Where it goes awry is with stress. When you get overly stressed and can’t escape, your brain puts out cortisol. Too much cortisol! It also cranks out epinephrine and nor-epinephrine from the Fight or Flight arm (sympathetic) of the autonomic nervous system. With that kind of stress and high cortisol, your gut gets leaky. More proteins leak through that normally would be held outside. When they leak through, your immune system reacts and gets over-stimulated, putting out all sorts of chemical messengers called cytokines that circulate back up to your brain and cause inflammation, not just in your gut, but also in your brain. The epinephrine acts as a multiplier of the cortisol effect to help create a vicious cycle of stress, injured gut, hyped up immune system and then a feedback to your brain where you get emotions of anxiety, chronic pain, fatigue. Think of the last time you were under stress. Did your tummy ache or feel all riled up? Did you get a cold? Did you feel exhausted and tired? Did you have more aches and pains? Headache? It’s likely you can easily think back and relate to an event like this.

How did you recover? Probably by your own native resiliency and common sense. But can you be more intentional the next time. Can you see the functioning triad of brain-gut-immune malfunction and how they all contribute to the cycle of perpetuating dysfunction? You get a vicious cycle set up that keeps turning the wheel of stress. If you can break the wheel’s turning at any point, you can interrupt the momentum. Try it.

Here are some tips. For example, we now know that you can turn on your parasympathetic system (calming, mellow, relaxed side) and counteract the synergistic inflammatory effect of the sympathetic system (fight or flight) by a variety of strategies. Breathing exercises can turn on your parasympathetic system in just a few minutes. Meditation takes longer but lasts much longer. Yoga does the same. Can you take up yoga? It’s anti-inflammatory! And a lot safer than pills. There’s more. A good night’s sleep also cools off inflammation and lowers cortisol. Gurgly upset gut? Probiotics will stimulate healing in your gut. Can you take probiotics for a couple of days? Can you add theanine (200 mg) to your bedtime routine, as well as some melatonin (3 mg) so that you get a great night’s sleep? Take theanine twice a day and see how much calmer you feel. It’s cheap and safe. Magnesium as a supplement will calm inflammation in your brain. (400 mg a day) Vitamin D turns down inflammation (4000 IU a day) and is strongly associated with less depression. Turmeric is increasingly being found to stifle inflammation. Can you take a good walk and get sweaty? Add all those together! Make it lifestyle?

WWW. What will work for me. We all find ourselves in a pickle from time to time. We feel stressed and frustrated, and then depressed. Can you make a more holistic attack on the problem at hand? More than just a good talk with a friend, can you think about how to sooth your churning gut, your ticked off immune system, your burning brain? I’m personally trying the theanine and melatonin combination for sleep. A good night’s sleep, and a lot gets smoothed out in the morning. Try it. And remember, the theanine works better is you take it twice a day. (Extract of green tea and been used in Japan for decades with no reported toxicity) I’ve not ever been described as mellow, but I feel more calm and on purpose. And cherish the talk with that good friend. That helps too.

Reference: American Academy AntiAging Webinar: Jan 10, 2011 Andrew Heyman

Where it goes awry is with stress. When you get overly stressed and can’t escape, your brain puts out cortisol. Too much cortisol! It also cranks out epinephrine and nor-epinephrine from the Fight or Flight arm (sympathetic) of the autonomic nervous system. With that kind of stress and high cortisol, your gut gets leaky. More proteins leak through that normally would be held outside. When they leak through, your immune system reacts and gets over-stimulated, putting out all sorts of chemical messengers called cytokines that circulate back up to your brain and cause inflammation, not just in your gut, but also in your brain. The epinephrine acts as a multiplier of the cortisol effect to help create a vicious cycle of stress, injured gut, hyped up immune system and then a feedback to your brain where you get emotions of anxiety, chronic pain, fatigue. Think of the last time you were under stress. Did your tummy ache or feel all riled up? Did you get a cold? Did you feel exhausted and tired? Did you have more aches and pains? Headache? It’s likely you can easily think back and relate to an event like this.

