A warning to anyone thinking of trying the low PRAL diet: if you’re not in a state of acidosis, it could push you into alkalosis, which you also don’t want to be in.
So please be cautious, a diet may not sound too risky, but these diets do real things in the body #TheAcidTest
Personally the low PRAL diet won’t be something I will try.
My lactic acid levels are elevated, yes, but that does not mean acidosis.
Typically between 2-4mmol/l are not indicative of lactic acidosis unless blood pH is also acidic patient.info/doctor/lactic-…
Levels of lactate between 2-4mmol/L may even be beneficial: “Lactate itself is not toxic or harmful & there is some evidence that Hyperlactatemia may be beneficial in some conditions, e.g traumatic brain injury & severe hypoglycaemia…as a metabolic fuel” ep.bmj.com/content/106/3/…
So whilst it’s interesting and gives clues as to what’s going on, caution is required for anyone attempting an intervention. Some may feel better with lower lactate, but others may feel worse.
I’ve also had the sodium bicarbonate level in my blood tested which shows no indication of acidosis or alkalosis so it’s not a balance I want to mess with.
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Hmmm 🤔 blood tests result pinged in, my phosphate is 0.83mmol/L and the Serum phosphate normal range is 0.83–1.63 mmol/l in healthy adults. Right on the edge of low/not low.
“Phosphate is involved in many critically important biochemical processes including energy metabolism, nucleic acid metabolism, cell signaling, bone formation, and maintenance of acid–base balance”
And this is probably why: “Increased renal clearance of phosphorus occurs in…hyperglycemic states”, which fits with my fasting Glycemia.
I’m always hot after I eat my evening meal so decided to check my PI and yep, best I’ve ever seen it (usually under 1.5)! Supports eating causing improved blood flow. But…my SPO2 is the lowest I’ve ever seen it. Never seen it go below 98%
Only other times I’ve managed to improve my PI% have been my using a hot water bottle on my abdomen (but it only went from 1.5% to 5.7%), or by laying down in bed & heating myself with a hair dryer, where my PI% went over 15% for the first time.
And I’ve been resting different fingers: each finger has different values but my left hand has consistently lower perfusion than my right, which ties in with blood tests where they can never find a good vein on the left!
Hospital trip yesterday about POTS. The doctor was also researcher in blood pressure so he was actually great & was very interested in the data I gave him on my BP, glucose & lactate. Couldn’t offer any help I haven’t already tried but ordered a ton of bloods & a tilt test.
Unfortunately my blood didn’t want to come out & I ended up at the hospital an extra 2 hours & extremely stressed. They finally got some out but as usual the phlebotomist was amazed at how my blood simply wouldn’t come out.
Fully exhausted and felt awful after, hoping the PEM won’t be too bad this coming week now 🤞🏻
As usual despite exhaustion, overdoing it meant I really struggled to sleep 😴 only managed it with a piece of melatonin gummy every few hours when I woke up wide awake.
Exercise is contraindicated for people with ME/CFS. Full stop.
Those with mild disease may be able to do some gentle exercise, or even occasional long walks, but the body simply doesn’t respond the way it should. Exercise = stress for the body. Healthy bodies adapt, ours don’t.
Cardio exercise especially always carries risk for those with ME/CFS. Even when it’s mild. The usual benefits that healthy people experience from adapting to exercise don’t occur. Cumulative physical stress from regular exercise with ME/CFS may lead to a decline in condition.
Most of us do too much, because we hate being limited, we don’t want to be. But we are.
When I say “exercise is contraindicated” I am referring especially to it being prescribed as treatment.
Movement is important, as much as can be safely done, but movement ≠ exercise.
Most of us are now familiar with #POTS but there are different types: hypovolemic, neuropathic & hyperadrenergic.
The hyperadrenergic form may be genetically determined & involves blood pressure increase when standing & elevations in adrenaline healthrising.org/blog/2018/08/1…
“Grubb’s 2011 study described hyperadrenergic POTS as having an increase in systolic blood pressure of ≥ 10 mm Hg during a tilt table test with rapid heart beat (tachycardia) or serum norepinephnrine levels that were greater than 600 pg/mL upon standing”
“the key symptomatic differences in hyperadrenergic vs non-hyperadrenergic POTS were increased dizziness, headache, and tremulousness in hyperadrenergic patients. (Tremulousness refers to trembling, quivering, or shaking hands, voice, etc.)”
“Compared to uninfected controls, COVID-19 patients of all age groups had severe GSH deficiency, increased OxS and elevated oxidant damage which worsened with advancing age. These defects were also present in younger age groups, where they do not normally occur”