the body, including genetics, stress, fitness levels and age.

Saturated fat intake

There is ongoing research and debate into whether saturated fat intake is directly linked to cardiovascular disease, with the hypothesis that this type of fat raises levels of LDL cholesterol. When we look into the detail, studies have shown that increased levels of saturated fat in the diet do indeed increase LDL cholesterol, but that this is made up of mostly the larger, more buoyant LDL particles, which are less likely to have a damaging effect on arteries than small dense LDL. 5

What has become clear, is that the results of studies into low saturated fat diets are greatly influenced by what types of food the saturated fat is replaced with and so we come to the crux of the issue.  If saturated fat is replaced by polyunsaturated fats (such as the omega 3 fats found in oily fish and certain nuts and seeds), or monounsaturated fats (found in olives and avocado), it can lower both LDL and HDL cholesterol. 6  However, by replacing the calories from saturated fat with carbohydates (particularly refined carbohydrates such as sugar, white flour and white rice), it can lead to a worse cardiovascular profile, with high triglycerides, more small LDL particles and lower levels of HDL cholesterol. 6,7

Food label sugar

Carbohydrate intake

When we consume carbohydrates, it triggers the pancreas to produce insulin, which directs glucose out of the blood stream and into cells, to be converted to energy.  Excess carbohydrate in the diet leads to excess glucose in the blood and can lead to cells becoming unresponsive to insulin, something we call insulin resistance.  Insulin resistance is implicated in the development of both diabetes and obesity and patients of these diseases are more likely to have higher levels of harmful small, dense LDL cholesterol. 2,8  Throughout several studies in which weight loss was induced by very-low-carbohydrate diets, it was observed that LDL cholesterol concentrations did not increase despite the high intakes of saturated fat on these diets. 5,6   This is important to clarify, as carbohydrates fall under several different brackets.  Refined carbohydrates, which elicit a high insulin response, are found to increase the level of small, dense LDL, while a high fibre diet is understood to have positive effects on cholesterol levels. 7,9

Heart health

While elevated cholesterol is obviously a concern that needs to be addressed, it is rather simplistic to focus solely on reducing LDL and increasing HDL using statin medication, as a preventative approach to heart disease.  Cardiovascular disease is complex, can develop over time and there are many other factors to consider with regard to the role cholesterol plays in its development,  particularly the balance of fats and types of carbohydrate in the diet.  At the other end of the reference range, low cholesterol is linked to stroke, depression and suicide, therefore it seems that there is a very narrow band which respresents a healthy cholesterol level. 10,11

Another area which is often overlooked, is thyroid function.  If you have a persistently high cholesterol level but eat a healthy diet, you may have an underactive thyroid.  Hypothyroidism decreases the speed at which your body uses fats, protein and carbohydrate and cholesterol and triglyceride levels may be increased with even mild hypothyroidism. 12,13

So what should I eat to maintain healthy cholesterol levels?

As always, you should focus on eating a diet that is rich in plant foods, with plenty of antioxidant-rich vegetables, herbs and spices.  Oily fish, nuts, seeds, avocado and olive oil are sources of the beneficial fats which help to balance cholesterol levels.  Choose your animal protein carefully, as the amount of cholesterol and saturated fat contained in meat is dependent on what the animal was fed.  Grass-fed animals tend to have a more beneficial fat profile, while meat from grain-fed animals is higher in saturated fat and cholesterol.  Eggs contain cholesterol but also choline, which helps to break down the cholesterol and they are a great source of protein, so enjoy them daily if you wish, but don’t fry them, as the fats the contain are easily damaged by oxidation.  Eat plenty of soluble fibre, found in oats, lentils, apples and most vegetables and keep refined carbohydrates and stimulants such as alcohol, caffeine and tobacco, which directly affect glucose levels, to an absolute minimum.

View List of References

    1. 1. Cohen D E (2008) Balancing Cholesterol Synthesis and Absorption in the Gastrointestinal Tract. The Journal of Clinical Lipidology, 2 (2): S1-S3. [Online] Pub Med Central (http://www.ncbi.nlm.nih.gov/pmc).2. Berneis K K, Krauss R M (2002) Metabolic origins and clinical significance of LDL heterogeneity.  The Journal of Lipid Research, 43: 1363-1379. [Online] The Journal of Lipid Research (http://www.jlr.org).3. Kontush A (2015) HDL particle number and size as predictors of cardiovascular disease.  Frontiers in Pharmacology, 6: 218. [Online] Pub Med Central (http://www.ncbi.nlm.nih.gov/pmc).4. Vickers K C, Remaley A T (2014) Thematic Review Series: High Density Lipoprotein Structure, Function, and Metabolism. The Journal of Lipid Research, 55 (1): 4-12. [Online] Pub Med Central (http://www.ncbi.nlm.nih.gov/pmc).5. Krauss R M, Blanche P J, Rawlings R S, Fernstrom H S, Williams P T (2006) Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. The American Journal of Clinical Nutrition, 83 (5): 1025-1031. [Online] The American Journal of Clinical Nutrition (http://ajcn.nutrition.org).6. Siri-Tarino P W, Sun Q, Hu F B, Krauss R M (2010) Saturated fat, carbohydrate, and cardiovascular disease. The American Journal of Clinical Nutrition, 91 (3): 502-509. [Online] Pub Med Central (http://www.ncbi.nlm.nih.gov/pmc).

      7. Parks E J, Hellerstein M K (2000) Carbohydrate-induced hypertriacylglycerolemia: historical perspective and review of biological mechanisms. The American Journal of Clinical Nutrition, 71 (2): 412-433. [Online] The American Journal of Clinical Nutrition (http://ajcn.nutrition.org).

      8. Siri P W, Krauss R M (2005) Influence of dietary carbohydrate and fat on LDL and HDL particle distributions. Current Atherosclerosis Reports, 7 (6): 455-459. [Online] Pub Med Central (http://www.ncbi.nlm.nih.gov/pmc).

      9. Harland J I (2012) Food combinations for cholesterol lowering. Nutrition Research Reviews, 25 (2): 249-266. [Online] Cambridge Journals (http://journals.cambridge.org).

      10. Holford P (2004) New Optimum Nutrition Bible, Piatkus Books Ltd, London

      11. Sansone R A (2008) Cholesterol Quandaries: Relationship to Depression and the Suicidal Experience. Psychiatry, 5 (3): 22-34. [Online] Pub Med Central (http://www.ncbi.nlm.nih.gov/pmc).

      12. Barona J, Fernandez M L (2012) Dietary Cholesterol Affects Plasma Lipid Levels, the Intravascular Processing of Lipoproteins and Reverse Cholesterol Transport without Increasing the Risk for Heart Disease. The Journal of Diabetes and Endocrinology, 3 (5): 57-69. [Online] Academic Journals (http://www.academicjournals.org).

      13. Rizos C V, Elisaf M S, Liberopoulos E N (2008) Effects of Thyroid Dysfunction on Lipid Profile. The Open Cardiovascular Medical Journal, 5: 76-84. [Online] Pub Med Central (http://www.ncbi.nlm.nih.gov/pmc).

Shape-shifting Candida albicans: yeast, fungus, or both?

What is Candida albicans and what causes an overgrowth?

Candida albicans is one of a variety of Candida species of yeasts which are found naturally in the human digestive and genitourinary tracts, mouth and skin 1, 2 and is one of the only types of fungal organism to cause disease in humans.2  When confined to specific sites within the body, in limited numbers and in a non-pathogenic (non-harmful) form, Candida albicans can thrive and presents no problems to its host. However, if the yeast establishes itself in other parts of the body, or alters its structure to become a more harmful fungal form, the human body launches an immune response in an attempt to attack and destroy the yeast cells.  Certain factors which disrupt the natural balance of bacteria in the digestive or genitourinary tracts may lead to an immune response to Candida, triggering production of anti-Candida antibodies.  Overgrowth of Candida can be caused by regular use of antibiotics, oral contraceptives or corticosteroids; stress; infection; high sugar and starch diets; and chlorinated water – essentially anything which suppresses the immune system or inhibits the growth of beneficial gut bacteria, both of which usually maintain Candida albicans at manageable levels. 1,3


How can Candida albicans be harmful?

‘Candida albicans is naturally present in both men and women and an overgrowth can lead to health issues of varying degrees of severity.’

When the immune system is compromised and particularly after antibiotic use, when levels of beneficial bacteria are diminished, Candida cells can proliferate rapidly and may also change from a yeast form to a fungal form, developing hyphae, or threadlike filaments which help them to adhere to the lining of the gut. 1, 4  If the gut lining is also compromised, the hyphal form of Candida albicans is able to penetrate through this important defence barrier and enter the bloodstream.4  From here, Candida albicans is able to further disrupt the immune system by disintegrating the membrane (outer layer) of certain immune cells.5  The yeast cells release toxic by-products, which can be linked to a wide variety of symptoms including headaches, sinus infection, fatigue, poor concentration, aching joints, thrush, rectal itching, decreased libido, skin complaints such as psoriasis or atopic dermatitis and commonly, a feeling described as ‘brain fog.’  These symptoms are so broad ranging and can easily be attributed to many other health issues, meaning that Candida overgrowth is often overlooked, unless it progresses to the extremely serious condition of invasive Candidiasis, which is a fungal infection of the blood, most often associated with severely immunocompromised and hospitalised patients and which can result in death.3

While the typical symptoms described above are obviously not life threatening, they can reduce quality of life and ongoing damage by Candida albicans hyphae (the fungal form) to the cells lining the digestive tract can lead to any number of other health issues.  It is therefore important to identify and treat a yeast overgrowth, while also considering any other factors which may be contributing to the imbalance of microorganisms in the gut, for example a hormonal imbalance, including pancreatic, thyroid and sex hormones.  Many pregnant women, or those taking the contraceptive pill or HRT find that they are more prone to vaginal or oral Candida infections,6 characterised by white spots on the infected skin cells,7 which is what people often associate with Candida. However, it is important to note that Candida albicans is naturally present in both men and women and an overgrowth can lead to health issues of varying degrees of severity, including localised mucosal infections within the mouth and genitourinary tract; widespread damage to the gastrointestinal system; or systemic invasion which affects the entire body, with the most severe form being a potentially fatal blood infection.7


How do I find out if I have a Candida overgrowth and what can I do about it?

