Tackling Alzheimer’s: who benefits from current spending?

by Jerome Burne

Is putting all our eggs in the drug basket really the best way to beat Alzheimer’s? Just as we can’t rely on drug companies alone to beat antibiotic resistance, so we can’t rely on a pharmaceutical silver bullet for Alzheimer’s. Tackling antibiotic resistance needs heavy investment in drugs that will be used sparingly for a short time. The pharma model prefers drugs for as many people as possible for as long as possible.

An equally unbridgeable strategic mismatch hampers drugs for Alzheimer’s. We need a way to reduce risk right now, preferably cheaply. Drugs can only offer promissory prevention in five to ten years at high cost. But evidence is mounting that taking lifestyle change and high dose vitamin seriously could have an immediate effect. Here’s some evidence why we need a rethink.

Evidence: Last month a big meeting of government and various dementia charities promised an Alzheimer’s treatment by 2020, saying that delaying dementia by five years would cut the number with the disease by one third. That would be great but so far a spend of about £25 billion researching Alzheimer’s drugs has produced virtually nothing useful.

Evidence: That meeting followed the G8 summit on dementia in London last September which was also exclusively about drugs. A statement calling for a shift to prevention signed by over 100 international dementia experts was effectively ignored. It emerged that for every £1000 pounds that UK Research Councils spent on Alzheimer’s just 1p went on studying prevention.

Can a problem as serious and intractable as Alzheimer’s really be tackled by all-too-familiar life-style advice?

Evidence: This week the Lancet published a report by the American Centres for Disease Control and Prevention saying that our epidemic of chronic diseases such as heart disease and diabetes were due to a small number of risk factors that were largely preventable including tobacco, poor diet, lack of exercise alcohol and high blood pressure. All (with the possible exception of alcohol) are also factors linked to Alzheimer’s. When you know what is causing a problem it surely makes sense to spend serious money tackling it.

Evidence: Last week saw the publication of a large analysis based on nearly 200 studies that put some impressive figures the contribution of lifestyle factors to dementia risk. (Epidemiologic studies of modifiable factors associated with cognition and dementia). These included lack of exercise (32%), a low level of education (24%), a low fish consumption (22%) and having a high levels of the amino acid homocysteine in your blood (22%). The only way to lower your level of homocysteine is by taking high doses of vitamin B. The official response to strong evidence that B vitamins may well cut dementia risk has been either ignored or ignorantly attacked (see below).

In an ideal world the government and charities would pick up and run with whatever looked promising as a treatment for Alzheimer’s. But if your agenda was finding a really profitable drug to treat the disease, then a treatment involving a vitamin that costs pennies might seem more of a threat. Sound too conspiracy theorist? Here’s some evidence.

Evidence: Four years ago a big randomised well run trial carried out at Oxford University showed that lowering the level of homocysteine with high levels of B vitamins could reduce the level of brain shrinkage in areas affected by Alzheimer’s by an astonishing 90%.

Evidence: It wasn’t definitive but it was something more specific than the drug companies had come up with so far and it offered something that people could do right away. It certainly deserved a follow up study in the UK. But four years later that has still not been done. In fact the Alzheimer’s charities have not only ignored it but misreported it. A recent review of all the evidence by Alzheimer’s Disease International says that the B vitamin RCTs had found the treatment “effective” but then falsely states in their conclusion that: ‘RCTs targeting elevated homocysteine levels…[have no] significant effect on cognitive function.’

That was bad enough and certainly hard to claim that this was all being done in the interests of patients. This week a study rubbishing the whole idea of using B vitamins to cut the risk of dementia came out. One of the authors was a high profile champion of statins.

Evidence: At first sight it looks like proper science. An analysis (Effects of homocysteine lowering with B vitamins on cognitive aging) of 11 trials involving 22,000 people designed to see if B vitamins could cut their risk of developing Alzheimer’s. Could this be the follow up of the 2010 paper? The conclusion was damming: ‘Homocysteine lowering by using B vitamins had no significant effect on individual cognitive domains or global cognitive function.’

Evidence: If that study had built on or tested what the original study had found that would have been disappointing but proper science. It might have varied the doses, it would probably have divided patients into high and low homocysteine groups as the study had shown clearly that only those whose homocysteine was high benefited from treatment. To be useful it would have given figures showing the difference between the scores of those in the placebo group and those getting the vitamins.

