How to avoid dementia

Most of us fear that we may develop dementia as we get older. I fear that I may have got it already, as my memory for names becomes even worse. One piece of good news is that, for around one third of people, it may be possible to prevent dementia simply by taking three forms of vitamin B. Vitamin B6, B12 and folic acid.

The research work on this was done at Oxford University, and was published earlier this year. I received a copy of the study about a month ago, and I read it with great interest. The key statements from the abstract are, as follows:

‘Our results shows that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD processes and that are associated with cognitive decline.

….we go further by demonstrating that B vitamin reduces, by as much as seven fold, the cerebral atrophy in those grey matter (GM) regions specifically vulnerable to the AD (Alzheimer’s Disease) process.’

Some of you may know that Jerome Burne blogged about this a while ago, which is what attracted my interest in the first place. It immediately fired me into instant action. Several weeks later I got hold of the full paper, which was published in the proceedings of the National Academy of Sciences. It is entitled: ‘Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment.’ Sorry to say that you have to pay to get the entire manuscript.

This study built on earlier work which also demonstrated a significant reduction in brain shrinkage using vitamin B(s) (at lower doses). The brain images themselves look particularly impressive, even to my untrained eye, with far less atrophy to see in the vitamin B treated group.

Unfortunately, this benefit only seems to be available those people who had a high level of homocysteine in their blood in the first place. A level found in about one third of the population.  For the other two thirds, taking vitamins does not seem to help.

Why do vitamin B(s) have this beneficial effect in this group?  Well, it has been known for a long time that people with high homocysteine levels are more prone to developing dementia. It is also known that B-vitamins lower the level of homocysteine the blood (look up Wikipedia if you want more detail on this complex area). However, just because a high level of homocysteine is found in people with dementia, does not mean that it truly is cause. It may be an innocent bystander. An association, rather than a cause.

However, the Oxford group, by lowering homocysteine and slowing brain atrophy, have gone a long way to prove that homocysteine does seem to be an actual cause of dementia. At least in about one third of people who have high levels in the first place. More importantly, the risk of dementia can be significantly reduced using a simple regime of B vitamins. A regime that appears to have no adverse effects – apart from a small degree of damage to the bank balance.

Why, you might ask, is no-one doing anything about this? Last week our glorious UK health secretary, Jeremy Hunt, announced that he was, sorry, we were, going to defeat dementia in twelve years’ time. Or some other such nonsense figure that he plucked from out of thin air. Did he mention research into vitamin B? No, he did not. Why not? Possibly because no-one made him aware of this research. Probably because he has no interest in dementia other than as a career enhancing, five minute, sound bite. He is such a busy, busy, man. Tomorrow he will be curing cancer. Sorry, we will be curing cancer.

A further important reason for the deafening silence in this area is because pharmaceutical companies cannot make money out of vitamins. Vitamins cannot be patented; therefore any profit margin is far too puny to be of interest to them. Which means that there will be no funding from the pharmaceutical industry to support any further research into B vitamins.

Even worse, if vitamins do work to reduce dementia this will significantly erode any pharmaceutical industry profits to be made. In commercial parlance vitamins would be called – ‘the competition’.

And what do we do to ‘the competition’ boys and girls?

We crush it sir?

‘Yes, that’s right, we crush it like an insect under our boot, don’t we boys and girls. Using any means possible……lock and load.’

I am sure a few Grima Wormtongues, sorry pharmaceutical company lobbyists, have already been whispering in various ears, denigrating this vitamin B research. ‘Very preliminary, not very convincing, we need a new approach, you need to support us, the pharmaceutical industry, only we can find a cure…….my precious…..’

Trust in me, just in me
Shut your eyes and trust in me
You can sleep safe and sound
Knowing I am around
Slip into silent slumber
Sail on a silver mist
Slowly and surely your senses
Will cease to resist
Trust in me, just in me
Shut your eyes and trust in me

(Kaa, the python the Jungle Book)

Wake up, wake up!

Of course Vitamin B is not a miracle cure for all forms of Dementia. In fact it is not a cure – in any recognised sense of that word. All that vitamin B(s) can do is to significantly slow the process of brain shrinkage. Once you have lost brain tissue, it does not come back.

In addition, these vitamins only work in about a third of the population, and only for Alzheimer’s Disease.  There are other causes of dementia, and vitamin B compounds will have no effect on them, at all. However, right now, it looks like by far best thing we have got. In fact, it is the only thing we have got. Alzheimer’s meds can slightly improve symptoms, but have no impact on the underlying disease process.

On the other hand, for the sake of a relatively simple blood test, and spending a couple of hundred pounds (or dollars) on vitamins a year, or however much they actually cost you, this decision is a no-brainer (sorry, couldn’t resist the pun).

Indeed, it is such an obvious thing to do that I have started to offer the blood test at my own clinic. (Yes, I suppose this counts as a Disclosure of Interest). Mainly because no-one in the NHS is the slightest bit interested. So someone had to do it.