‘The most important approach to treating Candida overgrowth is to boost the immune system…’

There are a few options for testing levels of Candida yeasts.  A blood test can check for the presence of anti-Candida antibodies, indicating both past and current overgrowth; a stool test is useful for showing levels of Candida present in the colon; and a urine organic acids analysis can detect compounds released by Candida yeasts, which are not normally produced by human cells.

The most important approach to treating Candida overgrowth is to boost the immune system: replenishing the beneficial bacteria which usually keep the yeast in check; addressing anything else which could be causing inflammation to the gut lining, such as poor digestion, food intolerances, alcohol or smoking; eating a diet rich in immune supportive nutrients, which enable immune cells to function optimally in their attempt to attack and destroy excessive yeast cells; and managing lifestyle factors which impact on the immune system, such as stress, sleep and chemical exposure.


Various diets are used to try to manage yeast overgrowth, of which the Candida diet is well known and involves the avoidance of sugar, fruit, starchy vegetables, grains, most dairy products, fermented foods, certain nuts, vinegar and processed meats.  I have seen mixed results with this approach, with some clients finding that severe and long-term restriction of carbohydrates reduces symptoms significantly, only for them to reoccur as soon as they re-introduce any kind of simple sugar into their diet.  If this approach is to be followed, it is essential to re-establish beneficial gut bacteria effectively; to use natural anti-fungal agents such as garlic and oregano oil carefully; and to support the repair of the gut lining with specific nutrients.  An alternative approach is to follow a low FODMAP diet, something often recommended to people experiencing digestive issues such as IBS.  FODMAP is an acronym used to describe specific short chain carbohydrates and sugar alcohols that are often poorly digested and subsequently fermented by bacteria in the colon, leading to the production of gas, bloating and pain associated with various digestive issues.   A low FODMAP diet excludes a variety of foods, including certain fruit and vegetables, grains and dairy products. Once again, replenishing beneficial gut bacteria, supporting the immune system and repairing the gut lining are vital parts of this process, with the aim of restoring balance within our delicate internal ecosystem, rather than trying to completely eliminate yeasts from the body.  In this way, the presence of naturally occurring Candida albicans in its yeast form does not need to be a threat to healthy individuals.

View List of References

    1. Corouge M, Loridant S, Fradin C, Salleron J, Damiens S, Moragues M D, Souplet V, Jouault T, Robert R, Dubucquoi S, Sendid B, Colombel J F, Poulain D (2015) Humoral Immunity Links Candida albicans Infection and Celiac Disease. PLoS One, 10 (3) e0121776. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
    2. Nobile C J, Johnson A D (2015) Candida albicans Biofilms and Human Disease. Annual Review of Microbiology, 69: 71-92. [Online] Annual Reviews (http://www.annualreviews.org/).
    3. Pfaller M A, Diekema (2007) Epidemiology of Invasive Candidiasis: a Persistent Public Health Problem. Clinical Microbiology Reviews, 20 (1):133-163. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
    4. Lu Y L, Su C, Liu H (2012) Candida albicans hyphal initiation and elongation. Trends in Microbiology, 22 (12): 707-714. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
    5. Thompson D S, Carlisle P L, Kadosh D (2011) Coevolution of Morphology and Virulence in Candida Species. Eukaryotic Cell, 10 (9): 1173-1182. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
    6. Paul L. Fidel, Jr., Jessica Cutright, and Chad Steele (2007) Effects of Reproductive Hormones on Experimental Vaginal Candidiasis. Infection and Immunity, 68 (2): 651-657. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
    7. Anaul Kabir M, Asif Hussain M, Ahmad Z (2012) Candida albicans: A Model Organism for Studying Fungal Pathogens. ISRN Microbiology, 538694. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).

Hypothyroidism: life with the parking brake on

Hypothyroidism, otherwise known as ‘underactive thyroid’ is one of the most common endocrine diseases, second only to diabetes.1  Symptoms vary widely and include tiredness, weight gain, dry skin, intolerance to cold, constipation, muscle weakness, impaired memory, poor concentration, depression, infertility and even hair loss of the outer third of eyebrows.2, 3  The thyroid acts as both the accelerator and brake pedal in the body and regulates energy and heat production, as well as normal growth, tissue repair and cell development.1

When investigating thyroid dysfunction, it is important to think of the endocrine system as whole, because the production and regulation of thyroid hormones are controlled by the same parts of the brain that manage hormones related to the reproductive system, adrenal health, cell growth and kidney function.  A part of the brain called the hypothalamus works behind the scenes, acting as an interface between the body and its environment, for example responding to temperature or stress.   The hypothalamus sends signals to the pituitary gland at the base of the brain, telling it to pass on instructions to specific organs or cells in the body, including the thyroid gland, to either stimulate or inhibit the release of hormones.  Although the pituitary gland is only the size of a pea, it is also called the ‘master gland’ because it is at the centre of this chain of communication.

Thyroid hormones

Hormones are essentially chemical messengers and the above diagram shows the main hormones involved in thyroid function.   The hypothalamus produces thyrotropin releasing hormone (TRH), which instructs the pituitary gland to release thyroid stimulating hormone (TSH).  TSH travels in the blood to its target organ, the thyroid gland, where it binds to receptors on the outside of the thyroid and causes it to secrete thyroid hormones.

‘…from a large pool of thyroid hormones, only a small number of them do the bulk of the work.’

Thyroid hormones are made from the amino acid tyrosine, joined to atoms of iodine.  They vary according to the number of iodine atoms they are joined to, with the majority of thyroid hormones having 4, hence the name T4, also known as thyroxine.  Molecules with 3 atoms of iodine are referred to as T3 and some T4 is converted to T3 in the liver and kidneys.4   Thyroid hormones are poorly soluble in water and almost 99% of those which are circulating in the blood are attached to carrier proteins.4   The small proportion which are not bound to proteins are called free T3 or free T4 and it is free T3 which plays the most active role in influencing body cells. In other words, from a large pool of thyroid hormones, only a small number of them do the bulk of the work.4

To illustrate how this all works together, imagine a cold winter’s day.  Your hypothalamus detects the drop in temperature and initiates the process through which your body can burn fat or glucose to produce energy and heat.  The hypothalamus sends a signal (TRH) to the pituitary gland, which then releases TSH into the blood, to pass on the message to the thyroid gland to secrete T4.  T4 is converted to T3, the active form of thyroid hormone, which is carried around the body by a carrier protein, then detaches and becomes Free T3, capable of instructing all cells to produce energy.  The process of energy production also releases heat, causing body temperature to rise, so you warm up!Cold hands

A classic symptom of an underactive thyroid is sensitivity to cold, in particular, cold hands and feet.2 A person with an underactive thyroid gland might be receiving signals from the hypothalamus and pituitary to produce thyroid hormones, i.e. they might have high levels of TSH, but there may be some issue further down the chain, whereby the thyroid does not or cannot secrete enough T4.  Even if adequate levels of T4 are being secreted and are available in the blood, the issue could be that this is not being converted to its active form of T3 and so it is very important to test T3 levels, not just T4.  Furthermore, there is another form of T3 called reverse T3 (rT3), which generally serves as the body’s brake pedal, slowing down metabolic processes at the cellular level and subsequently slowing down brain function, heart rate and the rate at which food is converted to energy.5, 6   Therefore, we also need to measure rT3, in case excess levels are causing weight gain, low energy, loss of libido, poor concentration and other symptoms.

So why might this communication breakdown occur?  There are many potential factors involved in primary thyroid failure, including genetics, illness and surgery, such as tonsillectomy which is performed very close the thyroid gland.  Pregnancy can affect thyroid hormones, particularly post-partum and certain medications such as lithium or high doses of corticosteroids can influence the chain of communication.7, 8   In addition, environmental toxins such as chlorine or fluoride, or heavy metals such as mercury and lead can also have a disruptive effect, by blocking the uptake of thyroid hormones into cells.7,9

Auto-immune conditions such as Hashimoto’s thyroiditis are the most common cause of hypothyroidism.1,2,3  Immune cells attack the thyroid gland, causing it to become inflamed and enlarged, sometimes resulting in a visible swelling, or goitre at the front of the neck.    Over time, damage to the thyroid gland can reduce production of thyroid hormones, causing hypothyroidism, but for many people, they are unaware of symptoms for years.  When the immune cells attack the thyroid, antibodies are produced and laboratory tests can check for the presence of these antibodies, to help ascertain the cause of hypothyroidism.  It is not always routine practice to check for anti-thyroid antibodies and yet, someone with normal levels of TSH and T4 may be suffering from Hashimoto’s thyroiditis, so it is well worth requesting this test at the same time as your thyroid hormone test.