How did you recover? Probably by your own native resiliency and common sense. But can you be more intentional the next time. Can you see the functioning triad of brain-gut-immune malfunction and how they all contribute to the cycle of perpetuating dysfunction? You get a vicious cycle set up that keeps turning the wheel of stress. If you can break the wheel’s turning at any point, you can interrupt the momentum. Try it.

Here are some tips. For example, we now know that you can turn on your parasympathetic system (calming, mellow, relaxed side) and counteract the synergistic inflammatory effect of the sympathetic system (fight or flight) by a variety of strategies. Breathing exercises can turn on your parasympathetic system in just a few minutes. Meditation takes longer but lasts much longer. Yoga does the same. Can you take up yoga? It’s anti-inflammatory! And a lot safer than pills. There’s more. A good night’s sleep also cools off inflammation and lowers cortisol. Gurgly upset gut? Probiotics will stimulate healing in your gut. Can you take probiotics for a couple of days? Can you add theanine (200 mg) to your bedtime routine, as well as some melatonin (3 mg) so that you get a great night’s sleep? Take theanine twice a day and see how much calmer you feel. It’s cheap and safe. Magnesium as a supplement will calm inflammation in your brain. (400 mg a day) Vitamin D turns down inflammation (4000 IU a day) and is strongly associated with less depression. Turmeric is increasingly being found to stifle inflammation. Can you take a good walk and get sweaty? Add all those together! Make it lifestyle?

WWW. What will work for me. We all find ourselves in a pickle from time to time. We feel stressed and frustrated, and then depressed. Can you make a more holistic attack on the problem at hand? More than just a good talk with a friend, can you think about how to sooth your churning gut, your ticked off immune system, your burning brain? I’m personally trying the theanine and melatonin combination for sleep. A good night’s sleep, and a lot gets smoothed out in the morning. Try it. And remember, the theanine works better is you take it twice a day. (Extract of green tea and been used in Japan for decades with no reported toxicity) I’ve not ever been described as mellow, but I feel more calm and on purpose. And cherish the talk with that good friend. That helps too.

Reference: American Academy AntiAging Webinar: Jan 10, 2011 Andrew Heyman

Well, this makes for a real Debbie Downer Date. Nothing fun left. That’s actually not quite true. There is just a ton of stuff out there that is delicious food, good for you, easy to find. We just have to start thinking differently as we make changes in our life style and patterns.

But first, the big picture. It’s all about the FAT. The RIGHT Fat. We need to stop thinking simplistically about fat as being bad because it’s high calorie. We have to get some nuance to the idea that fat is what our brains are all about. You have to have the right fat. Our brains are mostly fat. That’s the key. And our diets have changed dramatically in the last 100 years. Our meat used to have omega fatty acids in them that was good for our brains. Beef, raised on grass, is about the same as bison or deer or elk in regard to its fat content. They are about 7% fat content, of which a large portion is omega fatty acid (good for your brain, just like salmon). When you raise a cow, or deer, or elk or bison on corn and beans, they get a different fat in their meat, just like we do when we raise ourselves on corn and beans (and sugar and soda and fries). They turn their meat into a product that still has the exact same protein. That doesn’t change. But the fat changes from omega fatty acid to saturated fat. Your brain wants the omega fats, not the saturated fat. Your brain is about 40% by dry weight DHA and EPA, the two dominant omega-3 fatty acids found in fish oil. But fish oil is simply a natural food chain product starting with green algae in the ocean that gets eaten by little tiny fish, that get eaten by bigger fish. Green plants make DHA and EPA, whether in the ocean or on land. Our ancestors used to eat either those green plants, or the animals that ate them. And our brains are made from those healthy, essential fats.

What’s happened in America isn’t just the loss of the omega-3 fats but a flood of omega-6s. Omega 6 fats are the precursors to inflammatory signaling compounds called eicosinoids. They come from vegetable oils like corn oil, soybean oil etc. Omega-3’s are the precursors to the anti-inflammatory signaling eicosinoids. It stands to reason that you may want more anti-inflammatory products when the chronic diseases we all suffer from are based on inflammation.

