Thiamine Deficiency Disease Dysautonomia And High Calorie Malnutrition Pdf

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Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition explores thiamine and how its deficiency affects the functions of the brainstem and autonomic nervous system by way of metabolic changes at the level of the mitochondria. Thiamine deficiency derails mitochondrial oxidative metabolism and gives rise to the classic disease of beriberi that, in its early stages, can be considered the prototype for a set of disorders that we now recognize as dysautonomia.

Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition explores thiamine and how its deficiency affects the functions of the brainstem and autonomic nervous system by way of metabolic changes at the level of the mitochondria. Thiamine deficiency derails mitochondrial oxidative metabolism and gives rise to the classic disease of beriberi that, in its early. Thiamine deficiency derails mitochondrial oxidative metabolism and gives rise to the classic disease of beriberi that, in its early stages, can be considered the prototype for a set of disorders that we now recognize as dysautonomia. Derrick Lonsdale, and a recent collaboration with his co-author Dr.

(PDF)Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition 1st Edition

By Derrick Lonsdale and Chandler Marrs. Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition explores thiamine and how its deficiency affects the functions of the brainstem and autonomic nervous system by way of metabolic changes at the level of the mitochondria. Thiamine deficiency derails mitochondrial oxidative metabolism and gives rise to the classic disease of beriberi that, in its early stages, can be considered the prototype for a set of disorders that we now recognize as dysautonomia.

Derrick Lonsdale, and a recent collaboration with his co-author Dr. Chandler Marrs. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. This book and the individual contributions contained in it are protected under copyright by the Publisher other than as may be noted herein.

Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein.

In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. Thiamine, also known as vitamin B1, plays a fundamental role in energy metabolism.

It is the rate-limiting cofactor for no less than five enzymes involved in the initial steps of mitochondrial ATP production via the glucose, fatty acid, and amino acid pathways. Despite the critical and accepted role of thiamine in oxidative metabolism, however, the downstream effects of its deficiency are still poorly recognized, especially in clinical care.

Thiamine deficiency appears to have been relegated to the annals of history, a disorder that once plagued populations. Now, however, it is generally believed that it is no longer a relevant issue, thanks to modern nutrition.

We will provide evidence that this presumption is simply not true. In fact, it is precisely because of modern nutritional practices that thiamine deficiency is latent across populations. Derrick Lonsdale and a recent collaboration with his coauthor Dr.

Tiring of the bureaucratic interference he immigrated to Canada by joining the RCAF as a medical officer for a short service commission. On completion he was accepted as a pediatric resident at Cleveland Clinic and in was invited to join the pediatric staff. Lonsdale was a pediatric oncologist but switched his interest to studying the clinical and biochemical aspects of uncommon diseases known as inborn errors of metabolism.

A number of these diseases, if not all, cause severe mental retardation if they are not spotted at birth and this gave rise to the screening tests for newborn infants that are applied to every state in the United States. In some of them, the mental retardation can be forestalled by giving the infant a special diet. One of the rarest of these diseases is known as maple syrup urine disease branched-chain ketoaciduria , caused by an abnormal recessive gene.

The disease gets its name because there is a substance that occurs in the urine that smells exactly like maple syrup. Estimated to occur once in , births, the enzyme is a dehydrogenase that processes the branched-chain amino acids leucine, isoleucine, and valine. This enzyme has the same construction as pyruvic and alpha ketoglutarate dehydrogenases. The decarboxylating component in each of these enzymes requires thiamine and magnesium as cofactors.

The binding of the cofactors to the enzyme, like its gene, is also under genetic control. It is therefore sometimes possible to treat the corresponding disease by the epigenetic use of pharmacological doses of the respective cofactor. Epigenetics is a relatively new science that studies the effect of nutritional elements on the action of genes. Although epigenetics had not yet been discovered when the research reported here had been conducted, the clinical results from using thiamine and magnesium in megadoses tended to foretell its inception.

An initial diagnosis of maple syrup urine disease branched-chain ketoaciduria having been made, an epigenetic trial would be the first attempt at treatment. If this should fail, the special diet required to prevent mental retardation would have to provide the infant with an exact amount of the branched-chain amino acids that are essential to life.

This was the introduction to the value of thiamine for Dr. Lonsdale but it also introduced him to the extraordinary power of nutrition if tailored to the genetic needs of a given individual. From that point forward Dr. Lonsdale was committed to uncovering the connections between thiamine and metabolic health. The experience of Dr. Marrs is a bit more diverse. Her research career reflects a relentless pursuit of the root mechanisms and pathways that initiate disease, unbridled by conventional barriers.