Hashimotos goitre

From a nutritional perspective, deficiencies in the nutrients required for the production and uptake of thyroid hormones can affect hormone levels.  Essential fats are required for the uptake of thyroid hormones by cells.4   Tyrosine and iodine are both needed for production of T4, along with vitamins A and C, B vitamins, copper and zinc.4   Iodine is depleted in the soil of many countries, including the UK, Australia and NZ10 and iodine-related goitre is more prevalent in women than men.11   Certain foods are labelled as goitrogenic because they block utilisation of iodine by the body.2  They include raw brassicas such as broccoli, cabbage, kale, cauliflower and Brussels sprouts, plus soya beans, millet and pine nuts.9   At $88 per kilo, I’d advise anyone to go easy on the pine nuts, but don’t be put off eating your greens, as lightly cooking them renders their goitrogenic properties inactive2 and you would have to eat a large quantity of raw brassicas to experience an effect!

‘reverse T3 generally serves as the body’s brake pedal, slowing down metabolic processes at the cellular level and subsequently slowing down brain function, heart rate and the rate at which food is converted to energy.’

LevothyroxineThe conversion process of T4 to T3 in the liver and kidneys also requires copper, zinc and magnesium and may be inhibited by selenium deficiency2, 9  (selenium is also deficient in NZ soil and the NZ population),12 or excess levels of iodine.9   The liver and kidneys need to be functioning well in order to effectuate the conversion, so any compromise, particularly to liver health can be detrimental and is something to consider if you have experienced any digestive problems, which have a knock on effect on the liver.4  Similarly, if adrenal function is suboptimal and levels of the stress hormone cortisol are low, this can have a significant effect on the balance of thyroid hormones, resulting in high levels of TSH, as the brain tries to stimulate production, but T4 production by the thyroid gland is reduced and a greater proportion of whatever T4 is produced, is converted to rT3, the inactive form of T3, which slows down the body’s metabolic processes.  In addition, low levels of cortisol, which are often associated with chronic stress and adrenal insufficiency13 may further inhibit the conversion of T4 to active T3 in the liver and kidneys.

At the top of the chain, there is the possibility that damage to the hypothalamus or pituitary, caused by a tumour, radiation or infection for example, can result in insufficient levels of TSH being produced, which slows down the whole process.

MushroomsAs you can see, there is a lot to consider and it is important to identify where the breakdown in communication has occurred, rather than just fixing the problem by medicating with a synthetic version of thyroid hormone, which is the standard protocol.  Although hypothyroidism is relatively easy to treat from a medical perspective, many studies highlight problems with management of the condition, with under or over-replacement of thyroid hormone each creating its own issues.3,7 Another major issue is that levothyroxine, the most commonly prescribed synthetic thyroid replacement hormone, provides T4 only.  If a patient is unable to convert T4 to T3, then this may not solve the problem and while both natural and synthetic forms of T3 medication are widely available in the US, they are not generally approved or funded in the UK or NZ, which leaves many sufferers feeling no better while taking levothyroxine3, 14   and forces them to source their own alternatives.

“Many patients who present with symptoms of thyroid dysfunction return normal test results.”

SeaweedA vital tool for a correct diagnosis is a comprehensive test, which looks not just at TSH and T4, but also measures free T3, rT3 and also anti-thyroid antibodies.  Many patients who present with symptoms of thyroid dysfunction return normal test results, but in too many cases, budget does not allow for the full range of analytes to be tested and what is called ‘subclinical’ hypothyroidism remains undiagnosed.  There are two important points to note here. Firstly, there is much debate over what constitutes a ‘normal’ thyroid hormone range, given that hormone profiles vary by age, sex and ethnicity, at different trimesters of pregnancy and even at different times of day3, 10, 15.  The current accepted reference range for TSH in the UK and NZ is 0.4 to 4.0, while studies have indicated that 95% of healthy subjects have a TSH level below 2.5 and many scientists call for the reference range to be lowered.16   At the very least, it would be prudent to analyse results, guided by an ‘optimal’ reference range, which might highlight potential thyroid dysfunction in less extreme cases.

The second point which I tend to find with nutrition clients is that it is essential to analyse test results in conjunction with symptoms.  Time and time again, individuals receive ‘normal’ test results, yet their symptoms strongly indicate that there is an issue with their thyroid gland.  Again, this relates to the definition of ‘normal’ and while one person with levels of TSH at 3.8 may feel in optimal health, many others might continue to struggle with weight gain, fatigue, poor skin, or many of the numerous symptoms associated with an underactive thyroid.  Thyroid dysfunction is common among women over the age of fifty17 and many cases of subclinical hypothyroidism remain undiagnosed post-menopause, which is understandable given the broad range and overlap of symptoms associated with this period of hormonal change.  However, again it is important that testing is thorough and combined with analysis of symptoms, in order to achieve the correct diagnosis and medical or nutritional protocol.

Cabbages, close-upIn order to support your thyroid health, we can focus on the nutrients required to produce and facilitate the uptake of thyroid hormones.  The amino acid tyrosine is found in protein-rich foods such as almonds, pumpkin seeds, fish, chicken and also avocado.  Iodine is found in seafood and seaweeds such as kelp, nori, dulse and arame, while selenium and zinc rich foods include oysters, tuna, chicken, mushrooms, Brazil nuts, almonds, cashews, oats, brown rice, buckwheat and quinoa.2  You should avoid refined carbohydrates, which affect blood sugar and have an impact on adrenal hormones, sex hormones and thyroid hormones, but should include plenty of protein and essential fats from oily fish, nuts, seeds, eggs, avocado and flaxseed to help stabilise hormones.  If you have been diagnosed with an underactive thyroid, you should avoid eating large quantities of raw brassicas such as cabbage, kale and broccoli, but remember that lightly cooked green vegetables are a wonderful source of vitamins A and C, B vitamins and copper, which are needed for the thyroid gland to produce T4.9

Stress management and regular exercise are equally as important for maintaining hormone balance, particularly adrenal hormones and in some cases, it is advisable to focus on improving adrenal health before supporting thyroid function.  There is a clear correlation between food intolerances, gut permeability and auto-immune diseases, including auto-immune thyroid diseases such as Hashimoto’s.2  It is therefore crucial to support the gut by removing any foods to which the gut-based immune system is reacting and to heal the gut lining with nutrients such as l-glutamine.

In summary, the endocrine system is complex and should be considered in its entirety.  An imbalance of adrenal hormones may have an impact on thyroid function and vice versa.  Women with an underactive thyroid may find it harder to conceive and may struggle with the menopause.  Whatever the cause, hypothyroidism can mean misery for many people if it remains undiagnosed, untreated, or mismanaged.  It is important to conduct thorough testing through your GP, endocrinologist or nutrition practitioner and if medication is prescribed, to ensure that the dosage is regularly reviewed and adjusted, until you feel the benefits and see a reduction in symptoms.  Certain other medications and nutritional supplements can interfere with the absorption and effectiveness of thyroid medication, so always check with your medical professional before taking anything new.

View List of References

  1. Gurel A, Dogantekin A, Ozkan Y, Aydin S (2015) Serum apelin levels in patients with thyroid dysfunction. International Journal of Clinical and Experimental Medicine, 8 (9): 16394-16398. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  2. Pizzorno J E, Murray M T, Joiner-Bey H (2008) The Clinicians Handbook of Natural Medicine, 2nd Edition. Churchill Livingstone, USA.
  3. Chakera A J, Pearce S H, Vaidya B (2012) Treatment for primary hypothyroidism: current approaches and future possibilities. Drug design, development and therapy, 6: 1-11. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc)
  4. Malik R, Hodgson H (2002) The relationship between the thyroid gland and the liver. QJM, 95 (9): 559-569. [Online] QJM Oxford Journals (http://qjmed.oxfordjournals.org).
  5. Warner A, Mittag J (2012) Thyroid hormone and the central control of homeostasis. Journal of Molecular Endocrinology, 49: R29-R35. [Online] Journal of Molecular Endocrinology (http://jme.endocrinology-journals.org).
  6. Luongo C, Trivisano L, Alfano F, Salvatore D (2013) Type 3 deiodinase and consumptive hypothyroidism: a mechanism for a rare disease. Frontiers in Endocrinology, 4: 115. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  7. Roberts C G, Ladenson P W (2004) Hypothyroidism. The Lancet, 363 (9411): 793-803. [Online – abstract only] PubMed (http://www.ncbi.nlm.nih.gov/pubmed).
  8. Vanderpump M P J (2011) The epidemiology of thyroid disease. British Medical Bulletin, 99 (1): 39-51. [Online] British Medical Bulletin (http://bmb.oxfordjournals.org).
  9. Bajaj J K, Salwan P, Salwan S (2016) Various possible toxicants involved in thyroid dysfunction: a review. Journal of Clinical & Diagnostic Research, 10 (1): FE01-FE03. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  10. McNeil A, Stanford P (2015) Reporting thyroid function tests in pregnancy. The Clinical Biochemist Reviews, 36 (4): 109-126. [Online] Pub Med (http://www.ncbi.nlm.nih.gov/pubmed).
  11. Vanderpump M P J (2011) The epidemiology of thyroid disease. British Medical Bulletin, 99 (1): 39-51. [Online] British Medical Bulletin (http://bmb.oxfordjournals.org).
  12. Duffield A J, Thomson C D, Hill K E, Williams S (1999) An estimation of selenium requirements for New Zealanders. The American Journal of Clinical Nutrition, 70 (5): 896-903. [Online] The American Journal of Clinical Nutrition (http://ajcn.nutrition.org).
  13. Johannsson G, Skrtic S, Lennernas H, Quinkler M, Stewart P M (2014) Improving outcomes in patients with adrenal insufficiency: a review of current and future treatments. Current Medical Research and Opinion, 30 (9): 1833-1847. [Online – abstract only) PubMed (http://www.ncbi.nlm.nih.gov/pubmed).
  14. Saravanan P, Chau W F, Roberts N, Vedhara K, Greenwood R, Dayan C M (2002) Psychological well-being in patients on ‘adequate’ doses of l-thyroxine: results of a large, controlled community-based questionnaire study. Clinical Endocrinology, 57 (5): 577-585. [Online] PubMed (http://www.ncbi.nlm.nih.gov/pubmed).
  15. Surks M I, Boucai L (2010) Age- and race-based serum thyrotropin reference limits. The Journal of Clinical Endocrinology and Metabolism, 95 (2): 496-502. [Online] PubMed (http://www.ncbi.nlm.nih.gov/pubmed).
  16. Wartofsky L, Dickey R A (2005) The evidence for a narrower thyrotropin reference range is compelling. The Journal of Clinical Endocrinology and Metabolism, 90 (9): 5483-5488. [Online] PubMed (http://www.ncbi.nlm.nih.gov/pubmed).
  17. Pearce E N (2007) Thyroid dysfunction in perimenopausal and postmenopausal women. Post Reproductive Health, 13 (1): 8-13. [Online – abstract only] PubMed (http://www.ncbi.nlm.nih.gov/pubmed).

