(Protect The Brain.) What Was The Role Of Methylcobalamin In The Alzheimer’s Study?

Mom's hollyhocksReversal of cognitive decline:  a novel therapeutic program is a recent, small Alzheimer’s study reporting some treatment success using a multi-faceted regimen which addresses sleep, stress, nutrition, and supplements.  I enthusiastically encourage lifestyle change, particularly regarding food, to address health, and many of the things done in this study, my husband and I adopted about two and a half years ago into our lifestyle–with fantastic health results. I’ve been an evangelist ever since.  (It’s not the stuff they bombarded me with in pharmacy and medical school, by the way.)  Somebody who read that Alzheimer’s-related post posed a question regarding why methylcobalamin was used as a supplement:

Hi Terri, thanks for your great post. I love hearing about diet and lifestyle changes reversing disease. Lately I read about coconut oil and its usefulness in Alzheimer’s – Alzheimer’s Disease: What If There Was a Cure?  Terri, can you tell me why the methylcobalamin and CoQ10 were used?  What were their specific roles?”

In the study (follow the link above), there is a nice table listing all the specific interventions taken and why the researchers chose them.  If you are interested, I think it’s a good read.  There’s not too much detail, so today’s post on methylcobalamin and the last post regarding Co Q 10 definitely elaborate on a deeper level.

And let me tell you before we get started and I lose you to the jibber-jabber, these people were not eating breakfast cereal and drinking juice as part of the plan.  And neither should you or your kids.  My kids will never see a Pop-Tart again.

I see the researchers used methylcobalamine.  Why didn’t they just use the kind of vitamin B 12, cyanocobalamin, I have in my multi-vitamin?

Take 1
Because your vitamin sucks.  That’s why.
Take 2
Because cyanocobalamin is cheaper.
Take 3
My apologies.  There are different forms of vitamin B 12.  The vitamin B 12 commonly in our vitamins or in our injections is called cyanocobalamin and is not naturally occurring, but man-made.  The vitamin B 12 used in this study is methylcobalamin and is one of the forms active in our bodies.  Let’s talk about the differences in these two entities using an analogy about hats.

On hats
Sometimes you wear a hat.  You might wear a baseball cap.  Or a top hat.  Or a cowboy hat.  If you’re going to a formal restaurant with a great reputation and you wear a baseball cap, you won’t fit in.  In fact, you may not even be let in!  Well, cyanocobalamin, a synthetically made vitamin B 12, is wearing the wrong hat to the body’s party.  To change its cyanide (whoa) side-chain group to an appropriate hat requires lots of steps by the body.

On Methylcobalamin
Methylcobalamin is also a kind of vitamin B 12, and it is wearing the right hat to the body’s party!  Specifically it is vitamin B 12 with a  methyl group on it instead of a cyanide (whoa) group and has more success getting into the central nervous system than cyanocobalamin.  The vitamin B 12 in most Walgreen’s or CVS supplements is likely to be cyanocobalamin, the synthetic vitamin B 12.  (Man. I worked for CVS during medical school as a pharmacist to make money to cover Indian food and a movie.  I worked so hard there, I swear they were trying to kill me.  Made medical school feel like a breeze.)  Anyhow, here we go again (remember my folate posts), a synthetic vitamin supplement that needs converted by multiple steps to the active form.  Not a good idea if the active form is absorbable, effective, and not too cost prohibitive.

In an Alzheimer’s patient (heck, any of us for that matter!!!), oxidative stress (see last post for an oxidative stress easy explanation) is rampant and taking a toll on the biochemical pathways of the body.  Providing the active form of vitamin B 12 bypasses the reactions that have become broken and faulty due to oxidative stress.  (And providing dense nutrition and well-placed supplements can allow these broken and faulty reactions to be restored, like in the Alzheimer’s study.)  In addition, Alzheimer’s patients probably, being older patients, have low stomach acid, a condition which decreases vitamin B 12 absorption orally.  They may also be on the diabetic medicine metformin or the proton pump inhibitor Prilosec and thus have low stomach acid, exacerbating vitamin B 12 deficiency.  A GREAT REASON to change your diet and see if you can get OFF those medicines!

