So I've been reading through Dr. Kruse's blog posts and I have a couple of questions in regards to the PPP and fat oxidation.
1. Where does the idea that the PPP requires ketosis/fat adaptation come from? I can't seem to find any papers, books or studies suggesting that the pentose phosphate pathway is activated or induced by fat oxidation. If anyone could provide a citation for this, I'd be very appreciative.
2. What exactly are the advantages of fat oxidation instead of sugar oxidation? I know Jack suggests that fat provides more ATP, but couldn't you just eat more sugar and get the same amount of ATP? That makes little sense to me, especially considering Dr. Kruse's numbers are slightly confusing. Fats produce 4 times as much ATP as sugar per molecule however they are equal in terms of ATP per calorie. This gets confusing with Jack Kruse's numbers. Now, without this increased energy production, what exactly are the benefits of fat oxidation? Dr. Raymond Peat provides numerous benefits of sugar oxidation, (anti-cortisol, pro-thyroid, CO2). I don't necessarily agree with the sugar oxidation, but it's interesting nonetheless.

 

Interesting.

 

Hi QiGuy, I'd have to reread the PPP blogposts for your #1 question. For the other, sugar oxidation at the leaky complex 1 in the mitochondria produces all kinds of free radicals.
http://www.jackkruse.com/why-we-die-and-why-we-live/

 

Part 1 of you question remains a question for me too... I wish that someone who gets this would chime in? My only thought is that a hi fat diet supports the PPP in the sense that ROS are not generated ( as compared to carb diet) and PPP reducing power is not consumed and is thereby available for other processes. --- but this is a guess....

 

COLD IS THE NUMBER ONE WAY TO BEGIN PPP BETA OXIDATION: cold primordially upregulates beta adrenergic receptors as I said in CT 6 and is well known..........Peatatarians believe fructose is the only way to regenerate the reducing agent.........its not. http://www.ncbi.nlm.nih.gov/pubmed/1978808

 

Just said this in another thread here:http://forum.jackkruse.com/showthread.php?8934-Low-carb-insulin-resistance/page11
I will just post the entire comment I made about the fructose fat issue........

no......its a potassium issue.......and when I get to the Quantum puzzle blog you'll see why........BG is not the major issue. It can be when BG is present in higher temps body temps such as when cytokines are high. Your cytokines are low because you are CT machine. The longer you CT the higher your BG goes but you develop no issues with BG.........because insulin can not hurt you when you control cytokines.

When energy is used in a quantum cell, it operates coherently and cooperatively as a unit. It becomes destabilizes a bit from its metastable state, and this allows glucose and calcium, to move into the cell in droves. This tells you why I made a big deal about calcium ion frequency resonance in the EMF series. EMF uncouples this normally coupled coherent event.
Under the control of insulin, glucose adsorption sites on proteins and enzymes become exposed to the environment, and glucose can be burned to replenish the ATP or shunned if the cell is made IR as mentioned above in this thread. When glucose is the fuel, at the same time, carbon dioxide is produced, which functions to stabilize the resting living state. Here is where my cosmology links come back for you to consider........CO2 in cold causes matter in galaxies to condense under the force of the electromagnetic and gravitational forces of physics. In your body the same thing happens in the ABSENCE OF CYTOKINES OR INFLAMMATION. This effect is called the Bohr effect, increases the efficiency with which oxygen is unloaded from the red blood cells, curtailing the production of lactate and protons. Protons are positively charged and consider acids and they do not like Oxygen. In this highly energized coherent state, potassium is preferentially adsorbed to the ionized carboxylate groups on intracellular proteins. This satisfactorily explains why the administration of glucose and insulin can uncomfortably lower blood potassium levels............this is has huge implications for explaining rigor mortis:

NOW CONSIDER THIS: Carb whores think fructose is the only way to replenish glycogen.......not true. the PPP is the best way because it is the most reducing pathway using electrons to do so.......why does biochemistry miss it? Because modern humans beliefs have kept them from realizing that fructose is how you do it when cytokines are high and saturated fat electrons do it in the cold.........Seasons matter in biochemistry.

