Diary of Unknown Symptoms

Mystery of the Internal Vibration

Entry for July 20, 2006

I get a call from the doctor in the walk in clinic and the test results are in..FINALLY! The doctor has reviewed them and the results? NORMAL

What? I asked if she had all four results and she agreed that all four were now complete. Normal? How is this possible? I ask her to fax the results to my doctor since I am seeing him tomorrow.

No Beriberi. So why does Benfotamine have such an effect on my neurological symptoms?

I’ve checked the dosage to what the iridologist recommended. She divided my vitamins into two higher doses instead of three spread out during the day. And since I’ve been taking these divided doses, for the past two days I’ve had a weird mild chest pain around lunchtime. I haven’t bothered to replenish my niacin so could this be the problem?

I decide to take my night Benfotamine at lunch and the mysterious pain disappears almost instantly. What can I do now? If my Thiamine levels are okay why has the head pinching stopped never to return since I started Benfotamine? I’m starting to wonder if I’ll ever get an answer.

I’ll mention Riboflavin and Magnesium to my doctor tomorrow and let’s see where that leads… If that fails, I’ll ask for the referral to the Environmental Health Clinic to see Riina Bray.

How is it possible that a person who isn’t deficient in Thiamine need a Thiamine supplement???

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July 20, 2006 Posted by | Health | , , , , , | 2 Comments

Entry for July 06, 2006

Followed up with the doctor who did the test results for Beriberi. The secretary gave me a hard time saying that if I didn’t hear from them then the test result was normal. There is no way that it came back normal so it’s my guess that it’s not back yet.

I explained that it has been over two weeks and if it was fine, then I wanted to know. I think they should call everyone regarding the test results whether they are fine or not.

After a brief pause, she comes back on the phone and says they are still waiting for the Thiamine test.

Almost three weeks and still no results…

July 6, 2006 Posted by | Health | , , , | Leave a comment

Entry for June 25, 2006

Tonight I’m googling away to find any reported cases in Canada of Beriberi. I come across a case report from Toronto’s Mount Sinai journal of medicine. Now I don’t have Wernicke’s encephalopathy but it’s an interesting read because he was a non-alcoholic. The other interesting fact is that it’s mentioned that a Thiamine deficiency can be caused by a Magnesium deficiency. (Better look up those symptoms…)

MOUNT SINAI JOURNAL OF MEDICINE

Wernicke’s Encephalopathy in a Non-alcoholic Man

Wernicke’s encephalopathy, a serious neurological disorder caused by thiamine deficiency, is mostcommonly found in chronic alcoholics. We present a typical case of Wernicke’s encephalopathy in a non-alcoholic man. Our patient presented with altered mental status, slurred speech, fever, vomitingand headache of one-week duration. An infectious etiology of the symptoms was ruled out by spinal fluid cultures. The patient improved dramatically within 24 hours of administration of thiamine.

Introduction

WERNICKE’S ENCEPHALOPATHY (WE) is a serious neurological disorder caused by thiamine deficiency and is most commonly found in chronic alcoholics. Typically, patients have the “classic triad” of symptoms: oculomotor abnormalities, gait disturbance and global confusional state. However, some patients may not exhibit this triad. The diagnosis is then based on clinical suspicion and rapid reversibility of symptoms after administration of thiamine, or autopsy demonstration of the characteristic lesion. We report a case of Wernicke’s encephalopathy in a non-alcoholic man.

Case Presentation

A 34-year-old African-American man presented with altered mental state, fever, slurring of speech, vomiting and headache of one-week duration. The patient denied alcohol or drug abuse, protracted vomiting, starvation, hospitalizations or abdominal surgery and indicated that he ate a normal diet. He also denied any history of sexually transmitted diseases or promiscuity. He had had occasional headaches, but had never been seen by a doctor for this complaint. He claimed to be well otherwise. On examination, the patient was alert, but disoriented. His temperature was 102°F; his pulse and blood pressure were normal. He had bilateral ophthalmoplegia with vertical nystagmus, weakness of both lower extremities and gait ataxia. There was no neck rigidity or tenderness. No other focal neurological deficit was present. Complete blood count and serum electrolytes, including magnesium, were within normal limits.
The liver function tests showed normal enzymes and serum bilirubin levels with a low normal albumin.

