Brain Regions Involved in Anxiety

Anxiety has been hypothesised to be a survival mechanism by which threats are assessed and a more tentative and careful approach, following intense reflection, may confer advantages in dealing with situations. However, chronic anxiety, as can develop in humans and animals exposed to prolonged threat or multiple continued but different threats, can be debilitating and ultimately lead to dysfunction. Because of the detrimental effects of chronic anxiety in humans, interest in the regions of the brain involved has increased and research has tried to locate the main regions affected. In this regard much research has been performed on animal models. This research has highlighted the amygdala and the bed nucleus of the stria terminalis (BNST) as being central to the pathology of anxiety. For example, a higher amygdala weight is associated with greater levels of anxiety in animals and patients with anxiety show higher activation of the amygdala. The BNST likely regulates anxiogenic behaviour because it received prominent projections from the amygdala and routes these to the hypothalamus, which may be involved in activation of the hypothalamus-pituitary-adrenal axis. However, whilst these regions are central to the development of anxiety, there regions form part of a larger network of connections and these connections to the ventral hippocampus (vHPC), the medial prefrontal cortex (mPFC) and other regions are significantly involved in the development of anxiety. 

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Adhikari, A. 2014. Distributed circuits underlying anxiety. Frontiers in behavioural neuroscience, 8: 112
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Alcohol Addiction and Brain-Derived Neurotrophic Factor

Brain derived neurotrophic factor (BDNF) is a peptide hormone under the regulation of the cyclic AMP response element binding (CREB) protein. Evidence suggests that BDNF is required for neuronal health, synaptic plasticity, and may play a role in memory and learning. Chronic stress can reduce levels of BDNF because the major stress hormone cortisol is able to reduce cellular levels of CREB which in turn reduces the expression of the BDNF. Further, stress increases levels of oxidative stress in the brain because cortisol can increase expression of inflammatory cytokines, and a by-product of this is the generation of free radicals which is the cause of oxidative stress. Oxidative stress has been shown to downregulate neuronal levels of BDNF and this may have detrimental effects on synaptic plasticity,  neuronal health and memory. 

Moderate drinking increases levels of BDNF in the dorsal striatum, which in turn acts to inhibit alcohol intake through expression and activation of Mitogen-Activated Protein Kinase (MAPK). However at high intakes, alcohol lowers BDNF in the cortex and hippocampus, and the lower BDNF expression is associated with increased alcohol intakes in mouse models. Therefore whilst moderate drinking may protect the brain and improve memory, as intake rises the detrimental effect starts to negatively affect the individual such that not only is neuronal health and brain function compromised, but a greater desire for alcohol reinforces this process, causing further dysfunction with continued drinking. As drinking is often used as a strategy to counteract stress, these data would suggest that this can only be a successful strategy if the drinking is moderated significantly. 

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Logrip, M.L., Barak, S., Warnault, V. and Ron, D. 2015. Corticostriatal BDNF and alcohol addiction. Brain Research. 1628: 60-67
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Alcohol and Cognitive Impairment: Thiamine

Alcoholics and those with high intakes of alcohol such as chronic binge drinkers are at a greater risk of the neurological disorders including Wernicke­ Korsakoff syndrome (WKS). The damage associated with the structural brain changes seen in WKS include disturbed cognition, memory problems, reduced intellect and personality changes. One of the most serious effects of WKS is anterograde amnesia, which is the inability to learn from new memories, retrograde amnesia, which is the ability to recall memories from before the development of WKS, and impairment of several cognitive processes including concentration, learning and memory. As a result individuals can become easily distracted and unable to screen out unwanted information, whilst at the same time failing to focus on important information. These changes are associated with structural changes in the brainstem and the thalamus. Individuals with WKS also have problems separating sensations such as odours, colours or musical pieces and this is thought to relate to the fact that these perceptions originate in the thalamus. Further WKS sufferers also have impairments in language in the way they can analyse words and sentences and find it hard to evaluate at the orthographic graphic level by correctly using lower and upper case letters, at the phenomic level but understanding rhyming, or at the semantic level, to identify how words contextualise a sentence. 

One of the main factors that is thought to contribute to the development of WKS in alcoholics is a thiamin deficiency. This is significant because thiamine deficiency is known to be induced by chronic alcohol consumption in a number of ways including an increased excretion of the vitamin and a concomitant decreased absorption. Alcohol can also reduce intakes of thiamine rich foods because of the effects it has on inhibiting inhibitory control, which causes an increased intake of tastier but lower quality foods. As alcohol contains 7 kcals per gram, heavy drinkers often substitute food calories for alcohol calories, thus reducing their thiamin intakes significantly. Wernicke’s encephalopathy is a disease similar to WKS, that is known to be caused by thiamine deficiency in the absence of alcohol, and this condition can be reversed clinically by administration of thiamine. Thiamine deficiency is able to disrupt normal brain activity because it is required for glucose metabolism in the neurones, is required for the correct myelination of myelinated neurones and may be involved in maintaining membrane structure. Patients who present in hospital with chronic nutritional deficiencies including deficiencies of thiamine often have symptoms identical to WKS despite the absence of alcohol.  