The daily doses of vitamin B in this study were:

20mg vitamin B6
500mcg vitamin B12
800mcg folic acid

These are considerably higher than the recommended daily allowance (RDA) for these vitamins. But the RDAs for almost all vitamins were established as a bare minimum, many years ago, using virtually zero evidence. They remain unchangeable by any means known to man. I call them the ‘ten vitamin commandments,’ which have been engraved upon stone.

Until a group of idiots…sorry experts, decides to study the benefits of various vitamins in greater depth, we are going to be stuck with RDAs that make no sense, and will certainly not help you to delay, or even prevent, dementia. Until then, get a blood test to check homocysteine levels. Providing, that is, you can find anyone to do it. Then, if it is high, take vitamin B(s).  They can do you no harm, but they could do you a hell of a lot of good. Which is my kind of preventative medicine.

66 thoughts on “How to avoid dementia

  1. Jo

    “In fact, it is the only thing we have got. Alzheimer’s meds can slightly improve symptoms, but have impact on the underlying disease process.” Did you mean to put a ‘no’ in there?

    I have a lot of interest in this topic as my dad has AD. I was interested to hear of some benefits of fasting on dementia, but I guess we won’t see a lot of studies on this either.

    Reply
  2. Dan

    Has anyone studied whether people eat foods high in the above vitamins (B6, B12 and Folic Acid) have the same benefits as the vitamin study. There is a Tedx talk from a brain surgeon (or something to do with brain) who cured herself of MS. She found vitamins that slowed down the effects of MS and wondered if she ate food high in those vitamins if it would help further. Her theory was that food high in vitamins that helped her cause would contain other nutrients that would also be beneficial. This seemed to have worked because she was no longer confined to a wheelchair. Might be worth a look.

    Reply
  3. Alastair McLoughlin

    Great article – especially the Jungle Book reference!
    Interesting that raised homocysteine levels are related to hypothyroidism
    http://www.clinchem.org/content/47/9/1738.long

    and also raised cholesterol levels
    http://www.ncbi.nlm.nih.gov/m/pubmed/7240961/

    One endocrinologist suggests hypothyroidism is the most misdiagnosed and under diagnosed condition that we face mainly because people are exhibiting many symptoms of low thyroid function yet patients’ blood tests reveal they’re within the accepted range. May I suggest that some people just don’t function well even though they’re within acceptable blood testing limits. Another ‘commandment’ here: thou shall not prescribe thyroid medication even if the symptoms suggest it’s needed. Surely some mistake?
    (Just wondered if you were aware of the hypothyroid/homocysteine/cholesterol connection Dr Mc?)

    Reply
      1. Alastair McLoughlin

        (Sorry Dr K – I thought it was, but then I saw Mc somewhere on the page).
        I think this mis diagnosis and under diagnosis of hypothyroidism may be an often overlooked cause of the problems were talking about – at least in some cases anyhow. The symptoms of hypoT are wide and varied and symptoms taken in isolation (I’m sorry you can only tell the doctor of one problem per visit) will mean the completely wrong diagnosis being arrived at.
        For example migraines may be a symptom of hypoT. Is it ever mentioned? Well it wasn’t to me as a migraine sufferer for over thirty five years. I found out through my own research.
        So low thyroid function is a very big area that is by and large being ignored. Even blood tests are unreliable as they don’t tell us about hormone uptake. Thyroid function that is even slightly low will create problems that don’t seem to mean much in the standard range of testing.

      2. Dr. Malcolm Kendrick Post author

        I think you are right about this. I am become gradually more aware of the idea that the way we test thyroid function does not tell us much of what we want to know. But this is an area where the medical profession is now becoming very defensive/aggressive about. The whole armour argument is growing, and I think my colleagues are finding themselves on the wrong side of best practice.

      3. Alastair McLoughlin

        Thanks for your positive comments about the hypothyroid thingy.
        The situation is incredible: Many doctors are prescribing statins – and other medications – with amazing regularity, even if they’re not particularly needed or effective and yet when it come to sub-clinical hypothyroidism (and correct me if I’m wrong here) current guidelines to doctors do not allow them to prescribe levothyroxine to patients who exhibit many signs of hypoT – yet whose results still fall within the reference range. Instead symptoms are probably looked at in isolation and treated this way.
        I reckon you could start a whole new thread on this subject Dr K….and who knows…there might be another book in the making….

      4. GG

        As you say below, patients are being ‘sacrificed’. Routine, thyroid function tests do not consider the individual and how he/she feels. The attitude is one of as long the blood tests are ok then the patient must be too. Nothing could be further from the truth.

      5. Professor Göran Sjöberg

        Again!

        As a metallurgist I am getting more and more convinced that “evidence based” medicine is just a religion of profits rather than any sort of science.

    1. Spokey

      Are you aware of the work of Ray Peat? He connects almost every malady to stress hormones in his articles and is rather big on the thyroid angle.
      (PS, I loved every page of your book the Cholesterol Con Dr MK!)

      Reply
    2. anglosvizzera

      From what I have read, the reference range for thyroid is just based on some random sample – who’s to know whether some of those people are suffering from hypothyroidism already? That’s the problem with a lot of ‘reference ranges’ in my opinion….

