Thursday, 10 December 2015

Coffee and Health Part 1 – What is in coffee and how does it work?

It’s one of the most sought after commodities in the world right up there with crude oil and natural gas.  Whilst the former products are used to power cars, planes and industrial factories the humble coffee bean powers us human beings through the latest deadline, early morning, hangover or workout.  In the UK it’s estimated that we consume 70 million cups of coffee each day.  In recent years there has been a substantial growth in businesses specialising in coffee.  The turnover for these outlets was 6.2 billion pounds in 2013, a 6.4% growth from 2012, and 800,000 Britons report visiting a coffee shop at least four times per week.  This upward trend in the consumption of espresso style coffee substantiates the requirement to better understand the health implications of coffee, and the bioactive compounds in coffee.

I believe I come at this topic from a relatively unique perspective.  Not only have I got a fairly deep understanding of the hard science behind coffee and caffeine, I have also worked in a coffee shop on and off throughout my school and university years for eight years.  If I had to count the number of cups of coffee I have made it would most certainly be in the thousands, and similarly I have read hundreds of peer reviewed research articles on coffee.

So a little bit of background on coffee before going into the mechanics of how it does what it does.  Despite it now being grown in a number of countries, coffee originated in Ethiopia.  The coffee blend used to make your morning cuppa will always consist of Arabica beans which may also have added to them Robusta beans.  Arabica beans are very flavourful with less caffeine and tend to grow at higher altitude in comparison to Robusta beans.  Robusta beans are much more bitter and acidic than Arabica and contain much more caffeine, usually 50% or more, and typically grow at lower altitude.  The role of caffeine in plants is actually as a pesticide, hence robusta beans in lower areas have greater concentrations to protect the plant against a greater number or insects.

Coffee and caffeine typically go hand in hand how often have we heard the phrases “I need my caffeine fix”.  There is good reason for this caffeine has the predominant effect out of all the compounds in coffee.  Anyone who has had a strong cup of coffee will have felt that stimulant effect, that buzz that comes from consuming caffeine.  So I will now seek to explain what caffeine actually does in the body. 
The Formula of Caffeine 
When we look at the effects of any substance on the human body it’s important to consider the precise mechanisms of what is actually going on, to full understand the effect it is having.  This means getting quite deep into the science however I will try to make to make it as easy to read as possible.  The primary mechanism of caffeine is to act as an antagonist for adenosine receptors, more specifically the A1 and A2a receptors.  What this means is that caffeine binds to the adenosine receptor sites, therefore preventing adenosine from doing so.  Imagine coming into work to see a life size cardboard cut-out of yourself siting in your office, yes it may look like you and occupy the same space, but that doesn’t mean it can actually do the same job (having said this some days I feel a cardboard cut-out may be just as productive as me!).  This is essentially what happens with caffeine, on a molecular level it is structured very similarly to adenosine, so it binds to the same receptor sites but it can’t actually cause the same action that adenosine would.  
Caffeine Binding to Adenosine Receptor Sites  
The regular function of adenosine is to dilate coronary heart vessels, promote sleep, supress arousal and decrease renal blood flow.  Antagonism of adenosine receptors plays an important role in affect caffeine has on cognitive performance, alongside the inhibition of benzodiazepine receptor ligand (another neurotransmitter that slows down brain activity). Caffeine intake causes increases in neurotransmitters, including noradrenaline, dopamine, acetylcholine, glutamate and gamma-aminobutyric acid.  The increase in these neurotransmitters is what causes the “caffeine high” or “caffeine buzz”.  The net effect is a temporary increase in blood pressure and arterial stiffness, a feeling of alertness or stimulation and a mild diuretic effect.  Chronic consumption of caffeine leads to an up regulation in number and activity of adenosine receptors, also referred to as caffeine adaption.  This is the principle reason why habitual and non-habitual consumers tend to react differently to caffeine in studies.  It is also the reason why regular caffeine consumers often see themselves slowly increasing their intake.  As their body adapts they require more caffeine to get the same “buzz”.

The Structure of Caffeine Versus Adenosine
Another important consideration is the metabolism of caffeine, or the way the body processes caffeine.  Caffeine is absorbed rapidly from the small intestine, and is highly bioavailable.  It reaches peak plasma concentrations 30-45 minutes after consumption, and is delayed with food ingestion. Caffeine is metabolized into more than 25 metabolites in humans, mainly paraxanthine, theobromine, and theophylline.  Seventy two to eighty per cent of the metabolites from caffeine metabolism are paraxanthine.  Cytochrome P-450 1A2, located in the liver, is responsible for ≈ 95% metabolism in humans.  There are variances in the genes encoding for the enzymes that metabolise caffeine, this means that individuals will metabolise caffeine at different rates.  The normal half-life of caffeine is around 2.5-5 hours.  This means that if you consume 200mg of caffeine 2.5-5 hours later there will only be 100mg left in your system.  Carriers of the *1F allele variant metabolise caffeine slower than average, whereas carriers of the A2*1A gene metabolise caffeine at a higher rate.  Studies in regular caffeine consumers have often found increased activity of CYP1A2a, so they metabolise caffeine much quicker compared to non-caffeine consumers.  In fact the half-life of caffeine in these individuals have been reported to be as low as 1 hour.  Again in regular caffeine consumers, variances in the loci near BDNF and SLC6A4 have been detected which could impact consumption patterns by modifying the acute behavioural and reinforcing properties of caffeine.  So these consumers have genetic variances that actually make caffeine consumption seem more pleasurable.
A final factor (for now) when looking into this topic when it comes to coffee is, although caffeine is the main bioactive compound in coffee, there are a ton of other substances in there too!  Other important compounds in coffee include quinic acid, chlorogenic acid, citric acid, phosphoric acid, acetic acid, cafestol and kahweol.  Furthermore not every cup of coffee is created equally variances in blends, roasting process and preparation methods all impact the amounts of caffeine and other compounds in a cup of coffee.  This makes it difficult to thoroughly pool the research together, and draw definitive conclusions.  I have found that preparation method is something that is only staring to be considered in the research.

So there we have it a bit of back ground on coffee and caffeine, how it’s metabolised and what it’s actually doing in the body.  Coffee and caffeine remains a poignant focus of research for good reason.  It’s consumed in vast quantities and there are a number of questions that remain on its effect on short and long term health and performance.  What I’m hoping to do with these series of blog articles is bring evidenced based information on this debated, topic and hopefully provide some answers.  Stay tuned for the parts 2-4 which will be cardiovascular health and heart disease, sports performance and cognitive function. 

Sunday, 9 August 2015

The Future of Meat

I recently attended the Nutrition Society Summer conference entitled “The future of animal products in the diet.”  The conference was fantastic there was a huge diversity of speakers, coming at the issue’s from a myriad of perspectives.  The combination of informative presentations on the latest scientific research and lively debate, combined with a friendly “in it together” atmosphere made for a uniquely positive environment that I found to be very inspiring.  I am going to attempt to sum up, and give my opinion on, some of the main topics.