WWW. What will work for me? I’m trying to change my eating habits to avoid vegetable oils and add omega three fats. There is evidence that those folks who take at least a gram a day of fish oil have a brain that’s 1-2% larger than those who don’t. Want a bigger brain or a smaller one? I’m opting for the bigger helping. I’ve bought a grass raised cow from a farmer. It’s taking a year for it to grow. It will cost me about $ 3 a pound if I do all the delivery, pick up and sorting out. Sounds like a bargain for my brain. Can you buy local? Get together with friends. Help a Wisconsin organic farmer make a local living.

Reference: Brain Building Nutrition by Michael Schmidt Third Edition

To make order of my exploration, I want to first talk about what we shouldn’t do. We now know there are just lots of things our brain would prefer we didn’t expose it to. First and foremost, the inflammation and irritation that comes along with cigarettes is just a disaster. The cells that protect each brain cell are called glial cells. They are sort of like baby sitters for brain cells, covering them, protecting them, shielding them. When they get mad and get inflamed, they damage the brain cell underneath. Cigarettes are right up there as noxious. Whew. A freebe. I don’t smoke. But there’s much more.

Mercury, lead, cadmium and arsenic make up a toxic handful of heavy metals that damage brain cells. We used to get lead exposure from gasoline. Now lead comes from older house-paint flaking off and materials made below our protection standards. (Toys from China. Lipsticks?) Even Nigerian chocolate (where 70% of the world’s cocoa is grown and where you can still buy leaded gasoline) has lead contamination. Arsenic comes off of the green wood we make our decks with. Yup, that nice kid’s playground wood: filled with arsenic.

Mercury is in coal so coal fired power plants put it in the air. And then there are old filings from the 60s and 70s with mercury content in them. Cadmium comes from cigarettes. We all have variable heavy metal exposure not seen before in human history. Some of it rises to the level of toxicity. I just measured my toxic levels. It’s not pretty.
But more common to all of us are everyday poisons like fake fats that create a low level of irritation and inflammation. Trans fats and saturated fats are everywhere. They don’t cause immediate noticeable damage but they do set off inflammation in our arteries and they make our membranes function less smoothly. If your arteries are inflamed your brain is too.

What about glutamate? There is all sorts of controversy about glutamate because of MSG. Monosodium glutamate came to America in the 1960s and its consumption continues to skyrocket. Sort of on the same order as our brain diseases of Alzheimer’s, Parkinson’s and ALS. We like MSG because it makes food taste so good. The theory is that it causes excitatory cells to fire off, and fire and fire and fire, and then roll over and die. In experimental animal models exposed to the amount of MSG we have in our diet we can show the same sort of damage that shows up in Alzheimer’s. Not proven yet, but sure a lot of disturbing literature.

WWW. What will work for me. That’s the short starter list. Avoid cigarettes and smoking. Think about not using green pressure treated wood for surfaces you walk on. Read food labels and avoid MSG and all of its fake names like ‘hydrolyzed vegetable protein’. We didn’t even get to fake sweeteners. There is a lot you can do to help your brain. We’ll get to that.

Stand by for a battle-royal over Alzheimer’s disease (AD)-to take place in
the British High Courts of Justice, no less. Shortly, in a unique court case, NICE (National Institute for Clinical Excellence), the UK’s National Health Service drugs watchdog, will be challenged to defend its decision not to fund Alzheimer’s drugs intended for use in the early stages of the disease.

Ranged on the prosecution benches will be two big guns of the pharmaceutical industry, Pfizer and its marketing arm Eisai, aided and abetted by the Alzheimer’s Society, a vociferous patient support group that equally loudly proclaims itself to have no ties with any drug manufacturers.

What’s all the fuss about? Are the Alzheimer’s drugs any good at all, and are there any alternatives? And what causes the disease in the first place?

Dementia and Alzheimer’s

From near-obscurity only a generation ago, Alzheimer’s disease is now probably, after cancer, the most feared disease of old age. Alzheimer’s has been chillingly described as an affliction whose victims suffer the loss of qualities that define human existence.

