Just thought everyone should know. I might be dying soon, but you already knew that, lol.
I've gotten past the idea of dwelling on it and have accepted it for what it is, so I haven't been making a big deal about it. I don't remember the exact order of events, but I do remember the 'big one' was waking up one morning, bending over to clean a mess on the floor and lifting back up, I felt a sharp quick pain deep in my chest. Found that weird, so reattempted; it repeated. Ate some spinach, making sure to extract the juices for quick nitrate absorption, and wasn't able to repeat it, despite trying over and over again. Yep, this was the 'nitrate test', essentially, another person recommended to indicate the underlying issue (Or rule it out). Then I felt sleepy an hour later, so I went to bed, got up about 40 minutes later, and noticed I felt an incredible sense of 'dread'. Not anxiety, per se, as in a panic attack, but dread, as if something was pretty darn wrong. Found myself getting short of breath (hurried, shallow breaths) and this feeling lasted for about 4 hours and the underlying feeling persisted throughout the day. It's been pretty weird since, getting this pretty persistent middle back pain (Between the shoulder blades, pretty much corresponds to the area right above the sternum), occasionally chest burning and pressure sensations that last 30 seconds, woke up to incredible middle back pain and anxiety this morning, found I was a bit confused until I 'ran' the confusion off. I'm just going with it for now, because I think I might have just injured my midback and this morning sequalue is nothing particularly indicative of anything progressively sinister when doing the dead lift. And... ohoh... look, I just found the irony in the name of the exercise. Doing the deadlift, you might just end up dead. God, why didn't anybody warn me?! lol. I'm joking, I've obviously been slacking off on the exercise ever since getting back home and the early northern nights and the sparse hours to the day, typically mean I don't get much exercise in (Especially now the business is running in the exercise room).
Anyway, I found someone else's personal experience with waking with that 'feeling of dread'. He then started pouring out the sweat and later died. Granted, he was in his 60s/70s, but similar experience, just different personal timelines. And, I've seen other people's comments on waking with panic attacks, then two years later, waking up and not being able to breath. Yep, I'm insightful enough to know what's going on there - heart failure. Nocturnal panic attacks were simply the first obvious sign. Anyway, you might think that heart failure is incredibly rare for younger persons; Haha, this isn't true! It's actually pretty darn common.
Oh, that's right. The day before the big one, I was noticing this persisting mid pain and left arm numbness throughout the day. The next day, i figured it was probably because I was anxious throughout the entire day trying to get the huge backlog of orders out in a timely manner, but if that were true (it's merely anxiety and transient), I wouldn't expect the symptoms to be persistently prominent as they are now.
Anyway, just thought everyone should know, the midback is actually a pretty common initial site for cardiac pain to manifest, and that's because the heart is attached to the spine via ligaments. When the pain becomes more pronounced, it then normally starts appearing in the chest. The reason why midback pain is not normally associated with cardiac causes is likely because back pain is usually assumed to be normal and quite common and dismissed as such. No one ever suspects nearby organs might be causing it, until it later makes itself obvious as it progresses.
Anyway, I know the midback backpain is of cardiac origin because in certain positions, the pain pulses in sync with the heartbeat. In other positions, it's pretty constant (Until it fades after 10 seconds as your mind gets 'used' to the pain signal, and tunes it out). Normally, as least at the moment and most of today, it's not really noticeable.
And, how do I /really/ know the big one was heart related? I checked my EKG. Under normal circumstances, I'd suspect hypoglycemia, but with the constellation of symptoms, I'm suspecting something cardiac. Probably not a heart attack, per se, (Didn't see any of the classic indicative waveforms -> ST elevation, R wave really diminished, hyper acute T wave, inverted U wave, etc.), but definitely not a normal healthy trace. Anyway, I knew hypoglycemia was likely happening that day as that sugary greek yogurt tasted especially satisfying. I ran out of grains the day before, and coincidently ran out of fruit, and I was pretty darn busy, so I most likely didn't eat enough the day before.
I think I should really have a glucose meter on hand to complement the ECG. Coincidentally, it's what the emergency personnel use. If only the strips weren't so prohibitively expensive as they are in the USA.
Well, actually, R wave was half the usual height. Impaired left ventricular contraction and reduced cardiac output seems to match the symptoms, so I guess it was confirming something that wasn't looking good. I don't understand how exactly that would stop one from being able to hold their breath for more than 3 seconds? That morning, I just could not hold my breath for more than 3 seconds; even though my breathing appeared 'normal' by that time, I definitely could not hold it without gasping for air as if I was desperate for it. Any other time, any other day, I can easily hold it for more than 30 seconds.
If I had a CO2 meter, I could probably confirm if serum CO2 levels were too high. This would be suggestive of panicky hyperventilation. More medical devices I need; a blood glucose meter, and a CO2 meter.
- See, .5%. 1 out of 200. (Or, wait, is that actually .3%? 1 out of 300.)
I'm still speculating on the inability to hold my breath. Perhaps serum O2 levels were low (Didn't seem low earlier on the oximeter). Perhaps serum CO2 were high (Unconfirmed). Is there any other reason why one would be unable to hold your breath? The reason why one feels compelled to breath after so many seconds of holding your breath, is because O2 gets used up in the ATP process in the mitocondria of the many cells that metabolise (serum o2 and serum glucose), and serum CO2 is the cellular byproduct, and after 30 seconds or so, the O2 starts to decline and CO2 starts to build up (CO2 displaces the O2, so once CO2 becomes high enough, it compels the body to exhale the serum CO2 and inhale more O2). You can see the decline in O2 with an oximeter. You could also probably see the increase in serum CO2 with a CO2 meter.