Is eating meat healthy?
A lot of the talks were focused around the health implications of eating meat.  This involved looking at some of the individual nutrients in meats and epidemiological trends in disease incidences.  As most of us know meat is an excellent source of protein containing both essential and non-essential amino acids.  Depending on the type, meat can also be a good source of several micronutrients including magnesium, zinc, iron and B12.  Its certainly true we can also get these nutrients from plant sources however, the proteins and micronutrients in meat are highly bioavailable.  An excellent example is heam iron, which has a bioavailability of around 20-30% whereas iron found in plants is only around 5%.

A topic that came up several times was the health implications of consuming saturated fat, of which meats, alongside dairy, contribute a significant percentage to our diet.  The general consensus was that that saturated fat seemed to have a neutral effect on cardiovascular disease mortality incidence and risk markers.  If you want to know more I have written an article on this HERE.  Omega 3 was also talked about in depth.  Consuming adequate amounts of omega 3 should be, in my opinion, a huge priority in public health campaigns.  Again I have more details on Omega 3 HERE.  An advantage of meat consumption that kept cropping up was that animal sources of omega 3 are already in the active forms, EPA and DHA.  Humans have an extremely limited capacity to convert the 18 carbon omega 3 fatty acid alpha linolenic acid, found in plant sources like flaxseed, to the longer chain omega fatty acids EPA and DHA.  At this point I want to point out that we eat whole foods we don’t just consume single nutrients.  Although saturated fat may not have a significant influence on cardiovascular disease as we first thought, if you consume lots of salami containing high amounts of salt and nitrates this could be detrimental. 

When it comes to meat and disease incidence processed meat appears to be the bad guy.  High consumption of processed meat was linked to cardiovascular disease, stroke, diabetes and certain types of cancer.  A large question mark here is what exactly is defined as processed meat?  For example a question was raised as to the effects of processed fish, this appeared to highlight a gap in the current knowledge base.  For me this means trying to stick to whole cuts of fresh meat, and if you’re unsure ask your butcher they should be able to tell you exactly what has or hasn’t been done to their product.

Meat farming practices, feeding
In an effort to make farming meat more sustainable and the product more nutrient dense, there has been a lot of work done on feeding practices.  This is something humans have been doing for years essentially trying to get an animal’s weight to increase quicker.  This has been done through selective breeding of animals with a better feed efficiency (able to put on weight with less food).  It was explained in one of these lectures that feeding cows fish oil or micro algae was being used to increase the EPA and DHA content in beef.  For me I feel like this is adding an extra step that isn’t required if we just eat seafood.  If I wanted to go to London from Edinburgh I wouldn’t go via Moscow!  Slight hyperbole but I think that’s what we are doing here.  It’s quite sad that as a population we are so adverse to consuming fish that feeding cattle fish oil is what we are turning too.  Moreover the EPA and DHA content of this enhanced meat still paled in comparison to what is in fish.  From a sustainability stand point I don’t think this makes sense either, a lot of oceans are over fished so why give these fish to cattle to produce a beef product that has less EPA and DHA compared to the original fish.  On the other hand micro algae may be a slightly more promising option as at least this can be grown fairly easily, but again I just think people should try and eat fish.  Another issue with these find of changes to farming practices is it is unlikely that farmers would be able to implement any of these strategies without some sort of financial backing.

Meat Sustainability Carbon Footprint
This was a big topic during the conference.  The world’s population is expanded at a rapid rate growing around 1.14% each year.  This raises huge questions on how we are going to efficiently feed this expanding population.  To compound this we have the issue of global warming.  Now I am not an expert in this area at all and won’t pretend to be.  Producing meat on the scale we currently do has a huge carbon footprint and requires vast quantities of water.  We need to produce the feed itself, transport the animals and meat and also the animals have an impact themselves particularly cows due to the amount of methane they produce.

It has become a bit of a joke but cows do produce a lot of methane especially if you consider the fact that there is around 1.4 billion cows.  What is less funny is this image of an industrial farm in the states.  That green coloured "pit" in the middle is a whats known as a "waste lagoon".

Going forward this has to change and the solutions appear to be an overhaul of farming practices or reduce the demand i.e. eat less meat.

What should we do?
One of the best quotes from the conference was in my opinion….
"We don't need to demonise meat, but we should recognise its cost” - Professor Tim Benton
Personally I don’t think we should all become vegetarians.  I enjoy eating meat and it is a great source of several nutrients.  What I do support is a reduction in meat consumption and a mindfulness of what types of meat we are consuming and where it’s coming from.  I think western populations are often guilty of constantly wanting more more more, and this just isn’t sustainable.  The food and agricultural industries have a huge role to play moving forward as we seek to make meat consumption a more viable long term option.  However we as consumers need to take some responsibility for our current predicament and make some changes to our eating habits

So what can we do?
        Cut down on meat and consume more alternative protein sources - Current recommendations from the British Nutrition Foundation is to consume a maximum of 80g of meat per day.  Beans, legumes and pulses are all good sources of protein and are high in fibre.  Several meat alternatives exist too such as Quorn and hey if it’s good enough for Mo Farah.  I have to admit I didn’t have a particularly high opinion of Quorn but a talk from Dr. Tim Finnigan educated me on the food product, highlighting that Quorn is a complete protein with a high bioavailability (actually higher than some meat products). 

·      Prioritise fresh cuts of meat over highly processed products, and shop local.  Processed meat was consistently shown to have a negative impact on health.  By buying fresh cuts you are looking after your health and, if you buy from a butcher, you are supporting a local business.
·       Spend the same but buy less – go for quality of quantity and look for sustainably sources meat products.  Companies are usually quick to advertise if their meat is sustainable it just takes a little time to check over the labels.

·      Eat the whole animal – A mantra I have lived by over the last couple of years is if I am going to eat meat I am going to make an effort to consume a mix of cuts.  This includes eating organ meats on a fairly regular basis.  These are cheap and extremely nutrient dense and there is a ton of recipes out there to get them into your diet.  WARNING organ meat tends to be very high in vitamin A so it wouldn’t be advisable for anyone who is pregnant to consume any more than once per week.

·       Try eating some wild caught game – This is tricky to come by in the UK but its a much more sustainable meat.  The animal is usually fed on its natural diet and game tends to be both lean and nutrient dense venison being an excellent example.

Eating insects

There was a talk from Professor Arnnold van Huis, co-author of “the insect cookbook”.  At first, to me, this seemed like it was going to be a talk about the “novel” idea of consuming insects.  It turns out this is a legitimate option that many countries have already adopted.  Farming insects is a relatively easy and very sustainable practice, which has been practiced across regions of Asia for a number of years.  These insects can be fed to animals or consumed by humans, and are a source of protein and nutrients.  Supermarkets in the Netherlands have already started selling certain varieties of insects and cricket flour can easily be purchased from online retailers.   The issues moving forward here in the UK is ticking all the boxes on food regulations, but it seems the ball has been set in motion on this.  Another big issue is just getting past the notion of eating insects, which in western cultures is generally thought of as well a bit weird.  I will certainly be interested to see if insects hit our supermarkets in the future and how they will be received.  Professor  Van Huis has actually done a Ted Talk and it can be viewed here.