In view of the normal hemoglobin level (14.9 g/dL), serum folate was not done. Urine toxicology was negative. Although the patient declined to have an HIV test, he had normal CD4 counts with a normal CD4/CD8 ratio. Computerized tomography (CT) scan and magnetic resonance imaging (MRI) of the brain were normal. The patient was admitted to the intensive care unit with the differential diagnoses of meningitis, cerebrovascular event or Wernicke’s encephalopathy. He was empirically given cephtriaxone, vancomycin, and acyclovir because of fever, vomiting, altered mental state and lower extremity weakness, which suggested the possibility of meningitis or encephalitis. Cerebrospinal tap results were normal and all antibiotics were stopped immediately after the spinal fluid cultures were reported as negative. He was also given 100 mg of thiamine intravenously and started on oral thiamine supplementation of 100 mg daily. Within 24 hours the patient improved dramatically. He became alert and fully oriented. The ophthalmoplegia and vertical nystagmus resolved and the leg weakness improved markedly, with some residual ataxia. The patient was discharged home with continued outpatient physiotherapy.

Discussion

Wernicke’s encephalopathy is a common but preventable disorder due to thiamine deficiency. Alcoholics account for most cases, but thiamine deficiency may infrequently occur in patients with hyperemesis, starvation, hemodialysis,� cancer, acquired immune deficiency syndrome (AIDS), magnesium depletion, gastroplasty/gastric bypass surgery, rapid weight loss, anorexia nervosa, refeeding syndrome and prolonged intravenous feeding. Body stores of thiamine are only sufficient for up to 18 days. Thus, depletion can occur rapidly with restricted intake or prolonged vomiting.

The Canadian recommendation for thiamine intake is 1.1 mg per day, whereas the American recommendation is 1.4 mg per day. Thiamine is a co-factor of several enzymes, including transketolase and pyruvate dehydrogenase. Activity of the latter enzyme, a rate-limiting tricarboxylic acid cycle enzyme, is significantly reduced in autopsied brain tissue of Wernicke’s encephalopathy patients and from rats treated with a central thiamine antagonist, pyrimethamine. In animal studies, evidence suggests that such enzyme deficits result in focal lactic acidosis, cerebral energy impairment and depolarization of neurons resulting from increased glutamate in vulnerable brain structures. This depolarization may result in n-methyl-d-aspartate receptor-mediated excitotoxicity as well as increased expression of immediate early genes such as c-fos and c-jun, resulting in apoptotic cell death. Another mechanism may involve free radicals and alterations of the blood-brain barrier. Anatomical abnormalities in WE occur mainly in periventricular regions of the diencephalon, midbrain, brainstem and superior vermis of the cerebellum. In acute cases of WE, the lesions consist of symmetrical discoloration with petechial hemorrhages. Amnesia is related to lesions of the medial dorsal nuclei of the thalamus. Shrinkage of the mamillary bodies can also be seen.

Symptoms and signs indicative of WE usually include vomiting, nystagmus (horizontal more than vertical), medial and lateral rectus muscle palsies leading to unilateral or bilateral ophthalmoplegia, fever, ataxia and progressive mental deterioration that evolves to a global confusional state, coma, and death. Other manifestations of a nutritional deficiency, such as polyneuropathy, may also occur. Tachycardia and orthostasis may be related to an impaired autonomic nervous system or coexistent cardiovascular beriberi. The true prevalence of WE at autopsy is about 3%, much higher than what is diagnosed clinically in the general population. Acute WE should be suspected in all alcoholics with neurological symptoms, especially those with evidence of calorie or protein malnutrition and peripheral neuropathy. The classic triad of oculomotor abnormalities, gait disturbance and global confusional state occurs only in one-third of the patients. The diagnosis of WE is based on the clinical suspicion and rapid reversal of symptoms after the administration of thiamine. Decreased serum activity of erythrocyte transketolase and MRI (sensitivity 53% and specificity 93%) may be helpful in confirming the clinical diagnosis. Typically, there is an increased T2 signal of the paraventricular region of the thalamus and peri-aqueductal regions of the midbrain. There can also be enhanced T1 weighted spin-echo (SE) sequences after intravenous gadolinium administration in the acute phase of WE. Normal MRI does not exclude the diagnosis of WE. On the other hand, the sensitivity of the CT scan in detecting the characteristic lesion of WE is extremely low (13%), so it is not useful in the diagnosis of this entity. WE is a medical emergency and requires the immediate administration of thiamine in a dose of 50 – 100 mg, either intravenously or intramuscularly. Doses should be given daily, to build up the body reserves until the patient is able to resume a normal diet. The central nervous system is almost entirely dependent on glucose for its energy requirements. Thiamine is an important co-factor needed in several steps of glucose utilization. Therefore, loading of glucose in a thiamine-deficient person can�precipitate a neurological crisis (WE) or can cause rapid worsening of mild symptoms. To avoid this complication, thiamine should always be given prior to any intravenous glucose administration whenever this diagnosis is suspected. Patients who recover show improvement of oculomotor palsies within hours of thiamine administration. Ataxia improves more slowly. About one-half the patients recover incompletely and are left with a slow, shuffling wide-based gait and inability to take one step in quick succession after the other. Apathy, drowsiness and confusion diminish gradually. As these symptoms recede, an amnesic state with impairment in recent memory and learning may become more apparent in some cases (Korsakoff’s psychosis).

