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I have recently written an article on EPA fish oil and its role in Alzheimer’s disease, as there are currently around 700,000 people in the UK with dementia (it is believed that these figures are set to rise to one million in the next 10 years because of the ageing population) and new research adds to the weight of evidence that suggests that people who regularly include fish as part of their diet have a lower risk of developing dementia and, in particular, Alzheimer’s disease.
The human brain is a complex organ that controls our senses, our movements, receives information, analyses information, and stores this information as memories. Dementia, simply put, means ‘deprived of the mind’ and, contrary to what many of us consider an acceptable part of growing old, memory loss and dementia are not a natural part of the ageing process. Scientists are now suggesting that the omega-3 EPA, found in fish oil, can help. Like any organ, the brain needs nurturing, and if we provide our brain with the correct nutrients then we can help to ensure the function of our brain remains at its most efficient.
For those of you interested in finding out more about how EPA helps preventing memory loss, offering help for Alzheimer’s sufferers, the full article is available here: EPA fish oil and its role in Alzheimer’s disease risk
Whilst most people in the UK are familiar with alcohol-related liver disease as a result of heavy drinking, which is on the rise, many of us are unaware of the problems associated with another form of liver disease, non-alcoholic fatty liver disease (NAFLD) – also known as non-alcoholic steatohepatitis (NASH). A recent review of four human studies by a group based at the University of Edinburgh found that long-chain omega-3 fatty acids not only improve liver health and function, but also increase insulin sensitivity in people suffering from fatty liver disease.
I’ve recently published an article on Omega 3s and fatty liver disease and the study led by Dr Gail Masterton and I would be very interested to hear your feed back!
Currently there are around 700,000 people in the UK with dementia and it is believed that these figures are set to rise to one million in the next 10 years because of the ageing population. The National Institute of Health and Clinical Excellence (NICE) guidance is that people with dementia should only be offered antipsychotic drugs if they are severely distressed or there is an immediate risk of harm to the person or others. However the use of sedatives in dementia has repeatedly been condemned due to the increasing evidence that the use of such drugs in dementia patients significantly increases their risk of death. One such study published earlier this year followed 165 patients with Alzheimer’s disease living in care homes in Oxfordshire, Tyneside, London and Edinburgh. Patients who were already taking anti-psychotics either continued on their treatment, or given a dummy pill for a year and then followed up over a period of three years. After two years, 46% of patients who had been treated with anti-psychotics were alive compared with 71% on the placebo. Three years after the start of the study, fewer than a third of people on anti-psychotics were alive compared to nearly two-thirds taking the placebo (Ballard et al, 2009). A recent review ordered by the Department of Health outlines the over prescription of antipsychotic drugs to treat aggression and agitation in people with dementia and contrary to NICE guidance. The review authored by Professor S. Banerjee goes as far as suggesting that up to two thirds of those individuals with dementia receiving anti-psychotic drugs are prescribed them unnecessarily.
So why is it that pharmaceutical drugs, with such well documented findings in terms of their negative health effects, continue to be prescribed? It certainly appears that they are offered as a ‘quick fix’ regardless of the long term consequences. Originally discovered in the 1950s, anti-psychotics were found to block receptors in the dopamine pathway and used quite successfully in the treatment of schizophrenia and bi-polar disorder before being introduced as treatment for dementia where their actions serve as nothing other than “chemical restraints”. It seems shameful that pharmaceutical companies can benefit in such situations whilst nutraceutical companies struggle to get clearance for health claims from the Medicines and Healthcare products Regulatory Agency (MHRA). This government agency is responsible for ensuring that medicines and medical devices work and are acceptably safe, and consistently rejects claims for many well-known safe and commonly used nutritional products.
The benefits of fish oil and the role of long-chain fatty acids in brain chemistry and in dementia are generally accepted but not endorsed. Ironically the side effects of consuming fish oils include only relatively minor complications (gastrointestinal upset, nausea, headaches) when compared with the potentially very serious sides effects of some pharmaceutical products. Given that long-chain fatty acids are involved in the dopamine pathway influencing dopamine concentration, number of vesicles and D2 receptors, and have been beneficial in studies where the dopamine pathway is known to be involved such as schizophrenia and attention deficit hyperactivity disorder (ADHD), would it not be prudent to suggest a role of fatty acids as a regular or add-on treatment in individuals with dementia? The recent positive findings of the role of eicosapentaenoic acid EPA in reducing cerebral atrophy in Huntington’s disease is certainly indicative that non-pharmaceutical products need to be investigated and that their role in dementia, not only in the treatment but in the prevention of the condition, is sadly underrated at the expense of the patient.