Rather than conclude with a lengthy statement I’ll just sign off with this video which I think sums up the sustainability of meat quite well.  I will say that personally I probably am going to cut down my meat consumption a little, especially processed meat.  I am into my sport and I enjoy training and with that always comes the importance of consuming high quality protein.  By spending the same and eating less, focusing on sustainably sourced meat and alternative protein sources even as a fairly active person I don't think I have anything to worry about regarding protein intake.

Saturday, 20 June 2015


Indulgence and Binging
At one point or another we’ve all indulged in some less than ideal food choices, or in some cases gone on an all-out food binge devouring everything insight until a state of food coma is reached.  The food we indulge in will vary between individuals it may be massive curry, a slab of cheese cake or anything in between.  Unfortunately what follows is often an overwhelming feeling of guilt, reinforced by some physiological “symptoms” of overindulgence water retention, lethargy, mind fog etc. can all occur.  My opinion is we should be able to treat ourselves every now and then and not have to feel this way, it’s about maintaining balance and viewing food as an experience.  So here are some insights and tips from me when it comes to treating ourselves.

Be Mindful of What You’re Doing
This article isn’t designed to be an all access pass to the Chinese buffet, it’s about making conscious decisions on what we are doing and if it’s constructive towards our goals.  If your goal is fat loss and you overindulge therefore going above you calorie threshold, it’s important to be aware that what you’re doing isn’t constructive in terms of your individual goal.  However fat loss doesn’t boil down to individual days it’s about consistency over weeks, months or even years.  So going out with friends and having a burger with fries and milkshake on occasion won’t suddenly make you pile on the pounds, as long as you are consistent throughout the rest of your diet.  Just because you are dieting doesn’t mean you should miss out on social experiences and good food.  The problem tends to arise when this becomes and all too regular occurrence, this is when progress starts to slow down or regression occurs.  To wrap up this point be conscious of your decisions to indulge, how often it’s occurring and if it’s constructive, but don’t feel guilty about experiencing food and being social when the time comes.    

Pre Plan and Really Make the Most of it
This is a fairly subjective point, what you chose to indulge in is your own provocative but this is what I like to do.  If I’m going to indulge I usually try and plan to do so on social occasions whether it’s a family meal, a celebration or something of that nature.   These occasions are meant to be enjoyed and I don’t want to take away from the experience by worrying too much about my calories or macros.  Another time you may want to consider pre-panning your indulgence is scheduling re-feeds whilst dieting.  There is evidence that occasionally increasing calories whilst dieting can actually be helpful in terms of preserving lean tissue and losing fat.  The degree to which these are necessary, the frequency and the caloric intake will vary depending on individual psychology, physiology and goals.  For example someone who has had previous issues with food binging probably should be careful regarding the use of these days, or  for someone who has a degree of insulin resistance or issues managing blood sugar it may not be optimal for them to include re-feeds too often.
If you are going to indulge I think it’s important to make the most of it.  Splash out on some quality ingredients and foods to maximise taste and experience.  I’m always plugging the message of eating whole foods, and I believe that should apply to when we are treating ourselves too.  I’d much rather treat myself to good quality beef burger with bacon on homemade bread with sweet potato fries than on a MacDonald’s meal.  I know for a fact that I am going to enjoy the taste of that burger much more and it’s still going to be providing me with a lot of nutrients.  You’ve been working hard on your diet so when you’re treating yourself treat yourself right.

 Difference between Indulgence and Binging
It’s important to differentiate between a bit of a treat and an all-out binge.  As you can tell I am all for the occasional treat or re-feed but all out binges not so much.  The problem with all out binges is…
1.  They are often not planned, they tend to be impulsive due to severe hunger or cravings
2.  They lead to extreme caloric surplus which can be detrimental to weight loss goals
3. The “food hangover” the next day is much more severe with more guilt
4. Often one binge can lead to another supporting yo-yo dieting
To avoid food binging it’s important we understand why we sometimes get this insatiable need to eat copious amounts of food.  I think the most common reason is over restriction of calories or carbohydrate.  When we restrict energy or carbs it’s possible to experience hypoglycemia (low blood sugar).  When we have low blood sugar our bodies react by craving foods high in sugar, it needs that instant hit of fast absorbing carbs to maintain homeostasis.  This is why food binges tends to mainly consist of foods high in both refined carbohydrate and calories.  My tips for avoiding this again comes back to being mindful and thinking about what’s going on in your body.  If you’re having these crazy cravings recognise that you may be over restricting your calories or carbohydrate, solution consume an extra 100-300 calories from whole food carb sources such as potatoes, brown rice, quinoa, squash or fruit.  This should give your body the carbs and energy is shouting out for without the unplanned 3000kcal surplus.  Again don’t feel guilty about these extra carbs and calories, your body is showing signs of over restriction, and the added calories will likely not take you out of a caloric deficit.

Tips for the day after
So you’ve decided to treat yourself and the next day you’re not feeling too great. 
1.       Just to reiterate don’t feel guilty this can lead to unhealthy relationship with food, when really food is awesome
2.       Do something active go for a long walk or exercise
3.       Drink plenty of water, usually excess salt and sugar leads to water retention so we need to make sure we stay hydrated
4.       Don’t starve yourself to “make up for it” this will only lead to potential hypoglycaemia and another binge/cheat.  Sure have a lighter breakfast for me I usually have one less egg or 25g less oats nothing too restrictive.
So there we have it my thoughts on food indulgence.  To sum up yes its ok to indulge every now and then, try to avoid binging, be mindful and favour quality whole foods evening when treating yourself. 

Wednesday, 27 May 2015


In an earlier article I talked about the importance of focusing on nutrient density and quality and not just calories.  The first law of thermodynamics essentially boils down to:

Energy in (from food)-energy burned (physical activity and other metabolic processes) = energy balance

So if energy balance is positive, we gain weight and if it’s a negative we lose weight.  This has been the basis for many nutritional programmes whether the aim is to gain or lose weight.  I'm not here to argue with this rule as it’s completely correct, we must consider caloric intake for nutritional strategies.  What I do want to discuss is another major consideration we need to make when it comes to the food we eat.  The biological processes in our body are regulated by a number of hormones, and it’s important to understand these hormones and their functions for health, body composition and performance.  I am a strong believer that a better understanding of our bodily processes will lead to us making more positive diet and lifestyle choices.  In short knowledge is power. 
A hormone that most people will recognise is insulin.  Insulin one of the hormones responsible for the metabolism of carbohydrate, amino acids and fats.  It is a peptide hormone that is produced in the beta cells in the pancreas.