Summary

WE is uncommon in non-alcoholics, but not rare. One should have a high index of suspicion in patients with hyperemesis, starvation, dialysis, cancer, magnesium depletion, AIDS, gastroplasty/ gastric bypass surgery, rapid weight loss, anorexia nervosa, refeeding syndrome or prolonged intravenous feeding. Our patient had none of the aforementioned conditions. The recommended treatment is the administration of thiamine, and most patients respond within 24 – 36 hours.

June 25, 2006 Posted by | Health | , , , | Leave a comment

Entry for June 25, 2006

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Still waiting for the tests to confirm whether or not I have Beriberi but I thought I’d try contacting Health Canada to find out if they have any statistics on the number of reported cases in the past twenty years. I also contacted the US Department of Health with the same question.

Diet has always had a vital influence on health. Until as recently as the 1940’s, diseases such as rickets, pellagra, scurvy, beriberi, xerophthalmia, and goiter (caused by lack of adequate dietary vitamin D, niacin, vitamin C, thiarnin, vitamin A, and iodine, respectively) were prevalent in this country and throughout the world.

Today, thanks to an abundant food supply, fortification of some foods with critical trace nutrients, and better methods for determining and improving the nutrient content of foods, such “deficiency” diseases have been virtually eliminated in developed countries.

For example, the introduction of iodized salt in the 1920’s contributed greatly to eliminating iodine-deficiency goiter as a public health problem in the United States. Similarly, pellagra disappeared subsequent to the discovery of the dietary causes of this disease. Nutrient deficiencies are reported rarely in the United States, and the few cases of protein-energy malnutrition that are listed annually as causes of death generally occur as a secondary result of severe illness or injury, child neglect, the problems of the house-bound aged, premature birth, alcoholism, or some combination of these factors.

June 25, 2006 Posted by | Health | , , | Leave a comment

Entry for June 19, 2006

What to do when beriberi is suspected.

After you have carefully examined the patient and described the findings in all the systems, then you should give ‘flooding doses’ of thiamine (normal adult requirement is 0.4mg per 1000 kcal). Give 50 or 100 mg thiamine hydrochloride intravenously and then give 10 mg per day orally. Infants may be treated with adult doses (it is not toxic in very large quantities), or lesser doses if this is more convenient. Mothers of patients should always be given 10mg per day orally.

Dry Beriberi: (this is the form that has been experimentally induced in human volunteers). In dry beriberi there is a peripheral neuritis. It starts with parasthesia & pins and needles) of the feet, diminished touch sensation, and a feeling of ‘heat’ in the feet. Joint position, vibration and pain sensation are usually normal. The ankle and then the knee reflexes are lost and the patients have muscle weakness starting with the foot.

A vibration and muscle weakness starting with the foot. Those are the two first symptoms of Dry Beriberi. If my medical doctor actually listened to what I was saying, did a bit of research maybe this could’ve been solved a long time ago. He was only interested in following the gastric symptoms which I questioned all along. If he sent me to a specialist in the very beginning, would they have picked up on the fact that the vibration stopped when I ate pears and said “Ah, a nutritional deficiency”? Who knows…but it seems very logical to me but maybe that’s asking for too much. Doctor’s know very little about nutrition.

