Last year, there was an interesting story about a woman who could smell a certain odour that seemed to be given off by people with Parkinson's (primarily her husband).
"But he was in our control group so he didn't have Parkinson's. "According to him and according to us as well he didn't have Parkinson's. "But eight months later he informed me that he had been diagnosed with Parkinson's.
wow
It has wrecked my life, and I'm fairly convinced it is causing prolonged ketoacidosis. It's also likely that it's exposing me to greatly increased risk of Parkinson's disease, which killed my grandfather and is currently in the process of killing my uncle.
But enough of that sob story. One of the theorised causes of Parkinson's and diseases in the same class is the endogenous formation of persistent prions. Prions are proteins that are 'defective' and fold abnormally.
Your body will likely destroying/metabolise prions in fairly short order; a good thing because newly synthesised proteins (mostly from amino acid metabolism) 'learn' how to fold themselves from other proteins. If they happen to learn from a "prion", one that's likely avoided being metabolised for an abnormally long time, this behaviour can spread and proteins begin to behave abnormally, in some cases forming plaques on vein and arterial structures in the body.
This is obviously bad. It's arguably worse for someone in ketosis, as their brain is burning proteins for fuel door to depleted glyco-something (sorry, the name escapes me, it's the sugar your brain uses for energy). So now some of these prions migrate to various synapses (presumably the most energy hungry ones) and behind to form plaques on these synaptic structures.
In addition, my recent (totally amateur) theory is that ketosis increases the rate of prion occurrence. In ketosis, you're metabolising unusually high levels of amino acids/proteins. So more risk of a bad or incomplete enzymatic reaction. In many cases this metabolism occurs in red blood cells, where amino acids capture, and are broken apart by, hydrogen atoms (ions?).
So now you're entire system is under more oxidative stress, you're burning proteins and synthesising new ones at a high rate, is difficult to stay hydrated due to all these hydrogen atoms going missing, and one of the byproducts of some AA hydrogenation is ultimately acetone (paint striper). Also the metabolites are highly acidic, which unbalances your plasma pH levels and further interferes with normal metabolic processes. Interestingly is not necessarily unbalanced towards 'acid', as one might expect. The reasons are still unclear to me, but I'm guessing it's something like "homeostasis gone mad".
And acetone is what dogs can be trained to detect: to try and rid your body of the excess acetone, you start respiring (exhaling) acetone, with its trademark "over ripe fruit" smell.
It doesn't make sense to say newly synthesised proteins arises mostly from amino acid metabolism, metabolism involves both catabolism (breakdown) and anabolism (synthesis). Amino acid degradation results in glucose via gluconeogenesis or cellular energy (ATP), whereas amino acid synthesis is of course what is used for proteins, as proteins are made of amino acids. So yeah, doesn't really make sense. Perhaps you meant to say that newly synthesised protein uses amino acids of which are most often sourced from proteolysis?
As for red blood cells, they don't have any mitochondria, so they only metabolise glucose and other sugars (and anaerobically at that, due to their function of carrying oxygen). They certainly don't metabolise amino acids or proteins, so I'm not sure where you got that idea from.
I hope that helps.
I'm probably on the wrong end of the metabolic semantics here; I was specifically referring to hydrolysis (or is the correct term hydrogenation?) occurring in red-blood cells. If this is not considered part of normal metabolic processed then mea culpa. The particular (pro)drug I mentioned (likely) relies on this mechanism to cleave/dissolve a covalent bond between the two constituents of the prodrug, to produce a 'time-release' effect: the constituents being l-lysine and dexamfetamine/dextroamphetamine ('lisdexamfetamine').
For example, here's one of the few serious studies I've been able to find on its metabolism (i.e. not a single dose study that concludes 'yes, this leads to amphetamine in the blood'): http://www.tandfonline.com/doi/full/10.3109/21556660.2013.77... . There was another (better) one somewhere on pubmed, but I can't seem to find it atm (although it was also an in vitro study). I also found this, more general paper, quite interesting (although I'm guessing it's outdated?): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142344/
I admit, my understanding of the process by which amino-acids are synthesised in to proteins in vivo is not the best. I'm actually a little hazy on how I first arrived at the notion that an over-abundance of l-lysine could disrupt the Krebs-cycle. I probably came up with it during one of my long treks across Wikipedia, so it's very likely wrong....