How it works
When carbohydrate is digested it enters the blood stream, this triggers both the synthesis and secretion of insulin from the beta cells.  To go a little deeper into the mechanism glucose in the blood stream stimulates calcium ions to move into the beta cells, thus triggering a calcium-dependant exocytosis of insulin through microtubules releasing it into the blood stream.  Amino acids, particularly leucine, fatty acids and ketone bodies have all been shown to exert a weak stimulation of insulin secretion, however these are dependent on the presence of glucose in the blood to be effective.
Insulin has many functions, however its main role is to act as a transporter for glucose into cells.  Glucose is an energy source for all cells in the human body.  Skeletal muscle, cardiac muscle and adipose (fat) tissue are heavily reliant on insulin to deliver the glucose they require.  Insulin stimulates the translocation of glucose transport type 4 (GLUT 4) from within cells to the outside membrane allowing it to accept glucose and transport it into the cell.
So when we consume carbohydrate, blood glucose levels rise, insulin is secreted and glucose is taken up by the cells to be used as energy.  The body is constantly working to maintain a stable blood glucose level of around 4mmol/l.

The condition most associated with insulin is diabetes.  There are two main types of diabetes type 1 and type 2.

Type 1 is characterised by a loss of beta cells in the pancreas therefore reducing the organs ability to secrete insulin.  The condition is usually a result of an autoimmune reaction.  It generally develops in childhood or early adulthood, and requires treatment with exogenous (from outside the body) insulin.

Type 2 occurs as a result of cells becoming insulin resistant, which I will go on to explain in more detail.  It normally presents in adulthood, however it is becoming more frequently diagnosed in children.   Type two diabetics can sometimes go on to require insulin to manage their condition.  Type 2 diabetes makes up around 90% of all cases of diabetes.

Glycemic Index and Glycemic Load
When discussing insulin and nutrition glycemic index and glycemic load is often brought up.  According to Diabetes UK the glycemic index is “A ranking of carbohydrate-containing foods based on the overall effect on blood glucose levels. Slowly absorbed foods have a low GI rating, while foods that are more quickly absorbed have a higher rating.”  The scale goes from 0-100 with pure glucose being 100.  They define glycemic load as “A measure that takes into account the amount of carbohydrate in a portion of food together with how quickly it raises blood glucose levels.”  I quite like this is a measure, as it considers both the type of food and the portion size.  A low glycemic load is between 0-10, medium 11-19 and anything above 20 is considered to have a high glycemic load

Insulin Sensitivity/Resistance
So I have already mentioned the term insulin resistance so let’s delve into what it is.  Insulin resistance is a state in which the cells response to insulin is impaired.  As a result glucose cannot enter the cell and blood sugar levels remain elevated.  Now because blood glucose levels remain high the body reacts by creating and secreting more insulin, so now we have elevated levels of both blood glucose and insulin (hyperinsulinemia).  The pancreas will continue to release insulin until blood sugar levels drop back down to within normal limits.  With insulin resistance it’s not a case of you have it or you don’t, individuals will vary on a scale between being insulin sensitive and insulin resistant.  When someone has high insulin sensitivity it’s like insulin is communicating with the cells on the latest 4G smartphone, whereas being insulin resistance is not unlike the two bean cans tied together with string.  I should also point out our insulin sensitivity varies depending on a variety of factors including time of day, diet and training stimulus.

Insulin resistance is associated with an increased risk of a number of health conditions including diabetes, hypertension, atherosclerosis (a precursor to coronary heart disease), obesity and polycystic ovaries.

There are several genetic risk factors for insulin resistance, however diet and lifestyle plays a huge role in both the development and management of the condition.  Being overweight or obese and/or having a diet high in refined carbohydrate significantly increase the risk of an individual becoming more insulin resistant.  In terms of prevention a healthy balanced diet with an emphasis on single ingredient whole foods, alongside regular activity is certainly the way to go.  When an individual is already to some degree insulin resistant the dietary strategy becomes a little more complicated and debated.  Most recommendations are that when consuming foods rich in carbohydrate aim for those with a lower glycemic index (e.g. brown rice, beans, pulses and oats).  There is also evidence to support the use of low or moderate carbohydrate diets to manage and even reverse insulin resistance.  The purpose of this article is not to debate the varying dietary strategies, if you or someone you know is found to be insulin resistance or diagnosed as pre-diabetic, advice should be sought from primary care providers as dietary strategies should be ideally tailored on an individual basis.
Low Glycemic Index Foods
So to sum up here what we generally want is to maintain a high degree of insulin sensitivity and less insulin resistance.  To test for insulin resistance an oral glucose tolerance test can be performed.  This involves consuming a glucose drink in a fasted state and monitoring blood glucose levels before ingestion and 30, 60 and 120 minutes post ingestion.  The speed at which the body lowers blood glucose levels back to normal indicates how inulin sensitive or resistant an individual is.

Insulin as an Anabolic Hormone 
The final thing I wanted to touch on in regards to insulin is its use as an anabolic hormone.  Because insulin facilitates the transport of carbohydrate and amino acids into the cells it promotes an anabolic environment, as well as preventing catabolism.  It is essentially delivering your muscles the fuel they need to perform, recover and grow.  Strategically manipulating insulin is something body builders and athletes have been doing for years.  This is normally achieved by consuming fast acting (high GI) carbohydrate before and/or after work outs.  Now I would be completely naive to ignore the fact that insulin abuse is a problem in the body building community.    To take advantage of the anabolic properties of insulin some body builders give themselves insulin injections.  It’s certainly not something all of them do, however a survey of 450 body builders found that 10% admitted to abusing insulin.  This is extremely dangerous, it can cause hypoglycaemic events, pancreatitis, coma and even death.  So unless you require insulin for a medical reason, the risk of injecting more far outweighs any potential benefit.

So there we have a quick whistle stop tour about insulin and its role within the body.  Hope you enjoyed it.


Accurso, A., Bernstein, R., Dahlqvist, A., Draznin, B., Feinman, R., Fine, E., Gleed, A., Jacobs, D., Larson, G., Lustig, R., Manninen, A., McFarlane, S., Morrison, K., Nielsen, J., Ravnskov, U., Roth, K., Silvestre, R., Sowers, J., Sundberg, R., Volek, J., Westman, E., Wood, R., Wortman, J. and 
Vernon, M. (2008). Dietary carbohydrate restriction in type 2 diabetes mellitus and metabolic syndrome: time for a critical appraisal. Nutr Metab (Lond), 5(1), p.9.

Davies, A., Blakeley, A., Kidd, C. and McGeown, J. (2001). Human physiology. Edinburgh: Churchill Livingstone., (2015). Diabetes UK, UK Diabetes Resource, Diabetes Symptoms, Diabetes Diet, Gestational Diabetes. [online] Available at: [Accessed 25 May 2015].

Evans, P. (2003). Insulin as a drug of abuse in body building. British Journal of Sports Medicine, 37(4), pp.356-357.

Fox, S. (1996). Human physiology. Dubuque, IA: Wm. C. Brown.

Kumar, P. and Clark, M. (n.d.). Kumar & Clark's clinical medicine.

Westman, E., Yancy, W., Mavropoulos, J., Marquart, M. and McDuffie, J. (2008). The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab (Lond), 5(1), p.36.