People say they don’t want two-tier health system in Canada. Well guess what? It already is.

June 19, 2006 Posted by | Health | , | Leave a comment

Entry for June 19, 2006

I was vibrating when I went to bed and I was vibrating when I woke up. Hopefully it won’t be long until I hear back from the blood test. My own treatments of vitamins doesn’t appear to be working as fast as I’d like it to.

I have mentioned my theory of Beriberi to a few people and so far it is met with a lot of sceptical criticism. I’m hearing the usual “That can’t happen in the North American diet” or “That only happens in the far east because they eat rice”, and “You can’t have Beriberi because you don’t drink any alcohol and it only happens to chronic alcoholics”.

What people don’t realize is that Beriberi is caused by a nutritional deficiency. It’s not a foreign disease. Forget about the cause because it is irrelevant. I have some of the key symptoms and I believe the electromagnetic radiation irritated my stomach to the point that it was unable to absorb the vitamins and minerals from my diet. It’s only a guess but what else do I have?

I was probably low on B vitamins to begin with so it wouldn’t take much to push it over the edge.  I’ve had sensitivity to light, cracked lips and feeling tired all of the time for years. All classic symptoms of a B vitamin deficiency.

June 19, 2006 Posted by | Health | , , | Leave a comment

Entry for June 16, 2006

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To the walk in clinic and I explain to the receptionist that I would like to speak to a doctor about nutritional deficiencies. It’s a friday night so it’s not too busy and I’m called in within 5 minutes.

The doctor comes in, reads my file and says “I hear you would like to speak to a doctor…well, I am one.”  I thought that was funny and I like him almost immediately. I give him the coles notes version of my history of symptoms starting with the mysterious internal vibration. I tell him about the various tests and procedures done by my regular doctor that all came up with nothing. I explain about how my research indicates that it could be a nutritional B vitamin deficiency and it’s my hunch that I have Beriberi. I’ve read that there is a blood test and I would like it done.

He says he hasn’t heard the term Beriberi since medical school and admitted that he wouldn’t even know how to treat it. I’d say he’s an older man in his mid-fifties.  I told him that from what I’ve read, it’s very easy to treat with high doses of B1 vitamins and in some cases, vitamin injections. He’s heard of B12 injections but not B1. He mentions about folic acid and I told him about my research regarding the chemical reaction of B1 with folic acid so I would really like to have that tested as well.

He questions why I think I have a nutritional B vitamin deficiency and hesitantly, I mention about how I think electromagnetic radiation had an effect on my stomach and disturbed the normal absorption of vitamins and minerals from my food. I continue my story with the purchase of the wireless intercom system and how when I discovered the symptoms to be EMF, I bought a meter to test around the house. I was probably low with B vitamins to begin with and the EMF exposure created a nutritional deficiency. Then he asks about how I learned about electromagnetic radiation. So I explain the story about the global tv show and Dr. Riina Bray.

At the end of my story I told him how I thought it sounded like something from a science fiction novel and he agreed saying this was the first time he had ever heard a story like mine.

So he writes out the lab requistion form for a blood test.

June 16, 2006 Posted by | Health | , , , , , | Leave a comment

Entry for June 16, 2006

What is folate?

Folic acid, also called folate or folacin, is a B-complex vitamin most publicized for its importance in pregnancy and prevention of pregnancy defects.

Folic acid is one of the most chemically complicated vitamins, with a three-part structure that puts special demands on the body’s metabolism. The three primary components of folic acid are called PABA, glutamic acid, and pteridine. (Two of these components, glutamic acid and pteridine, help explain the technical chemical name for folate, namely pteroylmonoglutamate.)

As complex as this vitamin is in its structure, it is equally as complicated in its interaction with the human body. For example, most foods do not contain folic acid in the exact form described above, and enzymes inside the intestine have to chemically alter food forms of folate in order for this vitamin to be absorbed. Even when the body is operating at full efficiency, only about 50% of ingested food folate can be absorbed.

What is the function of folate?

Red blood cell formation and circulation support

One of folate’s key functions as a vitamin is to allow for complete development of red blood cells. These cells help carry oxygen around the body. When folic acid is deficient, the red bloods cannot form properly, and continue to grow without dividing. This condition is called macrocytic anemia, and one of its most common causes is folic acid deficiency.

