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Curcumin: Problems and promises

I take curcumin regularly. This is a nice visual representation of how it potentially acts as an anti-cancer agent providing all conditions requiring therapeutic efficacy are met. Bioavailability is key here to make the most of the therapeutic benefits of curcumin. If you take it as a supplement make sure it is paired with piperine and is taken in therapeutic doses. We need more in vivo studies in brain tumour patients to elucidate what would act as an optimal dose, crossing the blood brain barrier so I will continue to research this medicinal compound.  ‘Major reasons contributing to the low plasma and tissue levels of curcumin appear to be due to poor absorption, rapid metabolism, and rapid systemic elimination. To improve the bioavailability of curcumin, numerous approaches have been undertaken. These approaches involve, first, the use of adjuvant like piperine that interferes with glucuronidation; second, the use of liposomal curcumin; third, curcumin nanoparticles; fourth, the use of curcumin phospholipid complex; and fifth, the use of structural analogues of curcumin (e.g., EF-24). The latter has been reported to have a rapid absorption with a peak plasma half-life. Despite the lower bioavailability, therapeutic efficacy of curcumin against various human diseases, including cancer, cardiovascular diseases, diabetes, arthritis, neurological diseases and Crohnʼs disease, has been documented. Enhanced bioavailability of curcumin in the near future is likely to bring this promising natural product to the forefront of therapeutic agents for treatment of human disease.’ As the acclaimed philosopher Karl Popper explained, a good scientist should constantly be trying to prove themselves wrong in order to have a truly unbiased opinion. This forms the basis of pure, valid, reliable scientific research. If I am trying to prove myself right all the time without a healthy degree of skepticism I may ignore the challenges…

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An explorative essay: Can magnesium chloride raise seizure threshold?

Exploiting ionic changes in the epileptic brain to increase seizure threshold with oral supplementation of magnesium chloride Epilepsy is a serious neurological disorder marked by sudden recurrent episodes of sensory disturbance, loss of consciousness, or convulsions, associated with abnormal electrical activity in the brain. Seizures are associated with neuronal ionic changes (Schwartzkroin, 1998) that can be managed with increased efficacy through magnesium chloride supplementation. Magnesium supplementation should be part of an essential component of a management strategy for any type of epilepsy to raise seizure threshold and maintain trace element homeostasis. The form of magnesium that has been used most clinically and has the longest therapeutic use to treat epilepsy in the literature is magnesium sulphate, however this is not practical or convenient for patients with epilepsy. While there needs to be more research into other forms of magnesium to manage epilepsy, there remains adequate evidence to suggest that oral magnesium, particularly magnesium chloride, has numerous benefits to increase seizure threshold by modulating neuronal activity. Magnesium chloride is easy to ingest, convenient to apply, acts effectively as a central nervous system depressant, improves insulin sensitivity, and lowers plasma blood glucose. This essay will explain how these mechanisms can effectively contribute towards raising seizure threshold for patients with all types of epilepsy. ‘Non-synaptic mechanisms’ are an important consideration in an attempt to manage neuronal activity in epilepsy. This includes, but is not exclusive to ionic interactions that involve magnesium, potassium, sodium and calcium. Increases in the extracellular concentration of potassium in particular is of vital importance in order to consistently manage epileptic seizures however this is dependent on many cofactors. Magnesium is involved with over 300 enzymatic reactions and has numerous mechanisms of action that make it an effective standalone treatment to modulate neuronal excitability with great efficacy and safety. ‘Regulation…

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Optogenetics and cancer?

My life is already becoming much more productive and enjoyable since making alterations to my light environment. I feel the benefits going forward as I learn and apply more could play a significant role in optimising this metabolic approach to my situation.   I am undertaking a great deal of study into the potential of optogenetics for a variety of applications and would love to take this further as I progress at university. Ontogenetics has roles to play in glucose regulation, behaviour, and several other hormonal actions as well as having the potential to treat blindness and diseases relating to the eye. I have attached a number of links I find incredibly interesting to the Youtube video and I hope others share my enthusiasm for this approach in clinical settings to treat neurological disease. If you’re too lazy to look for the links here they are! Optogenetics and its potential for neurological disease management: optogenetics news story- optogenetics and glucose metabolism- optogenetics- optogenetics and disease, mental health- McCullum lake cancer cluster- melatonin and cancer-

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Think it’s all about food? Think again.

I’m collecting more information on how I can improve my light environment, this is pretty good.  Astrocytes are like many little clocks, mess up the times and it can change your genes. I was diagnosed with an astrocytoma so this information is gold.  Light is often more important than food, I understand this. The problem is probably that people can’t make much money out of this and it’s not trendy.

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I have become overly reliant on technology lately and this is not a good thing. From now on I will be limiting my use of all personal technology (phones, computers, TV) to the hours of 12-1pm, 3-4pm and 6-7pm. In this day and age I cannot cut my use completely unfortunately because as a society in this country we have become so dependent on it, however I believe cutting down will allow me to be more efficient with my time when I do use it and the times I am not using it. Also please see again this study on EMF and epilepsy. I am writing this at 12:25 so the limitation period has begun and the phone will be switched off again very soon. 🙂 

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Epilepsy and hyperbaric oxygen therapy- important considerations

I’m at the halfway point now! Today I start week 3 of my 6. Week 2 of my hyperbaric oxygen treatment was certainly more eventful than week 1, even at this early stage! This is both good and bad. I had experience of an oxygen toxicity seizure towards the end of HBOT last Monday and I was able to reverse this just in time before it became more serious. I knew this was a risk as I have reflex epilepsy but there are some interesting findings that I am documenting. Increase in ROS and RNS (among other complex mechanisms) obviously affects the epileptic brain and stimulates the central nervous system but we can manage this to get the benefits rather than increase risky complications using some clever management techniques I learned from research as I will explain. We must also remember that antioxidants have anticonvulsant benefits but reduce the efficacy of HBOT so a patient with reflex epilepsy must try to find a balance that is therapeutic to get the benefits of HBOT and not dangerous. I don’t take any antioxidants now including vitamin D which I usually take regularly and can be a useful anticonvulsant at therapeutic doses. If I have problems I will take magnesium chloride orally to act as a central nervous system depressant to ward off seizures when I experience an aura. I just slip off my mask and have a drink and rest for a few minutes, then continue using biofeedback techniques to stay calm. Now, I could have been really negative here if I was misinformed by thinking that this treatment was just not for me and may be making things worse but I see the seizure activity as a great thing even though its terrifying and makes me anxious. Interestingly as the week…

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