      As for RDAs, there is something called SONA (Suggested Optimal Nutritional Levels) which seems to be a more realistic guide to our daily needs:

      http://www.aunaturalenutrition.com/uploads/1/7/2/5/17259806/sonas.pdf

      Reply
  4. Edward Hutchinson

    There appears to be a free full text copy of the Gwenaëlle Douaud et ALL paper online HERE for those who enjoy reading full text papers.

    Metformin, one of the drugs used to treat (& prevent progression) of diabetes and is now also being touted as a preventative measure for cancer, has the effect of Inducing Vitamin B12 Deficiency
    There must be something to learn from the inverse relationship between cancer and dementia incidence but if the choice of decreasing the risk of one increases the risk of the other I’m not sure it’s such a good deal.
    There has to be a better way of reducing the risk of diseases involving dysfunctional glucose metabolism, (diabetes, cancer dementia) that doesn’t involve drugs?
    Trouble is a low carbohydrate, higher fat, real food diet approach isn’t going to make drug companies any money and will require health professionals and dieticians to acknowledge that current dietary advice needs changing.

    Reply
  5. celia

    It’s pretty sad that vitamins are so easily discounted. I heard on Monday’s BBC Today program that research had been carried out on multivitamins and they were found to be useless in helping heart disease and dementia. I hadn’t seen them as a cure anyway, but I figure something is better than nothing for my general health. Jonny Bowden seems to have taken a severe knocking re: the Catalyst documentary for selling supplements (how evil can you get?) So it’s good to know someone is doing some useful research on the relationship between B vitamins, homocysteine and dementia. I only wish things like this would get picked up when they are available.

    Reply
  6. Brenda Wyse

    There’s a higher incidence of dementia among older diabetics than other population groups.
    I wonder if this research needs to be approached with caution and quote from Jenny Ruhl’s book, “Blood Sugar 101”: “….it turns out that megadoses of Folic Acid, B6 and B-12 worsen the progress of diabetic kidney disease and raise the risk that people who have diabetic kidney disease will experience strokes.” Jenny Ruhl doesn’t state what constitutes a “megadose” although she goes on to recommend the use of tiny doses, compared to your suggestion in your blog. Unusually, for Jenny Ruhl, she does not cite her research sources on B Vitamins or at least, I have been unable to find her source in this one instance. Generally, every piece of advice she gives in her wonderful book is carefully researched with clear citations.
    I think it may be possible for kidney damage at a minimal level to exist in diabetics without the patient being aware of it, thus putting them at risk if supplementing at such high dosage? Perhaps in addition to the homocysteine level test, diabetics should also request regular kidney function tests which, in some areas, do not seem to be routine or regular?
    I love reading your blog and really appreciate the way you share your ideas. Your blog gave me the confidence to proceed with a low carb/higher fat diet and I now have normal glucose numbers without any medication. I had read Jenny Ruhl’s book but continued to hesitate to commit to higher fat in my low carb diet until I read sections of your blog. Recent blood tests for me, at least, confirm it’s a good and safe approach. Nope, it wasn’t the fat…. from reading your book and your blog I would guess that in my case anyway, stress was the original culprit. I am very grateful to have had access to so much helpful information, especially from “The Great Cholesterol Con”. So thank you for that, sincerely. I would be interested to learn what you think of the caveat above though?
    Yours sincerely
    Brenda Wyse

    Reply
      1. Craig

        FWIW I have heard that the Cyanocobolamin form of B12 is potentially toxic if kidneys are not functioning properly due to the cyanide group whereas methylcobalamin is safe. To complicate matters the hydroxycobalamin version can be used to scavenge cyanide but it also scavenges nitiric oxide which may cause other problems for arterial health. Whether the methyl form behaves like that is an interesting question??? Is the form of B12 in liver a more natural version? To my amazement, as I read on Wikipedia about methylcobalamin being used as a first-line treatment for diabetic neuropathy, I am left wondering why none of my GP’s ever bothered to mention this. I suppose that goes hand in hand with the bad advice about cholesterol and the statin prescriptions. Arrrgggh!

        Craig.

  7. dearieme

    I’m due an all-day endocrinology blood test soon. If I said “Now, my love, would you please just add a homocysteine test to your list” what are my chances of success?

    Reply
  8. Claire Birtles

    Hello Dr K
    Is it a routine lab test? And can it be controlled by lifestyle factors at all?
    (I am a practice nurse currently trying to get as many otherwise healthy patients off statin by stealth as is humanly possible without losing my job.)

    Reply
  9. TJ

    Where would one find vitamins of this potency? I am afraid that my “Nature Made” brand “Super B-Complex vitamins purchased in the states has but a fraction of the B12 and B6 that you call for.

    Reply
      1. Wendy

        Dr David Perlmutter, MD author of The Grain Brain – “The Surprising Truth About Wheat, Carbs and Sugar – Your Brain”s Silent Killer” – it says on the cover! He calls Alzheimer’s type 3 diabetes.