Once considered a rare disorder, it is now known to be the most common type of senile dementia, defined as physical damage to the brain in old age that results in major changes to reasoning, memory, personality and behaviour. Until recently, the only way to distinguish Alzheimer’s from other types of dementia was by post-mortem examination of the brain. A typical AD brain is found to be partly atrophied, with the brain cells clumped together in what are called ‘neurofibrillary tangles’ or ‘plaques’.

The second major type of dementia is vascular dementia, where the interruption of the brain’s blood supply, usually due to ‘mini-strokes’, causes brain cells to die. These two main types of dementia can now sometimes be distinguished from each other by brain scans using either magnetic resonance imaging (MRI) or positron-emission tomography (PET).

Senile dementia is not as inevitable as many people might imagine: between 25 and 50 per cent of individuals over 85 are spared it. Nevertheless, dementia is on the increase, so the drug companies claim, because of the simple fact that we’re all living longer. It is believed to be incurable.

Big Pharma’s offerings

Any prolonged chronic illness that is only ended by death is, of course, meat and drink to the pharmaceutical industry. And yet, perhaps surprisingly, there are relatively few drug treat-ments available for Alzheimer’s. First on the market was tacrine (marketed as Cognex) in 1993. Like virtually all of its successors, tacrine is a so-called cholinesterase inhibitor, which acts by artificially maintaining levels of acetyl-choline in the brain. This important brain chemical is known to be reduced by as much as 90 per cent in AD sufferers; it’s also believed to be important for memory, so finding a drug that can preserve the chemical in the brain makes sense.

In fact, the theory is fine-the trouble is the side-effects. After just a decade on the market, tacrine began to be no longer actively marketed after reports of severe liver toxicity. As much as 60 per cent of patients found the drug’s side-effects to be intolerable at high doses. The final nail in tacrine’s coffin was that, after all this, it really doesn’t work (JAMA, 1998; 280: 1777-82).

Since then, three other drugs have come onto the market, all of which attempt to do the same trick of increasing acetylcholine in the brain. As expected, these drugs are all deadly rivals. Pfizer’s Aricept (donepezil), has an advertising tagline that says ‘when Alzheimer’s hits home, Aricept can help’; Novartis’ Exelon (rivastigmine) claims to be ‘another step forward against Alzheimer’s disease’; and Shire Pharmaceuticals/Janssen’s Reminyl (galantamine) sells itself with the somewhat vague tagline ‘Reminyl is now’.

So far, Pfizer is the only manufacturer to have threatened a lawsuit against the recent NICE ruling that none of these drugs is really worth taking in the early stages of AD. Will the drugmaker win their case? Our prediction is no-and, frankly, because the evidence is stacked against them.

The only large-scale, truly independent clinical trial of Pfizer’s Aricept was carried out by a team of British researchers at the University of Birmingham. In a double-blind trial that lasted for more than two years, Aricept was tested head-to-head against a placebo in over 500 patients who had mild-to-moderate AD.

The study’s conclusions? Aricept works, but its benefits are very small-“below minimally relevant thresholds” (Lancet, 2004; 363: 2105-15). As study director Professor Richard Grey stated in the report: “Patients and their families would probably notice no difference if the drug was stopped.”

What’s more, even clinical trials funded by the drug companies them-selves failed to show much benefit with any of their products. For example, Oxford University researchers recently scrutinized data from 24 separate Pfizer-sponsored Aricept trials, involving more than 5000 patients at different stages of AD, and concluded that “the treatment effects are small and are not always apparent in practice”. Add to that the strong likelihood of “many adverse events” such as nausea, vomiting, diarrhoea, muscle cramps, dizziness, fatigue and anorexia, and it’s little wonder that there’s what the researchers politely refer to as a “debate” over whether Aricept is worth a candle (Cochrane Database Syst Rev, 2006; 1: CD001190).

The same Oxford scientists have also examined another of Pfizer’s claims-which is also supported by the strictly independent Alzheimer’s Society-that Aricept helps prevent the onset of AD, stopping what is classified as ‘mild cognitive impairment’ (MCI) from turning into full-blown Alz-heimer’s. The researchers’ conclusion? According to their report: “There is no evidence to support the use of Aricept for patients with MCI. The putative benefits are minor, short-lived and associated with significant side effects” (Cochrane Database Syst Rev, 2006; 3: CD006104).

