Urine Strips: When tested in urine, these strips will elicit a color change based on the level of ketones, namely acetoacetate, which is present in the urine. It is important to note that acetoacetate is different than the ketones present in the blood, namely, beta-hydroxybutyrate (βHB). Due to its nature, urine ketone testing may be a sufficient initial method to test ketone production; however, it is not the ideal method for determining the utilization of these ketone bodies, especially once “keto-adapted.”


Therapeutics: The ketogenic diet was originally developed in the 1920s as an alternative therapeutic option to treat children suffering from drug-resistant epilepsy. Since its inception, the utilization of the ketogenic diet has expanded as a therapeutic treatment for many other conditions such as Alzheimer’s disease, Parkinson’s disease, GLUT-1 deficiency syndrome, Bipolar disorders and even cancer.
So question….what if you are watching your sodium intake due to high blood pressure? From what I read here, there is a lot of salt/sodium involved (more than my normal intake), how do I deal with this issue if doing keto? I do not take any medications. About three years ago I found that my thyroid levels were on the low end of the normal range and it affected my blood pressure. So I lowered my sodium intake and increased my iodine/iodide intake. This has worked for me for the past three years, in the sense that after a month of being on bp meds, I no longer needed those meds and my thyroid levels have stayed around the mid-range of normal. I have always eaten healthy with some junk foods here and there, but apparently being pregnant kicked off a thyroid issue and weight gain. What are my sodium options with keto? How do I balance it so my bp doesn’t take a freefall nor a significant increase?
There are many ways in which epilepsy occurs. Examples of pathological physiology include: unusual excitatory connections within the neuronal network of the brain; abnormal neuron structure leading to altered current flow; decreased inhibitory neurotransmitter synthesis; ineffective receptors for inhibitory neurotransmitters; insufficient breakdown of excitatory neurotransmitters leading to excess; immature synapse development; and impaired function of ionic channels.[7] 
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