PLT Test Blog

Today’s post is about further refining antioxidant therapy. As we saw in a recent post, oxidative and nitrosative stress is a very common feature of autism and is treatable with OTC products. The cheapest antioxidant, N-acetylcysteine (NAC), looks to be the best one, but there are numerous others with exotic names and equally   exotic prices. Today we just look at selenium and molybdenum.   Selenium was on my to-do list for a long time because it affects some key enzymes call GP X (glutathione peroxodases). Molybdenum was enthusiastically recommended in a recent comment and this blog has previously touched on Molybdenum Cofactor Sulfurase (MOCOS). Rather surprisingly, there is a commercial product that contains NAC, Selenium and Molybdenum.   Selenium and GP X (glutathione peroxodases) There are eight different glutathione peroxodases , but GPx1 , GPx2 , GPx3, and GPx4 are all made from selenium. GP X speeds up the antioxidant reactions that involve glutathione (...

Today’s post highlights a paper with some very concise insights into how microglial cells become “activated” resulting in the “ exaggerated inflammatory response” that many people with autism experience on a daily basis.   This is very relevant to treatment, which is not usually the objective of much autism research. I recall reading a comment from John’s Hopkins about neuroinflammation/activated microglia in autism; they commented that no known therapy currently exists and that, of course, common NSAIDs like ibuprofen will not be effective.  But NSAIDs are effective. As we see in today’s paper, there a least 4 indirect cytokine-dependent pathways leading to the microglia, plus one direct one. NSAIDs most definitely can reduce cytokine signaling and thus, indirectly, reduce microglial activation. The ideal therapy would act directly at the microglia, and as Johns Hopkins pointed out, that does not yet exist with today's drugs.  If you read the research on various natural ...

I am returning to an old theme of mine, which is my hypothesis that the thyroid releasing hormone (TRH) may be of therapeutic value in autism.   I have been reading up on what some endocrinologists are doing the US and also looking a bit deeper into the underlying biology of the related hormones and thinking about my research sample of one, Monty aged 10 with ASD.   My original hypothesis was argued in an earlier post. The Peter Hypothesis of TRH-induced Behavioural Homeostatis in Autism Since none of the TRH researchers care to reply to my emails, I decided to refine and document my hypothesis further and then plan to go and see a child endocrinologist for myself.   In most countries, the doctor does the talking and the patient does the listening, so I know that I need something unusual; I called it “an open minded endocrinologist”. Peter’s TRH & Central Hypothyroidism Theory Research has documented which parts of the autistic brain are often damaged.   ...