The influence of gut bacteria on obesity

Gut bacteria are currently the subject of a huge amount of exciting and ground breaking research.  Scientists are now able to analyse hundreds of what are possibly a thousand or more species which live inside your body, making up your personal microbiome.  They are beginning to piece together the evidence which links certain gut bacteria profiles to various disease states, or potential risk of disease, such as cancer of the colon, autoimmune diseases, or autism 1, 2, 3, 4.  Obesity is now classed as a disease and research indicates that gut bacteria may be heavily implicated in its development, through various mechanisms associated with extraction of energy from food; inflammation; insulin sensitivity; and communication with the brain.

Energy harvesting

One of the many functions that beneficial bacteria carry out in the digestive tract is fermentation of indigestible dietary fibre, which produces short chain fatty acids (SCFAs), such as butyrate.  Butyrate is a vital source of energy for the cells which line the colon 5.  In other words, the combination of beneficial gut bacteria and a high fibre diet are of great importance for digestive health, as the fatty acids which are produced nourish the colon cells.  It is therefore not surprising that low concentrations of SCFAs have been found in patients with inflammatory bowel diseases such as ulcerative colitis, along with very different bacterial profiles to healthy subjects 6.

Studies on both mice and humans have shown that obese individuals have a different microbiome (mixture of bacterial species) to lean individuals and it seems that the gut bacteria in obese subjects are more efficient at extracting, or ‘harvesting’ energy from the diet 4,5,6.  Many studies use germ-free mice, animals which are born by caesarean section with a sterile gut and kept in a sterile environment. Obese mouseIt has been found that germ-free mice remain leaner than conventionally raised mice, even when eating a higher intake of food.  If bacteria from normal mice are introduced into germ-free mice, their body fat has been found to increase by 60% in just 10-14 days, even when food consumption is reduced 7.  Germ-free mice which were colonised with bacteria from obese mice saw significant increases in body fat 1, which supports the idea that certain types of bacteria are able to release more energy from food – energy which is then stored as fat.

Inflammation and insulin sensitivity

Butyrate, the SCFA produced by bacterial fermentation of fibre, is important for helping to keep the lining of the digestive tract intact 6.  A healthy mucosal lining ensures that partially digested food and bacteria does not pass through from the inside of the gut, into the bloodstream.  Any disruption to the balance of bacteria in the gut can cause inflammation 1, which damages the delicate lining and enables unwanted substances to find their way into the blood, where they trigger an immune response.  Further inflammation ensues.  Obesity is understood to be driven by inflammation, partly because the production of inflammatory chemicals by the immune system causes cells to become less sensitive to insulin 8.  If we consume food which is converted to glucose and cells do not respond to insulin, (i.e. they are resistant to insulin, which attempts to direct glucose into cells to be used as energy), then rather than allow blood levels of glucose to become dangerously high, the body converts glucose to fat and stores it, leading to weight gain.

Obese kidFaecal transplants are becoming more commonly used in medical procedures on humans, as well as mice, although trials are typically small in size (possibly due to lack of volunteers?!) One small study 9 analysed men who were insulin resistant (a condition which typically precedes the development of type II diabetes) and who received a faecal transplant from lean donors.  Those who received the transplant were observed to have a significantly improved sensitivity to insulin, as well as a much more diverse range of bacteria in their gut, particularly the species which produce the beneficial butyrate SCFA.

Communication with the brain

Gut bacteria have been shown to influence the neurotransmitter (brain chemical) serotonin 6, of which 90% is actually produced in the gut.  Serotonin plays a major role in regulating our mood, as well as our appetite and feeling of satiety, or feeling full after eating.  It helps to regulate insulin production by the pancreas 10 and is therefore implicated, in partnership with gut bacteria, in the progression of insulin resistance towards diabetes and obesity.

Dietary and lifestyle measures to address the obesity crisis

Obesity is a complex disease, but what is becoming clearer, is that inflammation is at the heart of the issue and that the microbiome has an influential role.  It is therefore crucial to minimise dietary and lifestyle factors which contribute to inflammation, such as sugar, wheat, processed vegetable oils, and artificial additives, as well as stress, poor sleep, antibiotics (disruption to the beneficial gut bacteria), or environmental toxins such as fertilisers and pollution.

Chicory  Prebiotic foods
Probiotic supplements can be an effective way to colonise the gut with beneficial bacteria and natural ways to boost your levels of bacteria include eating prebiotic fibre such as onions, garlic, leek, chicory, asparagus and banana, as well as fermented food and drinks such as kefir, kombucha, sauerkraut and tempeh.

KombuchaKefirTempeh stack

View List of References

      1. Zhang Y-J, Li S, Gan R-Y, Zhou T, Xu D-P, Li H-B (2015) Impacts of gut bacteria on human health and diseases. International Journal of Molecular Science, 16 (4): 7493-7519. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
      2. Sansonetti P J, Medzhitov R (2009) Learning tolerance while fighting ignorance. Cell, 138 (3): 416-420. [Online] Cell (www.cell.com).
      3. Tlaskalová-Hogenová H, Stepánková R, Hudcovic T, Tucková L, Cukrowska B, Lodinová-Zádníková R, Kozáková H, Rossmann P, Bártová J, Sokol D, Funda DP, Borovská D, Reháková Z, Sinkora J, Hofman J, Drastich P, Kokesová A (2004) Commensal bacteria (normal microflora), mucosal immunity and chronic inflammatory and autoimmune diseases. Immunology Letters, 93 (2-3): 97-108. [Online – abstract only] PubMed (http://www.ncbi.nlm.nih.gov/pubmed).
      4. Sekirov I, Russell S L, Antunes C M, Finlay B (2010) Gut microbiota in health and disease. Physiological Reviews, 90 (3): 859-904. [Online] Physiological Reviews (http://physrev.physiology.org).
      5. Sharma V, Garg S, Aggarwal S (2013) Probiotics and liver disease. The Permanente Journal, 17 (4): 62-67. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
      6. Hartstra A V, Bouter K E C, Backhed F, Nieuwdorp M (2015) Insights into the role of the microbiome in obesity and type 2 diabetes. Diabetes Care, 38 (1): 159-165. [Online] Diabetes Care (http://care.diabetesjournals.org).
      7. Tsai F, Coyle W J (2009) The Microbiome and Obesity: Is Obesity Linked to Our Gut Flora? Current Gastroenterology Reports, Sep: 307-313. [Online] ResearchGate (https://www.researchgate.net).
      8. Hotamisligil G S, Shargill N S, Spiegelman B M (1993) Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science, 259 (5091): 87-91. [Online – abstract only] PubMed (http://www.ncbi.nlm.nih.gov).
      9. Vrieze A, Van Nood E, Holleman F, et al. (2012) Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. Gastroenterology, 143: 913–916. [Online] CaelusHealth (http://caelushealth.com).
      10. Oh C-M, Park S, Kim H (2016) Serotonin as a New Therapeutic Target for Diabetes Mellitus and Obesity. Diabetes Metabolism Journal, 40 (2): 89-98. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).

Natural approaches to prevent urinary tract infection (UTI)

Almost half of all women will experience a urinary tract infection (UTI) in their lifetime.  The most common UTI is cystitis, an infection which develops in the lower urinary tract and affects the bladder and urethra.  However, it can extend to the upper tract, where the ureters and kidneys are located and is then known as pyelonephritis 1.  Symptoms include burning pain on urination; increased frequency of urination; foul smelling, or dark urine; bacteria, blood or pus in urine; and lower abdominal pain 2.  Certain groups are at increased risk, such as pregnant women, infants, the elderly, diabetics, or patients using urinary catheters and adult women are significantly more likely to experience UTI than men 3.

