Visitors' Questions and Dr Ryan's Answers
I've compiled this list of visitor's questions and my answers, in the hope it will be helpful to others:
This first, and very important, question has been asked three or four times now from readers in different countries...
Q: I've read on the web that a drug called etanercept might be a cure for Alzheimer's disease?
A: First let me say that the colleagues undertaking this interesting work are not claiming to have found "the cure" for Alzheimer's disease. But the findings are interesting and hopeful. The work is being conducted by Professor Tobinick and his colleagues at California's Institute for Neurological Research. What they have discovered is that over what now amounts to three years of study, and involving some 50 or so patients with various stages of developed Alzheimer's disease, injection of the drug etanercept - a drug that blocks the effects of tumour necrosis factor in the body - into the spinal canal (outside of the tissues surrounding the spinal cord), has resulted in apparent, sometimes dramatic, and seemingly sustained improvement in cognitive function.
Tumour necrosis factor alpha (TNF) is a so-called "cytokine" - a natural chemical that can influence immune reactions and inflammation in the body. Treatments aimed at suppressing the action of TNF are now in widespread use in medicine, often in the treatment of auto-immune diseases, such as rheumatoid arthritis, ankylosing spondylitis, severe psoriasis and bowel conditions. Doctors have long suspected that some of the illnesses that affect the brain and nervous system are also auto-immune conditions (where the body's own defences are damaging its own tissues), for example multiple sclerosis - and possibly Alzheimer's disease. For this reason it is revealing that anti-TNF treatment might improve patients with developed Alzheimer's disease. The pilot study by Tobinick and his colleagues, at the USC School of Medicine in Los Angeles, was first reported in 2006. Another study of the effects of the drug in a single 81-year-old patient with Alzheimer's disease is referenced below.
The big problem in giving anti-TNF therapy for brain disorders is that the current drugs - in this case etanercept - don't readily cross from the blood into the brain, where the disease pathology is taking place. This means that an ordinary injection will not work since the drug won't arrive at the inflamed areas within the brain. This is why the etanercept had to be given as an injection in the perispinal space in the neck, where it has been shown to enter the cerebrospinal venous cirulation and thus get into the brain. But the results do appear to be promising - and for two reasons.
First, they may point to the potential of a totally new avenue of treatment, in spite of the difficulties with the blood-brain barrier. Second, it tells us more about what is happening locally within the brain. The fact that an anti-TNF drug has had such an apparently dramatic effect, and so very quickly, sheds a new light on the actual pathology of Alzheimer's disease. Pathologists will undoubtedly learn much from this. One conclusion might be that ongoing inflammation of the auto-immune type may be playing an important role in Alzheimer's disease. This may also open up other potential routes to an effective treatment in the future.
What many doctors must now wonder is what might be the potential of such a therapy in patients with very early disease - would it prevent, or even delay, the progression of the disease. If so that would be a major medical breakthrough.
Let's hope so.
Tobinick E, Gross H, et al (2006). TNF-modulation for treatment of Alzheimer’s disease: a 6-month pilot study. MedGenMed 8(2): 25.
Tobinick E (2007). Perispinal etanercept for treatment of Alzheimer’s disease. Curr Alzheimer Res 4: 550-52.
Tobinick E (2008). Perispinal etanercept for treatment of Alzheimer’s disease. Curr Alzheimer Res 4: 550-52. Tobinick E (2008). Perispinal etanercept for treatment of Alzheimer’s disease. Curr Alzheimer Res 4: 550-52.
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Q: From a New Zealand reader: Dr Ryan... Thank you for introducing a complex subject in such an easy way to grasp. Getting the balance right between Omega-3s and other fats is going to be the challenge. We probably eat too much red meat (5 times a week), with snapper (a white fish) when we can catch it. It would be helpful to know how much saturated fat per ounce (25 grams) there is in beef, pork and lamb, and what the impact is on the 2 x 275 mg capsules of cod liver oil we have just begun to take.
A: I'm glad you find The Brain Food Diet useful. Red meat contains about a fifth of its grilled weight as fat, of which about half is saturated fat. So a five ounce fillet steak would contain about half an ounce, or 15 grams, of saturated fat. The other meats contain slightly less, but this would act as a general guide. I would suggest you reduce the red meat to three times a week. I would also suggest you eat fish twice a week, preferably oily -- but white fish is fine since you supplement your diet with cod liver oil capsules. Since you can't eat poultry, I would suggest maybe you try vegetarian twice a week. Remember that vegetarian curries and Chinese vegetarian meals can be very tasty. But be careful about adding full cream milk and cheeses with a high saturated fat content. These often contain more saturated fat, weight for weight, than red meat.
If you need more information, the US version of The Brain Food Diet has additional information on dietary balance. It is available as an e-book at a giveaway price (see US book page).
Good luck with your efforts to balance your diet.
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A: Yes, indeed I have read about this study in the journal Neurology. It's early days - but it will be exciting if it proves to be helpful to patients. As yet all we have is post-mortem observations on the brains of people who had been taking statins, which showed less in terms of the amyloid tangles and plaques than the pathologists would have anticipated. It's interesting from a theoretical standpoint, since it suggests that lipids, such as cholesterol, may play an important part in the causation of Alzheimer's disease - which might in turn might tell us more about how omega-3s help to reduce the risk. The great thing is that further research should readily be possible since there are millions of people currently taking statins.
Li G, Larson EB, et al (2007). Statin therapy is associated with reduced neuropathologic changes of Alzheimer disease. Neurology 69: 878-85.
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Q: from a Scottish reader living in Australia: Congratulations on your book, which I found fascinating. But I'm really struggling with getting the ratio of omega-6 to omega-3 right. Is there some simple formula, or am I just being a bit dense?
A: No - you're not being dense at all. In my opinion this is the single most difficult thing to get right. It's why I devoted half the book to explanation of day to day recipes and diet. Omega-6s and omega-3 are both essential to normal health. The important thing is just to get the ratio right. We eat far too much omega-6. In fact an American expert worked out that if we were to continue to eat as much omega-6 as we do in America, the UK, Australia and New Zealand, we would need to take the equivalent of ten spoonfuls of cod liver oil a day to get the right balance. What that tells us is that we need to greatly reduce our consumption of omega-6s.
These are found in most of the common cooking and salad oils, such as sunflower, soybean, corn and safflower oil. One very good way of reducing our intake is to swap to rape seed oil in cooking and salads. Rape seed oil has much less omega-6 and more plant-type omega-3s. Another simple tip is to greatly reduce the consumption of processed foods, such as doughnuts, muffins, pies, and pastries. It's always best to do your own cooking, so you know what goes into it.
Good luck!
Frank
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Q: from an English ex-pat living in Spain: I've read something in a newspaper about a protein called LR11. Do you know anything about this and what it might be doing in Alzheimer's?A: You'll know, from reading The Brain Food Diet, that EPA and DHA reduce the tendency for inflammation anywhere in our bodies, which may be a significant way in which they help reduce the risk of developing Alzheimer’s disease. Recently there has been an important new paper by Professor Cole and colleagues from
Ma Q-L, Teter B, et al (2007). Omega-3 fatty acid docosahexaenoic acid increases SorLA/LR11, a sorting protein with reduced expression in sporadic Alzheimer’s disease (AD): relevance to AD prevention. J of Neuroscience 27(52): 14299-307.
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