So, for the 15-20% who relapse you go on antibiotics for 10-14 days again, or you may find physicians using the tapering method. This is where your physician might ask you to go on antibiotics for a week or so, and slowly taper down the strength or amount of antibiotics over a month or so. You may also be asked to try a pulsing method which is similar except you might take antibiotics every other day while tapering down to lower levels of antibiotics. So, these methods will vary in time, so let’s assume it takes another 30 days. Now we’re up to what, 45 days?
A 30-d course of oral administration of a semipurified extract of the root of Withania somnifera consisting predominantly of withanolides and withanosides reversed behavioral deficits, plaque pathology, accumulation of β-amyloid peptides (Aβ) and oligomers in the brains of middle-aged and old APP/PS1 Alzheimer's disease transgenic mice. It was similarly effective in reversing behavioral deficits and plaque load in APPSwInd mice (line J20). The temporal sequence involved an increase in plasma Aβ and a decrease in brain Aβ monomer after 7 d, indicating increased transport of Aβ from the brain to the periphery. Enhanced expression of low-density lipoprotein receptor-related protein (LRP) in brain microvessels and the Aβ-degrading protease neprilysin (NEP) occurred 14-21 d after a substantial decrease in brain Aβ levels. However, significant increase in liver LRP and NEP occurred much earlier, at 7 d, and were accompanied by a rise in plasma sLRP, a peripheral sink for brain Aβ. In WT mice, the extract induced liver, but not brain, LRP and NEP and decreased plasma and brain Aβ, indicating that increase in liver LRP and sLRP occurring independent of Aβ concentration could result in clearance of Aβ. Selective down-regulation of liver LRP, but not NEP, abrogated the therapeutic effects of the extract. The remarkable therapeutic effect of W. somnifera mediated through up-regulation of liver LRP indicates that targeting the periphery offers a unique mechanism for Aβ clearance and reverses the behavioral deficits and pathology seen in Alzheimer's disease models.
Re the Low-High FODMAP terminology: Websites I’ve previously read about low FODMAP diets indicate the Elimination Phase is where you eat “No High FODMAPS” during this short period to see if symptoms improve (though some might eat no FODMAPS). You then go into the “Re-Introduction Phase” as you re-introduce high FODMAPS back into your diet to see which ones you might be able to eat and in what serving sizes while still enjoying the low FODMAP foods you can tolerate. After that, you’ll be eating a “Low FODMAP” diet that’s customized for you which allows you to eat foods you can tolerate when in in appropriate serving sizes.