Urinary tractEscherichia coli (E coli), one of the first bacteria to colonise in the human gut after birth, 4 is the predominant bacteria associated with UTI in adult women, while Enterobacteriacaea are more typically found in children experiencing a bladder infection 5. The main risk factor for UTI is sexual activity 6, but pregnancy also increases the risk, as well as structural abnormalities of the urinary tract.  Urine, which is excreted by the kidneys, is sterile until it reaches the uretha.  Problems arise when bacteria from faeces or vaginal secretions travel up the urethra and colonise in the bladder, or further up the urinary tract.  The inner surface of the bladder has antimicrobial properties and the pH of urine usually inhibits the growth of many bacteria, but it is important to minimise the risk of bacterial contamination, by completely emptying the bladder when urinating; wiping from front to back after using the toilet; by urinating before and after sexual intercourse; and avoiding sex while being treated for a UTI 2.

Cranberry juice has been well researched in relation to UTI and many studies show that it can reduce the recurrence of infection in women who have experienced regular UTI 6, 7, 8 and can reduce the number of recurrences in children 9.   Proanthocyanidins are compounds found in cranberries (and other berries such as blueberries), which prevent E. coli from sticking to the walls of the bladder and urinary tract.  Adhesion to the mucosal layer of cells which line various cavities in the body, such as the bladder and intestines, is necessary for most bacteria to multiply and to trigger infection 9.  The bladder is able to flush away bacteria which have not attached themselves and therefore, preventing the adherence of E. coli in particular, is of vital importance in preventing recurrent urinary health issues.

Cranberry juiceWhile unsweetened cranberry juice has been proved to be an effective preventative intervention, many studies report large numbers of participants dropping out of the experiments, which has been linked to the acceptability of consuming significant quantities of juice over time.  Cranberry juice may also interact with certain medications, so it is advisable to seek medical advice before commencing any preventative programme for UTI.  An alternative to drinking cranberry juice is to take a supplement of concentrated proanthocyanidins which are extracted from the fruit.  If used consistently over time, such products have been shown to have a preventative effect, reducing the number of UTI recurrences 1.

Another alternative is to take a supplement of D-mannose, which is suitable for both adults and children. D-mannose is a simple sugar, found in certain fruits (including cranberries, peaches, apples and oranges) and is found naturally in some cells of the body.  It is similar to glucose, but is metabolised differently and absorbed more slowly, so doesn’t have the same impact on blood sugar and isn’t stored in the liver as glycogen. Experiments have shown that, like proanthocyanidins in cranberries, D-mannose prevents E. coli bacteria from adhering to the walls of the bladder 10 and a 2014 study indicated that it was equally as effective as the antibiotic Nitrofurantoin in reducing recurrence of UTI in women, but with significantly less side effects 11.

Similarly, probiotic therapy has been tested in long-term studies looking at preventing recurrence of UTI.  Lactobacillus bacteria taken once a week in pessary form proved to be as effective as a variety of antibiotics taken daily for a year, in preventing recurrence of UTI, but without any side effects, compared to significant incidences of side effects reported by patients taking antibiotics 12.

When you consider the impact of antibiotics on the long-term health of the gut and the growing threat of antibiotic resistance, any natural alternative should certainly be considered as the starting point for treatment.  For UTI caused by E. coli, D-mannose is a good option, which can often provide effective treatment without the use of antibiotics.  Meanwhile, probiotics provide a way of maintaining ongoing healthy bacterial balance, as they compete with E.coli for adherence to the cells lining the gut and bladder 13. It is important to note that the safety of taking D-mannose in pregnancy has not been researched enough, while most probiotics are confirmed to be safe to use when pregnant.

fermented foods

From a dietary perspective, any measures which support the healthy functioning of the digestive and immune system may be beneficial for the prevention of UTI.  An American study 14 found that frequent consumption of fermented milk products was associated with low incidence of UTI recurrence, while no such association was found for fresh milk products.  Indeed, consumption of a range of fermented food and drinks such as sauerkraut, kefir, kombucha, tempeh and yoghurt promotes the growth of beneficial gut bacteria, which play a vital role in developing and communicating with our immune system.  Prebiotic foods such as onions, garlic (also known for its potent anti-bacterial properties), leek, chicory and asparagus, as well as resistant starch (found in cooked and cooled potatoes and rice, or in green bananas), provide fibre that beneficial bacteria ferment to produce energy, which further sustains both them and the cells lining the digestive tract 15.

Food allergies can cause inflammation in the urethra and bladder, making it harder to treat UTI, so it is important to identify and avoid foods such as gluten, which trigger inflammation in some individuals.  Sugar inhibits the immune system and fuels potentially harmful bacteria, so a diet based on natural, unprocessed foods is advisable.  Keeping properly hydrated ensures adequate urine flow to flush away bacteria, so it is recommended to drink at least 2 litres daily of water, herbal teas, vegetable juices and diluted, unsweetened fruit juices (pure, not concentrated).  Avoid soft drinks, alcohol and caffeine, which act as diuretics.

View List of References

    1. Othman M (2013) Cysticlean and Recurrent Urinary Tract Infection. Urology, 4 (4): WMC004203. [Online] WebmedCentral (www.webmedcentral.com).
    2. Pizzorno J E, Murray M T, Joiner-Bey H (2008) The Clinician’s Handbook of Natural Medicine, 2nd Ed., Churchill Livingstone, USA.
    3. Foxman B (2002) Epidemiology of urinary tract infections: incidence, morbidity, and economic costs. The American Journal of Medicine, 113 (1): 5-13. [Online – abstract only] Science Direct (www.sciencedirect.com).
    4. Kataoka K (2016) The intestinal microbiota and its role in human health and disease. The Journal of Medical Investigation, 63 (1-2): 27-37. [Online] Japan Science and Technology Information Aggregator Electronic (www.jstage.jst.go.jp).
    5.  Ronald A (2002) The etiology of urinary tract infection: traditional and emerging pathogens. The American Journal of Medicine, 113 (1): 5-13. [Online] Science Direct (www.sciencedirect.com).
    6.  Kontiokari T, Sundqvist K, Nuutinen M, Pokka T, Koskela M, Uhari M (2001) Randomised trial of cranberry-lingonberry juice and Lactobacillus GG drink for the prevention of urinary tract infections in women. British Medical Journal, 322: 1571. [Online] British Medical Journal (www.bmj.com).
    7. Avorn J, Monane M, Gurwitz J H, Glynn R J, Choodnovskiv I, Lipsitz L A (1994) Reduction of Bacteriuria and Pyuria After Ingestion of Cranberry Juice. Journal of the American Medical Association, 271 (10): 751-754. [Online – abstract only] Journal of the American Medical Association (www.jama.jamanetwork.com).
    8. Salo J, Uhari M, Hekminen M, Korppi M, Nieminen T, Pokka T, Kontiokari T (2012) Cranberry Juice for the Prevention of Recurrences of Urinary Tract Infections in Children: A Randomized Placebo-Controlled Trial. Journal of Clinical Infectious Diseases, 54 (3): 340-346. [Online] Oxford Journals Clinical Infectious Diseases (www.cid.oxfordjournals.org).
    9. Howell A B, Vorsa N, der Marderosian A, Foo L Y (1998) Inhibition of the Adherence of P-Fimbriated Escherichia coli to Uroepithelial-Cell Surfaces by Proanthocyanidin Extracts from Cranberries.  New England Journal of Medicine, 339: 1085-1086. [Online] New England Journal of Medicine (www.www.nejm.org).
    10. Altarac S, Papes D (2014) Use of d-mannose in prophylaxis of recurrent urinary tract infections (UTIs) in women. British Journal of Urology International, 113 (1): 9-10. [Online – abstract only] Wiley Online Library (www.onlinelibrary.wiley.com).
    11. Kranjcec B, Papes D, Altarac S (2014) D-mannose powder for prophylaxis of recurrent urinary tract infections in women: a randomized clinical trial. World Journal of Urology, 32 (1): 79-84. [Online] PubMed (www.ncbi.nlm.nih.gov).
    12. Reid G, Jass J, Sebulsky M T, McCormick J K (2003) Potential Uses of Probiotics in Clinical Practice. Clinical Microbiology Reviews, 16 (4): 658-672. [Online] PubMed (www.ncbi.nlm.nih.gov).
    13. Sekirov I, Russell S L, Antunes C M, Finlay B B (2010) Gut Microbiota in Health and Disease. Physiological Reviews, 90 (3): 859-904. [Online] Physiological Reviews (www.physrev.physiology.org).
    14. Kontiokari T, Laitinen J, Jarvi L, Pokka T, Sundqvist K, Uhari M (2003) The American Journal of Clinical Nutrition, 77 (3): 600-604. [Online] The American Journal of Clinical Nutrition (www.ajcn.nutrition.org).
    15. Topping D L (1996) Short-chain fatty acids produced by intestinal bacteria. Asia Pacific Journal of Clinical Nutrition, 5 (1): 15-19. [Online] PubMed (www.ncbi.nlm.nih.gov).