In addition to its support of red blood cell formation, folate also helps maintain healthy circulation of the blood throughout the body by preventing build-up of a substance called homocysteine. A high serum homocysteine level (called hyperhomocysteinemia) is associated with increased risk of cardiovascular disease, and low intake of folate is a key risk factor for hyperhomocysteinemia. Increased intake of folic acid, particularly by men, has repeatedly been suggested as a simply way to lower risk of cardiovascular disease by preventing build-up of homocysteine in the blood. Preliminary research also suggests that high homocysteine levels can lead to the deterioration of dopamine-producing brain cells and may therefore contribute to the development of Parkinson’s disease. Therefore, folate deficiency may have an important relationship to neurological health.

Research is now confirming a link between blood levels of folate and not only cardiovascular disease, but dementias, including Alzheimer’s disease.

One of the most recent studies, which was published in the July 2004 issue of the American Journal of Clinical Nutrition evaluated 228 subjects. In those whose blood levels of folate were lowest, the risk for mild cognitive impairment was more than tripled, and risk of dementia increased almost four fold. Homocysteine, a potentially harmful product of cellular metabolism that is converted into other useful compounds by folate, along with vitamin B6 and B 12, was also linked to dementia and Alzheimer’s disease. Individuals whose homocysteine levels were elevated had a 4.3 (more than four fold) increased risk of dementia and a 3.7 (almost four fold) increased risk of Alzheimer’s disease.(June 30, 2004)

Research teams in the Netherlands and the U.S. have confirmed that low levels of folic acid in the diet significantly increases risk of osteporosis-related bone fractures due to the resulting increase in homocysteine levels. Homocysteine has already been linked to damage to the arteries and atherosclerosis, plus increased risk of dementia in the elderly. Now, in a study that appeared in the May 2004 issue of the New England Journal of Medicine, researchers at the Eramus Medical Center, Rotterdam, Holland, and another team in Boston have confirmed that individuals with the highest levels of homocysteine have a much higher risk of osteoporotic fracture.

In the Rotterdam study, which included 2,406 subjects aged 55 years or older, those with the highest homocysteine levels, whether men or women, almost doubled their risk of fracture. The Boston team found that risk of hip fracture nearly quadrupled in men and doubled in women in the top 25% of homocysteine levels. Both groups found that folic acid reduced the risk of osteoporotic fractures by reducing high levels of homocysteine.

What factors might contribute to a deficiency of folate?

In addition to poor dietary intake of folate itself, deficient intake of other B vitamins can contribute to folate deficiency. These vitamins include B1, B2, and B3 which are all involved in folate recycling. Poor protein intake can cause deficiency of folate binding protein which is needed for optimal absorption of folate from the intestine, and can also be related to an insufficient supply of glycine and serine, the amino acids that directly participate in metabolic recycling of folate. Excessive intake of alcohol, smoking, and heavy coffee drinking can also contribute to folate deficiency.

How do other nutrients interact with folate?

Vitamins B1, B2, and B3 must be present in adequate amounts to enable folic acid to undergo metabolic recycling in the body. Excessive amounts of folic acid, however, can hide a vitamin B12 deficiency, by masking blood-related symptoms.

How is folate-deficiency anemia diagnosed?

Folate-deficiency anemia may be suspected from general findings from a complete medical history and physical examination. In addition, several blood tests can be performed to confirm the diagnosis. If the anemia is thought to be caused by a problem in the digestive tract, a barium study of the digestive system may be performed. Folate deficiency does not usually produce neurological problems; B12 deficiency does. Folate and B12 deficiency can be present at the same time. If B12 deficiency is treated with folate by mistake, the symptoms of anemia may lessen, but the neurological problems can become worse.

Natural forms of folic acid:

orange juice
oranges
romaine lettuce
spinach
liver
rice
barley
sprouts
wheat germ
soy beans
green, leafy vegetables
beans
peanuts
broccoli
asparagus
peas
lentils
wheat germ
chick peas (garbanzo beans)

How do I know if I’m deficent in folate? Untill I started eating healthy recently, the only thing I had on a semi-regular basis was romaine lettuce. I’m sure wheatgrass is a good substitute for the green, leafy vegetables.

