Marmite

Marmite is a yeast extract that is a by-product of the brewing industry. The ability to use the concentrated thrub from the brewing process to make marmite is attributed to the German scientist Justus Freiherr von Liebig. The thrub is the concentrated sediment that is present after the wort has been boiled and transferred elsewhere during the brewing process. In 1902 the Marmite company was started to manufacture marmite, and this process was reliant on the large brewing industry in Staffordshire to provide the raw materials, particularly in Burton Upon Trent. The traditional label for marmite contains an image that was based on an earthenware pot, that in French is called a marmite. The nutritional qualities of marmart have been demonstrated in many studies. For example, in the 1920s, marmite was successfully used to treat anaemia, a phenomenon more recently known to be due to the presence of B vitamins in the marmite. Pernicious anaemia is caused by a vitamin B12 deficiency, and marmite is an excellent source of the vitamin, along with other vitamins from the B family that are present in brewers yeast.  

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RdB

Franklin, J. L., Marmite: its place in medical history, Lucy Wills, and the discovery of folic acid. Hektoen International A Journal of Medicinal Humanities. 
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How Does Niacin Treat Lipid Disorders?

Nicotinic acid has been shown to have beneficial effects on blood lipid levels. In this regard nicotinic acid can normalise raised levels of blood lipids and reduce cardiovascular disease risk, when taken at pharmacological levels above its normal vitamin requirement. Evidence suggests that nicotinic acid is able to have favourable effects on lipids because it directly and noncompetitively inhibits hepatocyte diacylglycerol acyltransferase–2. As this enzyme is required for triglyceride synthesis, its inhibition reduces the synthesis of triglycerides and reduces very low density lipoprotein (VLDL) particles. As the VLDL particle is made of triglycerides and responsible for transporting them to the blood, this also reduces blood lipid levels. At the same time, intracellular apolipoprotein (apo) B containing lipoproteins (i.e. the VLDL particle) continue to be degraded. Further, as the low density lipoprotein particle is derived from the VLDL particle, this process also lowers levels of LDL. In addition, nicotinic acid also reduced catabolism of apolipoprotein (apo) A-I containing lipoproteins, which in effect is the high density lipoprotein (HDL) particle. This raises levels of HDL in the blood by increasing its halflife,and the raised levels of HDL are associated with a reduced risk of cardiovascular disease. In addition, niacin may also reduce levels of oxidative stress in the blood by improving the reductive capacity of vascular endothelial cells. Further niacin may also reduce the expression of inflammatory genes that give rise to inflammatory cytokines that are required for the development of inflammation in the arteries. 

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Kamanna, V.S. and Kashyap, M.L., 2008. Mechanism of action of niacin. The American Journal of Cardiology. 101(8): S20-S26
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Niacin as a Lipid Lowering Agent

Nicotinic acid is a vitamer of niacin that can prevent the development of pellagra. This is its essential function, and this effect is attributed also to nicotinamide, which also shares vitamer activity under the niacin group. Beyond its role as a vitamin, nicotinic acid also has a pharmacological profile when taken in higher amounts beyond its requirements for its role as a vitamin. These pharmacological effects include the ability to lower levels of certain lipids in the blood. In particular, nicotinic acid can lower levels of low-density lipoprotein (LDL) cholesterol, triglyceride, and lipoprotein(a), while raising levels of increasing high-density lipoprotein (HDL). Clinical studies suggest that use of niacin to control elevated levels of blood lipids can improve the health of the individual with regard to the cardiovascular outcomes expected. However, nicotinic acid is associated with elevated levels of blood glucose and so the use of high intakes is recommended only for those at high risk of cardiovascular disease, and should also only be taken over the short term under medical supervision. For most people this will not be necessary, as switching to a healthy, high quality diet in itself will be enough to lower blood lipid levels to the normal range. One part of this is that high quality diets cause weight loss, and as weight gain is associated with increased levels of blood lipids and an increased risk of cardiovascular disease, weight loss alone can be a significant part of cardiovascular health.  

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RdB

McKenney, J. 2004. New perspectives on the use of niacin in the treatment of lipid disorders. Archives of Internal Medicine. 164(7). 697-705
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The Role of Thiamine in Alcohol-Induced Brain Abnormalities

Alcoholics are at increased risk of thiamine deficiencies because of a combination of lower quality food intakes and a propensity for malabsorption and increased excretion of certain essential compounds. In the case of alcoholics, thiamine deficiency can lead to the formation of Wernicke-Korsakoff syndrome, which is characterised by aberrations in certain parts of the brain. The metabolic dysfunction that results from alcohol-induced thiamine deficiency can lead to permanent brain damage or even death. Thiamine is important to metabolic activity because it is required for nerve function, being pivotal in the generation of energy from glucose, a source of energy that neurones rely upon. However, to say that Wrnicke-Korsakoff syndrome only occurs in alcoholics is not true, as any person with a thiamine deficiency, particularly in the context of other nutritional deficiencies, can develop the condition. That being said, the neurodegeneration seen with thiamine deficiencies is more common in alcoholics, and may develop more thoroughly and more quickly in alcoholics compared to non-drinking contemporaries. There is also significant biochemical individuality whereby some individuals appear to be highly susceptible to a thiamine deficient state. 