Ballard C, Hanney ML, Theodoulou M, Douglas S, McShane R, Kossakowski K, Gill R, Juszczak E, Yu LM, Jacoby R; DART-AD investigators. (2009) The dementia antipsychotic withdrawal trial (DART-AD): long-term follow-up of a randomised placebo-controlled trial. Lancet Neurol. 2009 8:151-7.
Puri BK, Bydder GM, Manku MS, Clarke A, Waldman AD, Beckmann CF. (2008) Reduction in cerebral atrophy associated with ethyl-eicosapentaenoic acid treatment in patients with Huntington’s disease. J Int Med Res. 36:896-905
Each year on 10th October, the Mental Health Foundation marks the day by raising awareness about mental health and well-being. Whilst we would probably all consider ourselves as reasonably tolerant and open minded, there is still quite a significant stigma about depression. If we haven’t experienced depression directly, it’s highly probable that we know someone, perhaps a friend, relative or workmate, who suffers. Mental Health Statistics report that 1 in 4 British adults experience at least one diagnosable mental health problem in any one year and 1 in 6 of us experiences this at any given time. In 2001 the World Health Organisation (WHO) estimated that approximately 450 million people worldwide have a mental health problem, of which 154 million are affected by depression.One of the major side effects of depression is that the way we think about food changes and this can influence how we eat – both the types of food and how often. Because food can directly influence our mood, our diet is even more fundamental when we’re feeling low.
The Glycemic Index
The brain needs energy supplied at an even rate in order to function optimally. Sudden peaks in blood sugar will adversely affect behaviour, anxiety, depression, and fatigue, so it is particularly important for people with depression to keep their blood glucose levels even. Although commonly known for its diabetes and weight loss benefits, the glycemic index (most commonly referred to as GI index), which ranks carbohydrates according to their effect on blood glucose levels, is a good guide to informing us which foods to include as part of a healthy diet, and indeed which foods to limit.
While all carbohydrate foods are eventually broken down into glucose, quick-release simple carbohydrates (such as high sugar foods, glucose and fructose) are broken down more quickly into glucose than complex carbohydrates (such as wholemeal grains), releasing glucose rapidly into the bloodstream. Repeated ‘spikes’ of glucose can decrease insulin sensitivity, increasing the risk of type 2 diabetes, as well as promoting oxidative stress in the veins and arteries – a cause of coronary heart disease. After the highs come the energy-sapping blood sugar lows and, frequently, strong urges to reach for another sugary carbohydrate snack to perk us up. Indeed individuals who suffer from atypical depression (a subtype of depression) often overeat and report an almost irresistible craving for carbohydrates.
White sugar and other refined carbohydrates, such as those found in processed white bread and white pasta, white rice and most convenience foods, supply few nutrients to the body but use up important B vitamins, which are essential for our nervous and immune systems, as well as healthy digestion. Avoiding refined foods and sugar, as well as consuming foods with a low GI value, will help to keep blood sugar levels even. Perhaps a more accurate reference guide to prevent blood sugar spikes is the Glycemic Load(GL) ranking system, which is based on a food’s GI value and average portion size. For example, whilst an apple is not low GI, it has a low GL and will barely influence blood sugar levels.
Micronutrient deficiencies
It is extemely common for depression sufferers to have low levels of B vitamins and essential minerals such as zinc, selenium and magnesium. These water-soluble vitamins and minerals must be consumed daily to avoid depletion. Deficiency can, in turn, hinder the body’s ability to utilise specific omega-3 fatty acids, which are known to lift our mood by elevating serotonin and regulating levels of this important neurotransmitter.