  10. Craig

    Yet again a very interesting post. No mention of B1 in there?

    When I was first diagnosed as type 2 D. I consumed quantities of benfotiamine and allinamin (fursultiamine) to help with some neuropathy. The latter is a lipophilic form of thiamine which was developed as an accelerated cure for the vitamin B1 deficiency disease Beri-beri which can involve similar sorts of nerve damage to diabetic neuropathy. I understand that various lipophilic versions of B1 are given as an injection after alcolholic poisoning to prevent long term brain damage, memory loss etc. — I fear it may be too late for me!

    Vegemite is looking better all the time, but no B12 in that afaik unless you use the UK form, Marmite. Is it time to invest heavily in brewers yeast?

    Craig.

    Reply
    1. Professor Göran Sjöberg

      My wife is severely diabetic which was first recognised through her very serious peripheral neuropathy. With a very strict low carb high fat regime, and no medication, the peripheral neuropathy was gone in about half a year and her ability to drive in darkness also returned.

      Reply
  11. Steve Morrissey

    I was also intrigued by the articles about the B vitamins and dementia. I was also pleased that people were talking about prevention by looking at nutrition. The body is very complex and we do not understand all the mechanisms at work, unfortunately we do not understand nutrition too well. If mankind cannot agree about healthy ratios of fat, carbohydrates and proteins then I would submit that our understanding of the micronutrients is also lacking.
    I found that the Office of Dietary Supplements had a useful web site:-
    http://ods.od.nih.gov/factsheets/VitaminB12-HealthProfessional/#h8
    Vitamin B12 looks very safe as a supplement. There seemed to be some questions about high intake of B6 and folate, though some of the issues were connected to not taking enough B12.
    I was interested to see that a serving of liver could give people as much B12 as the supplements. And that liver also has high levels of B6 and folate. Add some green vegetables, onions and a glass of red wine and you probably get a very nice mix of nutrients! 🙂

    The RDAs for vitamins do seem to be linked to the minimum that one can get away with. I know that in the case of vitamin K that much higher intakes are needed to activate the non hepatic vitamin K dependent proteins.
    On the subject of dementia, if it can be shown that vitamin K2 can stop and/or reverse arterial calcification then it could potentially prevent/treat vascular dementia.
    Some studies have shown that low vitamin K diets are linked to impaired mental performance in older rats. Other studies have shown that people in the early stages of Alzheimer’s patients are low in vitamin K compared with matching controls (admittedly they are probably not consuming much in the way of green vegetables and so are short in many nutrients).
    I have mainly been spending time learning about vitamin K, however I don’t think vitamin K2 can solve Alzheimer’s disease on its own. And so I am interested in other important nutrients. I am also interested in the recent ideas proposing that Alzheimer’s is type 3 diabetes, so possibly removing sugar from the diet is prudent.
    Please let me know if you would like to see the references. This posting has been a lot quicker than my usual postings!
    Best Wishes
    Steve

    Reply
  12. Robert Park

    Just a couple of minor considerations. Probably one of the best forms of natural vitamin B is brewer’s yeast, so I am informed.

    Some years ago when I frequently suffered from angina the GP prescribed medication which gave me severe headaches and made me feel unwell. Later, by chance, I discovered that by taking folic acid at between 2-4 mg (and not mcg) it stopped the symptoms with no adverse side effect. Later still, I discovered that by ramping down on vegetable oils in my diet that I no longer suffered from heart problems! It was then that I also discovered that saturated fats were a buffer against ill-health.

    Reply
  13. Lauren Romeo, MD

    Nutritional supplements are not helpful if the patient is suffering from malabsorption, as an example, Celiac Disease. I try to re-establish gut integrity and then supplement. Great article.

    Reply
  14. Susan

    At 35 after taking Cipro for three days, I developed peripheral neuropathy. Over the next 5 1/2 years I developed many other neuropsychiatric symptoms, including all the symptoms of dementia minus hallucinations. Six months after becoming bedridden I found a book online written by a nurse and ER doctor in the USA called Could It Be B12?: An Epidemic of Misdiagnosis. The next day I started B12 injections plus folic acid and a B complex. The majority of my page and a half of symptoms were gone or greatly reduced in days though unfortunately the ones I have had the longest are still with me such as peripheral neuropathy and tinnitus. Later I read about Dr. Newport treating her husband’s dementia with coconut oil and I started a Paleo diet high in healthy fats, such as coconut oil. I was then able to return to work part-time.

    Anyway, my point is as a pharmacist I see many older patients being misdiagnosed or having their B12 deficiency undertreated. In Canada, cyanocobalamin tablets are now standard therapy even though there are no long-term studies or even studies focusing on neurological symptoms, all seem to focus on serum B12 levels (mine were always in the normal range!) The serum B12 test is used as a gold standard diagnostic tool by much of the medical profession even though it is not (one study has shown it misses 35% of B12 deficient patients). It should only be used with MMA and Hcy (which are much more expensive so used sparingly), giving it about 99.8% accuracy according to one study. For me a daily injection of B12 and a change to a low carb high fat diet have been key.