What are deficiency symptoms for folate?

Because of its link with the nervous system, folate deficiency can be associated with irritability, mental fatigue, forgetfulness, confusion, depression, and insomnia. The connections between folate, circulation, and red blood cell status make folate deficiency a possible cause of general or muscular fatigue. The role of folate in protecting the lining of body cavities means that folate deficiency can also result in intestinal tract symptoms (like diarrhea) or mouth-related symptoms like gingivitis or periodontal disease.

So folate helps maintain healthy circulation of the blood throughout the body by preventing build-up of a substance called homocysteine which can lead to a higher risk of coronary heart disease, stroke and peripheral vascular disease.

Another one of my “weird” symptoms is when I hold my hands over my head for more than ten seconds. I start to feel a mild numbing sensation down the length of my arms and I’m sure it’s due to a lack of blood circulation.

I think I’ve proven that I do have circulation issues so maybe I’m deficient in folic acid too. Beriberi sounds very serious and if it’s what I have then I should get a blood test to confirm it. On the way home I’ll drop into the walk in clinic and see if I can convince the doctor for a blood test. At the very least, I will be able to rule out if it comes up negative.

June 16, 2006 Posted by | Health | , , , , , , | Leave a comment

Entry for June 15, 2006

Beriberi – this is caused by thiamin deficiency and affects the cardiovascular, muscular, gastrointestinal and nervous systems. As well as the above symptoms, a person with ‘dry’ beriberi may have: nerve degeneration, nervous tingling throughout the body, poor arm and leg coordination, and deep pain in the calf muscles. Symptoms of ‘wet’ beriberi include: an enlarged heart, heart failure and severe oedema (swelling).

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Beriberi causes different symptoms in different people. One form, called dry beriberi, causes nerve and muscle abnormalities. Symptoms include a prickling (pins-and-needles) sensation in the toes, a burning sensation in the feet that is particularly severe at night, and pain, weakness, and wasting (atrophy) of muscles in the legs.

Brain abnormalities due to vitamin B1 deficiency occur primarily in alcoholics. Brain abnormalities may develop when a chronic vitamin B1 deficiency is suddenly worsened by a rapid, substantial decrease in the vitamin B1 level (which can be caused by an alcoholic binge) or by a sudden increase in vitamin B1 requirements (which may occur when an undernourished alcoholic is fed intravenously).

Prognosis:

Wet beriberi: Improvement is observed in the first 6-24 hours after thiamin administration.

Cyanosis disappears, Heart rate reduces, Respiratory rate reduces. Diuresis and reduction in heart size may be apparent within 1-2 days.

In cases of dry beriberi and Korsakoff psychosis, the complete resolution of the neurologic symptoms can take several months.

oh great…the complete resolution of the neurologic symptoms can take several months. Well I’ve waited this long. Maybe I’ll think about getting a test done to prove this diagnosis once and for all.

One study on human starvation found that in thiamine vitamin B. deficiency, symptoms such as lack of well being, anxiety, hysteria, depression, and loss of appetite preceded any clinical evidence of beriberi. Other studies using the Minnesota Multiphasic Personal Index (MMPI) have also demonstrated that adverse behavioral changes precede physical findings in thiamine deficiency. Indeed, thiamine treatment—as much as 300 mg—is used to treat Wernicke’s encephalopathy (cerebral beriberi), an acute brain disorder whose early stages are characterized by mental confusion, an inability to think of words, and fabrication of “facts” (Winter and Winter, 1988).

Confusion, forgetfulness, and irritability—symptoms often diagnosed as Alzheimer’s disease—may actually be an easily treated vitamin B deficiency. Untreated, the deficiency can lead to irreversible spinal cord degeneration, other neurologic problems, and serious anemias. If your patient is a vegetarian, such a deficiency may result from inadequate compensation for a lack of red meat. Elderly patients may be deficient owing to malabsorption of the vitamin. A B 2 deficiency can be diagnosed with a blood or urine test. Once detected, a monthly intramuscular B2 injection is recommended.