Evidence: Remarkably it did none of those things. Instead what it actually showed was that if you treat healthy people on a variety of doses of B vitamins, using a measure of memory that can’t detect the small changes you’d expect to find in healthy people and ignore the fact that people with low levels of homocysteine don’t benefit from B vitamins you won’t cut the risk of Alzheimer’s. Hardly surprising. It certainly tells you nothing about the trial done four years ago and certainly doesn’t justify the conclusion that lowering homocysteine with B vitamins has no benefit.

Evidence: From one perspective though it was a roaring success. It attached a prestigious name Professor Sir Rory Collins (recently in the news as an aggressive champion of the benefits of statins (see here: https://healthinsightuk.org/2014/05/22/eminence-based-medicine-defends-the-status-quo-on-statins/) to a report with the conclusion: Dementia. B vitamins. No benefit. Since both doctors and journalists rarely read further than the abstract, the impression that B vitamins don’t work is out there. (More details.)

And that’s not the only piece of evidence that there is a concerted effort to discredit the B vitamin effect by whatever means necessary. An even more shoddy dismissal of B vitamins /Alzheimer’s link was performed about six months ago. Again it plausible to assume that by generating a wholesale condemnation of B vitamins it was a huge success.

Evidence: The study, which involved giving multi vitamins containing a modest amount of B vitamins to 6000 healthy doctors, came with this ringing editorial that provided the scare headlines but which didn’t remotely reflect what the studies actually found .

‘Antioxidants, folic acid, and B vitamins are harmful or ineffective for chronic disease prevention, and further large prevention trials are no longer justified. Most supplements do not prevent chronic disease or death, their use is not justified, and they should be avoided.’(‘Enough Is Enough: Stop Wasting Money on Vitamin and Mineral Supplements’)

Evidence: A finding about multivitamins given to well-educated, well-nourished people not ‘at risk’ of dementia tells you nothing about ‘most’ supplements” and nothing about the benefits of high doses of B vitamins given to people know to be at risk. What happened was that over eight years the cognitive levels of placebo and drug groups stayed almost the same. Again not a surprise.


The fact that those supposedly fighting the scourge of Alzheimer’s can not only ignore good evidence for the effectiveness of prevention but then try very incompetently to discredit the one approach that has a good randomised trial supporting it should make anyone personally involved with Alzheimer’s alarmed and angry.

It also points to one of the serious flaws in our system of evidence based medicine. If the drug approach does yield a pill that shows up in randomised trials to be better than a placebo at slowing the development of Alzheimer’s it will be hailed as a triumph for the evidence-based approach to the problem. The fact that a range of promising, cheaper, most likely far less toxic non-drug approaches were ignored won’t be seen as a failure. But it is.

Jerome Burne

Jerome Burne

Jerome Burne is the editor of HealthInsightUK. He is an award-winning journalist who has been specialising in medicine and health for the last 10 years and now works mainly for the Daily Mail. His most recent book “The Hybrid Diet” was written with nutritionist Patrick Holford, published 2018. Award: 2015: Finalist for 'Blogger of the Year' Medical Journalists' Association.


  • You write
    “The only way to lower your level of homocysteine is by taking high doses of vitamin B. The official response to strong evidence that B vitamins may well cut dementia risk has been either ignored or ignorantly attacked”
    I agree B12 (and B vit complex) is most important but it’s worth knowing one of the Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes is reduction of HbA1C.
    There is also evidence for other strategies such as a low-glycemic index diet, fructose reduction, resveratrol, correction of Vitamin D deficiency, Fenugreek, aerobic and resistance training Vitamin C, and Dietary fibre which all have long-term beneficial effects on HbA1c however as none of these strategies for HbA1C reduction would benefit big Pharma I’m sure they also will continue to be ignored.

    • Editorial

      Thanks for those comments – yes there certainly is evidence for a number of other life-style interventions and the low carb/paleo one is particularly interesting as there is some sensible evidence to suggest that Alzheimer’s may well involve insulin resistance; some researchers are referring to it at diabetes type3. There is a trial (ongoing I think) looking at giving insulin as a treatment. That has had serious funding. Lowering carb intake to a fairly low level has not.
      Time for a campaign calling for a proportion of funding be devoted to promising/plausible non-drug approaches, not to be done by people with a vested interest/history of rubbishing such potential treatments.

    • I have never been clear as to how to reduce fructose intake while still consuming plenty of fruit.