What of Aricept’s two other rivals, however? Again, independent studies of the clinical data have exposed the drug companies’ marketing hype.

With MCI, for example, Polish researchers concluded earlier this year that the efficacy of all three cholinesterase-blocking drugs was “questionable”, especially given the high incidence of side-effects, some of which-as in the case of Reminyl-apparently can be fatal (Neurol Neurochir Pol, 2007; 41: 13-21).

As for full-blown AD itself, three groups of independent researchers all agree that the three drugs, although having slightly different modes of action, all produce broadly similar effects-or rather, a lack of effects. Their benefit to Alzheimer patients is variously described as “not large” (Cochrane Database Syst Rev, 2006; 1: CD005593), “limited” (Tijdschr Psychiatr, 2006; 48: 17-26) and “small” (Drugs Aging, 2007; 24: 155-67).

Nevertheless, Aricept remains the market leader in a highly profitable $3 billion a year business that is fore-casted to grow exponentially.

But there’s one new drug that is beginning to challenge Aricept. It’s called memantine (marketed as Ebixa, Axura, Namenda and Akatinol). Strictly speaking, it’s not a drug, as it’s derived from the naturally occurring mineral adamantine, and it also works in a different way from its pharmaceutical rivals. Developed by Merz, a German manufacturer of natural health products, the compound appears to protect brain cells against glutamate, the amino acid that is thought to be toxic to the brain in excess amounts and to trigger Alzheimer’s.

Clinical trials of memantine have been promising, showing it to be particularly effective in moderate-to-severe AD, although it generally only slows mental decline rather than reverses it (Drugs, 2006; 66: 1515-34). Detailed testing has found that it appears to benefit attention and information-processing speed more than memory (Int J Geriatr Psychiatry, 2006; Nov 20; epub ahead of print).

Its side-effects are hardly greater than a placebo tablet, with a slight tendency to produce tiredness and dizziness. It is widely used in Germany, often in preference to the standard drugs; however, in Britain, it is still considered experimental.

Alternative treatments

Meanwhile, gradually emerging into the limelight are a number of promising plant-based treatments, some of which turn out to have properties that seem almost tailor-made for AD.

Take the humble culinary sage plant, Salvia officinalis. In addition to having potent antioxidant and anti-inflammatory effects, sage is known to have anticholinergic effects similar to Aricept’s. When tested against placebo in a recent clinical trial, 60 drops of sage oil a day was often found to be better than Aricept at maintaining mental functioning in people with mild-to-moderate AD-and without any side-effects (J Clin Pharm Ther, 2003; 28: 53-9). Sage oil can also improve memory in younger people, too.

Lemon balm (Melissa officinalis) has been found to bind to the brain receptors believed to be involved with anxiety, thus reducing the agitation symptoms seen with AD. Particular strains of the plant have also proved able to slow the decline of mental functioning (Curr Pharm Des, 2006; 12: 4613-23). However, although some proponents recommend these plants as aromatherapy for Alzheimer sufferers, the evidence is considered “inconclusive” (Aust NZ J Psychiatry, 1999; 33: 789-99).

The classic herbal memory-enhancer is Ginkgo biloba, which has been proven in numerous clinical trials to benefit mental faculties in people of all ages. Germany is where it’s most used for Alzheimer’s, as even German conventional doctors consider it prefer-able to the pharmaceutical drugs on offer.

Although it’s by no means a miracle-worker, Ginkgo has been shown to benefit virtually all AD patients to some degree, and about a third of them quite significantly. The recommended dosage is 240 mg/day of the Ginkgo extract codenamed ‘EGb 761’; the benefits normally show up within six months (Pharmacopsychiatry, 2003; 36: 297-303). It’s even been suggested that Ginkgo might help prevent the onset of AD but, so far, no research has been done to test its possible role in Alzheimer’s prevention.