Saturday, 9 May 2015

Nutritional Supplements

Nutritional science has come a long way in the last few decades.  Researchers are constantly finding new patterns and mechanisms, in the pursuit of improving and optimising health.  Coinciding with the advances in the field, the supplement industry has exploded.  Twenty years ago you might have been lucky, or unlucky enough to have grandma force feed you some cod liver oil.  Now supplements stores are popping up on the high street and online with a myriad of vitamins, minerals, plant extracts, individual amino acids and so much more.  The purpose of this article isn’t to detract from or promote a particular supplement but more to address the use of supplements in general.  I will however be using some examples to illustrate a point, I have no affiliation with any products or brands.   Do we need supplements?  When can they be useful?  Are they safe?

The oxford dictionary defines a supplement as “a thing added to something else in order to complete or enhance it.”  So we take supplements to complete or enhance our diet and that’s what I want to focus on first.  I don’t believe we should look to dietary supplements to compensate for a poor diet.  Popping a multi vitamin does not make up for not consuming fruit and vegetables.  It may be better than nothing but is the notion of “I’ll just take this pill, eat whatever and be fine” promoting a healthy attitude?  My personal take is we should only consider supplementation in the following scenario’s

·         It would be extremely difficult to get the required amount through diet alone. (e.g. creatine has been shown to enhance performance but it would be extremely difficult to get the required dosage through just food).
·         You have a deficiency that would be difficult to address through diet alone (e.g. most of our vitamin D comes from being synthesised within our skin cells and requires sunlight particularly of the UVB variety which we lack in the UK most of the year).
·         You have an ailment where a specific nutrient in a specific quantity could help (e.g. the amino acid lysine can be used to fight of cold sores).
·         You have got your diet down to a tee and are really looking to optimise your health and performance.

If you are in the situation where you have been taking supplements to try and compensate for a poor diet, I think it’s time to start looking introspectively at what you’re currently doing.  

I have a few pet peeves when it comes to supplements and the way they are marketed
The first is, it seems we are always looking for a magic pill.  There is no greater example of this than the slimming pills that are currently on the market.  As much as there may be some evidence to support the ingredients in some, they send a terrible message to anyone trying to lose weight.  Losing weight isn’t about taking a pill and watching the fat just drop off, it’s about making sustainable lifestyle changes.  The problem is often people think they can just take a pill and eat whatever they like.  This isn't entirely the supplement industry’s fault, we ourselves have to be realistic.  If it were that easy why rates of obesity continuing to rise?  Facing up to reality and making changes isn't easy but it’s the first step to becoming healthier and happier, the answer isn't in the bottom of a slimming pill tub.

Secondly the benefits of certain supplements are often sold based on what I would call “half sciences”.  This would be a claim that is based on some scientific evidence but maybe doesn't tell the whole story.  An example of this would be collagen supplements. Our skin is made up of a lot of collagen hence it is popular supplement choice for those striving for healthy skin.  What is often not mentioned is that collagen is comprised of several amino acids, meaning it gets broken down in the gut like any other protein.  So once its broken down it needs to be reformed to make collagen, which is an incredibly complex biological process.  Furthermore once its broken down your body doesn’t care that you have consumed a collagen supplement, that could have been any protein rich meal full of amino acids.  Also if you lack the other nutrients required for collagen formation particularly vitamin C collagen supplements won’t necessarily lead to that perfect complexion.  So collagen supplements aren’t useless in fact several studies have found positive results in term of skin health, however it’s not as simple as we often lead to believe in the advertising. 

The price of supplements is a tricky subject.  Generally you get what you pay for, cheap supplements for the most part are not the same quality as more expensive varieties.  Some supplements can be quite pricey, which is why I urge people to do the research into exactly what each supplement contains and what are the potential benefits, do you really need it?  It goes back to the magic pill perception I mentioned earlier.  Often people view supplements as an easy option so they spend a fortune on them, when in reality a diet and lifestyle change could be more effective.  I generally tend to find the more educated an individual becomes in nutrition the less supplements they take and more specific they are about their supplements.  Currently the only supplements I take are Vitamin D in a subliqual form and fish oil.  There other supplements I may take for a specific purpose for example creatine or alpha lipoic acid but for the moment those are the only two.  This hasn’t always been the case let me rattle off the list of supplements I have taken in the past: fish oil, multi vitamin, 5 HTP, l-carnitine, BCAAs, green tea extract, acai berry extract, CLA and ZMA.  Again I’m not saying these aren’t good supplement choices, however I believe I was putting too much stock into the benefits they proposed rather than looking into my own diet and lifestyle habits.  This has been a big focus for me this year, to take stock of what I’m eating and what I’m doing activity wise and try and optimise that for me and my goals as best I can. As I’m kind of figuring that out then and only then will I consider adding in some additional supplements to further enhance my diet.

An important thing to consider when you’re doing your research is where is the information coming from.  If its from a supplement store or someone affiliated with a supplement company, bare in mind at the end of the day they are trying to sell you something.  Take your time check the credentials of the person selling you the supplement are they qualified to advise you on the supplement? do they actually know their stuff?  If it is an online article do they provide references to scientific literature, just saying “studies show that” really isn’t enough.

It’s important to get supplements from credible companies.  This is especially true when shopping online.  It’s so easy to set up an online store these days, anyone can do it.  This leads to a lot of non-regulated supplements being sold, these theoretically could have just about anything in them.  In fact I know in recent memory, some pre-workout supplements in America were found to have illegal stimulants in them.  The moral of the story is to not only research your particular supplement of choice, but also the retailer and company producing the products to ensure you are getting a legit supplement.

One final thing is to be wary of particularly high doses of anything.  Generally what we are looking for is what’s known in medicine as the lowest effective dose.  This is the dose large enough to illicit a positive reaction, but low enough that is causes the least amount of potential side effects.  It’s a case of you certainly can get too much of a good thing.  For example a recent study picked up by the media looked at vitamin E and cancer incidence.  I was expected that giving vitamin E supplements would reduce the incidence of cancer, due to its antioxidant action.  The results actually showed that taking a vitamin E supplement boosted the risk of developing high grade prostate cancer.  Now there were several flaws in the study design and the way the study was portrayed in the media.  For a full breakdown I urge you to watch this video, which explains the flaws very well.

What I took from this was that we should be wary of taking high doses of anything.  Be careful if you feel you need to increases the dosage, do it very slowly with small increments to find that lowest effective dose and do so under a medical professionals supervision. 

To conclude supplements can be great, there are so many benefits they can illicit.  However, they shouldn’t be relied on to make up for a poor diet.  Make sure you do your research, and preferably get your information from a unbiased or reliable source.

Thursday, 30 April 2015

The Saturated Fat Debate

Recently as part of a nutritional science module I was given several options of essay subjects, and one of them really jumped out at me.
1)        Nutrition science continues to evolve and we should always challenge the accepted view when new evidence emerges. Discuss this statement, using examples of controversial areas within the subject area of public health nutrition.

