Alzheimer’s – drugs or vitamins?

  • 6 Aug 2015
  • Reading time 5 mins
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There’s a blatant example of double standards going on right now with dementia. You will recall that the first ‘disease modifying treatment’ – B vitamins given to those with pre-dementia (mild cognitive impairment or MCI) dramatically reduces shrinkage of the Alzheimer’s brain areas by nine times and virtually stops further memory loss. This study was part-funded by Alzheimers Research UK (ARUK).

But then, last week, we are told by ARUK’s Eric Karren that a new drug, solanezumab is the ‘first disease modifying treatment’. Obviously, his memory isn’t very good. But what of this drug that is designed to clear out amyloid protein from the brain? Does it work? Well, there is an effect but it is very small in comparison to that reported with homocysteine lowering B vitamins. Firstly, there’s no change in rate of brain shrinkage, which is critical if the drug is going to modify the disease process, not just marginally slow it down. There’s also barely any improvement in memory. But you wouldn’t know this from the press coverage. “First treatment to slow Alzheimer’s disease unveiled in landmark breakthrough,” enthused the Telegraph. Newsweek was only slightly more restrained: “New drug shows promise for early-stage Alzheimer’s.” “Hugely significant…first drug actually slowing down the course of the disease …verge of a radical breakthrough.” Said another ARUK spokesman. For the full story see ‘Tale of Two Treatments’.

The press stories hit before the study was published so people who know how to analyse the complex results of this study are only now reporting what actually happened. Margaret McCartney, writing for the British Medical Journal, puts this in perspective. In one test those on the drug, out of a possible score of 30, scored 1 point higher than those on a placebo. In the other two tests – possible scores 90 and 56 - the difference was never more than 2 In contrast, there was a virtual cessation of any further memory loss in the B vitamin study.

Also, on a very important measure, the Clinical Dementia Rating (CDR), there was no change between the drug and the placebo, which is bad news because it means no-one actually got better. To give you a comparison the difference between the placebo group (28%) and the B vitamin group (58%) reverting to zero on the CRD was 30%. In other words B vitamin treatment doubled the proportion of people reverting to zero on the CDR according to Dr Celeste de Jager. In this drug study there is no difference compared to those on placebo.

The best memory test result for the drug, the MMSE and ADAS-Cog tests, showed a 34% slowing down of decline in scores compared to those on placebo over 18 months. In the B vitamin trial, those starting with high homocysteine had a complete prevention of any further decline in episodic memory and in semantic memory over 2 years.

But the most worrying result of all for the drug makers is the lack of change to the rate of brain shrinkage. They reported a non-significant 2% reduced rate of brain shrinkage in those on the drug compared to the placebo. In contrast, in the B vitamin study there was an average 30% reduction in the rate of brain shrinkage, which went up to 53% in those with raised homocysteine, and 73% in those starting with good omega-3 levels given B vitamins, compared to placebo.

Big pharma has put most of its eggs into the story that amyloid protein, which produces amyloid plaques found in the brains of those with Alzheimer’s, is the ‘cause’. It’s the same kind of mythical story as cholesterol and heart disease.

The brain produces more amyloid protein as a response to something going wrong. That thing going wrong is most likely to be poor methylation (that’s what homocysteine levels reflect and B vitamins correct) and increased inflammation (a side-effect of lack of omega-3). The drug reduces amyloid protein. In other words, it eats the scar but doesn’t treat the cause of the injury. Meanwhile, scientists at the University of California have been seeing what giving lots of omega-3 does to those with cognitive impairment. Well, it actually helps the body get rid of amyloid protein. So, omega 3 does what the drug does, but without the side-effects. The B vitamins may help stop the formation of amyloid protein in the first place.

So, is there even a need this drug? Yes. To make Eli Lilly, the inventors of Prozac, lots of money. And that money gets circulated to the charities, who help do the research, and the government with taxes, and key decision makers with nice consultancies. It also funds studies purposely designed to provide ammo to kill off the B vitamin and omega-3 story, and the PR to spread the word. Then these the potential for side-effects. Solanezumab is a monoclonal antibody drug, which has to be given by injection every few weeks. These drugs are associated with haemorrhage, which occurred in a small percentage of people in this study. By the time you factor in side-effects, as yet not fully researched, I think this drug is quite useless and certainly not in the same league as homocysteine-lowering B vitamins and omega-3s.

By the way, if you want to keep your brain, your mood, memory and mental energy optimal come to my one-day seminar Optimum Nutrition for the Mind on Saturday November 14th. Also, I strongly suggest you do Food for the Brain’s free online the Cognitive Function Test which also works out your preventable risk factors and gives you a personalised report of key changes to make to reduce your risk.