EPA, a long-chain omega-3 fatty acid found in fish oil, not only influences serotonin and dopamine in the brain, but is also converted to powerful anti-inlammatories via a series of enzyme-mediated steps. It is these enzymes that rely on the presence of B vitamins and essential minerals in order to function, without which the body’s production of natural anti-inflammatories is minimal, and can even result in the production of inflammatory substances. Combining a good nutritional vitamin and mineral supplement with 1 gram EPA daily (or 4 capsules Vegepa) can help to balance serotonin levels and alleviate the symptoms of depression.
Carbohydrate cravings are also linked with low levels of chromium, which helps to regulate blood sugar levels and reduce cravings. This is because for blood sugar to provide energy, it must be escorted into each of our cells where the energy conversion takes place. Insulin then ‘unlocks’ the cell, allowing glucose to pass in. But there is a missing link. Insulin doesn’t work properly unless biologically active chromium is present as a cofactor (much like a catalyst).
With many modern food processing methods, up to 80% of chromium is lost – particularly with whole wheat and raw sugar when they are processed to white flour and refined sugar. If we regularly opt for these refined foods over their healthy wholegrain relatives, chromium levels within the body can easily become depleted.
Whilst it is likely a low priority during episodes of low mood to concentrate on our eating habits, following a few general guidelines can help to restore healthy brain chemistry and minimise sugar-induced mood swings.
- Avoid processed foods.
- Keep red meat to a minimum or eat organic (red meat is high in inflammatory omega-6 unless animals are fed on natural grass).
- Drink plenty of water, as the brain needs to be hydrated to function at its best.
– Don’t forget your ‘five a day’. Make sure you get plenty of vitamins and minerals by eating a wide variety of fresh fruit and vegetables. If you eat them raw they’ll supply even more nutrients.
– Eat two portions of oily fish weekly to top up on omega-3, containing the natural antidepressant EPA, or take 2 capsules of Vegepa morning and night.
If you found this article interesting, you might like to read more about anti depression foods.
Another juicy head line this week. This time it’s the Daily Express reporting the findings of a study led by Dr Carl Lavie and published in the Journal of the American College of Cardiology. The outcome of the study suggests that eating oily fish can help ensure a long life, as it slashes the risk of heart failure by a third and as a result of these findings there is a push for everyone in Britain to be taking omega-3 (about time too). So we are told that people with existing heart problems should take at least 800 to 1,000mg of omega 3 each day – the amount found in three to four 3oz portions of oily fish a week. The news story then goes on to quote that half that amount of fish would provide enough omega-3 for healthy people – so 400-500mg, “the equivalent of one supplement capsule”.
So I can now hear the thunder of feet rushing down to Holland and Barrett a bid to snap up their EPA 1000mg fish oil capsules. This has to be good value for money surely? Firstly, they come in a tub so big that it nearly take up the whole basket leaving very little space for your ginseng and dried apricots (but you do get change from a tenner). Secondly, the pot clearly states “EPA 1000mg” so it’s all good – isn’t it? Well no! This is where the public get misled and some what confused (and I get annoyed). My first point that I feel needs clarification is the statement – “equivalent of one supplement capsule.” This is confusing and misleading. Firstly capsules mostly come in two sizes, 500mg and 1000mg (like our H&B example above). Secondly there is a huge variation in the quality of supplements. Generic fish oil (including Mr Holland and Mr Barrett’s “EPA 1000mg”) is simply oil that has been extracted from the flesh of fish and filtered but not molecularly distilled or concentrated. These types of supplements are cheap and tend to be easy to spot on the shelves, generally containing 180mg EPA and 120mg DHA per 1000mg of fish oil. Indeed, a far cry from the boastings of “EPA 1000mg” (which actually refers to the size of the capsule and not the EPA content!).