Drawing from her early entrepreneurial ventures in the technology sector, as a graduate student, she founded and directed the UNLV Maternal Health Lab to conduct clinical and Internet-based research on maternal health and mental health. Her lab research identified a pattern of aberrant late pregnancy adrenal androgen concentrations that would predict postpartum psychiatric disturbances, while her clinical research suggested a necessary reorganization of clinical symptomology within that diagnostic paradigm.

Marrs founded Lucine Health Sciences, a health research and media company that publishes the online journal Hormones Matter and conducts postmarket, direct-to-patient medication safety and efficacy studies. It is through her work on medication adverse events that Drs. Marrs and Lonsdale began to collaborate and uncover evidence of thiamine deficiency in patients suffering from medication or vaccine adverse reactions.

This book represents a culmination of what we both have learned. A major part concerns the clinical and biochemical research covered between and while Dr. Lonsdale was at Cleveland Clinic. This research was published originally in The finished books were stored in a warehouse that caught fire and only a handful of them were saved.

Lonsdale took early retirement from the Cleveland Clinic as Associate Emeritus and entered a private practice specializing in nutritional therapy. This type of medicine is now known as alternative complementary medicine, and he was able to continue adding to his rapidly increasing awareness concerning the role of vitamins in treating common diseases.

He discovered the extraordinary role of thiamine and magnesium deficiency in causing conditions where the standard laboratory studies were negative or deemed to be because of other causes.

The changes in brain function were so diverse that Dr. Lonsdale came to be aware that this kind of deficiency was the great imitator of different conditions, each of which was considered to be a separate disease in its own right. This was particularly obvious in children and in a symposium was published to commemorate the synthesis of thiamine. From that symposium, Zbinden stated that published papers had reported attempted thiamine therapy in different diseases with varying degrees of success.

Lonsdale found that high-calorie malnutrition was so common that he felt it necessary to republish the material, but also update it with new insights gleaned between and his retirement in and subsequently with his collaboration with Dr.

Over the last few years we have begun working together to untangle the nutrient deficiencies and mitochondrial damage associated with medication and vaccine adverse reactions, specifically those capable of triggering dysautonomia. Dysautonomic symptoms have been reported following HPV vaccination. With subsequent research, Dr. Marrs has been able to map many of the mechanisms involved in these reactions.

We will be detailing those mechanisms throughout the book. This book is about thiamine and how its deficiency affects the functions of the brain stem and autonomic nervous system by way of metabolic changes at the level of the mitochondria.

We will provide evidence that thiamine deficiency underlies some of the dysautonomic syndromes and make the provocative suggestion that disordered oxidative metabolism may represent a common part of the etiology in both the genetic and acquired forms of dysautonomia. It is well established that beriberi evolves from thiamine deficiency. A review of clinical and laboratory findings of the dysautonomias demonstrates tremendous similarities with beriberi.

Inasmuch as the autonomic system regulates organism-wide homeostasis, dysautonomias are marked by a variety of seemingly disparate and often erratic symptoms. From heart rate irregularities to cerebellar ataxia, sleep—wakefulness disturbances to salt and mineral dysregulation, and everything in between, the system-wide autonomic disturbances make diagnosis of these conditions difficult for all but the most astute clinician. This is in large part caused by the underlying contributing etiology—mitochondrial dysfunction where disordered oxidative metabolism is key and thiamine and other nutrient cofactors are critical.

Over the subsequent chapters we will review the research and provide clinical studies to support this. Today there is increasing interest in the role of mitochondria in health and disease. Mitochondria sit at the nexus of health and disease and, in many ways, moderate the complex interactions between the organism and its environment.

As will be discussed later in the book, we have obtained information on how trauma, infection, and poor nutrition can interact together in damaging mitochondrial function. They deplete critical cofactors, compromising mitochondrial function and evoking disease processes that extend beyond our current medical conceptualizations of anatomically discrete etiologies. Nutrients, especially thiamine, matter to mitochondrial functioning. In , Dr. Lonsdale hypothesized that thiamine and magnesium deficiencies were keys to disease.

These cases, as well as many others involving vaccine or medication reactions, were also published on HormonesMatter. Each of them was shown to have an abnormal erythrocyte transketolase that proved thiamine deficiency or abnormal homeostasis.

These young people were later found to express single nucleotide polymorphisms in thiamine transporter genes. All of them were top-class students and athletes before they became crippled by POTS. We concluded that the effects of marginally high-calorie malnutrition, particularly in the brightest and the best energy-requiring brains, coupled with genetic risk and the nonspecific stress of vaccination, precipitated POTS, one of the dysautonomic syndromes that is rapidly becoming more common.

The combination of malnutrition, genetic risk, and vaccination appeared to be necessary to precipitate POTS, masking as beriberi. This observation had misled the early investigators who were trying to elucidate the cause of this ancient scourge that had affected people for thousands of years. Because several individuals succumbed to the first symptoms of the disease concurrently, they concluded that the cause was a mysterious infection.