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RdB

Martin, P.R., Singleton, C.K. and Hiller-Sturmhöfel, S., 2003. The role of thiamine deficiency in alcoholic brain disease. Alcohol Research & Health. 27(2): 134
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Niacin Vitamers

Niacin describes a group of vitamins that are required for correct metabolic activity. Failure to obtain enough niacin in the diet results in the development of pellagra, which is characterised by dermatitis, diarrhoea and dementia, and if left untreated will lead to death. Treatment of pellagra is simply a case of returning adequate niacin to the diet. This can be done by addition of any of the compounds that share niacin activity which effectively means nicotinic acid or niacinamide. These are described as vitamers of niacin. Organic electron carriers such as nicotinic adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) also show niacin activity, but are much less bioavailable compared to nicotinic acid and niacinamide, and so these latter two compounds are the forms of niacin that are favoured nutritionally. One explanation for the lower bioavailability of NAD and NADP is that they are labile in acidic conditions as might be found in the stomach. One real world example of where this is important is in the maturation of corn, whereby bioactive forms of niacin are transformed into less bioavailable forms, reducing the nutritional value of the corn in terms of its niacin activity. Nicotinamide riboside is found in milk but its contribution to human nutrition is not fully understood. 

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RdB

Gregory, J.F. 2012. Accounting for differences in the bioactivity and bioavailability of vitamers. Food & Nutrition Research. 56(1): 5809
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Vitamers

Vitamins are essential organic chemicals that are required by humans (and animals) to prevent specific named diseases. For example, thiamine prevents the development of beriberi and niacin prevents the development of pellagra. However, most vitamins actually exist in multiple forms and these forms are called vitamers. For example, the deficiency disease caused by a deficiency of vitamin E is lipid peroxidation. However, vitamin E is actually a group of 8 different chemicals that all share the same activity. These are alpha, beta, gamma and delta tocopherol and alpha, beta, delta and gamma tocotrienol. Niacin too is made up of a number of forms including nicotinic acid and niacinamide, both of which can prevent pellagra. The various vitaminer may have slightly different effects and their relative potencies can vary. For example the fungal form of vitamin D, named ergocalciferol, is not as potent in humans as the animal form of vitamin D, named cholecalciferol. However both forms prevent the development of the deficiency diseases rickets in children and osteomalacia in adults. Folate activity is shared by as many as 10 naturally occurring variants of the vitamin, and this exemplifies the large number of vitamers that are present naturally in foods.   

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RdB

Gregory, J.F. 2012. Accounting for differences in the bioactivity and bioavailability of vitamers. Food & Nutrition Research. 56(1): 5809
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Alcohol and Thiamine

Alcohol abuse can cause significant nutritional deficiencies for two main reasons. Firstly, individuals that abuse alcohol tend to obtain much of their energy needs from alcohol and their behaviour to find, consume and recover from drinking alcohol tends to negate time they might otherwise spend eating or preparing food. As a result alcoholics tend to have nutrient poor diets that contain empty calories supplied mainly from alcohol. In addition, alcohol can prevent the absorption of many nutrients and at the same time increase excretion rates, and these factors increase the risk of obtaining a vitamin deficiency. In alcoholics, one of the most likely deficiencies has been shown to be for thiamine, which can result in the development of beriberi, a form of neurological disorder. 

As thiamine deficiency worsens, the neurological changes characteristic of beriberi can deteriorate into the development of Wernicke’s encephalopathy, a disorder of the brain that results in ocular mobility problems such as nystagmus and ophthalmoplegia, ataxia, as well as confusion, drowsiness and coma. When alcohol intakes are high and thiamine intakes are low, the development of Wernicke’s encephalopathy can be reasonably common. And can lead to long term brain damage if drinking continues. Alongside Wernicke’s encephalopathy, Korsakoff’s psychosis can also be present, which is characterised by anterograde and retrograde amnesia, disorientation, poor recall, impairment of recent memory and confabulation. The development of both conditions results in a condition known as Wernicke-Korsakoff syndrome, which can be effectively treated with high dose thiamine therapy, which reverses the neurological problems. 