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Langlais, P.J. 1995. Alcohol-related thiamine deficiency: Impact on cognitive and memory functioning. Alcohol Health and Research World. 19(2): 113
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The Acute Effect of Alcohol on Cognition

Ingestion of alcohol is well evidenced to alter behaviour and change aspects of psychology. For example, impairment of cognition required for divided attention tasks occurs at relatively low intake of alcohol. This may be the reason that alcohol is particularly damaging to driving ability even at low intakes, despite much higher intakes being required to impair reaction times. One aspect of this is the ability of alcohol to alter brain functions that in turn increase the propensity to undergo behaviour likely to increase alcohol intake further. Under normal circumstances, inhibitory control prevents behaviours that are self-damaging and detrimental to the individual. However, at doses of alcohol that are below the threshold for causing significant global impairment of cognitive performance, alcohol can increase automatic alcohol-related cognitions. In this way, alcohol can impair the executive function of inhibitory control, which is the ability to inhibit motor responses that are already initiated. This inhibitory control is a significant part of preventing impulsive behaviour, and therefore by reducing inhibitory control, alcohol can significantly increase impulsive behaviour. A blood alcohol content of only 0.06 %, produced by relatively modest intakes of alcohol can cause inhibition of inhibitory control, and the result of the downstream impulsivity may lead to a desire to seek further alcohol intakes, thus overriding the normal cognitive function that would prevent this behaviour. This is one of the strongest arguments that suggest that alcoholics should avoid alcohol completely if they wish to break their habit. 

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Field, M., Wiers, R.W., Christiansen, P., Fillmore, M.T. and Verster, J.C. 2010. Acute alcohol effects on inhibitory control and implicit cognition: implications for loss of control over drinking. Alcoholism: Clinical and Experimental Research. 34(8): 1346-1352
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Nutrition for Eye Health

Nutrition can play an important role in the health of the eyes. Damage to the eyes can occur over the lifetime of the individual and one of the main drivers of eye disease is free radical generation, which can in turn lead to oxidative stress. Free radicals can damage various parts of the eyes, with the retina, vitriolic gel and lens being particularly susceptible. Cataracts, glaucoma, vitriolic degeneration and age-related macular degeneration (AMD) are all eye diseases that affect these portions of the eyes. Risk factors that can accelerate these diseases include those that increase free radical generation such as sunlight, smoking, poor diet and obesity. To counteract the damage from free radicals a number of nutrients can be taken that have antioxidant effects. Lutein and zeaxanthin are carotenoids found in fruits and vegetables that can have a significant positive effect on eye health because they accumulate in the eye, particularly the retina, and here they protect the eye from damage. This function is similar to the role they play in plants, where they protect plant tissues from the generation of free radicals caused by excessive sunlight. Other nutrients that have antioxidant effects that may benefit the eye include green tea catechins, anthocyanins, resveratrol, and Ginkgo biloba. A healthy diet high in fruits and vegetables can provide high amounts of these and other antioxidants and those who wish to protect their eyesight should consider increasing these types of foods in their diets. 

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Rhone, M. and Basu, A. 2008. Phytochemicals and age-related eye diseases. Nutrition Reviews. 66(8): 465-472
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Tryptophan Nutrition: Niacin

Niacin is a general name for nicotinic acid (pyridine-3-carboxylic acid) and nicotinamide (niacinamide or pyridine-3-carboxamide) and niacin is considered an essential vitamin that is grouped with the B vitamins. Niacin is considered a vitamin because its absence can result in the deficiency disease pellagra, and this can be reversed through addition of niacin to the diet. However, whilst niacin (as a group) is considered a vitamin, nicotinamide can be synthesised in the liver from tryptophan, and then the resulting nicotinamide is distributed to other tissues around the body to perform its metabolic role in energy production. The synthesis of nicotinamide can be affected by a number of factors including disease, other nutrients, toxins and chemicals. Roughly 67 mg of tryptophan is needed to produce around 1 mg of nicotinamide in the liver, a ratio that is increased during late pregnancy when there may be an increased requirement for the vitamin. Therefore whilst niacin is considered a vitamin, a dietary intake of adequate tryptophan, in the absence of factors that increase requirement, can allow for enough niacin to cover the metabolic requirement of the vitamin. 

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Fukuwatari, T. and Shibata, K. 2013. Nutritional aspect of tryptophan metabolism. International Journal of Tryptophan Research. 6: IJTR-S11588
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How Complex is Good Nutrition?