June 15, 2006 Posted by | Health | , | Leave a comment

Entry for June 15, 2006

Dear Dr. Google…

I’ve been taking high doses of niacin for over a month and although there is some improvement, I still have the mysterious internal tremor and low stomach acid. I forgot to take my acidophilus this morning and I had the head pinching. It disappeared when I took the acidophilus so something is obviously still wrong. Maybe it’s not a niacin deficiency at all? I have nervous system symptoms that are effected by diet. It has to be a nutritional deficiency, I just don’t know what kind.

With the Iridology charts and the deep lines at the top of my iris suggesting something effecting the cerebrum part of my brain, I start looking up symptoms with the cerebrum. With iridology some practitioners feel they can diagnose severe disease well before symptoms present themselves. So let’s see what I find out. I start reading about a whole bunch of scary neurological disorders and nothing matches my symptoms. It has to be a nutritional deficiency.

I start googling vitamin deficiencies and I look up every one. A, B, C, D, E, K etc. After reading them all and not finding anything as a possible match, I decide search for vitamins deficiencies that can effect the brain or more importantly, the cerebrum. This time I come across a more detailed decription of a Vitamin B1 (Thiamin) deficiency.

Vitamin B1 Deficiency

Vitamin B1 (thiamin) deficiency may result from a deficiency in the diet. People whose diet consists mainly of polished (refined) white rice are at risk of vitamin B1 deficiency, because polishing removes almost all of the vitamins. Alcoholics, who often substitute alcohol for food, are at high risk of developing this deficiency.

Symptoms

Early symptoms are vague. They include fatigue, irritability, memory impairment, loss of appetite, sleep disturbances, abdominal discomfort, and weight loss. Eventually, a severe vitamin B1 deficiency (beriberi) may develop, characterized by nerve, heart, and brain abnormalities.

Brain abnormalities due to vitamin B1 deficiency occur primarily in alcoholics. Brain abnormalities may develop when a chronic vitamin B1 deficiency is suddenly worsened by a rapid, substantial decrease in the vitamin B1 level (which can be caused by an alcoholic binge) or by a sudden increase in vitamin B1 requirements (which may occur when an undernourished alcoholic is fed intravenously).

Diagnosis and Treatment

The diagnosis is based on symptoms. Tests to confirm the diagnosis are not readily available. All forms of the deficiency are treated with vitamin B1 supplements.

A balanced diet containing all essential nutrients will prevent a thiamine deficiency and the development of beriberi. People who consume large quantities of junk food like soda, pretzels, chips, candy, and high carbohydrate foods made with unenriched flours may be deficient in thiamine and other vital nutrients. They may need to take vitamin supplements and should improve their diets. Usually there are other deficiencies in the B vitamins that will also need treatment.

Excess thiamine is excreted by the body in the urine, and negative reactions to too much thiamine are rare. Thiamine is unstable in alkali solutions, so it should not be taken with antacids or barbiturates.

Thiamine should be taken daily, with the dose depending on the severity of the disease. Additional supplements of B vitamins, a multivitamin and mineral complex, and Vitamin C are also recommended. Other alternative therapies may help relieve the person’s symptoms after the thiamine deficiency is corrected.

So maybe I had multiple B vitamin deficiencies? Another web site talks about how a B1 deficiency can lead to a disease called Beriberi :

Beriberi – this is caused by thiamin deficiency and affects the cardiovascular, muscular, gastrointestinal and nervous systems. As well as the above symptoms, a person with ‘dry’ beriberi may have: nerve degeneration, nervous tingling throughout the body, poor arm and leg coordination, and deep pain in the calf muscles. Symptoms of ‘wet’ beriberi include: an enlarged heart, heart failure and severe oedema (swelling).

Thiamine Deficiency And Dependency

The coenzyme thiamine pyrophosphate, the active form of thiamine (vitamin B1), participates in carbohydrate metabolism through decarboxylation of -keto acids. Thiamine also acts as coenzyme to the apoenzyme transketolase in the pentose monophosphate pathway for glucose. Deficiency causes beriberi with peripheral neurologic, cerebral, cardiovascular, and GI manifestations.

Another site lists another set of symptoms:

Deficiency Symptoms: Depression, constipation, impaired growth in children, shortness of breath, numbness of hands and feet, weakness, fatigue, nervousness, sensitivity to noise, loss of appetite.