Since we now know that the disease is caused by thiamine deficiency, we have to conclude that exposure to the ultraviolet light acted as a stress factor and precipitated the disease in marginally malnourished individuals. That a stressor can initiate disease is an important precept.

Actions always mediate reactions and in physiology those reactions are biochemical in nature. No matter the form that the stressor takes, it will require an adaptive response. So a stressor can be defined as any environmental factor that requires an adaptive response to the effects of living in a hostile environment.

The biochemical mechanisms that they evoke would not only initiate symptoms of a latent biochemical or genetic risk, but also might be capable of inducing new disease processes.

Case histories, appearing later in this book, bear this out. The evidence suggests that the answers lie with the mitochondria and more specifically in disordered oxidative metabolism, the process by which food is converted to cellular fuel. Dietary vitamins and essential minerals are critical cofactors for the enzymatic reactions participating in mitochondrial respiration and energetics. Mitochondrial functioning therefore can be compromised significantly by nutrient deficiency. When the mitochondria are damaged or inefficient their decline in function leads to diminished cellular efficiency.

The Role of Thiamin in High Calorie Malnutrition

Derrick Lonsdale born is a pediatrician and researcher into the benefits of certain nutrients in preventing disease and psychotic behavior. According to Lonsdale, thiamine is a special vitamin because as the cause of beriberi it is one of only four vitamins associated with a named pandemic deficiency disease. Of these four vitamins, only thiamine requires transport proteins to diffuse throughout the body. A thiamine derivative called TTFD is a thiamine precursor that does not require transport proteins to freely diffuse. Lonsdale was a practitioner in pediatrics at the Cleveland Clinic for 20 years.


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Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition

Dysautonomia refers to a disease where the autonomic nervous system is dysfunctional. This may be a central control mechanism, as in genetically determined familial dysautonomia Riley-Day Syndrome , or peripherally in the distribution of the sympathetic and parasympathetic systems. There are multiple reports of a number of different diseases associated with dysautonomia.

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Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition - Ebook

Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition explores thiamine and how its deficiency affects the functions of the brainstem and autonomic nervous system by way of metabolic changes at the level of the mitochondria. Thiamine deficiency derails mitochondrial oxidative metabolism and gives rise to the classic disease of beriberi that, in its early stages, can be considered the prototype for a set of disorders that we now recognize as dysautonomia. This book represents the life's work of the senior author, Dr. Derrick Lonsdale, and a recent collaboration with his co-author Dr. Chandler Marrs. Presents clinical experience and animal research that have answered questions about thiamine chemistryDemonstrates that the consumption of empty calories can result in clinical effects that lead to misdiagnosisAddresses the biochemical changes induced by vitamin deficiency, particularly that of thiamine.

All have male gender preponderance and obesity has been linked to cognitive dysfunction. High calorie malnutrition, defined as calorie yielding foods with insufficient non-caloric nutrients, is common in America. The objective of this review is to show that this type of malnutrition, particularly with the consumption of simple carbohydrate foods, induces thiamin deficiency, often also with magnesium deficiency, providing a common etiological component for these diseases, analogically compared with variations on a symphonic theme in music. Conclusion: High calorie malnutrition is affecting millions of people, involving the inordinate consumption of sugar and fat as empty calories. All simple carbohydrates are metabolized in the body as glucose, with thiamin as the rate limiting factor in the three enzymes that make up pyruvic dehydrogenase and as a cofactor in transketolase. Other non-caloric nutrients are also crucial in oxidative metabolism.

By Derrick Lonsdale and Chandler Marrs. Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition explores thiamine and how its deficiency affects the functions of the brainstem and autonomic nervous system by way of metabolic changes at the level of the mitochondria. Thiamine deficiency derails mitochondrial oxidative metabolism and gives rise to the classic disease of beriberi that, in its early stages, can be considered the prototype for a set of disorders that we now recognize as dysautonomia. Derrick Lonsdale, and a recent collaboration with his co-author Dr. Chandler Marrs. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. This book and the individual contributions contained in it are protected under copyright by the Publisher other than as may be noted herein.

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Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition explores thiamine and how its deficiency affects the functions of the brainstem and autonomic nervous system by way of metabolic changes at the level of the mitochondria. Thiamine deficiency derails mitochondrial oxidative metabolism and gives rise to the classic disease of beriberi that, in its early stages, can be considered the prototype for a set of disorders that we now recognize as dysautonomia. Derrick Lonsdale, and a recent collaboration with his co-author Dr. Chandler Marrs. He immigrated to Canada in and in he was accepted as a pediatric resident at Cleveland Clinic, Cleveland, Ohio. In he was appointed to the pediatric staff where his clinical research led to his commitment to uncovering the connections between thiamin metabolism and metabolic brain disease.

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Derrick Lonsdale

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