 

Fructose is used when cytokines are high to replenish ATP and fats are used when cytokines are low.........fats use electrons and fructose uses protons to get there. The electron pathway is way more efficient. The key issue becomes temperature............

 

30 yrs ago this was shown..........The experiments described in the article by Miller and Bryce. “Adaptations to a high-fat diet that increase exercise endurance in male rats.” Journal of Applied Physiology (1984) vol. 56 (1) pp. 78-83 refute the simple theory of the Peatatarians. So compelling are these results that lard manufacturers may start advertising their products as performance fuels. The rats fed lard in this experiment far out performed the rats fed a high carbohydrate diet. This is why human performance rises in ketosis. Have a look at the Stanford cold glove data........athletes wearing their glove to cool their blood to induce fat burning increase their performance by 100-300%. It stays in the paleo blind spot.........because no one is fat or cold adapted to hit it.......but the data is out there if you look. The Stanford cooling glove got lots of press 2 yrs ago and now all elite military systems are employing it in training.

 

My main problem with Peat and the paleo performance crew is that they really believe there is a true need to replenish glycogen........for performance..........YOU DONT NEED GLYCOGEN WITH FAT..........ATP IS THE KEY METRIC AND FRUCTOSE CANT HANG WITH SATURATED FAT in this area.

 

The biggest factor in this ability is the molecular clock. It is easy to explain, once you realize that you can’t access the fat burning pathway when your molecular sense of timing is off.

This is what I laid out in detail in EMF 4.

When you molecular clocks are off you can never benefit from true fat burning because you are burning glucose and fructose neither of which make enough ATP to move electrons in your semiconductors well when your redox potential is low. When your molecular clock is off so is your redox potential in all cell membranes and especially your mitochondria. When this happens you have poor collagen function (no triple helix), poor water structure with no charge separation, poor hormones panels because they are a mirror of how well or poor you move electrons or protons within your semiconductors, and relatively small chance of living chemically reduced within the PPP. It is about electrons and ATP.....not macro's. Fats give you the most electrons............

If you dont you will first get sick and then you die slowly on the vine………..

My take on exercise then becomes simple to understand……once you fix the semiconductor issues in your body even partially……collagen and water begin to react better to stressors……you then can exercise…….why? Any stress, pressure, movement, massage, increases muscle, tendon, and cartilage actions in a semiconductor is to generate a piezoelectric signal (BECKER's KEY POINT)…….A piezoelectric signal can change light to a mechanical signal or an electrical signal to a mechanical one and that changes chemical energy to an electric signal that the brain can translate in its language as an electromagnetic computer (EE6) …….if your semi conductors are limited in holding its charge or broken or severely hampered (Leptin Resistance or high cytokine levels for any reason) then you need to back off exercise and focus on getting your conditions of existence to be able to access the PPP with ease……….to move electrons well to increase your overall redox potential.........FAT DOES THIS BEST. NO ONE NEEDS GLYCOGEN WHEN IT IS A COLD AND KETOTIC WORLD THAT BATHE YOUR SEMICONDUCTORS

 

The Pentose-phosphate pathway has a wide range of purposes in the cell. It provides a constant supply of NADPH, which is used in biosynthesis. The pathway also produces Ribose-5-phosphate, which is required for nucleic acid synthesis. Also in the Pentose-phosphate pathway two glycolytic intermediates are formed:
1. Fructose-6-phosphate (the PEAT WAY) and
2.Glyceraldehyde-3-phosphate. (THE KRUSE WAY VIA FATS)

Regulation of the Pentose Phosphate Pathway:
Due to the first step of this pathway being reversible, it is highly regulated. As a result the enzyme Glucose-6-phosphate dehydrogenase is inhibited by NADPH and also by fatty acid esters of coenzyme A.