Immediately I thought about saturated fat and heart disease.  I said to myself “Finally this is the motivation you need to actually go out and do a ton of reading on the subject to get a full understanding”.  There is loads of books, articles and media posts going round addressing this subject.  What I’m hoping to do with this article is present an objective view of the scientific evidence behind saturated fat and heart disease, and generally shed some more light on fairly complex debate.  So here it is a kind of adaption of the essay I wrote for this module.
I think there is a couple of things I should explain before delving into the article.

LDL (low density lipoprotein) Cholesterol – often referred to as “bad” cholesterol.
HDL (high density lipoprotein) Cholesterol – often referred to as “good” cholesterol.  HDL cholesterol scavenges and removes LDL cholesterol

Relative Risk (RR) - measures the magnitude of an association between an exposed and non-exposed group. It describes the likelihood of developing disease in an exposed group compared to a non-exposed group.
n-3 PUFA – Omega 3 Fats
Foods that are high in saturated fat include....
Red meat
Processed Meat
Animal Fats

Nutritional science is constantly developing as more research is conducted and analyzed.  This requires governing bodies and health advisory committees to adapt when new evidence presents itself.  Saturated fat (SF) has been a focus of public health, as part of nutritional strategies to prevent cardiovascular disease (CVD).  The current guidelines in UK are that SF should contribute no more than 11% to total energy, Current intakes are 12.6%.  It is commonly accepted that SF raises plasma LDL cholesterol, a common risk factor for CVD.  Recently clinical and epidemiological research has been published that appears to dispel the link between SF and CVD.    You may have seen these studies portrayed in media, none more prominent than the headline “Eat Butter” on the front of the Time magazine accompanied by this image showing the apparent change in stance of the scientific community.
Undoubtedly this contradictory message leads to confusion.  I’ve spent a bit of time studying nutrition and the headlines perplexed me, I was thinking how could everything we have been told about saturated fat be untrue.  I think for the sake of the general public just looking to lead a healthy happy life we need to re-evaluate the evidence regarding SF and CVD so a clear evidence based public health approach can be made.
How does Saturated Fat potentially increase risk of CVD?
A diet high in SF reduces esterification of cholesterol and leads to higher concentrations of non-esterified cholesterol.  In response to this, hepatic concentration of LDL receptor mRNA is reduced, consequently LDL receptor activity is reduced leading to raised plasma LDL.  In the development of CVD LDL particles are oxidized within the arterial matrix.  Oxidised LDL leaks into, and accumulates in the sub endothelial space.  Macrophages preferentially take up the oxidised LDL forming foam cells.  Foam cells deposit accumulated oxidised lipids between the endothelium and the arterial smooth muscle, causing stenosis.  This can lead to both ischemic heart disease and cerebrovascular accident.   Imagine LDL particles as drunk drivers there is a greater risk these guys are going to crash into the side of the arteries and cause a massive tail back.  HDL essentially acts as the police or the AA cleaning up after these inconsiderate atherogenic little buggers. 

Contradictory Evidence
Before I go into the contradictory evidence its important to outline why we need saturated fat and cholesterol, what positive bodily processes are they required for?  saturated fats are structural components of sphingolipids and ceramides, which are important components of cell membranes, skin and myelin.  Myelin is particularly interesting in my opinion, it acts as an insulator around the axis of a neuron.  This is why the use of statins ha been associated with higher risk of dementia.  There is lots of other potential benefits to consuming adequate saturated fat including butyric acid which has been linked to protection from cancer and production of caprylic acid, which acts an antiviral agent.
Two large meta-analyses have found evidence that SF intake is not linked to CVD incidence or mortality.   An analysis of prospective cohort studies, including 347,747 participants with a mean follow up of 14.3 years, found that SF intake was not associated with an increased risk of CVD (RR 1.00).  A systematic review and meta-analysis including data from prospective cohorts, observational and randomised control trails, concluded that there currently was not enough evidence to support saturated and polyunsaturated fat (PUFA) guidelines in relation to coronary heart disease (CHD). The study included data from 659,298 participants.  In the prospective cohort data, when the top and bottom thirds of dietary intake were compared CHD RR was 1.02 for SF, 1.00 for monounsaturated fat (MUFA), 0.87 for PUFA, 0.98 for Omega six fat and 1.16 for trans fatty acids.  Furthermore in the studies that measured fatty acid bio markers SF was associated with a RR of 1.06.  Both of these papers relay heavily on prospective epidemiological data.  These require dietary assessment methods where under and over reporting of food intake is common, and they do not account for variability in diet over time. 

A review into the effect SF has on blood lipids from epidemiological, animal and human studies, pointed out the inconsistencies in blood lipid data.  Some trials reporting negative effects and others reporting either neutral or positive effects related to SF intake.  Furthermore various biomarkers have been used to assess CVD risk including total LDL, total cholesterol to HDL ratio and LDL particle size, creating more inconsistency.  The authors proposed that the negative effect of SF on blood lipids was related to a lack of n-3 PUFA, rather than SF alone.  This hypothesis was based on evidence that SF works synergistically with n-3 PUFA, leading to an increase in n-3 PUFA concentration in plasma and liver lipids.  This theory is mostly based on animal studies however some human trials were cited.  A postprandial trial on 59 participants found that when SF was combined with a docosahexaenoic acid rich n-3 PUFA formula, reductions in non-esterified fatty acids occurred compared to SF alone.  Postprandial means the measurements were taken shortly after feeding, so no long term follow up was performed.  The study cannot fully support the hypothesis that SF and n-3 PUFA work synergistically, only that n-3 PUFA may negate some of the negative effects of SF.  More research is required to support this theory and to establish mechanisms and dose response’s.  This study does highlight that previous research on SF has often failed to consider how n-3 PUFA could affect plasma lipid levels.  A large number also did not consider that a particular fat group will never be isolated in the diet.  Using biomarkers as risk factors for CVD is limiting as the effects of diet on CVD risk are mediated by, many pathways with blood lipids being only one.  Although these biomarkers do provide some evidence of increased CVD risk, CVD incidence and mortality are needed to assess the effects of dietary contributors to CVD. 

So biomarkers are fairly good tool for measuring CVD risk, however really we need to be using CVD deaths and incidence as an end point for the most reliability and validity.  Do you see the problem here?  Well if were are doing a randomised control trial we cant ethically give humans something we think might do them harm, so we have to relay on prospective epidemiological studies which follow people and try and figure out trends.  The problems with epidemiological studies are its difficult to accurately assess food or nutrient intakes, and there is so many factors that contribute to CVD risk outside of saturated fat intake its difficult to control for all those factors.  The alternative is animal models which again contribute to the evidence base, but effects do not always translate to free living humans.  You see what I mean when I said it’s a tricky subject.