    Regards,

    Susan

    Reply
  15. TC

    Alastair McLoughlin raises the issue of hypothyroidism. The medical profession’s shortcomings in relation to statins and cholesterol are likewise in play on this issue. Virtually all of the endocrinology community seem to believe that hypothyroidism is a condition that can be identified or excluded by a simple blood test (TSH) and then treated with levothyroxine exclusively . However that may be only the case if the source of the problem is inadequate production of the requisite hormones by the thyroid. For many, the hypothyroid symptoms arise from impairment of the body’s mechanisms for converting thyroxine (T4) to liothyronine (T3), the active hormone used by all cells in the body. In other words, the thyroid may produce adequate thyroxine but the body fails to convert it efficiently to the active hormone (T3). The endocrinology community for whatever reason seem unable to comprehend this and as a result refuse to treat hypothyroid sufferers in this category because their TSH is in the “normal” range. As a consequence, such patients usually have to resort to self-treating and sourcing their thyroid medication (e.g. Armour, Erfa, liothyronine) from the internet in order to resolve their symptoms. In many cases, the symptoms can be extremely debilitating, leading to job loss, disruption of family life, divorce etc.

    There are a few practitioners in the UK who do understand the issue and have restored many sufferers (including my daughter) to good health. Unfortunately one of them, Dr Gordon Skinner, passed away recently following a stroke. He had been hounded by the GMC for many years over his non-mainstream approach involving in-depth examination of the patients’ signs and symptoms and treating them with thyroid medication even if the TSH blood test was in range. Every time he appeared before the Fitness to Practice Panels, the GMC was swamped with vast numbers of testimonials from patients whose lives had been restored through him. Like a true Scotsman, he courageously defended himself against the GMC and its so called experts and managed to thwart the GMC in its efforts to strike him off. Nevertheless, the GMC continued to pursue him remorselessly until the end of his life and one has to wonder whether the inevitable stress contributed to his stroke. A great Scotsman who was prepared to stand up against the mainstream naysayers for the benefit of his patients.

    We need more people like Dr K and Dr Skinner who are able to see beyond the end of their noses.

    Reply
    1. Ali

      Totally agree! I have only just managed to get Nature-Throyd after decades of suffering on Levothyroxine. The transformation was astounding, like going from black and white to full spectrum in HD. I believe that my eyesight and teeth would not have deteriorated so badly if I’d had this medication sooner, as well as family life and career. The mistreatment of thyroid conditions in the UK is a disgrace, I am pretty sure that a large majority of people written off as senile just need to get their thyroid sorted.

      Glad to see that vitamins and fats/coconut oil are mentioned in this discussion. Hope people are aware that some B vits should not be taken late in the day, or they will keep you awake.

      If only more GPs would read this.

      Reply
  16. Laura

    Great article, Dr. K. I just started taking B vitamin supplements after reading “Lipitor, Thief of Memory,” because I thought it couldn’t hurt. There have been members of my family who developed AD, so hopefully, taking the B vitamin supplements will help protect me somewhat.

    I am well acquainted with the issues from hypothyroidism. When I was around 20, I kept going to doctors saying that I had issues and it wasn’t until I developed a goiter that anyone would address it. I have been on synthroid for decades now, but my body temperature is never over 98, unless I have a fever (I usually run around 97 degrees). My doctor and I had a discussion about my high LDL and my suggestion that we address the probable root cause, which is my hypothyroidism (that is if she was concerned about my LDL, since I am not) and she told me that since my numbers were in range, that I did not have hypothyroidism and she wanted me to take statins. I politely declined.

    Reply
  17. Brendan

    From :Hippocampal memory processes are modulated by insulin and high-fat-induced insulin resistance.
    http://www.ncbi.nlm.nih.gov/pubmed/20176121

    Insulin regulates glucose uptake and storage in peripheral tissues, and has been shown to act within the hypothalamus to acutely regulate food intake and metabolism. The machinery for transduction of insulin signaling is also present in other brain areas, particularly in the hippocampus, but a physiological role for brain insulin outside the hypothalamus has not been established. Recent studies suggest that insulin may be able to modulate cognitive functions including memory. Here we report that local delivery of insulin to the rat hippocampus enhances spatial memory, in a PI-3-kinase dependent manner, and that intrahippocampal insulin also increases local glycolytic metabolism. Selective blockade of endogenous intrahippocampal insulin signaling impairs memory performance. Further, a rodent model of type 2 diabetes mellitus produced by a high-fat diet impairs basal cognitive function and attenuates both cognitive and metabolic responses to hippocampal insulin administration.

    HUh? Diabetes is caused by high fat? High fat causes insulin resistance?

