Gasping for air: Stages of hypoxia

In a sense life is a slow to rapid asphyxiation and ironically bouts of asphyxiation are often accompanied by oxidative burst injuries.

In addition, and equally ironically, if we avoid hypoxia and find ways to oxygenate tissues better, we may live longer, but oxygen itself (iron helps) dooms us. And though we are healthier if our tissues are better oxygenated, are we any happier? Maybe not, but possibly so because we can enjoy life more than the “walking dead,” which is what I call those suffering with hypoxia. We die with too little oxygen or we die from a lifetime with too much oxygen or too little defense from the ravages of oxygen rich living.

There are degrees of hypoxia – and thus stages of hypoxia. As we age, our tissues become more hypoxic, and if we do things wrongly, we become more hypoxic more quickly. As tissues become more hypoxic, HIF1 expression increases, mitochondria are selectively degraded, pyruvate dehydrogenase is inhibited by phosphorylation, and cells are reprogrammed to run degenerative metabolism that is a milestone on the way to degenerative diseases like autoimmune diseases, type II diabetes, and cancer.

As we age, our VO2 max decreases noticeably (perhaps 10%) every decade.

What we are doing wrongly accelerates our eventual downfall. Smoking is an obvious thing, and if smoking leads to either COPD or emphysema, it is extremely hypoxic.

But there is so much more. The simple failure to consume sufficient essential fats means that the intricate inner membrane mitochondrial protein structures so critical to running proper OXPHOS are off.

The simple lack of daily fasting (not eating just one meal in 5 hours or less) means that autophagy is inhibited, allowing more junk and particularly more junk mitochondria and junk mitochondrial proteins to accumulate in our cells.

Feasting from an unfasted state accelerates the development of degenerative metabolism – high fat plus poor antioxidant defenses tends to shunt metabolism away from mitochondrial oxidation, while overconsumption of sugars stimulates glycolysis, the production of reactive aldehydes, and lactic acid fermentation, and if coupled with numerous nutrient deficiencies (especially thiamine), sugar fermentation is favored even more over TCA/OXPHOS.

Not consuming enough of critical nutrients such as B12, iron or copper, leads to a near anemic state, and this increases hypoxia, and hypoxia via HIF! favors lactic acid fermentation over TCA/OXPHOS.

Aggravating any degree of anemia are multiple errors one can make in developing circulatory deficiencies, leading to local hypoxias, wherever flow is impeded in any way, including of course basic problems with eNOS.

Breathing contaminated air (especially carbon monoxide) and eating food and drink contaminated with even low levels of respiratory poisons eventually takes it toll. Failure to monitor these critical low level poisonings by routine urinalysis with HPLC-MS means that it is all happening invisibly, and because of this more is blamed on “aging” than is actually deserved.


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