The propensity for those with a commercial interest in nutrition is to overly complicate the basics and thus obfuscate how simple it is to care for your health. In fact, basic nutrition for health is very easy and there is no reason why most people cannot benefit from the health advantages of a healthy diet, should they choose. Of course, the onus is on the individual to stick to the eating strategy that facilitates health, something many are not prepared to do. These individuals are the food that feeds the snake oil salesman, as he promises easy options and magic pills. For whilst understanding what to eat is fairly easy, the notion of abandoning fast food, tasty snacks, sugary and fatty foods, and those that are heavily processed to sacrifice nutritional quality for taste, is perhaps too much for many. This is why many never manage to obtain true health and why ailments are common in those who inhabit the Western nations and consume the typical Western diet. In essence eating healthily involves avoiding processed foods, consuming fresh produce, perhaps based around plant foods, and obtaining adequate protein, minerals, vitamins, essential fats and energy, in order to allow the body to grow and heal itself. The avoidance of chronically high levels of stress and toxins and pollution are also a high priority for health, but many are unable to sacrifice the rat race for the good of their bodies. Therefore as with all things, you take your choice and pay the price. Eat well my friends. 

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The Effects of Macronutrients of Sleep

Macronutrients include protein, carbohydrate and fat. Macronutrients play an important role in health, particularly for protein and fat which contains essential nutrients. It has been understood for some time that alterations to the ratios of macronutrients in the diet can have a significant influence on the metabolism of the individual, with evidence that hormonal secretions are significantly influenced by the types, amounts and ratios of macronutrients in the diet. Sleep is one important aspect of health that may be significantly influenced by macronutrient ratios. In one study researchers administered a high fat, high protein or high carbohydrate diet to a group of individuals to assess the effects on sleep parameters over 4 day periods. The results of the study showed that the high protein diet was significantly associated with free waking periods during sleep. In contrast, the high carbohydrate diet was significantly associated with reduced sleep latency. This suggests that during sleep the food that has been consumed in the previous wakeful period plays an important role in certain sleep parameters, and this could be used as a basis to improve sleep quality in those with particular sleep problems.

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Lindseth, G., Lindseth, P. and Thompson, M. 2013. Nutritional effects on sleep. Western Journal of Nursing Research. 35(4): 497-513
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Nutrition for Vitreous Degeneration

Vitreous degeneration refers to the degradation of the posterior part of the eye. One of the symptoms of this can be the increasing number of ocular floaters seen by the observer, in addition to eye discomfort or pain. The vitreous gel at the posterior of the eye can degrade as a result of age and other factors and part of the process is believed to involve the degeneration of the cartilage that is fundamental to the integrity of the vitreous layer. Oxidative stress and cellular changes including increased production of proteolytic enzymes may be fundamental to triggering or facilitating the development of severe degradation. Some studies have assessed the effects of nutrition on the presence of floaters in the eye, as this is one of the key symptoms and a good measure of vitreous degeneration. One study administered 125 mg L-lysine, 40 mg vitamin C, 26.3 mg Vitis vinifera extract, 5 mg zinc, and 100 mg Citrus aurantium or placebo for 6 months, to subjects that were experiencing vitreous degeneration. The results of the study showed that the supplemental programme was significantly able to reduce the discomfort in the eyes and the amount of floaters experienced by the subjects, compared to the placebo. The study authors also reported that other parameters in the eye, such as photopic functional contrast sensitivity with positive contrast polarity, improved following supplementation. 

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Ankamah, E., Green-Gomez, M., Roche, W., Ng, E., Welge-Lüßen, U., Kaercher, T. and Nolan, J.M. 2021. Dietary Intervention With a Targeted Micronutrient Formulation Reduces the Visual Discomfort Associated With Vitreous Degeneration. Translational Vision Science & Technology. 10(12): 19-19
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Cellular Effects of Raspberry Ketones

Raspberry ketones have been evidenced in animal studies to protect from the damaging effects of overconsumption of energy. In addition, studies in animals show that raspberry ketones can also reduce body fat in overweight animals. In human studies, similar effects are seen with raspberry ketones, and these include the ability to cause weight loss and protect from fatty liver and insulin resistance. Because of these effects, it is interesting to speculate on the possible cellular mechanisms by which these effects can occur. A number of cellular studies have attempted to elucidate this aspect of the pharmacology of raspberry ketones and have published evidence that supports a weight loss effect. For example, in one study the researchers observed an increase in lipolysis and an increase in fatty acid oxidation in cell culture models. In addition, raspberry ketones increase the expression of adiponectin, and adipocytokine, which has been shown to have anti obesity effects in humans and animals. The study authors concluded that raspberry ketones may be a potentially useful supplement in the treatment of obesity and could be used therapeutically to increase fat oxidation and protect from weight gain. 

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Park, K.S., 2010. Raspberry ketone increases both lipolysis and fatty acid oxidation in 3T3-L1 adipocytes. Planta medica. 76(15): 1654-1658
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