    Reply
    1. Steve Morrissey

      Animal studies on diet are a bit of a minefield. Apart from the fact that other animals are different to humans the wording by many researchers can be imprecise. High fat diet can mean normal diet plus additional fat and so it is quite different from an isocaloric diet with a high proportion of fat. When I see a diet described as high fat and no further explanation I tend to assume that it is a high calorie diet with plenty of fat and plenty of carbohydrates.
      The paper referred to does not mention any caloric control, it mentions that the rats were able to eat ‘ad libitum’ , so it is very feasible that the rats given the higher fat diet ate more and going by the data most of their calories were coming from carbohydrates.
      In addition the fat used in studies can vary, for instance it could be a pro inflammatory fat like corn oil, an anti inflammatory omega 3 oil or it could be mono-unsaturated fat like olive oil. And this means that the results can vary a great deal depending on the type of fat and whether the animals used are adapted for a high proportion of fat or not.
      So a good number of the studies can probably be filed under the letter B as Dr K has suggested!
      I hate imprecise terms since then one isn’t learning anything. My background has been mathematics and computing, and in those disciplines the logic and the terminology has to be precise otherwise you get nowhere.

      Reply
  18. Christopher Palmer

    “Hippocampal memory processes are modulated by insulin and high-fat-induced insulin resistance.”

    “File under….bollocks.”

    Yes, quite.

    I note the lead author is Ewan McNay.

    Lead author Ewan McNay receives/received funding from the Alzheimers Society. It is also quite ironic that he is placed at Albany Med School in New York, where, some four decades ago some much better designed research established that cholesterol is not at all atherogenic while a cholesterol derivative, cholestane triol, is. Cholestane triol is the most potent atherogen of the three possible oxidised cholesterols and establishing this has paved the way for Dr Kilmer McKully to come to understand an important link.

    Dr McCully (whose name should be preceded by the term ‘Saint’) is the excellent pathologist who first identified the link between homocysteine and atreriosclerosis and who has devoted his career to the homocysteine theory of heart and vascular disease. He, and others, have identified homocysteine as another atherogenic biochemical.

    The way it works is this:

    Methionine is a an amino acid which can be metabolised to homocysteine and B vitamins are important to managing homocysteine this homocysteine that results legitimately. If B vitamins are in short supply (not enough in diet, or are consumed by other legitimate antioxidant processes in the body) then homocysteine levels rise. Homocysteine appears to bear upon cholesterol (a good and vital biochemical) to result in cholesterol becoming oxidised to oxycholesterols including the most atherogenic oxycholesterol which is cholestane triol. Cholestane triol, it would seem, is the atherogenic biochemical that modifies cell behaviour and thence induces the formation and advance of the tell-tale fatty plaques of cardiovascular disease or the calciferous plaques of arteriosclerosis. Homocysteine is an agonist in the process by virtue of its capacity to oxidise ‘healthy’ cholesterol to atherogenic cholestane triol.

    The homocysteine – cholestane triol axis gets interesting since B vitamin deficiency can be traced to failing supply or alternate physiological demand and consumption; smoking, for instance, can be a drain. Them homocysteine gets interesting because it appears to link with cortisol. Rising levels of cortisol are acknowledged, with little contention perhaps, to elevate levels of homocysteine. Cortisol gets interesting because it associates with other endocrinologcal balances including insulin. Cortisol can amplify gluconeogenis (conversion of proteins to glucose or blood sugar) by a factor of six to ten fold, and high levels of cortisol and elevated levels of insulin appear to sit hand in glove. Cortisol may rise for all manner of reasons; emotional stress, anxiety, pressures of work, insecurity, fear etc, but other causes of elevated cortisolemia can be linked to lessor known factors too. For instance:

    Earthing has been demonstrated to encourage normalisation of several physiological factors including cortisol, and we may wonder if ‘isolation’ (absence of earthing) permits chronic dys-cortisol-emia (lasting cortisol imbalance), and in ‘Lights Out’ Wiley and Formby present a plausible hypothesis that the combination of urban living and artificial light has bearing upon our physiology because aspects of the endocrine system are sensitive to light and to the natural circadian rhythms natural light adheres to. In effect they say cortisol levels are commanded to some extent by day length and by seasonal variations in day length. Hence artificial light induces dys-cortisol-emia by the factors of insufficient hours of sleep (nine hours or more is needed), artificial long days and hours of ‘light’, and light pollution whereby absence of adequate dark, even while sleeping, is a barrier to the circadian normalisation and rhythm of hormones whose ‘pyramid’ seems to be topped by cortisol.

    Steve Redgrave, the Olympic multi-gold-medallist (quite atypically) developed type-2 diabetes mid career. To fuel his training he had to consume 8000 calories per day. He didn’t do it consuming fat especially, but ate a lot of pies cakes and biscuits. The details offered were sketchy but I think the terms indicated shop-bought and not home-made. Rower Sir Stephen Redgrave consumed a lot of carbs with a lot of n-6 PUFAs. According to the thesis of Barry Groves this would put Redgrave at risk, but regard for the cortisol connection now has me thinking these dietary factors were compounded by over-training, too little rest, and absence of grounding (especially while sleeping). Each of these factors would contribute to chronic hyper-cortisol-emia and chronic dys-insulin-emia. If cortisol (allied with any cascading factors) bears upon type-2 diabetes then Redgraves case history would no longer seem so atypical as it did.