Give a shout-out to sprouts!

mung bean sproutsIn terms of packing a nutritional punch, there are few foods which score as highly as sprouted seeds and pulses, like sprouted broccoli, alfalfa, radish, mung beans, chickpeas and lentils.  The process of germination, or sprouting, is demonstrated to increase levels of nutrients, including vitamins, minerals and protein, while reducing anti-nutrients such as phytates and tannins 1.  After just 3 days of sprouting, it is suggested that a small quantity of sprouted cruciferous seeds such as broccoli, may potentially deliver the equivalent cancer-protective nutrients as a much larger quantity of mature vegetables of the same variety 2.

Germination is a complex process during which various compounds in the seed, grain or legume change dramatically.  Fats, carbohydrates and proteins within the seeds are broken down in order to provide energy and amino acids for the developing plant 3.  These changes increase the availability of essential nutrients and bioactive compounds, such as phenols, which in mung beans, can increase by 2010% after sprouting 1.  Antioxidant activity of chickpeas is shown to increase significantly after germination 1, while radish sprouts are reported to have the most potent antioxidant capacity 4.  Sprouts have a high protein content (21-28%) and are a good source of calcium, phosphorus and certain vitamins such as vitamin C, which increases during the sprouting process 4, 5.  Indeed, across many parameters, the nutritional content of sprouts are significantly higher than their seed format 3, 4, 11, with some nutrients being assessed at 10 to 100 hundred times greater than in the mature plant2.

Sprouting seeds

Just as humans require antioxidant nutrients to balance the oxidative damage caused by everyday body functions and factors like stress, pollution or dehydration, plants also protect themselves with antioxidant compounds, which offset the damage caused by photosynthesis, respiration and other cellular reactions 5.   The sprouts of cruciferous vegetables such as radish and broccoli are good sources of the body’s most important antioxidant, glutathione, which is produced by the liver and can neutralise free radicals 6.   Broccoli sprouts have also been used in studies to demonstrate the potential anti-viral properties of the sulphoraphane compound which they contain 7.

”Sprouted pulses are more easily digested, without the common side effects of bloating and gas”

One way in which plants protect themselves from being eaten by insects is with compounds such as tannins, which act as a deterrant or toxin 8.  Like other types of phenolic compounds, tannins can influence the colour, smell or bitterness of leaves and protect against UV damage 9.   They are known as ‘anti-nutrients’ because they can interfere with the way humans absorb certain vitamins and minerals.  Phytates provide an important form of energy storage for plants and are found primarily in the hulls of seeds 10.  However, they can have a similarly negative impact on human mineral levels, as they bind to calcium, magnesium, iron and zinc, making them unavailable for absorption. Soaking and sprouting seeds is shown to reduce the levels of both tannins and phytates 1,4,10, which is why it is also beneficial to soak other plant foods such as nuts, beans and grains.  Removing the hulls of seeds reduces levels of phytates even further and is easily done after sprouting 10.

Mung beans in bowl

Furthermore, sprouting is shown to increase the fibre content of seeds, while reducing the proportion of carbohydrates (possibly used for energy in the germination process), meaning that sprouted seeds have a fantastic nutrient profile, high in vitamins, minerals, protein and fibre, while being low in fat and carbohydrate 3.  They are also more easily digested by humans 3, without the common side effects of bloating and gas which can be caused by consuming non-sprouted pulses.

”Soaking and sprouting seeds is shown to reduce the levels of both tannins and phytates , which is why it is also beneficial to soak other plant foods such as nuts, beans and grains.”

Overall, the evidence is clear that adding sprouted plant foods to our diet is a simple, inexpensive and delicious way to boost our nutrient levels.  They are best eaten raw (in salads, wraps and smoothies), but may be lightly steamed, added to stir-fries, soups and stews, or even ground into flour.  Sprouts are widely available in supermarkets, but the sprouting process only takes a few days and is simple and cheaper to do at home.

Alfalfa is very easy to sprout if you are new to this process and is a lovely, mild addition to salads and other dishes.  Organic alfalfa seeds are available in health food stores and some garden centres, along with inexpensive sprouting trays or bags.  Simply soak a tablespoon of seeds in a bowl of water for around 8-12 hours.  Place the seeds in the sprouting tray or bag and rinse carefully, ensuring that you drain the water completely.  Leave in a bright spot, but out of direct sunlight and continue to rinse and drain them at least twice a day for 3 days. (I find that if I leave them near the kitchen sink, it’s easy to remember to do this and it only takes a minute.  If you forget to rinse them, they can be susceptible to mould).alfalfa sprouts

By day 2, you should see roots and shoots starting to emerge and by day 3, tiny green leaves will start to show.  Once the leaves are bright green and the sprouts are between 2-5cm long, they are ready to be eaten (usually around day 4 for alfalfa, but this varies with each type of seed or bean). Rinsing and gently rubbing the sprouts helps to remove the brown seed hulls and you should then store the alfalfa sprouts in an airtight container lined with kitchen paper and keep them refrigerated.

Once you have mastered alfalfa, you can apply the same method to chickpeas, lentils, quinoa, adzuki beans, pumpkin seeds, sesame seeds and even raw, unpasteurised almonds or peanuts.  Use them in your usual recipes, while enjoying the additional nutrient content.

View List of References

  1. Tarzi B G, Gharachorloo M, Baharinia M, Mortazavi S A (2012) The Effect of Germination on Phenolic Content and Antioxidant Activity of Chickpea. Iranian Journal of Pharmaceutical Research, 11(4): 1137-1143. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  2. Fahey J W, Zhang Y, Talalay P (1997) Broccoli sprouts: An exceptionally rich source of inducers of enzymes that protect against chemical carcinogens. Proceedings of the National Academy of Sciences in the United States of America, 94(19): 10367-10372.  [Online] PNAS (www.pnas.org).
  3. Uppal V, Bains K (2012) Effect of germination periods and hydrothermal treatments on in vitro protein and starch digestibility of germinated legumes. Journal of Food Science & Technology, 49(2): 184-191.  [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  4. Shah S A, Zeb A, Masood T, Noreen N, Abbas S J, Samiullah M, Alim A, Muhammad A (2011) Effects of sprouting time on biochemical and nutritional qualities of Mungbean varieties. African Journal of Agricultural Research, 6(22): 5091-5098.  [Online] African Journal of Agricultural Research (academicjournals.org/AJAR).
  5. Zielinski H, Piskuta M K, Michalska A, Kozlowska H (2007) Antioxidant capacity and its components of cruciferous sprouts. Polish Journal of Food and Nutrition Sciences, 57(3): 315-322. [Online] Polish Journal of Food and Nutrition Sciences (pan.olsztyn.pl/journal).
  6. Galano A, Alvarez-Idaboy J R (2011) Glutathione: mechanism of its non-enzymatic defense action against free radicals. Royal Society of Chemistry Advanced, 1: 1763-1771. [Online-abstract only] Royal Society of Chemistry (http://pubs.rsc.org).
  7. Muller L, Meyer M, Bauer R N, Zhou H, Zhang H, Jones S, Robinette C, Noah T L, Jaspers I (2016) Effect of Broccoli Sprouts and Live Attenuated Influenza Virus on Peripheral Blood Natural Killer Cells: A Randomized, Double-Blind Study. PLoS One, 11 (1): e0147742. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  8. Barbehenn R V, Constabel P (2011) Tannins in plant-herbivore interactions. Phytochemistry, 72(13): 1551-1565. [Online – abstract only] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  9. Chon S U (2013) Total polyphenols and bioactivity of seeds and sprouts in several legumes. Current Pharmaceutical Design, 19(34): 6112-6124. [Online – abstract only] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  10. Nakitto A M, Muyonga J H, Nakimbugwe D (2015) Effects of combined traditional processing methods on the nutritional quality of beans.  Food Science & Nutrition, 3(3): 233-241. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  11. Tang D, Dong Y, Ren H, Li L, He C (2014) A review of phytochemistry, metabolite changes, and medicinal uses of the common food mung bean and its sprouts (Vigna radiata). Chemistry Central Journal, 8: 4. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).

Acne: ‘diabetes of the skin’

Acne vulgaris is an inflammatory skin disease which is most often associated with the onset of puberty, 1 affecting around 85% of teenagers. 2 However, it has become increasingly common in the past 50 years, notably among adult women. 3   The precise mechanisms of acne development are still not fully understood, but it is characterised by overproduction of sebum (the oily secretion produced by sebaceous glands in the outer layer of skin); disruption of the cells which line hair follicles; and inflammation; in conjunction with hormonal and bacterial influences. 4,3,5

Sebaceous gland

Recent studies have focused on the role that insulin-like growth factor (IGF-1) plays in acne.  IGF-1 is a hormone which promotes cell growth and is naturally higher during puberty. 6   Elevated levels of IGF-1 lead to increased sebum production and over-production of the cells which surround sebaceous follicles, 4 with subsequent clogging of pores.  Bacteria such as Propionibacterium acnes, which is normally present in the skin, may become trapped in clogged pores, leading to infection and the redness and swelling of acne lesions.1  Consumption of cow’s milk results in a significant increase in blood levels of IGF-1, 7 while epidemiological studies show that acne is absent in populations consuming paleolithic diets, with low glycaemic load and no consumption of milk or dairy products. 6,8  Whey protein extracts are of particular concern, with various studies focusing purely on acne development in users of whey protein supplements. 9,18  Whey protein extract from cow’s milk contains 6 different growth factors, hence its use for increasing muscle mass, but which could also be the reason why whey protein supplementation is linked to the onset of acne. 18

”epidemiological studies show that acne is absent in populations consuming paleolithic diets, with low glycaemic load and no consumption of milk or dairy products.”