How do saturated fats compare with other fatty acids and carbohydrate?
When evaluating the recommendations to lower SF intake, it is important to consider the nutrients that replace them.  Current guidelines are to replace SF with MUFA and PUFA. 
To investigate the implications of these dietary changes, eleven cohorts were pooled encompassing 344,696 participants with follow ups varying between four and 10 years.  Five percent total energy from SF was replaced by PUFA, MUFA or carbohydrate.   PUFA was associated with significant reductions in cardiac death and coronary events, RR 0.74 and 0.87 respectively.  Replacement with carbohydrate was associated with a significant increase in coronary events and a non-significant reduction in coronary deaths RR 1.07 and 0.96 respectively.  MUFA replacement was no associated with any change in CVD.

Substituting SF with PUFA has yielded positive results. A systematic review and meta-analysis of RCTs, including data from 13,614 participants, found an overall RR for myocardial infarction or coronary death of 0.81.  Furthermore a meta-regression found that study duration played a significant factor with longer duration studies showing greater benefit.  This is important as most dietary guidelines are encouraged to be followed over a lifespan.  If longer duration translates to greater reductions in risk, the evidence for replacement of SF with PUFA is valuable from a public health perspective. In addition it has been estimated that countries following a westernised diet could expect a mean reduction of 0.06mmol/l in total cholesterol, translating to a 2-3% reduction in CVD incidence by replacing 1% of total energy from SF with 0.5% of PUFA. 
The evidence that replacing SF with MUFA providing a benefit to cardiovascular health is inconclusive.  In human trials MUFA is predominantly derived from meat and dairy products, which are also high in SF, this could explain the lack of protective association.

Evidence that replacement with carbohydrate is mixed.  This could be down to a lack of evidence addressing the specific type of carbohydrate that is being consumed.  In a cohort of 53,644 low glycemic index carbohydrate replacement was associated with an OR of 0.88 for myocardial infarction, this association was not statistically significant.  In the same cohort high glycemic carbohydrate replacement was significantly associated with an OR of 1.33 for myocardial infarction.  This is supported by blood lipid data from a human cohort of 4301, which showed high carbohydrate intake to be associated with significantly higher LDL levels.  Furthermore fibre density was inversely correlated with very small, small and medium LDL particles.  Replacing SF with high glycemic carbohydrate increases total triglycerides and decreases HDL and LDL particle size.  The mechanisms behind this effect are currently not known, however these changes do present a higher risk for CVD.  It is particularly concerning that high glycemic carbohydrate decreases LDL particle size as these are more atherogenic, even in populations at low risk of CVD. Another important factor to consider is the metabolic health of an individual.  Carbohydrate replacement in otherwise healthy individuals is more likely to bring about benefits than in overweight or obese populations, who a have higher prevalence of insulin resistance.

Examples of Refined Carbohydrate Foods

Is it Important to Differentiate between Saturated Fatty Acid Types and Sources?
There is growing evidence that it may be important to differentiate between subclasses of SF.    Lauric (12:0), myristic (14:0) and plamitic (16:0) acids are considered hypercholesterolemic.  Stearic acid (18:0) has a neutral effect on LDL cholesterol, as it is readily de-saturated to oleic acid.  A meta-analysis of 60 clinical trials found that the increase in total cholesterol as a resultant of lauric acid intake, was largely due to an increase in HDL.  This subsequently reduced the total cholesterol to HDL ratio.  Nutritional guidelines in France have increased SF targets to 12% of total energy, with lauric, myristic and palmitic acids, limited to no more than 8% energy.  It is too early to assess if this change in policy has been effective.  One of the difficulties with this type of message is how well it translates to food items as foods contain varying proportions of each SF.  Without appropriate food education or food labelling the guidelines may not translate to the general public.  The information could be useful for food industry reformulation, when a solid fat is needed (e.g. baked goods) stearic could be encouraged to replace other saturated or trans fatty acids.

A major food group that has been focus of debate is dairy products.  There are a number of items in this food group which are high in SF (e.g. cream and cheese).  A meta-analysis of prospective cohorts revealed that high consumption of dairy products, was associated with lower risk of ischaemic heart disease RR 0.79.  There was limited data on specific dairy items.  butter and cheese, two dairy items high in SF, were associated with reductions in vascular events RR 0.93 and 0.90 respectively, neither were statistically significant (Elwood et al., 2010).  Another example of a food item high in SF that has been shown to be beneficial for cardiovascular health is dark chocolate.  Dark chocolate has been shown to the beneficial in observational, mechanistic and RCT studies.  The effect of the SF in these foods may be counterbalanced by the content of protein, calcium, polyphenols and other nutrients. This shows that when considering nutritional guidelines, it is important to consider the entire nutrient matrix of a food item.  In conclusion there is some evidence to support increase in SF recommendations.  This is largely based on prospective cohort studies that are heavily reliant on dietary assessment methods, which can be inaccurate.  In terms of risk biomarkers, the fact that SF raises total and LDL cholesterol is well established by evidence from metabolic studies, but this paradigm may be too simplistic.  Clinical studies will need to consider total cholesterol to HDL ratio and LDL particle size, when assessing CVD risk.  There is still a need for more high quality epidemiological studies, using cardiovascular mortality and events as an end point to support a change in SF guidelines. 

Foods Containing High Levels of each Saturated Fat subtype
Lauric Acid - Pal kernel oil, coconut oil, coconut flesh and butter.
Myristic Acid - Coconut oil, palm kernel oil, coconut flesh, unsalted butter and cream
Palmitic Acid - Palm kernel oil, shortening unsalted butter, lard and beef tallow.
Stearic Acid -  Beef tallow, lard, pork fat, chocolate

There is strong evidence that replacing SF with PUFA reduces CVD risk.  Future studies need to differentiate between n-3 PUFA and n-6 PUFA as they appear to have varying metabolic effects in terms of CVD risk with n-3 PUFA having a more favorable effect.  Nutritional guidelines to consume two portions of oily fish per week encourage this change.  If you want to know more about n-3 PUFA check out my article on Omega 3.

Replacing SF with carbohydrate appears to have a negative effect on cardiovascular outcomes.  Very little evidence exists examining the quality of carbohydrate being introduced, and this has an impact on subsequent CVD risk, and needs to be a focus of future research. 

More food based studies would translate effectively to public health and the general public.  These would also fully encompass the whole nutrient profile of a food group.  This method could be used to assess the effect of MUFA from vegetable and fruit sources, as seen in the Mediterranean diet, on CVD.  If the evidence base does become strong enough to warrant a change in guidelines, the French guidelines would still require reduction in average SF intakes (12.6% to 12%) and would also draw attention to foods high in the more hypercholesterolemic SF.  Food based recommendations would convey a more simplistic message that is more likely to be adopted by the public.

Many other factors need to be considered when evaluating the evidence on a single nutrients contribution to CVD risk.  CVD is a multifactorial condition with many contributing factors.  Furthermore better treatments and changes in associated risk factors will have also played a role in CVD trends.  CVD is a leading cause of premature mortality and morbidity in the UK, so diet advice should aim to reduce this burden however, other prominent issues must be considered in these guidelines e.g osteoporosis, obesity and diabetes. 