    The insulin / cortisol / homocysteine / cholestane triol axis and any likely association with the HPA axis does look like a promising field for understanding many a modern disease including Alzheimers.

    But let’s have another laugh at Ewan McNays expense:

    McNays latest work was reported in New Scientist (2945) although McNay conceded in email that the work had not been written up and nor had it been peer-reviewed nor published. He also suggested he induced diabetes in his lab rats by feeding them butter (I have asked he makes an entry in his Health and Safety records on the basis I nearly died laughing). You see insulin, insulin resistance, and hyperinsulinemia seems to accompany the advance of beta-amyloid plaques seen in Alzheimers. Hence Alzheimers is seen in association with type-2 diabetes.

    Something called an oligomer has been identified as a molecular pre-cursor to beta-amyloid. The race is on and the race pays Ewan McNays salary. Pharmaceuticals companies want to develop oligomer disruptors and so now the government (sorry ‘we’) are going to increasingly fund research and development of oligomer disrupting pharmaceuticals so every diabetic can be be prescribed oligomer disruptors, just as a preventative precaution, mind, in addition to their metformin they could do without if only the preventative advice on heart disease didn’t prevent them from coming off high carb / high n-6 PUFA diets to elect go high fat / low carb which reverses insulin resistance and cuts risks of dementia too.

    I saved the best for last. Ewan McNay deployed the memory test for rats to experimentally asses onset of diabetic-ally induced mental decline (dementia) in his lab rats. This ‘test’ involves training rats to associate a darkened enclosure with electric shocks. So, introduce a trained rat to this enclosure and they ‘freeze’. Those who freeze for the longest are judged to have good memory, and those rats that freeze for shorter durations are judged to be suffering from memory impairment and mental decline (Alzheimers). Sophisticated isn’t it? Of course later dissection confirms presence of beta-amyloid plaques.

    McNay and his team had little regard for cortisol and homocysteine (or for the demands upon B vitamins for homocysteine metabolism) and half-scared his rats to death inducing Alzheoers in diabetically stressed rats just so he could produce the molecular precursor to beta-amyloid, ‘oligomer’, to pave the way for oligomer disrupting pharmaceuticals. Part of his brief is to discredit the involvement of glycemia, hyperinsulinemia, excess carbs and (likley) AGEs in diabetes and dementia for no other reason than these point to the root cause, and anything that points to root cause permits a low-input solution to the problem. Removing any ‘f’ to be found in the root of cause is not nearly so lucrative as introducing treatments to target links higher up the causal chain.

    In an email response to my questioning McNay conceded he could perceive of no reason why he should want to earth his rats.

    Here is that reason Ewan:

    http://74.63.154.231/here/wp-content/uploads/2013/06/The-effect-of-earthing-on-human-physiology-Part-1-2006.pdf
    http://journals.sfu.ca/seemj/index.php/seemj/article/view/9/7
    http://74.63.154.231/here/wp-content/uploads/2013/06/Sokal__Sokal_earthing_influence_physiology-2010.pdf
    http://earthinginstitute.net/research/

    The bias to be found in Alzheimers research is fraud. Incidence of Alzheimers clearly favours certain peoples living in certain parts of the world. Evidence enough Alzheimers is entirely man-made. The fix is simple. Avoid the man-made factors that cause it.

    Statins, metformin, and the upcoming oligomer disruptors are all licensed drugs claiming to offer benefits that could be achieved in far more naturally oriented (and less profitable) ways. They are fiction, really, carefully crafted to return profit with no functional benefit.

    Merry Christmas, indeed. Stuff the turkey? Nah, stuff my principles!: Just as soon as the markets reopen I’m intent on investing all I have in big pharma. It’s the only rational way left to go. Oh, what a lovely world.

    Reply
  19. Christopher Palmer

    Homocysteine and Alzheimer’s disease:
    http://www.ncbi.nlm.nih.gov/pubmed/12849121

    Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer’s Disease:
    http://www.nejm.org/doi/full/10.1056/NEJMoa011613

    Homocysteine and Alzheimer’s Disease:
    http://www.diazyme.com/homocysteine-and-alzheimers-disease
    “[ …] using data from the Framingham Heart Study, found that 30% of people showing the highest tHcy levels had twice the risk of developing Alzheimer’s disease as people with average levels, although even mild elevations appeared to add some Hcy and Alzheimer’s Disease In a cross-sectional study […]”
    “[…] it is possible that Hcy is toxic to brain cells, possibly by excessive stimulation, resulting in neuronal damage due to CNS ischemia (Figure 13).”
    Yes, and it is probably worthy of curiosity if Hcy can bear upon cholesterol in brain cells and/or synapses and result in the oxidation of all important pure cholesterol to result oxycholesterols including cholestane triol.

    Nobody should rush to conclusions, but entertaining possibilities is no bad thing. Alzheimers is micro-vascular disease of neurological tissues in which saturated fats nor pure cholesterol play no part (in keeping with CVD). However high-carb, low B vitamin availability, oxidative stress, cortisol, insulin, homocysteine, AGEs (perhaps), and cholestane triol (not implausibly,) would seem to harbour some causative association.

