Nutritional Brain Bomb - Thiamine Deficiency

Yes, I will get back to the carbohydrate insanity series shortly.  But in the comments of the second post, Jack Kruse and Itsthewooo noted that studies with respect to alcohol, blood sugar and violence could be confounded by other nutritional deficiencies.  Which is absolutely true.  I have to say, it is rare to see scurvy or other famously maritime deficiency diseases aside from the serious long-term alcoholics who frequently populate the emergency room.  As one of my attendings in medical school put it, the "Three B diet" (beer, bologna, and bread) is not one likely to come up roses when thrown into a nutritionist's calculator.

So since I seem to be blogging an awful lot right now, I thought I would throw in an instructional primer on brain issues and thiamine deficiency, also known as Wernike's Encephalopathy (and if you are very unlucky, Korsakoff's Psychosis).  And a new subset of patients aside from chronic alcoholics need to worry about this issue too - as I mentioned in The Healthy Skeptic Podcast Chris Kresser Dot Com Podcast Episode 13, there are many case reports in the literature of psychosis and weird psychiatric and neurologic syndromes popping up in gastric bypass patients several years after the surgery - though copper, iron, and B12 are all problematic for post gastric bypass patients, so, apparently, is thiamine (vitamin B1).

Wikipedia Commons

Alcohol interferes with the intestinal absorption of thiamine, so that people who obtain the majority of their calories from alcohol are unlikely to get quite enough thiamine.  A "clinical pearl" taught in medical school is to double (in your mind, not in the chart!) the amount of alcohol someone tells you he or she drinks.  (Hundreds of honest people now vow to halve the amount of drinking they admit to� then realize in truth they already have been�).  I've heard every sort of vast quantity of alcohol use daily from "a quart of Jack" or "a 30-pack of beer" to "17 boilermakers" and "whatever I can get my hands on."   (Shoot - another "clinical pearl" segue, for any medical students or residents reading this blog - the opposite is actually true for any savvy opiate abusers - often the dose of methadone given to prevent withdrawal is scaled to the amount the patient says he or she uses, rather than using vital signs and clinical picture as is the gold standard, so he or she will often increase the self-reported amount to get more methadone off the bat.  And ALWAYS call the methadone clinic to confirm the chronic dose before you write the order for the hospital stay - 160 mg of methadone is a common clinic dose but can stop the breathing of someone not used to that much.)

So who cares if you don't get enough thiamine?  Well, as we know, your brain loves energy.  As do the rest of your nerves.  And good old vitamin B1 is a cofactor to a zillion energetic reactions.  If you burn glucose, you desperately need your thiamine.  To quote Harrison's Principles of Internal Medicine, 14th Edition (yes, I am old, page 2455):

Thiamine is a cofactor of several enzymes, including transketolase, pyruvate dehydrogenase, and alpha-ketoglutarate dehydrogenase.  Thiamine deficiency produces a diffuse decrease in cerebral glucose utilization and results in mitochondrial damage� electron microscopy shows disintegrating mitochondria, chromatin clumping, and swelling of degenerating neurons�consistent with excitotoxicity.

Yikes!  Even if the bigger words are mysterious, let me assure you that the picture is very bad.  Dying, rotting neurons and a smokey ruin of your precious brain.  Certain areas of the brain, such as the mammilary bodies and parts of the cerebellum seem particularly vulnerable, as they may have some of the highest glucose utilization in the brain.  The heart, being a high energy-using fellow itself, is also vulnerable to thiamine deficiency.  Nervous system symptoms from thiamine deficiency is also called "dry beriberi"  whereas cardiovascular involvement is known as "wet beriberi" or "sailor's asthma."

What are the symptoms?  Classically, the clinical triad is paralysis of certain eye movement muscles known as "ophthalmoplegia,"  problems with balance and walking (often a wide-based, shuffling gait) known as "ataxia,"  and confusion.   Only 1/3 of patients will present with all three - most are very disoriented, inattentive, and sometimes agitated.  If a profoundly thiamine-deficient patient shows up in the emergency room and is given straight-up D5 IV drip (D stands for dextrose - which is basically glucose) - this will confound the problem and worsen the symptoms - which can include stupor, coma, and death. (ER docs and nurses really try hard not to kill folks by giving them the standard IV in the emergency room).   This is why someone with a history of alcoholism will instead be given a "banana bag" - which contains folate, 100 mg thiamine, magnesium, and a multivitamin solution, which makes the bag yellow instead of clear like most IV solutions (thus the name).  Acute thiamine deficiency (Wernike's encephalopathy) can be cured with 50mg thiamine a day until normal eating resumes.

Chronic thiamine deficiency is not curable and can result in a particular type of brain syndrome called Korsakoff's psychosis.  The afflicted will have poor memory and confabulate like crazy - meaning, you ask him a question, and he will not know the answer, but he will make one up!

Well, most of you who are not members of the antique navies of the world and also without a 17 boilermaker a day habit or other genetic deficiencies of the pentose phosphate pathway will never experience such severe thiamine deficiency that you will get such dramatic symptoms.  But the case of vitamin B1 does serve to illustrate the importance of appropriate nutrition for our noggins to work correctly.

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