Hyperbaric oxygen therapy diabetes / obesity hypothesis – part three including references

Concluded from part 2 including references.

Glycogenesis, Gluconeogenesis and Glyceroneogenisis

Borrowing from past college nutrition lectures, where microbiology and physiology were also studied, and from online content for wording, I present brief definitions below. These are presented as a layman with quoted secondary citation.  

Glycogenesis [19 – Encyclopaedia Britannica] – can be described as the process of glycogen creation, in which glucose molecules are added to chains of glycogen for storage. This process is activated during rest periods following the Cori Cycle in the liver and also activated by insulin in response to high glucose levels, for example after a carbohydrate-containing meal. IE Placing polysaccharide into cells which forms glucose on hydrolysis. The making of glycogen from sugar.

Gluconeogenesis (GNG) [20 – Silva et al – 2009] is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates. From breakdown of proteins, these substrates include glucogenic amino acids from breakdown of lipids (such as triglycerides), they include glycerol (The backbone of lipids known as triglycerides); and from other steps in metabolism they include pyruvate and lactate.

Gluconeogenesis is one of several main mechanisms used by humans and many other animals to maintain blood glucose levels, avoiding low levels (hypoglycaemia). Other means include the degradation of glycogen (glycogenolysis),[1] fatty acid breakdown and fatty acid catabolism.

Glyceroneogenesis [21 – Nye et al 2008] is a metabolic pathway which synthesizes glycerol 3-phosphate or triglyceride from precursors other than glucose. Usually glycerol 3-phosphate is generated from glucose by glycolysis, but when glucose concentration drops in the cytoso (The cytosol or cytoplasmic matrix is the liquid found inside cells) it is generated by another pathway called glyceroneogenisis. Glyceroneogenesis uses pyruvate, alanine, glutamine (Alpha keto and amino acids). Glyceroneogenesis can be observed in adipose tissue and also the liver. It is a significant biochemical pathway which regulates cytosolic lipid levels. Intense suppression of glyceroneogenisis may lead to metabolic disorder such as type 2 diabetes

As mentioned, from a non-medical perspective, any understanding of the above 3 concepts is layman in nature and comments are as such.

In short and in layman’s terms,

Glycogenesis is the creation of glycogen which is a stored form of polysaccharide glucose in the muscle cells and liver. This is the inward journey of nutrients on their way through the liver and being converted into usable sugar in cells containing mitochondria, as a secondary storage means for energy in the body.

Gluconeogenesis is the internal process by which the body creates useable glucose from stored energy sources including proteins and fats (triglycerides) It produces glucose in the blood stream which, in heathy individuals with normal insulin response, is then available to cytoso.

Glyceroneogenisis is the process similar to gluconeogenesis but Instead of producing fructose 1,6- bisphosphate as gluconeogenesis does, Glyceroneogenisis converts dihydroxyacetone phosphate to glycerol 3-phosphate. This happens with the aid of Alpha Keto and Amino acids in the liver and adipose tissue. It’s the similar early stages of both Glyceroneogenisis and gluconeogenesis that are relevant to this discussion. HBOT is speculated to be an up regulator of Glyceroneogenis in adipose tissue as opposed to treating with down regulation of the process in the liver to reduce the triglyceride being released in to the bloodstream from the liver.

It’s that mechanism or process of Glyceroneogenisis, and its shared processes with gluconeogenesis, that causes type 2 diabetes when it fails or become supressed in the adipose tissue. And it fails because there is no signalling to trigger the process when blood sugar levels remain high because of poor insulin response. Without a reduction in blood sugar levels this process is not triggered. [18]

HBOT stimulates this process in adipose tissue, providing relief from suppression of the cycle allowing cells to respond better to natural insulin, cell gateways to open, allowing blood sugar levels to come down after moving sugars into the intra cellular fluid. Thus, lowering blood sugar levels and triggering glyceroneogenisis and gluconeogenesis. The pathway for converting fat back to sugar and using it up as energy at the intracellular level via means of better Adenosine Triphosphate (ATP) function and better regulated intra cellular energy use.

Insulin response is key to breaking the obesity cycle. Without effective insulin response, glyceroneogenisis is not triggered in adipose tissue and it stalls. In some cases, the body burns fat directly leaving behind ketone acids, (not to be confused with healthy ketosis), which can cause further damage to the kidneys. Artificially increasing insulin levels works as a short-term measure, but also further desensitises cells and further inhibits glyceroneogenisis in adipose tissue. A reasonable argument in favour of HBOT as a treatment method. Lower blood sugar results in lower insulin levels in type 2 diabetics, allowing for a better balance between glyceroneogenisis in the liver and adipose tissue.

Consideration must be given, for that which has been considered a potentially dangerous side effect for hypoglycaemic patients, is actually a positive treatment for hyperglycaemic ones.

Dive supervisor and chamber operator teaching dictates that one should watch out for blood sugar drop outs and unconsciousness. Why not put this to use for people who don’t want to take Metformin or who are unable to, or indeed for those who have become desensitised to its effects over time and also as a replacement for either naturally, (vine leaf) or artificially increasing insulin in the blood stream as a form of treatment.

The effect will be twofold at least. A loss of weight, and also effective insulin response management.

An interesting study to look at was conducted and published by the Rubicon Foundation which states;


This would suggest an improved use of glycogen as energy, resulting in rapid weight loss, following replacement of that glycogen from adipose tissue, following treatment.

Stem Cells, Genetics and Mitosis

As a diver, it starts to get beyond my scope of study when we reach topics such as genetics. It is proposed that such a connection nonetheless exists. Owing to various life experiences, I have encountered the subject of genetics before and have had to develop my own understanding of them to a level where I could at least have a conversation.

