DHA, Fish and Alzheimer’s: Press Misinformation

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.

Can bacon and eggs really help my hangover?

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!!

Coffee debate update

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.

Coffee Controversy: is it good or is it bad for you?

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.

Statins – Should all over 50s get anti-cholesterol drugs?

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.

Peripheral Neuropathy in Diabetics; what steps can we take to avoid it?

You might already be aware that of the many deteriorative conditions related to diabetes; ‘peripheral neuropathy’ is perhaps the most common, with an estimated 60-70% of diabetics reportedly experiencing symptoms. ‘Neuropathy’ describes damage, whether moderate or severe, to the peripheral nervous system (the ‘external’ portion of the nervous system, situated beyond the brain and spinal cord), which transmits information directly from the brain and spinal cord to the rest of the body.

Our nervous system acts very similarly to an electrical cable; with the nerve’s ‘impulse’ adopting the role of the electrical wire itself, and the ‘myelin sheath’ (the ‘skin’ of the nerve), mimicking the insulation surrounding the wire. If the wire becomes damaged, then the nerve signal will not travel efficiently along the wire, nor will it transmit the intended messages as instantaneously. This delay results inevitably in the ‘classic’ symptoms of neuropathy; namely; tingling, numbness, ‘burning’ and pain.

A causative link has been drawn between neuropathy and deficiencies of long-chain polyunsaturated fatty acids within the body. Indeed, insulin itself plays a pivotal role in the metabolism of EFAs (essential fatty acids), by alerting the genes necessary for enzyme-conversion to begin the process of converting short-chain fatty acids into a bio-available (i.e. usable by the body) long-chain fatty acid.

Where insulin is absent, or enzyme-activity impeded, the enzymes needed to create specific fatty acids cannot be produced and a deficiency results. Of the myelin layer which protects our vulnerable nerves, an estimated 75 % is composed exclusively of EFA’s (these are termed ‘essential’ because the body cannot generate them independently, but must instead source them externally from the diet). Depletion of this fatty, insulatory layer, leads to severe nerve damage (Neuropathy).

Nutrition, as all Diabetics are painfully aware, is central to the manufacture of insulin and for creating the right ‘biological environment’ to encourage enzyme conversions to take place. By boosting or supplementing our dietary levels of long-chain fatty acids we can essentially sidestep the risk that the enzyme-mediated conversions will fail to progress past the initial hurdle.

Fatty acid supplementation nourishes the myelin sheath, and prevents further degeneration of inter-cellular communication; it reduces the risk of developing Neuropathy, and actually reinvigorates nerve endings to overcome numbness and the likelihood of eventual tissue loss. However, EPA, a specific omega-3 fatty acid found in fish oil that appears to have significant beneficial effects on diabetic neuropathy and serum lipids as well as other diabetic complications such as nephropathy (kidney damage) and macroangiopathy (damage to the blood vessels). EPA plays a role in the compaction, stabilization, and maintenance of myelin sheaths by regulating the production of proteolipid protein or PLP. PLP is literally the ‘glue’ that hold in place the sheets of protective fats that cover the nerve axon. Loss of PLP is associated with many conditions that have nerve damage including Multiple sclerosis, Alzheimer’s disease and Huntington chorea.

OmegaForce is a patented formulation of omega-3 and 6 long-chain fatty acids with a multitude of health-enhancing properties, including anti-inflammatory and pain-relieving actions. For more information on the relationship between EPA deficiency and the pathogenesis of Diabetic Neuropathy, please go to www.igennus.com