What of the other ‘smart drugs’ that are sometimes claimed to be memory-enhancers for the able-bodied? Of these, only nicergoline (derived from ergot) appears to have any evidence of benefit, with up to a threefold improvement on some performance measures in AD (Cochrane Database Syst Rev, 2001; 4: CD003159). Vinpocetine and piracetam, although better known, don’t appear to have been adequately tested in Alzheimer’s patients to come to any firm conclusions.

On the near horizon, the curry spice curcumin is being investigated as a potential anti-AD compound, after it was recognized that people in India have lower rates of the disease. Lab tests by neurologists at UCLA have already shown that curcumin can repair brain cells damaged by AD, and clinical trials are currently underway
(J Alzheimers Dis, 2006; 10: 1-7).

Traditional Chinese medicine offers two sets of herbal mixtures: Yi-Gan
San is a combination of seven different plants, headed by angelica root; and
Ba Wei Di Huang Wan (BDW) com-prises eight herbs, including cinnamon and peony. Initial research shows that they may be useful in AD (Evidence-Based Complement Altern Med, 2006; 3: 441-5).

There is currently excitement over one Chinese herb in particular, a rare club moss called Huperzia serrata.

Five years ago, an extract of the moss-huperzine alpha (Hup-A)-was tested in more than 200 Chinese diagnosed with mild-to-moderate AD. The results were described as “remarkable”. After taking 400 mcg of Hup-A for less than three months, 60 per cent of the patients were observed to be “clinically on the mend”. Only about a quarter of patients failed to respond. Side-effects were “mild and transient” and, in any case, affected very few of the patients (Zhonghua Yi Xue Za Zhi, 2002; 82: 941-4).

How does Hup-A work? It’s thought to increase acetylcholine levels in the brain. But, in fact, it’s much better than that. It penetrates the brain more effectively than the current drugs, and lasts longer. It also has a wider range of effects, including protecting cells against further damage from inflammation and oxidation (Acta Pharmacol Sin, 2006; 27: 1-26). Here again, a clinical trial is currently ongoing.

The Chinese also use acupuncture for Alzheimer’s, and there is evidence that it may work (Zhongguo Zhen Jiu, 2005; 25: 390-2). In a Westernized variation of this, doctors have tested TENS (transcutaneous electrical nerve stimulation) therapy. Applied to various parts of the body (even the face), TENS has been shown to have some value, particularly in the early stages of AD. However, according to the Japanese doctors using it, the therapy needs to be repeated to sustain benefits beyond six months (Front Med Biol Eng, 2002; 11: 237-47).

Hopeful horizons

One possible AD treatment is chelation therapy. Often derided as mere quackery, chelation has been used for decades by frontier-spirited cardiologists to combat heart disease. The treatment involves transfusing a chemical cocktail into the bloodstream that will bind itself to harmful agents and carry them away. Chelation’s earliest use was to remove toxic levels of lead from workers in the battery and paint industries, but it’s now finding a revival in Alzheimer’s patients.

The argument is this: if metal toxicity is involved in AD, then chelation may be able to bind and flush away the harmful metals before they can cause brain damage.

One of the first trials of chelation used clioquinol as the chelating agent. The results were promising, showing a slight clinical improvement after three weeks (Dement Geriatr Cogn Disord, 2001; 12: 408-14). However, the results of the only subsequent trial were less encouraging (Cochrane Database Syst Rev, 2006; 1: CD005380).

Despite these disappointing findings, a whole slew of researchers across the globe-from Osaka University to Harvard-are actively pursuing the chelation route in hopes of making a breakthrough. Some scientists are even suggesting using ‘nanoparticles’ to trick the brain into allowing more powerful chelating agents past its barriers (Neurosci Lett, 2006; 406: 189-93).

The fact that researchers are being forced to consider such high-tech solutions says two things: the existing treatments aren’t working; and Alzheimer’s may be a rather tougher nut to crack than we thought.

Tony Edwards

The most drastic types of memory loss are dementia and Alzheimer’s disease, the results of two different types of brain damage identifiable on brain scans.