Acne has been referred to as ‘diabetes of the skin’ by scientists since the 1950s. 3 Insulin is necessary for the body to convert glucose into energy, but excess insulin in the bloodstream can cause an increase in IGF-1, 6 which in turn promotes skin cell growth.  Increased insulin also raises levels of androgens (male hormones, including testosterone, which women usually produce in lesser amounts).10 Androgens are implicated in increased sebum production and excessive skin cell turnover,1,11  both of which can trigger acne.  Diet plays a vital role, as high glycaemic foods such as sugar, white bread, white potatoes and white rice cause insulin levels to rise, but may also affect other cell proteins such as mTORC1 and Fox01 proteins, which regulate cell growth, sebum production, insulin sensitivity and hormone activity: 6 all factors implicated in the development of acne.  A low carbohydrate diet is recommended, 12 avoiding any refined or processed foods and limiting dairy, while focusing on good quality protein, essential fats and anti-oxidant rich vegetables.

Oily fish

An important dietary factor that influences inflammation, is the relative intake of omega 6 to omega 3 polyunsaturated fatty acids in food. Omega 3 fats reduce the production of inflammatory signalling molecules in sebaceous glands; 4,10 inhibit mTORC1 (a protein which can signal sebaceous glands to produce more sebum); 4 may help to maintain IGF-1 levels (thus preventing over-production of skin cells); and are also antibacterial, inhibiting the growth of Propionibacterium acnes and Staphylococcus species of bacteria which are involved in acne. 13  Modern diets tend to be higher in omega 6 fats (from vegetable oils used in processed foods), as well as saturated fats and trans fats, all of which can be converted to inflammatory substances called prostaglandins, while omega 3 fats have an anti-inflammatory effect on the body. 4,10 Observational studies have noted low occurrence of acne in populations who eat high amounts of omega 3-rich oily fish such as salmon, mackerel, herring, fresh tuna and anchovies. 14

”If the liver is overburdened, the lungs or skin may be used as an alternative route to remove toxins, so skin problems are often an indication that the liver needs supporting.”

Various nutrients have been found to be low in patients with acne, including chromium, selenium, vitamins A and E, and zinc. 5,15,16   In women with polycystic ovarian syndrome, acne was decreased following supplementation with chromium 15 and selenium. 16  Chromium is found in wholegrains, brown rice, eggs, meat, fish, mushrooms and Brewer’s yeast and has been shown to help balance blood sugar levels, while selenium is an important antioxidant found in Brazil nuts, fish, seafood, poultry, brown rice and mushrooms.   Vitamin A (found in oily fish, eggs and liver) and the vitamin A pre-cursor, beta carotene (found in dark green, yellow and orange vegetables) help cells to function and reproduce normally, replacing themselves roughly every month. 17   Vitamin E (found in soya, avocado, olive oil, nuts and seeds) helps to maintain hormone balance, is an important antioxidant nutrient and also helps to prevent scarring from acne.  The acne fighting properties of zinc (found in oysters, oats, meat, poultry, nuts and beans) are believed to be due to its ability to reduce inflammation and to kill bacteria, as well as its involvement in hormone production and androgen regulation. 1, 5 Green tea has been used topically in studies and found to be effective in improving mild to moderate acne, which is attributed to the antiseptic and anti-inflammatory properties of its flavonoids and tannins. 2,4

oysterTwo crucial factors, which are often overlooked in skin health, are the liver and digestive tract.  The liver fulfils over 400 functions in the body, of which detoxification is one of the most important.  All toxins which are produced by or enter the body are managed by the liver, which eliminates them via various processes.  If the liver is overburdened, the lungs or skin may be used as an alternative route to remove toxins, so skin problems are often an indication that the liver needs supporting.  Cutting back on sugar, alcohol and processed foods is beneficial, as well as increasing water intake and consuming a wide variety of vegetables which contain vital nutrients required for detoxification processes.


An imbalance of bacteria in the gut, or digestive issues such as constipation can also put pressure on the liver, with subsequent impact on skin health.  Bacteria and yeasts may release toxins in the digestive tract, leading to intestinal inflammation, 19 which in turn puts pressure on the liver.  Inflammation can also promote insulin resistance in cells that control blood glucose, 20 which brings us back to the link between elevated insulin; over production of skin cells and androgens; and acne.shiitake01Overall, an anti-inflammatory diet is recommended to address the underlying causes of acne, with many studies concluding that a paleolithic diet is the best approach.  It is advisable to investigate any potential digestive dysfunction and to support liver health, while consuming plenty of unrefined, wholefoods and essential fats, including oily fish, nuts and seeds, as well as a wide variety of fruit and vegetables, focusing on sources of vitamin A, vitamin E, chromium, selenium and zinc.

View List of References

  1. Pizzorno J E, Murray M T, Joiner-Bey H (2008) The Clinicians Handbook of Natural Medicine, 2nd Churchill Livingstone, USA.
  2. Nasri H, Bahmani M, Shahinfard N, Moradi Nafchi A, Saberianpour S, Rafieian Kopaei M (2015) Medicinal Plants for the Treatment of Acne Vulgaris: A Review of Recent Evidences. Jundishapur Journal of Microbiology, 8(11): e25580. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  3. Rubin M G, Kim K, Logan A C (2008) Acne vulgaris, mental health and omega-3 fatty acids: a report of cases. Lipids in Health and Disease, 7: 36. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  4. Melnik B C (2015) Linking diet to acne metabolomics, inflammation, and comedogenesis: an update. Clinical, Cosmetic and Investigational Dermatology, 8: 371-388. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  5. Mogaddam M R, Ardabilj N S, Maleki N, Soflaee M (2015) Correlation between the Severity and Type of Acne Lesions with Serum Zinc Levels in Patients with Acne Vulgaris. Biomedical Research International. [Online- Epub ahead of print] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  6. Melnik B C, Zouboulis C C (2013) Potential role of FoxO1 and mTORC1 in the pathogenesis of Western diet-induced acne. Journal of Experimental Dermatology, 22(5): 311-315. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  7. Melnik B C, Schmitz G (2009) Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Experimental Dermatology, 18(10): 833-841. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  8. Melnik B C (2012) Diet in acne: further evidence for the role of nutrient signalling in acne pathogenesis. Acta-Dermato Venereologica, 92(3): 228-231. [Online- abstract only] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  9. Melnik B C (2011) Evidence for acne-promoting effects of milk and other insulinotropic dairy products. Nestle Nutrition Workshop Series Pediatric Program, 67: 131-145. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  10. Kaimal S, Thappa D M (2010) Diet in dermatology: Revisited. Indian Journal of Dermatology, Venereology and Leprology, 76(2): 103-115. [Online] Indian Journal of Dermatology, Venereology and Leprology (www.ijdvl.com).
  11. Imperato-McGinley J, Gautier T, Cai L Q, Yee B, Epstein J, Pochi P (1993) The Journal of Clinical Endocrinology and Metabolism, 76(2): 524-528. [Online- abstract only] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  12. Kwon H H, Yoon J Y, Hong J S, Jung J Y, Park M S, Suh D H (2012) Clinical and histological effect of a low glycaemic load diet in treatment of acne vulgaris in Korean patients: a randomized, controlled trial. Acta-Dermato Venerelogica, 92(3): 241-246. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  13. Desbois A P, Lawlor K C (2013) Antibacterial Activity of Long-Chain Polyunsaturated Fatty Acids against Propionibacterium acnes and Staphylococcus aureus. Marine Drugs, 11(11): 4544-4557. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  14. Khayef G, Young J, Burns-Whitmore B, Spalding T (2012) Effects of fish oil supplementation on inflammatory acne. Lipids in Health and Disease, 11:165. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  15. Jamilian M, Bahmani F, Siavashani M A, Mazloomi M, Asemi Z, Esmaillzadeh A (2015) The Effects of Chromium Supplementation on Endocrine Profiles, Biomarkers of Inflammation, and Oxidative Stress in Women with Polycystic Ovary Syndrome: a Randomized, Double-Blind, Placebo-Controlled Trial. Biological Trace Elements Research, Epub ahead of print. [Online- abstract only] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  16. B. Razavi M, Jamilian M, Kashan Z F, Heidar Z, Mohseni M, Ghandi Y, Bagherian T, Asemi Z (2015) Selenium Supplementation and the Effects on Reproductive Outcomes, Biomarkers of Inflammation, and Oxidative Stress in Women with Polycystic Ovary Syndrome. Hormone and Metabolic Research, Epub ahead of print. [Online- abstract only] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  17. Beckenbach L, Baron J M, Merk H F, Loffler H, Amann P M (2015) Retinoid treatment of skin diseases. European Journal of Dermatology, 25(5): 384-391. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  18. Carvalho Pontes T, Fernandes Filho G M C, de Sousa Pereira Trinidade A, Sobral Filho J F (2013). Incidence of acne vulgaris in young adult users of protein-calorie supplements in the city of João Pessoa–PB.  Anais Brasileiros de Dermatologia, 88(6):907-912. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  19. Reinoso Webb C, Koboziev I, Furr K L, Grisham M B (2016) Protective and pro-inflammatory roles of intestinal bacteria. Pathophysiology [Online- Epub ahead of print] PubMed (www.ncbi.nlm.nih.gov/pubmed).
  20. Cavallari J F, Denou E, Foley K P, Khan W I, Schertzer J D (2016) Different Th17 immunity in gut, liver, and adipose tissues during obesity: the role of diet, genetics, and microbes. Gut Microbes, 2(7): 82-89. [Online] PubMed (www.ncbi.nlm.nih.gov/pubmed).

