It's wrong. Why are you talking about cyanide, a deadly, industrial poisonous gas?

"Well I read statches when heated form acrylamide. Enzymes catalyse ''cooking' so I thought it'd be a byproduct in the body as well."

Acrylamide is formed on the barbecue grill @ 500 degrees temperature, but definitely not in our bodies - that notion is strictly out of question. Period.

"I know these scenarios are extremely implausible and unlikely, but unlikely things do and can occur so they must be considered before we are so quick to dismiss SHC."

You know how absurd your theories are. Why don't you go ahead and test them out if you're that passionate about this pseudo-condition?

I gave another theory... the body constantly produces Hydrogen Peroxide and Acetone as a metabolic byproduct. When these two chemicals combine they produce Acetone Peroxide. Acetone Peroxide is insoluble in water, and will hence accumulate. It isn't toxic but is an explosive and can burn spontaneously, even underwater, in the slightest amounts.

Could you show me an article that states humans produce acetone as a waste product?

Here:

Human Metabolome Database

Search ''Acetone''.

It's pretty common knowledge in the world of biochemistry and especially to diabetics. If you look up hydrogen peroxide, you will see HMDB also declares it as another endogenous byproduct.

Let's say you form aqueous acetone peroxide. Then what happens?

Acetone peroxide can detonate or catch fire spontaneously, and it can explode even when wet.
Acetone peroxide is insoluble - you can't actually form an aqueous solution of it. Because of this, it can accumulate easily.

Please provide source.


Where will it accumulate? Inside cells? If that happens, macrophages will come and destroy that cell.

Hi GaiaGirl95,

How come you're not logging into your account instead of posting as a guest?

I don't currently have my home PC right now, which my login data is stored on. I should get it back by tomorrow though. For now I can only reply as a guest.

And a YouTube video titled ''Acetone Peroxide Explosion Montage'' shows AP detonating when underwater.

Explosion Video of the Week: TATP | Popular Science says: ''Note: TATP is still explosive when it's wet, so it's probably one of the reasons for the TSA's draconian rules about liquids.)''

How much AP is required to cause an explosion? If you can think of any disorder that produces the chemicals needed to make AP within the cell, then you probably got something going, but all of these thoughts are assumptions. Theories are not built on assumptions. In addition, what fuels AP once it is burning /releasing energy?

AP is its own oxidizer.. so it will continue to burn until it has used itself up.
Only about a gram or so is required to achieve a fire from AP. AP is insoluble, so if cells are producing a higher than normal concentration of acetone and HP (can happen. Catalase deficiency + diabetes?) in your cells, then by logic you should be accumulating AP.

Now all you have to do is prove if there are any proven biochemical pathways that will produce acetone and HP. If you can, then you are a ticking time bomb!

From PUBCHEM: Compound Summary for: CID 180
Acetone
Also known as: 2-propanone, propanone, Dimethyl ketone, Methyl ketone, Pyroacetic ether, Dimethylformaldehyde, beta-Ketopropane, Dimethylketal
Molecular Formula: C3H6O   Molecular Weight: 58.07914   InChIKey: CSCPPACGZOOCGX-UHFFFAOYSA-N
A colorless liquid used as a solvent and an antiseptic. It is one of the ketone bodies produced during ketoacidosis.   From: MeSH''


NCIBI.GOV:
''The cellular production of hydrogen peroxide.''

''1. The enzyme-substrate complex of yeast cytochrome c peroxidase is used as a sensitive, specific and accurate spectrophotometric H(2)O(2) indicator. 2. The cytochrome c peroxidase assay is suitable for use with subcellular fractions from tissue homogenates as well as with pure enzyme systems to measure H(2)O(2) generation. 3. Mitochondrial substrates entering the respiratory chain on the substrate side of the antimycin A-sensitive site support the mitochondrial generation of H(2)O(2). Succinate, the most effective substrate, yields H(2)O(2) at a rate of 0.5nmol/min per mg of protein in state 4. H(2)O(2) generation is decreased in the state 4-->state 3 transition. 4. In the combined mitochondrial-peroxisomal fraction of rat liver the changes in the mitochondrial generation of H(2)O(2) modulated by substrate, ADP and antimycin A are followed by parallel changes in the saturation of the intraperoxisomal catalase intermediate. 5. Peroxisomes supplemented with uric acid generate extraperoxisomal H(2)O(2) at a rate (8.6-16.4nmol/min per mg of protein) that corresponds to 42-61% of the rate of uric acid oxidation. Addition of azide increases these H(2)O(2) rates by a factor of 1.4-1.7. 6. The concentration of cytosolic uric acid is shown to vary during the isolation of the cellular fractions. 7. Microsomal fractions produce H(2)O(2) (up to 1.7nmol/min per mg of protein) at a ratio of 0.71-0.86mol of H(2)O(2)/mol of NADP(+) during the oxidation of NADPH. H(2)O(2) is also generated (6-25%) during the microsomal oxidation of NADH (0.06-0.025mol of H(2)O(2)/mol of NAD(+)). 8. Estimation of the rates of production of H(2)O(2) under physiological conditions can be made on the basis of the rates with the isolated fractions. The tentative value of 90nmol of H(2)O(2)/min per g of liver at 22 degrees C serves as a crude approximation to evaluate the biochemical impact of H(2)O(2) on cellular metabolism.''

Peroxisome - Wikipedia, the free encyclopedia
D-amino acid oxidase and acyl-CoA oxidase produce H2O2:

acyl-CoA + O2 \rightleftharpoons  trans-2,3-dehydroacyl-CoA + H2O2