In order to achieve anything close to the 400-500mg of omega-3 through consuming just one supplement capsule, then we need to be looking at pharmaceutical grade products. These oils undergo rigorous molecular distillation and can achieve as much as a 70% concentrated blend of active ingredients (namely EPA and/or DHA). Molecular distillation not only concentrates these fatty acids but also ensures that the oil is free from contamination and from vitamin A. Because of the processes involved and the amount of active ingredients in each capsule, the price goes up, but then you are paying for a quality product. Even then, a 70% oil falls short of achieving the concept of ‘one capsule is enough’. Not all supplements are the same and cheaper products will not give the benefits that the article suggests. EPA and DHA compete for the sn-2 site of phospholipids, and therefore the ratio of EPA to DHA within any supplement becomes important in influencing which fatty acid is the most active in any preparation. My second point…
This goes back to my “black or white” theory. Fatty acid metabolism and the role that these fats play in cardiovascular health is intensely complicated and it is no wonder that the public can find tabloid information confusing. EPA and DHA have very different mechanisms of action and therefore to generalise the effects of ‘omega-3’ as a whole is over-simplifying the issue. Indeed, many studies are now taking DHA and placing it gently to one side in order to focus on the activities of EPA. Whilst yesterday’s news is interesting it’s far, in fact, from novel, which is partly why I roll my eyes. In regards to taking an EPA-only product, a good line of support for the role of EPA in cardiovascular health for this comes from the Japan Eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS trial) which was the first large-scale, prospective, randomized trial of a combined treatment with a statin and EPA for the prevention of major coronary events. These studies take highly purified preparations in doses of around 2g daily to obtain the results that are subsequently published in major journals. This information, it seems to me, is then portrayed to the public via a game of Chinese whispers, with the resulting message being generally down played. The article furthers exemplifies my point that there is a general need for the public to be aware of the variation in the quality and dosage of omega-3 supplements.
The general public are reliant on the media for their most recent update on “what to eat and what not to eat” and so it’s terribly important that studies are reported objectively and fairly – and, of course, that we are given the whole picture. It is not a very new concept that eating fish such as salmon, sardines and mackerel may offer an element of protection against developing dementia and indeed the media has reported on a number of studies showing that people who consume a significant amount of oily fish or fish oil are less likely to develop Alzheimer’s disease. This week’s headline, “Fish may not be Alzheimer’s answer” suggests, however, that Alzheimer’s patients may not benefit from eating fish, despite this “brain food” reputation.
Our understanding of the significant health benefits associated with fish oil supplementation has come a long, long way since scientists’ original discovery, back in the 1950s, that cod liver oil was a rich source of fatty acids. Researchers have since then progressed far beyond the basic understanding that fish oil is a promoter of general good health, and moved onto the next phase of innovation – investigating which particular elements within this oil are biologically active and whether a physical deficiency in this bioactive element results in some degree of physical deterioration. Indeed, fish oil contains two major fatty acids EPA and DHA and it is only really in recent years that these important fatty acids have been investigated individually rather than dumping them in the same boat with the generic label of omega-3.
DHA is the most abundant omega-3 fatty acid in cell membranes, present in all organs and most abundant in the brain and retina. In contrast, EPA is present in minute quantities. It could be easily assumed that DHA is the more dominant of the two fatty acids and put all of our focus here. However whilst DHA has a primarily structural role, EPA plays an important functional role. In actual fact whist EPA and DHA are both considered to be important regulators of immunity, platelet aggregation and inflammation, their influencing bi-products arise from very different pathways and it is therefore not surprising that their mechanism of action will differ.
So what is my problem with the latest headline? Well what’s very misleading with this is the loose use of the word “fish”. The study didn’t even have a vague whiff of fish about it but was conducted using a DHA supplement and a dummy placebo. The importance of this is that the information put forward to eager ears gives the impression that all that mackerel eating is a waste of time. But hear me out. This study took but one of the major fatty acids associated with fish oil, showed no benefit, but happily used the word fish to summarise the findings. If we recall, fish oil contains two important fatty acids, DHA and EPA. It is becoming increasingly clear that the marked differences between the effects of EPA and DHA mean that we can no longer generalise the effects of ‘fish oil’ as a reservoir of omega-3. EPA not only plays a major role in cell signalling but also contributes to the compaction and stabilisation of neurones. Indeed previous studies have shown that high plasma EPA concentration may decrease the risk of dementia and that EPA can actually reduce the atrophy associated with the shrinking brain. I’m not objecting to their findings that DHA is not the fatty acid which plays a role in dementia, rather it’s the fact that the message implies that it we should now question or even rule out the protective role of fish altogether. But when we dig deeper and unravel the scientific evidence and put that on our plates to eat, we see that things are a little more convoluted than we initially thought – well, if you read the recent headlines, that is. Just because the bigwigs are now telling us that DHA won’t save our brains (this week at least) it doesn’t mean that we should now disregard our efforts to include fish as part of our diets in our bid to prevent age-related mental decline. I, for one, shall be continuing to get my twice weekly portions in and I hope you will too. Do remember that once again, it’s not black or white, to fish or not to fish.