Insomnia: what to eat for better sleep


Defined as ‘the inability to obtain an adequate amount or quality of sleep’, insomnia can have debilitating effects on daily life.  Difficulty falling asleep, waking during the night, or waking very early, can be linked to a multitude of factors, including stress, menopause, depression, medication, physical pain and consumption of caffeine and alcohol.1-8   Sleep experts advise us to practise good ‘sleep hygiene’ habits, such as banishing technology from the bedroom; keeping the environment dark, quiet and cool; and maintaining a regular wind down routine before bedtime.  However, it is also important to consider nutritional influences on sleep patterns.

”…dramatic fluctuations in blood sugar can either prevent you from getting to sleep, perhaps through feeling hungry or irritable, or wake you up with your heart and mind racing.”

Sugar, caffeine and alcohol all have a stimulatory effect on the body,9 causing blood sugar levels to surge, insulin to be released and glucose to either be directed into cells where it can be converted to energy, or stored as fat.  Blood sugar levels then drop significantly, triggering the release of the stress hormones adrenalin and cortisol, which increase the heart rate and release stores of sugar into the blood, preparing the body for action.  Such dramatic fluctuations in blood sugar can either prevent you from getting to sleep, perhaps through feeling hungry or irritable, or wake you up with your heart and mind racing.  Blood sugar can be maintained at balanced levels by eating regular meals and snacks, combining unrefined carbohydrates (such as wholegrain oats, brown rice and lentils instead of products containing white flour or sugar), with protein and essential fats (from oily fish, nuts, seeds and oils).10,11

Certain foods can influence the production of hormones and neurotransmitters (brain chemicals) which govern the sleep cycle.  Melatonin is the primary sleep hormone, produced by the tiny pineal gland in the brain, in response to darkness.  Caffeine may suppress melatonin production for up to 10 hours.12  Melatonin is made from the neurotransmitter serotonin, which in turn is made from 5-hydroxytryptophan (5-HTP).  5-HTP is derived from the amino acid tryptophan, which is found in protein-rich food, particularly turkey, chicken, tuna, eggs, oats, cottage cheese, tofu, beans, nuts, seeds, avocado and banana.13  5-HTP can be supplemented, but is contra-indicated with anti-depressant medications.14

”…eat a small snack containing carbohydrate before bedtime, such as half a banana, or an oatcake with cottage cheese.”

In order to convert amino acids such as tryptophan into hormones and neurotransmitters, the body requires some carbohydrate, which triggers insulin to help transport them into brain cells,15 so it can be useful to eat a small snack containing carbohydrate before bedtime, such as half a banana, or an oatcake with cottage cheese.  This will have the added benefit of helping to maintain blood sugar levels throughout the night.  The conversion of amino acids into brain chemicals also requires B vitamins,16 which are depleted by stress, sugar, alcohol and medication such as the contraceptive pill.  Good sources of B vitamins are fish, poultry, lean meat, eggs, beans, lentils, wholegrains, nuts, seeds and soya products.

”tryptophan… is found in protein-rich food, particularly turkey, chicken, tuna, eggs, oats, cottage cheese, tofu, beans, nuts, seeds, avocado and banana.”

Magnesium is known as ‘nature’s tranquiliser,’ thanks to its relaxing effect on the body.  Magnesium deficiency is very common, due to intensive farming causing depleted levels in soil and subsequently in plant foods.17 It is found in highest amounts in dark green leafy vegetables like broccoli, cabbage, spinach and kale, as well as in nuts and seeds, especially almonds and pumpkin seeds. However, it is relatively hard for the body to absorb adequate amounts of magnesium from food,18 particularly if the digestive system is compromised in any way.   A supplement of magnesium and calcium in a ratio of 2:1, taken half an hour before bedtime, can have a positive effect on sleep.  Herbal supplements may also be effective for some people and include valerian, hops, passionflower and lemon balm, although supporting evidence for their efficacy is less conclusive.19, 20 As with all supplements, it is best to seek professional nutrition advice, particularly if you are taking any medication.

View List of References

  1. Pillai V, Roth T, Mullins H M, Drake C L (2014) Moderators and Mediators of the Relationship Between Stress and Insomnia: Stressor Chronicity, Cognitive Intrusion, and Coping. Sleep, 37: 1199-1208. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  2. Kravitz H M, Zhao X, Bromberger J T et al. (2008) Sleep disturbance during the menopausal transition in a multi-ethnic community sample of women. Sleep, 31: 979-990. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  3. Ancoli-Israel S (2006) The impact and prevalence of chronic insomnia and other sleep disturbances associated with chronic illness. The American Journal of Managed Care, 12: S221-229. [Online] The American Journal of Managed Care (http://www.ajmc.com).
  4. Buysse D J (2008) Chronic Insomnia. The American Journal of Psychiatry, 165: 678-686. [Online] The American Journal of Psychiatry (http://ajp.psychiatryonline.org).
  5. Wilcox S, Brenes G A, Levine D, Sevick M A, Shumaker S A, Craven T (2000) Factors related to sleep disturbance in older adults experiencing knee pain or knee pain with radiographic evidence of knee osteoarthritis. Journal of the American Geriatrics Society, 48: 1241-1251. [Online – Abstract only] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  6. Drewes A M (1999) Pain and sleep disturbances with special reference to fibromyalgia and rheumatoid arthritis. Rheumatology (Oxford Journals), 38: 1035-1038. [Online] Rheumatology (http://rheumatology.oxfordjournals.org).
  7. Drake C, Roehrs T, Shambroom J, Roth T (2013) Caffeine effects on sleep taken 0, 3, or 6 hours before going to bed. Journal of Clinical Sleep Medicine, 9: 1195-1200. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  8. Park S Y, Oh M K, Lee B S, Kim H G, Lee W J, Lee J H, Lim J T, Kim J Y (2015) The Effects of Alcohol on Quality of Sleep. Korean Journal of Family Medicine, 36: 294-299. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  9. Battram D S, Graham T E, Richter E A, Dela F (2005) The effect of caffeine on glucose kinetics in humans – influence of adrenaline. The Journal of Physiology, 569: 347-355. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  10. Blaak E E, Antoine J M, Benton D, Bjorck I, Bozzetto L, Brouns F, Diamant M, Dye L, Hulshof T, Holst J J, Lamport D J, Laville M, Lawton C L, Meheust A, Nilson A, Norman S, Rivellese A A, Theis S, Torekov S S, Vinoy S (2012) Impact of postprandial glycaemia on health and prevention of disease. Obesity Reviews, 13: 923-984. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  11. Collier G, O’Dea K (1983) The effect of coingestion of fat on the glucose, insulin, and gastric inhibitory polypeptide responses to carbohydrate and protein. The American Journal of Clinical Nutrition, 37: 941-944. [Online] The American Journal of Clinical Nutrition (http://www.ajcn.org).
  12. Wright K P, Badia P, Myers B L, Plenzler S C, Hakel M (1997) Caffeine and light effects on night time melatonin and temperature levels in sleep-deprived humans. Brain Research, 747: 78-84. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  13. USDA Agricultural Research Service (2008). USDA national nutrient database for standard reference. [Online] (http://www.nal.usda.gov/fnic/foodcomp/search/)
  14. Hinz M, Stein A, Uncini T (2012) 5-HTP efficacy and contraindications. Neuropsychiatric Disease and Treatment, 8: 323–328. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  15. Richard D M, Dawes M A, Mathias C W, Acheson A, Hill-Kapturzak N, Dougherty D M (2009) L-Tryptophan: Basic Metabolic Functions, Behavioral Research and Therapeutic Indications. International Journal of Tryptophan Research, 2: 45-60. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  16. Zadeh S S, Begum K (2011) Comparison of nutrient intake by sleep status in selected adults in Mysore, India. Nutrition Research and Practice, 5: 230-235. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  17. Fan M S, Zhao F J, Fairweather-Tait S J, Poulton P R, Dunham S J, McGrath S P (2008) Evidence of decreasing mineral density in wheat grain over the last 160 years. Journal of Trace Elements in Medicine and Biology, 22: 315-324. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  18. Fine K D, Santa Ana C A, Porter J L, Fordtran J S (1991) Intestinal absorption of magnesium from food and supplements. The Journal of Clinical Investigation, 88: 396-402. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  19. Bent S, Padula A, Moore D, Patterson M, Mehling W (2007) Valerian for Sleep: A Systematic Review and Meta-Analysis. The American Journal of Medicine, 119: 1005-1012. [Online] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).
  20. Taibi D M, Landis C A, Petry H, Vitiello M V (2007) A systematic review of valerian as a sleep aid: safe but not effective. Sleep Medicine Reviews, 11: 209-230. [Online – Abstract only] PubMed Central (http://www.ncbi.nlm.nih.gov/pmc).