ASTRUP, A., DYERBERG, J., ELWOOD, P., HERMANSEN, K., HU, F., JAKOBSEN, M., KOK, F., KRAUSS, R., LECERF, J., LEGRAND, P., NESTEL, P., RISERUS, U., SANDERS, T., SINCLAIR, A., STENDER, S., THOLSTRUP, T. AND WILLETT, W., 2011. The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? American Journal of Clinical Nutrition.  January, vol. 93, no. 4, pp.684-688.

BROWN, J., SHELNESS, G. AND RUDEL, L., 2007. Monounsaturated fatty acids and atherosclerosis: Opposing views from epidemiology and experimental animal models. Current Atherosclerosis Reports.  December, vol. 9, no. 6, pp.494-500.

CHOWDHURY, R., WARNAKULA, S., KUNUTSOR, S., CROWE, F., WARD, H., JOHNSON, L., FRANCO, O., BUTTERWORTH, A., FOROUHI, N., THOMPSON, S., KHAW, K., MOZAFFARIAN, D., DANESH, J. AND DI ANGELANTONIO, E., 2014. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk. Annals of Internal Medicine.  March, vol. 160, no. 6, pp.398-406.

DIAS, C., GARG, R., WOOD, L. AND GARG, M., 2014. Saturated fat consumption may not be the main cause of increased blood lipid levels. Medical Hypotheses.  December, vol. 82, no. 2, pp.187-195.

ELWOOD, P., PICKERING, J., GIVENS, D. AND GALLACHER, J., 2010. The Consumption of Milk and Dairy Foods and the Incidence of Vascular Disease and Diabetes: An Overview of the Evidence. Lipids,.  April, vol. 45, no. 10, pp.925-939.

FERNANDEZ MLWEST KL., 2005.  Mechanisms by which dietary fatty acids modulate plasma lipids.  The Journal of Nutrition.  September, vol. 135, no. 9, pp2075-2078.

GERBER, P. AND BERNEIS, K., 2012. Regulation of low-density lipoprotein subfractions by carbohydrates. Current Opinion in Clinical Nutrition and Metabolic Care.  July, vol. 15, no. 4, pp.381-385.

HOOGEVEEN, R., GAUBATZ, J., SUN, W., DODGE, R., CROSBY, J., JIANG, J., COUPER, D., VIRANI, S., KATHIRESAN, S., BOERWINKLE, E. AND BALLANTYNE, C., 2014. Small Dense Low-Density Lipoprotein-Cholesterol Concentrations Predict Risk for Coronary Heart Disease: The Atherosclerosis Risk in Communities (ARIC) Study. Arteriosclerosis, Thrombosis, and Vascular Biology.  February, vol. 34, no. 5, pp.1069-1077.

Hooper, L., Kroon, PA., Rimm, EB., Cohn, JS., Harvey, I., Le Cornu, KA., Ryder, JJ., Hall, WL., Cassidy, A.,  2008.  Flavonoids, flavonoid-rich foods, and cardiovascular risk: a meta-analysis of randomized controlled trials.  American Journal of Clinical Nutrition.  July, vol. 88, no.1, pp 38-50.

LEGRAND P, MORISE A, KALONJI E., 2011.  Update of French nutritional recommendations for fatty acids.  World Review of Nutrition and Dietetics.  August, vol. 102, pp 137-143.

MENSINK, RP., ZOCK, PL., KESTER, AD., KATAN, MB., 2003.  Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials.  American Journal of Clinical Nutrition.  May, vol. 77, no. 5 1146-1155.
MOZAFFARIAN, D., MICHA, R. AND WALLACE, S., 2010. Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. PLoS Med.  March, vol. 7, no. 3, p.e1000252.

NHS., 2013. Ideas to reduce fat in your kids’ diet | Change4Life [online]. [Viewed 13 April. 2015].  Available from:

HUNTER, J., ZHANG, J. AND KRIS-ETHERTON, P., 2009. Cardiovascular disease risk of dietary stearic acid compared with trans, other saturated, and unsaturated fatty acids: a systematic review. American Journal of Clinical Nutrition.  November, vol. 91, no. 1, pp.46-63.

JAKOBSEN, M., DETHLEFSEN, C., JOENSEN, A., STEGGER, J., TJONNELAND, A., SCHMIDT, E. AND OVERVAD, K., 2010. Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index. American Journal of Clinical Nutrition.  June, vol. 91, no. 6, pp.1764-1768.

JAKOBSEN, M., O'REILLY, E., HEITMANN, B., PEREIRA, M., BALTER, K., FRASER, G., GOLDBOURT, U., HALLMANS, G., KNEKT, P., LIU, S., PIETINEN, P., SPIEGELMAN, D., STEVENS, J., VIRTAMO, J., WILLETT, W. AND ASCHERIO, A., 2009. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. American Journal of Clinical Nutrition.  February, vol. 89, no. 5, pp.1425-1432.

JIANG, X., YANG, Z., CHANDRAKALA, A., PRESSLEY, D. AND PARTHASARATHY, S., 2011. Oxidized Low Density Lipoproteins-Do We Know Enough About Them? Cardiovascular Drugs and Therapy.  October, vol.25, no.5, pp 367-377.

KOLBUS, D., RAMOS, O., BERG, K., PERSSON, J., WIGREN, M., BJARKBACKA, H., FREDRIKSON, G. AND NILSSON, J., 2010. CD8+ T cell activation predominate early immune responses to hypercholesterolemia in Apoe-/- mice. BMC Immunology.  December, vol.11, no.1, pp 11-58.

LOYD-WILLIAMS, F., 2008. Estimating the cardiovascular mortality burden attributable to the European Common Agricultural Policy on dietary saturated fats. Bull World Health Organ.  July, vol. 86, no. 7, pp.535-541.

NETTLETON, J., LEGRAND, P. AND MENSINK, R., 2015. ISSFAL 2014 Debate: It Is Time to Update Saturated Fat Recommendations. Ann Nutr Metab.  January, vol. 66, no. 2-3, pp.104-108.

NEWENS, K., THOMPSON, A., JACKSON, K., WRIGHT, J. AND WILLIAMS, C., 2011. DHA-rich fish oil reverses the detrimental effects of saturated fatty acids on postprandial vascular reactivity. American Journal of Clinical Nutrition.  August, vol. 94, no. 3, pp.742-748.

SIRI-TARINO, P., SUN, Q., HU, F. AND KRAUSS, R., 2010. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition.  March, vol. 91, no. 3, pp.535-546.

SONESTEDT, E., WIRFALT, E., WALLSTRAM, P., GULLBERG, B., DRAKE, I., HLEBOWICZ, J., NORDIN FREDRIKSON, G., HEDBLAD, B., NILSSON, J., KRAUSS, R. AND ORHO-MELANDER, M., 2011. High disaccharide intake associates with atherogenic lipoprotein profile. Br J Nutr.  Ocotber, vol. 107, no. 07, pp.1062-1069.

THE DEPARTMENT OF HEALTH., 2014.  The National Diet and Nutrition Survey.  London.  TSO.