Evidence suggests that the risk of Alzheimer’s and dementia is lower in those who have been intellectually active in their lives (Proc Natl Acad Sci USA, 2001; 98: 3440-5), although there are notable exceptions such as the novelist Iris Murdoch. Nevertheless, by and large, the higher the educational achievement in youth, the better the mental functioning later in life. Post-mortems show that college graduates tend to have a lower risk of Alzheimer’s and dementia (Brain, 1999; 122: 2309-19).

One risk factor for Alzheimer’s is serious head injury earlier in life (Alzheim Dis Assoc Disord, 1998; 12 [suppl 3]: S10-5). In a comparison of soccer players with swimmers and runners (athletes less likely to incur head injuries), over 30 per cent of the soccer players had impaired memory compared with less than 10 per cent of the swimmers and runners (JAMA, 1999; 282: 971-3).

Assessing the various stages of age-associated memory loss involves simple question-and-answer tests such as the Mini-Mental State Examination (MMSE), which consists of 30 items testing short-term memory. It’s most useful in assessing less-educated people. A more sensitive test for aged graduates is the ‘delayed recall’ test, in which a list of words has to be remembered 20 minutes later.

HEALTHY LIVING
We know how – we just don’t
In a study of 153,000 Americans, it was revealed that only 3 per cent follow all four of the so-called ‘golden rules’ for healthy living. Although many of them followed one or more of these rules, very few observed all four, which are: not smoking; maintaining a healthy weight (a body mass index of between 18.5 and 25); eating five or more vegetables and fruits every day; and exercising for at least 30 minutes, a minimum of five days every week (Arch Intern Med, 2005; 165: 854-7).

DEPRESSION
Therapy is as good as drugs
Cognitive therapy works just as well as drugs in cases of even the most severe depression. Researchers assigned 240 patients with severe depression to receive either drugs or cognitive therapy for 16 weeks. Both groups fared equally as well, and each was helped far more than those in the placebo group (Arch Gen Psychiatry, 2005; 62: 409-16).

AGEING EYESIGHT
Seeing clearly with vitamin E
Lens opacity, a common problem of getting old, can be slowed down or even prevented by regular supplementation with vitamin E. Researchers found a direct correlation between lens opacity, and the long-term use of vitamin E and a higher riboflavin or thiamine intake when they tested 408 women aged between 52 and 74 (Arch Ophthalmol, 2005; 123: 517-26).

Earlier published studies had revealed that the drugs increased the risk of stroke and heart problems; yet, despite this downside, they were still considered to be far safer than conventional antipsychotics.

The newly found suppressed trials revealed that the four drugs were associated with 276 deaths for every 1000 elderly patients with dementia, which would suggest that they could be far more dangerous than the previous generation. The drugs had been taken for only up to three months before the patients had died.

The studies were carried out as far back as two years ago, and the USC researchers say they can find no good reason why they have never been published. All had used the scientific ‘gold standard’ of randomised, double-blind trials, where the patient did not know if he was being given a drug or a placebo. However, all but one had been sponsored by one of the drug companies that manufacture the drugs being studied (JAMA, 2005; 294: 1934-43).

Researchers at Columbia University in New York tested the drug on 361 patients with early Parkinson’s and, as expected, found that levodopa helped to alleviate the stiffness, tremors, spasms and poor muscle control associated with the neurodegenerative disorder.

However, on scanning the patients’ brains, they discovered that the drug was actually causing damage to nerve endings – in particular, to the dopamine receptors that play an important role in controlling symptoms.

In other words, while patients need the drug to ease symptoms, they are also accelerating the progress of the disease. So far, this paradox has left scientists stumped, with a big question mark hanging over how the long-term use of levodopa will affect patients with Parkinson’s (N Engl J Med, 2004; 351: 2547-9).

Another drug under the microscope is rivastigmine, usually prescribed for people with Alzheimer’s. A research team in Istanbul decided to try it for mild-to-moderate dementia related to advanced Parkinson’s. While 19.8 per cent of patients improved in symptoms, 13 per cent got worse. To top it off, 29 per cent reported nausea, 17 per cent suffered vomiting and 10 per cent had tremors (N Engl J Med, 2004; 351: 2509-18).