      I noticed that just today there is an announcement that a new test for dementia may become available using 10 protein markers in the blood. It would be interesting to know if this test will be as predictive as measuring homocysteine levels.

  • I also wonder whether our long recommended low fat diet and drive to reduce our blood cholesterol with statin drugs are implicated in the incidence of dementia. Seems logical to me consider our brains contain large amounts of fat.

    • Editorial

      Indeed some researchers talking about Alzheimer’s as type 3 diabetes.

      • I know a guy who suffered the memory/cognitive side effects of statins (as well as muscle problems). Fortunately he has recovered after abandoning statins. However, is there any possibility that people could be diagnosed with dementia when they are actually suffering from statin poisoning – possibly ending up in care homes and being fed their statins every day?

        • Editorial

          There are certainly reason to think it possible. Cholesterol is an integral part of the cell walls of neurons, there are plenty of reports of people experiencing some sort of “brain fog” on statins. A new generation of statins that lower cholesterol more effectively but via a different route have had cognitive impairment flagged up as a possible side effect. As you are probably aware drug companied are not to reliable in their recording of side effects so if evidence is hard to come by

          • I think what I am trying to get at, is this.

            If someone is assessed for dementia but actually has brain side effects, is the diagnostic process precise enough to separate these two possibilities?

          • Editorial

            I think you mean is it possible to be diagnosed with Alzheimer’s but to actually be suffereing from the side effects of statins. I’m no expert but I’d say probably not. The standard test for Alzheimer’s is a paper Q&A – which just tells you your performance is dropping, not why. There are some more research level tests that look at proteins in the spinal fluid and MRI scans that look for plaques and tangles (the classic signs) in the brain. But as far as I know non of these would clearly distingush the causes – plaques and tangles for instance can show up but the patient has no memory issues at all. No idea about the highly publicised latest test that detects certain proteins in the blood – possible if it really does detect Alzheimer’s reliably that it might distinguish the two. Many of the side-effects of statins will reverse once you stop taking them – can they cause long term damage? Possibly but don’t have details. Point is that the body is good at making cholesterol – it is a vital lipid – so once you’ve stopped the lack can be made up.

        • If it helps, David, I think what Duane Graveline has written about statin toxicity and the indiscriminate way in which these drugs target the biosynthesis of mevalonic acid strongly indicates the nature of statin side effects could easily be mistaken for age related decline in capacity for memory and/or cognition. Dementia comes in various guises and I wonder how readily the medical profession can distinguish between the types.

          Cholesterol is so ubiquitous to biology, to cells, and to human physiology that its is sheer folly to think that cholesterol could be so functional in one instance and so cytotoxic in the next.

          Reading Graveline and thinking hard about prospects I think physiological side effects will arise in 100% of takers, and the usual interpretation of a side-effect which insists it has to be a physical or mental symptom to be detected and reported is woefully remiss. The physiological consequences of taking a statin are a mix of reversible and irreversible, perhaps, as lasting genetic interference seems a plausible prospect. The tricky deal is taking suspicions beyond plausible conjecture to evidence backed surety. Heres Graveline final paragraph of The Stain Damage Crisis (book).

          “And this entire black thing is masquerading as premature senility. Is it any wonder doctors, when hearing these patient complaints of tiredness, weakeness, wobbly-kneed with burning pain and numbness, poor coordination and terrible memory, respond with a predictable, “You are over fifty now and have to expect these kinds of things.” The various processes statins initiate take years to develop. So far the medical community is comfortable with blaming God for these premature disabilities and deaths and turns a deaf ear to these complaints. And I cannot yet prove a thing.”

          I’m not entirely convinced that merely cessation of ststin therapy will reverse all the changes that may have been initiated while on them. Homocysteine and certain oxides of cholesterol are implicated in the atherogenesis that marks the beginning and advance of cardiovascular disease, while much the same body of work provides evidence that exonerates cholesterol from direct involvement in the process. This means too things, the fat/cholesterol hypothesis is nonsense, and there is no case for lipid modification through prescription of statins, nor was there ever. Literature exists that makes that plain.

    • Indeed. Dr Stephanie Seneff, Senior Research Scientist at MIT, wrote a paper on this in 2009: http://innereye.eu/nuts/?p=241 . Here was her experience of getting it published: http://innereye.eu/nuts/?p=255 .

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