Why Ketosis is not a “one-size-fits-all” Approach

Why Ketosis is not a one-size-fits-all Approach

Intro

As I get deeper into my studies of genetics and epigenetics, evolutionary biology and the quantum field theory, I’m more inclined to embrace a “one-size-does-NOT-fit-all” approach to optimal living. That’s why I currently think that not everyone will do well in a ketotic state.

First of all, even though many of us are very similar genetically, there are variances that can make us respond differently to environment stimuli and to food.

Why not?

I will connect this thought with a recent blogpost of Peter from Hyperlipid. He discusses a research study on Arctic populations who exhibit a deleterious mutation in the CPT1A gene [1].

This gene encodes for the liver enzyme carnitine palmitoyltransferase 1A, which is responsible in the transport of long chain fatty acids into the inner mitochondrial membrane. A mutation in the gene may lead to a dysfunctional enzyme or the enzyme not being created at all.

This in turn can negatively impact the delivery of long-chain-fatty-acids inside the mitochondria, making fat metabolism very difficult.

“As a result, these fatty acids cannot enter mitochondria and be converted to energy.”[2]

During times of fasting or even during sleep (overnight fasting) this deficiency can “lead to low blood sugar and hypoketosis”[2]. I think this can be fatal, but there are ways to mitigate the condition. For more info, check out Peter’s blogpost.

Secondly, I think that long-term ketosis should not be the holy grail of optimal living unless one is able to see the bigger picture and do it properly. If your hormone signaling is disrupted (preponderantly in women), then you should focus on improving hormonal signaling through different approaches and not stick to ketosis when you see it not working.

Increasing the diversity of good bacteria in your gut (eliminating gut dysbiosis), fixing cortisol signaling, improving your circadian clock are only few approaches that could be helpful. And this should make you see that the entire concept of optimal health goes beyond food.

There’s no perfect health diet for all, or even for the majority of people. There’s no strict ketosis or carb-loading as single best approaches to build muscle. There are many ways to do it. In fact, sometimes it’s healthier to move away from food.

Hint: If you don’t cope with the idea of fasting, you may be a sugar burner.

Muscle, Ketones, and Protein

Conversely, if all parameters are optimal and you can do ketosis, prolonged ketosis and keto-adaptation will allow your muscles to efficiently use ketones for fuel (thus reducing protein and sugar intake would be rational) making them insulin resistant to a certain point. This is elegantly shown in a blogpost from Bill at caloriesproper.

That is one of the reasons that I do not find it normal to be obsessed on protein intake if you are keto-adapted. Yet again, very few folks have perfected this status.

Your body does not require as much protein as people on the forums and groups are talking about. You do not need to activate insulin, IGF-1, and mTOR pathways to build muscle. It is not the only way. Besides, not many people know that these pathways are also responsible for the proliferation of cancerous tumors.

Tumors often occur when DNA is not replicated correctly. This leads to new cells that are deficient (and do not undergo apoptosis). They keep on replicating at faster pace. This is present in every human, to a certain degree. Lifestyle choices and environmental stimuli differentiates between tumors growing out of control (fueled partially by the pathways mentioned above) and cells that are being fixed or killed when the body prioritizes healing and repair processes.

I would personally focus on activating the AMPk pathway allowing the body to focus on repair and healing and more efficiently using the protein I provide to build muscle. Increasing GH levels while AMPk is activated (can be achieved by prolonged fasting – 18+ hours) can be one way to do it more rationally. This is not easy because if you constantly increase your insulin levels, it may have a powerful negative effect on hunger and cravings and may not let you go without food for more than a couple of hours.

When your muscles become partially insulin resistant, the little sugar you provide through food (fibre-rich-nutrient-rich carbohydrates) mostly goes to your brain to satisfy 25-35% percent of its daily energy needs. A keto-adapted individual or a person undergoing prolonged fasting will provide the rest of 60-75% of brain fuel from ketone bodies and other substrates.

George Cahil brilliantly explains the mechanism in his papers on fasting and starvation [3].

Back to the Basics

There may be other mutations similar or different to the CPT1A deficiency that would prevent for an efficient fatty acid metabolism. This would urge to carefully seeking nutritional approaches that are compatible with life; and ketosis would be not a good solution.

I made the case in a recent article that if it were to choose from a low-carb approach and a keto-approach to nutrition (other factors being optimal), it would be better to go ketotic because it is easier and more efficient if you are able to stick to it.

But if there’s one common ground that we should all try to agree on, that is of reducing the amount of sugar we consume in our diets.

Conclusion

When it comes to eating habits, I personally want to stick to ketosis and maintain my keto-adaptation status for as long as I find it beneficial and compatible with the other areas of my life because it allows me to: fast for prolonged periods of time, consume less protein, it gives my muscles the ability to burn ketones, and it dramatically reduces hunger and cravings allowing me to maintain higher energy levels throughout the day.

References:

1. Clemente, F. J., Cardona, A., Inchley, C. E., Peter, B. M., Jacobs, G., Pagani, L., … & Kivisild, T. (2014). A selective sweep on a deleterious mutation in the CPT1A gene in Arctic populations.

2. CPT1A – U.S. National Library of Medicine.

3. Cahill Jr, G. F. (2006). Fuel metabolism in starvation. Annu. Rev. Nutr., 26, 1-22.

4. McCue, M. D. (2010). Starvation physiology: reviewing the different strategies animals use to survive a common challenge. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 156(1), 1-18.

Photo: here

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2 Responses to Why Ketosis is not a “one-size-fits-all” Approach

  1. I would only quibble with your use of the term “deleterious” for the Inuit mutation. For Inuit living their traditional lifestyle, it was a useful adaptation. Not so much anymore.

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