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RdB

Agabio, R., 2005. Thiamine administration in alcohol-dependent patients. Alcohol and alcoholism. 40(2): 155-156
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The Effects of Freezing and Toasting on Bread: Glycaemic Response

The glycaemic index is a measure of the rate and size of the rise in blood glucose following consumption of a carbohydrate food. Generally, lower blood glucose responses are associated with health, and foods that cause large positive perturbations in blood glucose trend to be foods that can contribute to the disease process. This process includes the development of insulin resistance, a phenomenon that results from cells protecting their integrity in the face of excess glucose by reducing its uptake. This process results in the more glucose remaining in the blood, and this can cause disease progression. Bread generally has a high glycaemic index, with white bread showing a similar glycaemic response to liquid glucose. Strategies to lower the glycaemic index of bread can therefore provide health benefits to the consumer. Eating other foods with the bread, particularly protein foods, is highly effective at lowering the glycaemic index. Another solution is to consume acidic foods with the bread, as acids tend to generally slow digestion and absorption of carbohydrates. Lastly, studies show that freezing and defrosting, toasting, and toasting following freezing are all effective at lowering the glycaemic index of bread. This likely relates to changes in the way that the carbohydrates in the bread interact with one another, and in particular may reflect changes to the moisture content. 

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RdB

Burton, P. and Lightowler, H.J. 2008. The impact of freezing and toasting on the glycaemic response of white bread. European Journal of Clinical Nutrition. 62(5): 594-599
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Treating Alcohol Withdrawal

Alcohol withdrawal symptoms can range from mild to severe, and can include tremors, seizures and delirium. The withdrawal symptoms are a result of the removal of the sedating effects of alcohol, which acts on targetts in the γ-amino butyrate (GABA) and N-methyl-D-aspartate (NMDA) glutamate neurotransmitter systems. One important effect of alcohol withdrawal is the kindling phenomenon that results in progressively worsening withdrawal symptoms on each recurrent detoxification. It is thought that this is related to long term damage to the neurones during detoxification, and each subsequent period of cessation increases this damage cumulatively. It has been suggested that this worsening of withdrawal symptoms increases the likelihood that the subject will experience cravings that are likely to drive them to start drinking again. For this reason it is important that the subjects take every opportunity for the abstinence of alcohol to be successful and they avoid further cycles of drinking and detoxification. Medical treatments for alcohol use benzodiazepines for the reason that they can activate the GABA system and in this way replace the sedating effects of alcohol. However, for this reason benzodiazepines are themselves addictive and they also have a narrow therapeutic window. Many herbs and nutrients can activate the GABA system and so nutritional strategies can also be successful. For example passionflower and camomile both activate the GABA system and so they could be beneficial at treating alcohol withdrawal as part of a healthy diet. Because alcohol addiction causes nutrient deficiencies, a balanced and healthy diet is a priority for any successful alcohol cessation plan. In particular, high levels of B vitamins, particularly thiamine, are necessary for correct neuronal activity in the brain. 

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RdB

Bayard, M., Mcintyre, J., Hill, K. and Woodside, J. 2004. Alcohol withdrawal syndrome. American Family Physician. 69(6): 1443-1450
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Sudden Alcohol Withdrawal

Addiction to alcohol can be a serious debilitating condition that leads to a slow deterioration in physical and mental health. Because of the damage that alcohol does to both the user and the people around them, individuals who abuse alcohol often realise that it is necessary to stop drinking. However, sudden cessation of alcohol abuse can be dangerous as it can create a number of symptoms termed alcohol withdrawal. These symptoms range from extreme to mild, but it is often not possible to determine how an individual is going to react. Acute symptoms include insomnia, autoimmune hyperactivity, hand tremors, hallucinations, seizures, psychomotor agitation, depression and anxiety. In addition, the withdrawal of alcohol often occurs with a more chronic memory impairment caused by nutritional deficiencies that lead to Wernicke-Korsakoff syndrome, which is characterised by severe cognitive impairment, delirium, abnormal gait and eye muscle paralysis. 

Following the acute symptoms, more protracted symptoms may ensue and it is often this period that convinces an individual to begin drinking again. Protracted withdrawal syndrome is characterised by symptoms that can last up to 1 year and can include all of the symptoms seen in acute withdrawal. However, alcohol can also have a sedating effect by acting on the glutamate and GABAergic systems in the brain. Alcohol activates the GABA system by acting on GABAA receptors, and as levels of alcohol fall, the levels of GABA in the brain fall, and this reduces the sedation of the individual, something which can lead to the development of anxiety and insomnia. Alcohol also inhibits the N-methyl D-aspartate (NMDA) glutamate receptor that is involved in excitability in the brain. When alcohol is withdrawn, the system becomes overly active and this can be a cause of seizures. Overactive glutamate receptors are also thought to  exert neurotoxic effects and so alcohol withdrawal can lead to neuronal damage and brain dysfunction. As NMDA receptors are also involved in memory, the activation of NMDA receptors can complicate the memory impairment seen from the Wernicke-Korsakoff syndrome. 

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RdB

Trevisan, L.A., Boutros, N., Petrakis, I.L. and Krystal, J.H. 1998. Complications of alcohol withdrawal: pathophysiological insights. Alcohol Health and Research World. 22(1): 61
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