Understanding lies in the knowledge that the body cells are regularly replaced by new cells every so often and in differing time scales depending on which cells we are talking about. The new cells copy the old cells and so on. For the purposes of this discussion neurons will be left out for now. While I have my own thoughts and beliefs on the regeneration of neurons they are somewhat unsubstantiated save fringe science studies into epigenetics and neuroplasticity, although modern research does claim to be able to convert glial cells into neurons but that’s another discussion. (Since this writing, further studies have confirmed this.) [23 Boldrini et al – 2018]

There are two sides to this section.

The known fact that our bodies replace cells from time to time, and also the known fact that those cells are ‘copied’ in accordance with the DNA or RNA present in the cell being copied. This is why scar tissue remains scar tissue for life. Whether that is regular scar tissue or, say for example, scaring to the myelin sheath in multiple sclerosis patients. Hence the medical standpoint that MS is only manageable and not reversible. We also know that HBOT stimulates the release of stem cells which are essentially brand new, ‘un-programmed’ cells likened with a foetal state cell.

It is also theorised that HBOT treatments effect genetic expression and effect the protein inside a cell. In the time leading up to becoming a diabetic the genetic expression of cells is to respond to insulin. Over time and excessive exposure to very high levels of insulin, and an imbalance in glyceroneogenisis between the liver and adipose tissue, those cells become less sensitive to insulin following a change in genetic expression brought about by a desensitisation to insulin. The result is a metabolic disorder.

In type 2 diabetics, there is generally plenty of insulin around, as generally the pancreas still functions. The body just doesn’t respond to it like it did before. This can also explain sudden hypoglycaemia and even unconsciousness in some patients whose blood glucose drops by as much as 10 mmol/l upon pressurisation. (referenced above). In fact, it is a described side effect and technicians and attendants are warned to keep an eye out for it even in non-diabetic patients. Sudden improvement in insulin sensitivity makes available an adequate supply of insulin in the blood to the cells that weren’t responding until pressurisation. [1 – Heyboer et al 2017]

Is the perception of an irreversible condition, perhaps owing to the gradual change in genetic expression over time, to a point where the condition is seemingly irreversible because any new cells are simply copies made of the faulty ones they are replacing. What if they weren’t? What if the cells being replaced were at optimal function at the time of replacement? Surely, they would be copied with a different genetic expression reversing at least that one cells insulin resistance?

Could the result of long term treatment be, that as cells are replaced with new ones, from an increased release of stem cells cascading as a result of HBOT, [24 – Thom et al – 2018] , those new cells are replaced at least at a higher level of function as it pertains to insulin response, thus providing a permanent, and if not complete, then partial and sustained reversal of the condition?

Treatment would then be multi-faceted. It would treat the immediate issue of poor insulin response, to reduce blood sugar in the immediate, thus preserving existing capillary structures and halting damage cause by high levels of glycated haemoglobin. While also treating consequential conditions like foot ulcers, problematic wounds, retinopathy, kidney disease and chronic kidney disease (CKD) by means of revascularisation of the kidneys and also potentially treat cells at a genetic level, leaving new cells in a better state of function and expression than their predecessors. They would then be able to signal the metabolic process better than before on their own without treatment. Thus undoing the cellular damage caused in the first instance.

Have any studies been conducted of the long-term effect of HBOT on the ongoing change in cellular response to insulin and the associated metabolic functions that go with it? Existing research suggests that more data are needed, but also suggests this is indeed the case.

Following long term treatment, perhaps 3 to 4 months, it could then prove valuable to maintain a program of regular home treatments in the form of Mild HBOT and soft shell chambers to maintain an ongoing effect.

Dare I say… Conclusion

I conclude, at least to my own sensibilities and thoughts, that hyperbaric oxygen therapy would indeed improve ATP function, up regulate glyceroneogenisis in adipose tissue, support metabolism in the long term and re-write the genetic expression of damaged cells, providing a long-term reversal of metabolic challenges such as type 2 diabetes, brought about by insulin resistance and uncontrollable obesity. Making life a lot more pleasant for many.

The referenced study at [25] here would seem to support these ideas. [25 – Wilkinson et al – 2015]

Thoughts on Pollution

As an aside and addition to these comments on localised pollution.

Some time ago I contacted the European Air Quality Commission as well as Public Health England to no avail.

This is rather an anecdotal aside but worth a comment since medical professionals I have discussed it with agree.

In 2016 I travelled to New Zealand where the air was cleaner than where I live in the UK. I had no problem losing weight. I lost around a kilogram a week for about 10 weeks before my return to the UK.

Nothing else had changed. I remained on the same low carb diet I had been, my activity was stable. The only change was location and consequently air quality.

Doctors and I speculated that owing to factory effluent in the area I live in, in the UK, and NHS Drager measurements of high carbon monoxide in my blood (18ppm), that what was an already challenged metabolism, was pushed just that little bit further and compromised beyond the point of being able to self-regulate the whole metabolic process and glucose cycle.

Consequently, I have put a lot of it back on in the 8 months since my return. As we know carbon monoxide bonds with haemoglobin 100 times more efficiently than oxygen does, (Hence the only good treatment for CO poisoning is HBOT). Lower oxygen transport to cells leads to lower metabolic function and while it may only be a few percentage points on TPo2 levels it could, in some cases, be the difference between losing weight gradually and not losing weight at all and perpetuating the problem.

This further supports, that even if only a small measure of difference, HBOT treatments could well move patients just over that line between downward spiral; and upward improvement in their lives.


© Copyright 2017

Funding Statement: The author declares that no funding was received for, and no conflict of interest exists in, the production of this article.


  1. Marvin Heyboer et al – 2017
  • US Navy Diving Manual Revision 7 – Naval Systems Command – 2017 – Volume 1 Underwater Physiology and Diving Disorders
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