OK.  But what does the methylcobalamin do?

Some studies show that Alzheimer’s patients have low vitamin B12 levels.  A low vitamin B 12 level can lead to damage of myelin, the protective coating of our nerves.  Improving vitamin B 12 status can help in myelin regeneration.  That’s likely to be important, but what they say they were after in this study was lowering homocysteine levels.  Homocysteine, an amino acid, can be elevated in Alzheimer’s disease.  High homocysteine is destructive in the brain.  It overactivates receptors in the neurons known as NMDA (glutamate) receptors and leads to cell death.  It leads to DNA damage and programmed cell death.  It keeps the inhibitory neurotransmitter GABA from doing its job.  It interferes with the important blood brain barrier.  High homocysteine levels are implicated in dementia and just overall decline in thinking ability (cognitive decline).

Low vitamin B 12 and high homocysteine levels can be linked.  A low vitamin B 12 level can result in high homocysteine levels.  Vitamin B 12, specifically methylated vitamin B 12–methylcobalamin, is necessary to take this homocysteine and turn it back into something called methionine.  Methionine then starts a cascade of reactions which provides necessary protection from oxidative stress, which we talked about in the last post.  Oxidative stress is prevalent in Alzheimer’s disease (and most people eating  sugar and grain-rich diets).

Extra credit paragraph:  Converting homocysteine to methionine requires methylated vitamin B 12 (methylcobalamine) AND a methyl group from 5-Methyl THF or “folate.” (Folate post 1 and folate post 2.)  (Eat real food.  Eat your greens and broccoli.  Eat your meat.)  From methionine, SAM is formed, which goes on to assist in many methylation reactions.  For those of you who are getting started in this alternative health area, you may have went googly-eyed over the forums where people start talking about methylation and methylation pathways.  You wanted to pull your hair out and tell them to stop it.  This homocysteine to methionine is a methylation process.  And don’t feel bad.  I used to stop reading right there too.  I didn’t want to go through those pathways again by choice!  But it’s all an onion.  Layer by layer by layer we learn if we persist.


Methylcobalamin was used as part of a multi-faceted approach to reverse symptoms and brain changes in Alzheimer’s dementia.  There was some preliminary success!  Many of the changes we can implement in our own lives and our children’s lives, without popping a pill!  Methylcobalamin helps lower homocysteine and power our “detoxification” systems.  Food sources are mostly, if not entirely, considered to be meats.  Liver is king.  If you are vegan or vegetarian, I encourage you to read up on vitamin B 12 so you do not get deficient.  Also, if you don’t like meat, you pop prescription medicines which could interfere with B 12, or you eat a crummy diet.  This is important.  It is your brain we are talking about here.

And just some last ideas to chew on.  Vitamin B 12 absorption decreases as we age.  Acid reflux medicines can interfere with vitamin B 12 absorption.  Vitamin B 12 lab values can be in normal range and a patient still be vitamin B 12 deficient.

Be diligent.  Don’t use the internet as your doctor.  My blog posts are not meant to be medical advice or treatment advice.  I stay at home and fold laundry, while reading “Go, Dog, Go” all day; don’t trust me.  Discuss all health changes with your favorite doctor.




1.  The Neuropsychiatry of Vitamin B12 Deficiency in Elderly Patients.  Christian Lachner, M.D.; Nanette I. Steinle, M.D.; William T. Regenold, M.D., C.M.  The Journal of Neuropsychiatry and Clinical Neurosciences 2012;24:5-15. doi:10.1176/appi.neuropsych.11020052


2. Low vitamin B-12 status in confirmed Alzheimer’s disease as revealed by serum holotranscobalamin.  H Refsumi, AD Smith.  J Neurol Neurosurg Psychiatry. 2003;74:959-961 doi:10.1136/jnnp.74.7.959


3.  Methylcobalamin Facilitates Collateral Sprouting of Donor Axons and Innervation of Recipient Muscle in End-to-Side Neurorrhaphy in Rats.  Wen-Chieh Liao,  Yueh-Jan Wang,  Min-Chuan Huang,  Guo-Fang Tseng.  September 30, 2013.  DOI: 10.1371/journal.pone.0076302


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