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Thiamine

Regarding H2S, oxidative stress, liver failure and other malnutrition syndromes….. 

Glycogenolysis is the biochemical breakdown of glycogen to glucose whereas glycogenesis is the opposite, the formation of glycogen from glucose. Glycogenolysis takes place in the cells of muscle, and liver tissues in response to hormonal and neural signals….

H2S has long been regarded as a strong toxin that inhibits mitochondrial respiration. H2S generates a state of oxidative stress. H2S causes blockage of electron transfer within the mitochondria.

Beriberi

Beriberi is characterized in its early stages by dysautonomia, appearing as postural orthostatic tachycardia syndrome (POTS). This well documented modern disease cannot be distinguished from beriberi except by appropriate laboratory testing for thiamine deficiency. Blood thiamine levels are usually normal in the mild to moderate deficiency state.

Examples of Dysfunction in Beriberi

The calf muscle often cramps with physical exercise. There is loss of the deep tendon reflexes in the legs. There is diminished visual acuity. Part of the eye is known as the papilla and pallor occurs in its lateral half. If this is detected by an eye doctor and the patient has neurological symptoms, a diagnosis of multiple sclerosis would certainly be entertained.

Optic neuritis is common in beriberi. Loss of sensation is greater on the front of the body, follows no specific nerve distribution and is indistinct.

Foot and wrist drop, loss of sensation to vibration and stumbling on walking are all examples of symptoms that would be most likely ascribed to other causes.

Breathlessness with or without exertion would probably be ascribed to congestive heart failure of unknown cause or perhaps associated with high blood pressure.

The symptoms of this disease can be precipitated for the first time when some form of stress is applied to the body. This can be a simple infection such as a cold, a mild head injury, exposure to sunlight or even an inoculation.

Is Thiamine Deficiency Common in America?

 It is extremely common. There is good reason for it because sugar ingestion is so extreme and ubiquitous within the population as a whole. Ingestion of sugar is causing widespread beriberi, masking as psychosomatic disease and dysautonomia. The symptoms and physical findings vary according to the stage of the disease. For example, a low or a high acid in the stomach can occur at different times as the effects of the disease advance. Both are associated with gastroesophageal reflux and heartburn, suggesting that the acid content is only part of the picture.
A low blood sugar can cause the symptoms of hypoglycemia, a relatively common condition. A high blood sugar can be mistaken for diabetes, both seen in varying stages of the disease.

It is extremely easy to detect thiamine deficiency by doing a test on red blood cells. 

The lower part of the human brain that controls the autonomic nervous system is exquisitely sensitive to thiamine deficiency. It produces the same effect as a mild deprivation of oxygen. Because this is dangerous and life-threatening, the control mechanisms become much more reactive, often firing the fight-or-flight reflex that in the modern world is diagnosed as panic attacks. Oxidative stress (a deficiency or an excess of oxygen affecting cells, particularly those of the lower brain) is occurring in children and adults. It is responsible for many common conditions, including jaundice in the newborn, sudden infancy death, recurrent ear infections, tonsillitis, sinusitis, asthma, attention deficit disorder (ADD), hyperactivity, and even autism. Each of these conditions has been reported in the medical literature as related to oxidative stress. So many different diseases occurring from the same common cause is offensive to the present medical model. This model regards each of these phenomena as a separate disease entity with a specific cause for each.

Without the correct balance of glucose, oxygen and thiamine, the mitochondria (the engines of the cell) that are responsible for producing the energy of cellular function, cannot realize their potential. Because the lower brain computes our adaptation, it can be said that people with this kind of dysautonomia are maladapted to the environment. For example they cannot adjust to outside temperature, shivering and going blue when it is hot and sweating when it is cold.

So, yes, beriberi and thiamine deficiency have re-emerged. We have forgotten history and appear doomed to repeat it. It is high time that the situation should be addressed more clearly by the medical profession.

SIBO, IBS and Constipation Unrecognized Thiamine Deficiency?

Malnutrition Induced Malnutrition

Together, these factors no doubt contribute to the phenomena of “malnutrition induced malnutrition”, a term coined by researchers to describe how thiamine deficiency can lead to all other nutrient deficiencies across the board. In other words, a chronic thiamine deficiency can indirectly produce an inability to digest and absorb foods, and therefore produce a deficiency in most of the other vitamins and minerals.  Thiamine is notoriously  missed by doctors and nutritionists. To summarize, B1 is necessary in the gut for:

• Stomach acid secretion and gastric emptying
• Pancreatic digestive enzyme secretion
• Intestinal brush border enzymes
• Intestinal contractions and motility
• Vagal nerve function

40 million people are intoxicated on any given day in America and the CV19 lockdown hasn’t helped…..

Alcoholism/Thiamine

Wernicke–Korsakoff Syndrome

A deficiency in the essential nutrient thiamine resulting from chronic alcohol consumption is one factor underlying alcohol–induced brain damage. Thiamine is a helper molecule (i.e., a cofactor) required by three enzymes involved in two pathways of carbohydrate metabolism. Because intermediate products of these pathways are needed for the generation of other essential molecules in the cells (e.g., building blocks of proteins and DNA as well as brain chemicals), a reduction in thiamine can interfere with numerous cellular functions, leading to serious brain disorders, including Wernicke–Korsakoff syndrome, which is found predominantly in alcoholics. Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells. People differ in their susceptibility to thiamine deficiency, however, and different brain regions also may be more or less sensitive to this condition. 

Approximately 80 to 90 percent of alcoholics with WE develop Korsakoff’s psychosis, a chronic neuropsychiatric syndrome characterized by behavioral abnormalities and memory impairments (Victor et al. 1989). Although these patients have problems remembering old information (i.e., retrograde amnesia), it is the disturbance in acquisition of new information (i.e., anterograde amnesia) that is most striking. For example, these patients can engage in a detailed discussion of events in their lives but cannot remember ever having had that conversation an hour later. Because of these characteristic memory deficits, Korsakoff’s psychosis also is called alcohol amnestic disorder. It is still somewhat controversial, however, whether Korsakoff’s psychosis always is preceded by WE or whether it develops in fits and starts, without an overt episode of WE.

Although WKS in developed countries occurs most commonly among alcoholics, other groups of patients are also at risk of developing the disease. For example, all people who are malnourished (e.g., because they have AIDS or are undergoing cancer chemotherapy) or who have a metabolic disease leading to impaired thiamine absorption (i.e., uptake) or utilization can develop thiamine deficiency. Patients with severe kidney disease who are undergoing regular dialysis are also prone to encephalopathy, and a substantial portion of them have been found to suffer from thiamine deficiency (Hung et al. 2001). Finally, patients who receive intravenous infusions of carbohydrates (e.g., the sugar dextrose) may experience episodes of thiamine deficiency, particularly if they are already at risk of receiving inadequate levels of this nutrient because they are alcoholics, as thiamine is used in the metabolism of those carbohydrates (see Ferguson et al. 1997).