Inhibits Absorption: Tobacco, stress, fever, coffee, alcohol, surgery, raw clams

Enhances Absorption: B-complex, sulfur, manganese, niacin, B-2, folic acid, C, E

And then another says one of the Neurologic signs is a….TREMOR.

Pathophysiology
Nutritional disease results from Thiamine deficiency

Symptoms : Weakness, irritability, Nausea, Vomiting, Burning feet, Pruritus

Signs

Neurologic: Tremor, Diminished reflexes in lower limbs, Muscle atrophy

Cardiac: Congestive Heart Failure, Pedal Edema , Pleural Effusions

And yet another:

The following systems are most affected by beriberi:

Gastrointestinal system

When the cells of the smooth muscles in the digestive system and glands do not get enough energy from glucose, they are unable to produce more glucose from the normal digestion of food. There is a loss of appetite, indigestion, severe constipation, and a lack of hydrochloric acid in the stomach.

Nervous System

Glucose is essential for the central nervous system to function normally. Early deficiency symptoms are fatigue, irritability, and poor memory. If the deficiency continues, there is damage to the peripheral nerves that causes loss of sensation and muscle weakness, which is called peripheral neuropathy. The legs are most affected. The toes feel numb and the feet have a burning sensation; the leg muscles become sore and the calf muscles cramp. The individual walks unsteadily and has difficulty getting up from a squatting position. Eventually, the muscles shrink (atrophy) and there is a loss of reflexes in the knees and feet; the feet may hang limp (footdrop).

Cardiovascular system

There is a rapid heartbeat and sweating. Eventually the heart muscle weakens. Because the smooth muscle in the blood vessels is affected, the arteries and veins relax, causing swelling, known as edema, in the legs.

Musculoskeletal system

There is widespread muscle pain caused by the lack of TPP in the muscle tissue.

A thiamin deficiency also produces Warnicke-Korsakoff syndrome, sometimes called cerebral beriberi, a disorder of the central nervous system.

Muscles shrink (atrophy) and there is a loss of reflexes in the knees and feet? Could this explain my Plantar Fasciitis? A B1 deficiency is linked to the Gastrointestinal system and the Nervous System. The two things I have symptoms for. The two things I’ve been telling the doctors about and now I have a link to the cerebrum.

What is Wernicke-Korsakoff syndrome?

Wernicke-Korsakoff syndrome (WKS) is a neurological disorder. Wernicke’s Encephalopathy and Korsakoff’s Psychosis are the acute and chronic phases, respectively, of the same disease. Wernicke-Korsakoff syndrome is a combination of  Korsakoff’s syndrome which constitutes confusion, aphonia and confabulation and Wernicke’s encephalopathy which is nystagmus, opthalmoplegia, coma and, if untreated, death. It is also known as cerebral beriberi, which is beriberi (thiamine deficiency disease) in the brain. This results from severe acute deficiency of thiamine superimposed on a chronic deficiency. Usually found in malnourished chronic alcoholics.

Korsakoff’s syndrome, with symptoms of severe anterograde and retrograde amnesia, is caused by damage to mammillary bodies and other brain regions due to deficiency of thiamine. This is most often caused by chronic alcoholism, though other conditions including severe malnutrition, have been known to cause it. An association of Gayet-Wernicke and Korsakoff’ syndromes frequently observed in alcoholic, nutritionally deficient patients with the Gayet-Wernicke syndrome. Patients develop symptoms of the Korsakoff syndrome, mainly amnesia with a tendency to confabulate with or without polyneuropathy.

I don’t think I’ve gotten to the point of the Wernicke-Korsakoff syndrome so it appears what I could have is a B1 deficiency that may led to it. Scary stuff…and it’s starting to make a bit more sense.

I’ve had this very weird feeling in my head almost from the time when the other symptoms started happening around July 2005. If I tilted my head back and kept it there for 5-10 seconds, when I try to bring it back, my head has a heavy sluggishness feeling. Almost like the fluid trying to balance itself. It dosen’t happen all of the time and I didn’t quite know how to explain it so I never mentioned it. The Cerebellum is the part of the brain below the back of the cerebrum and it regulates balance, posture, movement, and muscle coordination.

Down to Shoppers Drug Mart to pick up 100 mg of B1 suppliment.

June 15, 2006 Posted by | Health | , , , , , , , , , , , , | Leave a comment

   

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