Interesting, if O2 and CHO create CO2, what happens to the H? It must also be producing water. And, hey, it is according to https://en.wikipedia.org/wiki/Glycolysis
Huh, interesting, it seems fructose drives up Triglycerides. Apples are noteworthy for their high fructose content, what's the research on that?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093779/
Results:
Total polyphenols and fibers were 485 mg/kg and 4.03 g/100g in fresh apple respectively. After 8 weeks, significant statistical differences were observed considering the TG and VLDL levels between two groups, but no significant differences were observed regarding TC, LDL-C, HDL-C, Apo (B), Lp (a) and LDL/HDL ratio.
Conclusions:
Consumption of Golden delicious apple may be increased serum TG and VLDL in hyperlipidemic and overweight men. We need more studies to assay the effect of apple consumption on serum TC, LDL-C, HDL-C, Apo (B), Lp (a) and LDL/HDL ratio.
Interesting, I wonder if glucose has a similar affect on Triglyceride production as fructose? It seems that glucose would have to be converted into fructose before it could be converted into triglycerides, and that probably doesn't happen that much since glucose is the body's preferred source of energy.
Anyway, seems like now might be a good time to limit apple consumption, lol. (Might as well, it's not a tropical fruit and definitely doesn't have as much magnesium and potassium as tropical fruits, and has disproportionately more sugar)
http://onlinelibrary.wiley.com/doi/10.1111/j.0954-6820.1972.tb05338.x/abstract
Sucrose caused a significant increase of triglyceride concentration above that measured during fructose and starch diets. Diabetics were not included into the sucrose group, however. The fractional removal rate of plasma triglycerides was identical during all three diets but the triglyceride production rate showed a rising trend during fructose and, particularly, during sucrose diet as compared to starch. Because of the limited number of subjects studied so far, these results do not justify any definite conclusions.
This would sort of make sense, since sucrose is split into glucose and fructose by the body. What about dietary glucose (i.e., corn)?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682989/
When dietary glucose and fructose have been directly compared at ∼20–25% of energy over a 4- to 6-wk period, dietary fructose caused significant increases in fasting TG and LDL cholesterol concentrations, whereas dietary glucose did not, but dietary glucose did increase serum glucose and insulin concentrations in the postprandial state whereas dietary fructose did not.
Wait, you're telling me sucrose/fructose consumption (But not glucose, i.e., unadulterated natural corn) is the main culprit behind LDL? (And, not animal consumption like I've seen elsewhere.) Well then, that could then more easily explain the association with excessive sugar and fructose consumption and mortal illness.
Research found that within three weeks, among 4,587 people who came to the Pritikin Longevity Center, LDL cholesterol fell on average 23%. Non-HDL dropped 24%. Children respond well, too. In one study,7 the LDL cholesterol levels of American kids plummeted 25% after two weeks at Pritikin.
Now I'm so curious. How is starch converted into serum glucose? (I wonder if I can find it up there)
healthyeating.sfgate.com/types-carbohydrates-turn-sugar-3322.html
Plants form starches, which are also called complex carbohydrates, by stringing together sugars. When you eat starchy foods, the starches are broken down into sugars, including glucose, maltotriose and maltose, by an enzyme called amylase found in your saliva and small intestine.
Okay, how is maltose metabolized? [metabolic pathway]
https://en.wikipedia.org/wiki/Maltose
In humans, maltose is broken down by the enzyme maltase so that there are two glucose molecules from which the glucose metabolism obtains energy.
So, really, it just directly breaks down into two glucose molecules with no other byproducts?
What about maltiose metabolism?
Maltotriose is a trisaccharide (three-part sugar) consisting of three glucose molecules linked with α-1,4 glycosidic bonds
Oh, so probably the same thing. It's just broken directly down into three glucose molecules.
Glucose
Maltose
Maltriotiose
Anyway, this is fascinating, because the carb rich starchy plants are largely the root vegetables. Carrots, Green Peas, Sweet Potatoes(Okinawa Staple), Potatos, Cassava(African staple), etc.; the fruits themselves are largely rich with sucrose, with apples and pears leaning towards fructose and corn towards glucose. Anyway, this is fascinating, because the longest living cultures primarily consumed starchy foods. The exception being (most) American and South American tribal cultures, consuming maize/corn [which is comprised of mostly glucose].
What's also interesting about the fact that sucrose/fructose will significantly increase LDL/Triglycerides, but not glucose[nor its double or triple chain form as common when consuming starchy plants: maltose and maltitriose], is that Staphylcoccus Aureus will consume and grow in the presence of sucrose/fructose but not glucose. I assume at least some of this bacteria interfaces with the immune system in the digestive tract, causing inflammation. This suicide mission of phagocytes in engulfing the staph, causes the dead phagocytes to stick to the kidney and vessel walls in calcium cholesterol deposits. I'm not sure if any of the dead phagocytes get pushed out through the urine. The question of how this process is connected to increased LDL/Triglycerides would be interesting to know, if it's connected at all (Seems like it probably is, unless fructose is connected to LDL somehow outside of its association with the dead phagocyte(killed staph aureus)->calcium/cholesterol deposit. Perhaps LDL is created when cholesterol is used to create the calcium/cholesterol deposit to entomb and attach the dead phagocyte to the vessel walls. This would also explain why dirty foods, such as burgers and cow/pig meat, also increases LDL - through the bacteria -> dead phagocyte -> calcium/cholestorol deposit -> LDL cholesterol as byproduct connection.).