The answer is actually yes, but the question is how? Well there are three main steps in the processing of that large gin and tonic that is placed in your hand in the back room of the “Six Bells” on a Friday night. Firstly alcohol (AKA ethanol) isn’t actually all that bad for you. However when we drink, ethanol is processed in the liver and converted to acetaldehyde, a toxic and highly reactive compound. Acetaldehyde is then further converted into acetate, a harmless form of acetic acid (the acid which gives vinegar its sour taste and pungent smell). There are two enzymes involved in this process, alcohol dehydrogenase (converting alcohol to acetaldehyde) and acetaldehyde dehydrogenase (converting acetaldehyde to acetate). Ideally we would want to convert alcohol to acetaldehyde slowly to avoid build up, and then convert this toxic product as quickly as possible to harmless acetate. However, acetaldehyde dehydrogenase needs another substance called glutathione (a potent antioxidant), which contains high quantities of cysteine. Together, acetaldehyde dehydrogenase and the glutathione reduce acetaldehyde to acetate. Our bodies can cope efficiently as long as we don’t consume too many drinks too quickly. However, the liver’s stores of glutathione can quickly run out if large amounts of alcohol enter the system too quickly and the body struggles to keep up with the conversion of acetaldehyde to acetate, levels of acetaldehyde rise and result in that nasty hangover headache, feeling of fatigue and rather unpleasant dodgy tummy feeling! Cysteine is an amino acid found in most high-protein foods such as pork and eggs. So if you found yourself in a position of a little too much too quickly the night before the Sunday morning fry up (use olive oil, not vegetable oil) will provide the building blocks needed for the liver to replenish its depleted glutathione stores and help mop up those left-over toxins. But as I’ve said before, moderation is really the key to drinking. Make sure you line your stomach well (alcohol is an irritant), pace yourself, drink plenty of water and try to remember that a healthy liver can get rid of about one unit of alcohol an hour. So remember, that whilst that double gin and tonic may have only taken fifteen minutes to drink, your poor liver did not finish processing it for around another two hours!!
So the coffee debate continues. Today’s headline in The Telegraph shouts an enthusiastic message that drinking coffee could reverse the signs of Alzhiemer’s disease. The trial led by Dr Gary Arendash, an American neuroscientist presents evidence that indicates that caffeine not only helps to stave off the disease, but can actually treat it. The defining hallmark of Alzheimer’s disease is the accumulation of β-amyloid protein plaques in the the areas of the brain responsible for memory (the cortex and hippocampus). These ‘sticky’ deposits are known to damage nerve cells, interfere with nerve signalling and therefore memory. Caffeine, it appears, actually reduces the production of β-amyloid protein and therefore would reduce the production of plaques. So that’s the good news folks. The bad news is that this groundbreaking research was conducted using mice. Not bad news as such if you’re a coffee drinking mouse who can’t remember where you’ve left your cheese. These findings do however support an earlier study published in January this year. Led by Marjo H. Eskelinen the study found that among 1,400 Finnish adults followed for 20 years, those who drank three to five cups of coffee per day in middle-age were two-thirds less likely than non-drinkers to develop dementia, including Alzheimer’s disease. So for the time being I shall continue to enjoy my morning cafetière, not only because I enjoy the ritual and the taste but because it may, just may help me retain my memory in years to come.
I seem to have witnessed recently several identical conversations regarding coffee drinking. Is it good or bad for you? It’s not the coffee debate per say that intrigues me but this need for something to be so black or white, good or bad. I think it depends in part on where or from whom we get our information and the message that source wants to portray. It is true that coffee has well-documented side effects including anxiety, insomnia, tremor and palpitations. But on the plus side drinking coffee appears to improve alertness and some reports suggest that drinking 3 cups a day may even, reduce the risk of type 2 diabetes, protect against cancer and offer protections against dementia including reducing the risk of developing Alzheimer’s and Parkinson’s disease. So we have the good and the bad.