    Reply
  20. Tom Lin

    Amazing story, thank you Christopher!
    Need to ask for homocysteine next time, although the average doc would grunt: “Why? Total Chol is enough for you…”
    Sad to say, I have been thinking the same, no more Apple, just big pharma. No way to beat them…

    Reply
  21. anglosvizzera

    We don’t stand a chance. What with modern food depleted of essential vitamins and minerals, the contentious link between aluminium (think ‘flu jabs’ and their adjuvants) and dementia, the link between statins and ‘dementia-like side effects’, the possible link between wifi/mobile phone radiation (that’s becoming increasingly impossible to avoid) and the non-thermal effects on the brain (to do with calcium and cell membranes….) – in the words of Private Frazer, “We’re all doomed!”

    Reply
  22. Elenor

    I always describe the whole ‘test the pituitary (TSH) to learn something about the thyroid’ this way. They say ‘if your pituitary has “put out the call” (i.e., if you have “adequate” TSH) directing the thyroid to act (produce thyroid hormone); why then, your thyroid HAS acted, and you’re fine; here, have an anti-depressant!’ That’s like saying: if the farm wife yells out the window to the farmhands that lunch is ready, why then — the farmhands have eaten! Whether or not they heard the call or acted on the call — that yell is “proof” that they have eaten.

    {shrug} You (patients/people) have to educate yourselves and act for yourselves, because your doctors can’t or won’t. I actually do not (entirely) ‘blame’ the docs for following the wrong-headed and damaging ‘standards of care’ — because their first loyalty has to be to providing for their OWN families. When the conflict is: treat your patients in opposition to the ‘standard of care’ and maybe come to the malign (and often vicious!) attention of the local medical board, and maybe lose your profession and income; as against: {sigh} and follow their requirements while doing the least damage (rather than the best action) you can for your patients…

    Dr Mike Eades (whom of course you know) has a great little vignette that I also use all the time:
    ‘Let me sum up the take-home message with an unrelated story that oddly illustrates the point. When I was taking flying lessons years ago, the tower once told me to cross one runway we were stopped short of and proceed to the next one. I goosed the engine and started across. My instructor pushed on the brakes and stopped us and asked me what I was doing. I said, “The tower told me to proceed to runway 15L.” My instructor said, “Yes, but you didn’t look for traffic coming in on runway 15R (the runway we had to cross) before proceeding. Here’s what you’ve got to learn. If the pilot makes a mistake, the pilot dies; if the control tower makes a mistake, the pilot dies. Always check for yourself.”‘

    Reply
  23. Roberta

    “Last week our glorious UK health secretary, Jeremy Hunt, announced that he was, sorry, we were, going to defeat dementia in twelve years’ time. Or some other such nonsense figure that he plucked from out of thin air. Did he mention research into vitamin B? No, he did not. Why not? Possibly because no-one made him aware of this research. ”

    I wrote to my MP , Nicola Blackwood, concerning this issue bay in May. she replied “You have made some very important suggestions for the improvement of people’s health and I have passed on a copy of your correspondence to the Rt Hon Jeremy Hunt, Secretary of State for Health, and asked him to respond to the specific points that you raise”

    In due course I received a reply from Jeremy Hunt which carefully avoided answering any of my points. I threw away the letter in disgust. I recall it did mention funding for research on drugs.
    Jeremy Hunt was aware but chose to ignore it,

    Ther

    Reply
  24. anglosvizzera

    Dr Kendrick, there has been some research done by a Dr Emanuel Cheraskin (Professor Emeritus at Alabama Medical School) about optimum levels of vitamins and other dietary supplements to maintain health, reduce susceptibility to disease, slow down the ageing process and maintain vitality.

    The theory that was developed is known as SONA (Suggested Optimal Nutrient Allowance) and was based on a 15 year study of 13,500 participants which started in the 1970s.

    See this paper – http://www.science.edu/CheraskinPaper/CheraskinPaper.pdf

    Reply
  25. homepage

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    Reply
  26. Patricia

    My husband’s B12 level is 269 and his homocysteine is 5.2. He took statins for over 12years and stopped a year ago. Have you looked into the possibility of statins lowering homocysteine and lowering B12 levels?. Because low B12 frequently means high homocysteine. You do say in your book that statins appear to protect against heart attacks.
    If lowering homocysteine helps to prevent heart attacks and strokes we should all be taking B vitamins and I do know B3 has been used by doctors for lowering cholesterol. Niacin the real story by Abram Hoffer makes you wonder why vitamins are so readily ruled out Diagnosing and treating B12 deficency utube is well worth watching.
    Pat.

    Reply
  27. Leon R.

    ” Then, if it is high, take vitamin B(s). They can do you no harm, but they could do you a hell of a lot of good.”

    Unfortunately not true: a pubmed search will reveal that high concentrations in the blood of B12, folic acid, choline (and maybe other B-vitamins) are associated with an increased prostate cancer risk.
    Unfortunately often, what is good for one risk factor is bad for another.
    Seems we have to die from something…

    Reply

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