Glycerol is a precursor for synthesis of triacylglycerols and of phospholipids in the liver and adipose tissue. When the body uses stored fat as a source of energy, glycerol and fatty acids are released into the bloodstream. In some organisms, the glycerol component can be converted into glucose by the liver and, thus, provide energy for cellular metabolism.
Before glycerol can enter the pathway of glycolysis or gluconeogenesis (depending on physiological and environmental conditions), it must be converted to their intermediate glyceraldehyde 3-phosphate in the following steps:
Glycerol To Glycerol kinase To Glycerol-3-phosphate To Glycerol-3-phosphate dehydrogenase To Dihydroxyacetone phosphate To Triosephosphate isomerase To Glyceraldehyde 3-phosphate

Now the next step.......in understanding:

FATS STOP THE NEED FOR THE physiologic FRUCTOSE PATH...................What is this tied to? COLD and the activation of Brown fat that liberates fats!!!! Cold empties adipocytes to make the reducing elements........need for maintanence of the redox potential. This is tied to sympathetic nervous system response to cold. I spoke about this in CT 6

 

This means in nature...........cold and fat are a metabolic couple.......when you are a modern human you break this couple routinely and you never see efficient part of the PPP......... GOT IT?

 

Its all in a biochem book........but the Peat folks only read the parts they get and understand. They buy beliefs not benefits.

 

I believe that qualifies as a boom!



Chilled Head

 

This is important for people to understand but I believe Peat is correct for some people for a couple of months (summer) per year that the fructose pathway can access the PPP(Seasonal eating anyone?). Most of the people who derive benefit from the Peat way are totally warm adapted but lose results over time. I have a few as patients these recovering Peatarians and their stories are quite interesting.

 

The fructose pathway in my view is how humans adapt from summer to autumn......these two seasons are where fructose laden foods are..............and how long they are available are tied to your location on the planet..............but this is all immaterial when you realize that our modern beliefs and beahvior allow us to constantly live outside the dictums of the photoelectric effect with respect to both food and temperature. Peat gives half truths...............the rest of the story and the part for health reversals is in the other pathway for modern humans.

 

OK.......................next step in understanding PPP was not to come until next yr................but here ya go: This glycerol 3 phosphate molecule has a special shuttle that PeataTarians forget. Paleo too. This is a metabolic pathway controlled by transition metal maxwell demons. It allows electrons to skip cytochrome 1. Using it allows cytoplasmic NADH to enter the electron transport chain. Little known area of the PPP is in play here folks...........

They happen to have two special glycerol 3 phosphate dehydrogenases which make up the shuttle. Free in the cytosol there is cytosolic G3P dehydrogenase, which actually uses NADH to add a pair of hydrogens to a glycolysis intermediate (dihydroxyacetone phosphate) to form G3P directly.

The other G3P dehydrogenase really does dehydrogenate G3P, back to dihydroxyacetone phosphate. But this second G3P dehydrogenase is embedded in the outer surface of the inner mitochondrial membrane. KEY POINT!!! Anyone guess why? Think what I told you special in the quantum electron blog 2 years ago about FADH2? And it contains an FAD/FADH2 moiety which takes these two hydrogens and uses them to reduce the CoQ couple, feeding electrons in to the electron transport chain. FADH2 is our special fat pathway quantum tunneler......it allows glucose to act like saturated fat when the shuttle is active in cold environments or during starvation.

When the shuttle is working we pump electrons from cytosolic NADH directly in to the mitochondrial respiratory chain through the FADH2 tunneler. When you do this............it is electron only required and no pumping of protons. Anybody see WHY yet?

The G3P shuttle is the key to understanding the QED mystery of the PPP.

In leptin sensitive cells with low cytokines the signal to reject excess energy from food picks on glucose at cytochrome one because it is first in the chain. When it happens we get the development of insulin resistance from superoxide production of cytochrome 1, specifically at the iron sulphur cluster N-1a (Transition metal alert) . Lady evolution used Occams razor and made it simple............ to access this by burning saturated fats (NOT PUFA's) to generate a lot of FADH2. When you do this little molecular demon trick it cause backward bidirectional flow of a few electrons through complex I and it completely shuts down the Peatatarian carbohydrate pathway unknown to the Peatatarians.

You can make glucose act as if it were butter through the G3P shuttle.

 

The metabolic pathways chart is helpful for me to follow this discourse but of course it is missing some of Jack's finer details. Make sure to zoom in to clearly see the PPP and glycolosis--Top half center area.
http://www.sigmaaldrich.com/content/dam/sigma-aldrich/docs/Sigma/General_Information/metabolic_pathways_poster.pdf

 

How are BG levels regulated in this model?

 

Temperature and fats........