Coffee, however, like the majority of food stuffs we consume, is a complex composition. The side effects often associated with a steaming cup of java are actually the result of caffeine, which belongs to a group of stimulants called xanthenes. In moderation, caffeine can have very positive effects. It gives us more energy, heightens our ability to concentrate and makes us think more clearly and can even elevate our mood. That doesn’t sound so bad. But as with most things it merely boils down to moderation. If we drink caffeinated coffee in moderation it can increase alertness and mental stamina. If we drink too much too quickly, however, we are faced with the unpleasant side effects: nausea, confusion and excitability, which can be wholly unpleasant.
As with most things in life it’s not as simple as black or white. We need to look at the diet as a whole. Most foods we eat will have positive and negative factors, of which we are constantly being reminded by the tabloid headlines. Often telling just one side of the story, these messages can be somewhat confusing and frequently leave people rather bewildered as to what to consume and what to avoid. It’s a case of being sensible, taking everything in moderation and listening to the messages your body tells you. If you get the shakes after your morning espresso then that’s your body saying stop now, that’s enough.
Today’s Daily Mail headline announced the question “should all over 50s get anti-cholesterol drugs?” Normally statins are only prescribed to people who are considered to be at significant risk of a heart attack or stroke. In fact, it seems that these drugs can cut the risk of heart attack by 30% even in healthy people. So what are statins exactly? These are drugs that are known as HMG-CoA reductase inhibitors. HMG-CoA is an enzyme that is involved in the production of cholesterol in the liver. Ruducing or inhibiting the function of this enzyme therefore prevents cholesterol production. Statins (usually synthetic) are similar to HMG-CoA and mimic the actions of this enzyme but prevent the pathway progressing to the production of cholesterol and more than six million adults in the UK use them.
So far so good, until I open up the paper to page two where I am met with the words “although side effects are rare, they can include muscle pain and damage to the liver and kidneys.” I guess this is what infuriates me. With the majority of pharmaceuticals there will be the downside list of side effects or contraindications that steal some of the glamour from a treatment programme. Take NSAIDs, for example; these are common over-the-counter anti-inflammatory drugs, like Ibubrofen.
Whilst one of the most common over-the-counter drugs and used by millions, NSAIDs are associated with several side effects, of which many are probably not known by the common user. Whilst the frequency of side effects varies among NSAIDs, the most common side effects are nausea, vomiting, diarrhoea, constipation, rash, dizziness and headache (interesting that we often take them when we have a headache!). NSAIDs may also cause fluid retention, leading to oedema. The most serious side effects are kidney failure, liver failure, ulcers, an increased risk of heart attack and prolonged bleeding after an injury or surgery.
So why is it that if there is a natural alternative which we can take for both of these drugs and without the associated side effects, that we are not advised? Let me speak firstly about cholesterol. In the 1970s Danish researchers discovered that in spite of their high-cholesterol, high-fat, diet Greenland Eskimos had an astonishingly low incidence of cardiovascular disease (as well as arthritis and other chronic inflammatory diseases). When analysing blood samples it was discovered that they had low levels of LDL (bad cholesterol) and low levels of VLDL (triglyceride), but high levels of HDL (good cholesterol). It appeared that their high intake of omega-3 was responsible for this low risk of heart disease. Since this research emerged, much focus has been centred on the role of omega-3 fatty acids and, more recently, specifically the role of EPA in lowering cholesterol levels. EPA reduces cholesterol production by inhibiting the activity of another enzyme called acyl-CoA but without the side effects associated with statins. EPA also acts as an anti-inflammatory in a similar mechanism to that of NSAIDs, but again without the side effects. So my message today is to boost your EPA levels on a long-term basis and you may well lower the possibilities of having to resort to pharmaceuticals with all sorts of side effects.
Increase your fish intake and adopt a more Eskimo-like diet! For those who don’t like fish, you can opt for a high-EPA supplement. Purified fish oils actually are a useful alternative to oily fish consumption and, unlike most oily fish, are contamination-free.
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