Thursday, September 25, 2014

Uncoupling control in defence of FFAs

I've been reading this review on beta hydroxybutyrate and am struck by the concerns expressed throughout about the potential damage caused by free fatty acids, due to uncoupling, a sentiment I have picked up in several of Veech's publications which are heavily cited in the review.

I was particularly struck by how two papers I've recently discussed were described, so it's topical for me. One was the puzzling toxicity of a LCKD diet as published by Wang et al. This is the one using vegetable shortening of indeterminate trans fat concentration, a point sadly un-noted (or considered unimportant?) by the review. And second is the Kuwait study, described as LCKD in the review, which was not exactly glycogen depleting for a rodent.

Aside: This cited study starved rats for three days before ischaemia/reperfusion. That should have depleted glycogen AND raised raised FFAs (neither of which was checked, but any lipophobe should expect uncoupling combined with backup anaerobic glycogen reserve loss to be disastrous in ischaemia/reperfusion) as well as predictably increasing B-OHB. Combined starvation changes in fact reduce the damage produced and improve recovery. End aside.

So I'm a little ambivalent about the review and how much of the rest of their ideas I might take at face value.

Ultimately, thinking about free fatty acids, we have to talk about the control of uncoupling.

Recall this image from this study in part 29 of the Protons thread:

Free fatty acids are essential for proton transport across the inner mitochondrial membrane to uncouple oxygen consumption from ATP synthesis and to maximise electron flow down the electron transport chain with minimal resistance and minimal non essential superoxide generation.

No free fatty acids, no uncoupling. Free fatty acids are core to uncoupling.

But they are far from the only factor. For protons to be transported through the channel of the UCP by free fatty acids the channel must undergo a conformational change, which is highly dependent on the ATP status of the cytoplasm and the mitochondrial matrix.

So we have this picture from this very impressive study:

ATP in the cytoplasm fits in to a specific binding site, with each phosphate moiety of ATP fitting up against a specific arginine, all three aligning results in closure of the channel and inhibition of uncoupling, whatever the FFA concentration. Here is what the authors say:

"Moreover, residues R79 and R279 correspond to the arginines involved in nucleotide binding and protein inhibition in UCP1. According to the three-step binding model proposed for UCP1, β-phosphate of PN [phospho-nucleotide] binds first to R182 (helix IV, loose binding). The second step is the binding of γ-phosphate to R83 after protonation of E190 (tight binding). After the subsequent binding of α-phosphate to R276 (helix VI) the protein switches to the inhibited conformation"

Cytoplasmic ATP (and GTP) inhibit uncoupling. But not all of the time, despite the fact that there is normally always enough cytoplasmic ATP to inhibit uncoupling. So yet another factor comes in to play.

It is quite possible to inhibit the inhibition of uncoupling produced by cytoplasmic ATP.

You do this with mitochondrial ATP. ATP binding from the mitochondrial side of the channel interferes with the binding of cytoplasmic ATP but cannot reach the R83 arginine itself to close the channel. So elevated mitochondrial ATP keeps the uncoupling channel open, even in the face of rather high cytoplasmic ATP levels.

The logic to this is that if there is plenty of ATP within the mitochondria there is no need to preserve delta psi and it's fine to uncouple. If there is ATP in the cytoplasm but very little in the mitochondria the implication appears to be that ATP synthase is not generating enough mitochondrial ATP, i.e. we are either hypoxic or over-uncoupled. Continued glycolysis generates ATP on the cytoplasmic side so allows the uncoupling channel to close using this cytoplasmic ATP.

It's pretty logical.

So. Under hypoxia, whatever the level of FFAs, what happens to uncoupling?

It stops due to a lack of mitochondrial ATP. Should you fear FFAs? Only if you think you will continue to uncouple respiration under hypoxia. The balance of mitochondrial to cytoplasmic ATP should shut down uncoupling very rapidly when needed.

Just say no to Crisco (if that's how Wang et al got their result).

It has long worried me that in Veech's seminal paper on glucose, insulin and ketone metabolism in an isolated heart preparation the group was very, very careful to run the study without any involvement of free fatty acids. For those of us living in a temperate latitudes, lounging on the beach under a coconut palm while waiting for lunch to drop on our heads is not an option. Have you ever been to Lowestoft beach? No ketones without elevated FFAs at latitude 52 deg N on the North Sea coast. Fasting, or living on meat for a while, seems more likely than eating MCTs outside the tropics. I fail to see how the body would manufacture the miracle of ketones at exactly the same time as it releases the devil incarnate of free fatty acids.

Some folks like free fatty acids. Me, for one.

Some of us like uncoupling too, in the right place, at the right time.



mommymd said...


Guillermo Fernandez said...


Trying to fit everything within your proton thread, I understand that cells facing either starvation or a starvation mimetic diet such as a palmitate based one would increase superoxide production leading to insulin resistance plus increased uncoupling. This in turn leads to glucose deprivation in the cytosol and an upregulation of beta oxidation which is effectively less efficient in ATP generation per unit O2. After the whole process stabilizes you end up with a higher number of mitochondria producing enough ATP to balance cytosolic ATP consumption rates, working at a lower delta Phi, generating less ROS but fulfilling energy demands.
Coping with sudden hypoxic conditions as occur during ischemia would require increasing the efficiency of ATP production per unit O2. Nevertheless I do not see much difference between a lower number of mitochondria burning glucose compared to a larger number burning mostly fat as both produce the same required ATP (I can even think that a larger number would have the advantage of accessing O2 more efficiently).
I am only concerned about dynamics but I share your guess that uncoupling would be shut off easily as soon as mitochondrial ATP concentration decreases; probably that process would help improving efficiency.
Do you see any room for a sudden reversal of insulin resistance and the upregulation of glucose utilization that would imply a higher ATP production per unit O2? Should you think so, have you thought about the signals involved?
Thanks for another great post!

js290 said...

Nature was not ever going to misuse or waste a better ATP source. Nature as a lipophobe is a faith based proposition.

Pathway of mitochondrial β-oxidation
The oxidation of fatty acids yields significantly more energy per carbon atom than does the oxidation of carbohydrates. The net result of the oxidation of one mole of oleic acid (an 18-carbon fatty acid) will be 146 moles of ATP (2 mole equivalents are used during the activation of the fatty acid), as compared with 114 moles from an equivalent number of glucose carbon atoms.

Jack Kruse said...

MS is a disease of unfettered uncoupling Peter. This releases more IR light and causes demyelination. Good stuff.

Guillermo Fernandez said...

Someone is either missing the point or confusing C with O2….
The advantage of fat as a fuel is that it provides extensive stores of calories in a high density form. Fat is not hydrated and therefore it weighs much less per unit calorie than protein or carbohydrate (9 Cal/gm of fat vs. 4 Cal/gm of carbohydrate or protein). This also holds per unit C. A 6-carbon glucose molecule produces 36 to 38 ATP on average providing a ratio of 6 ATP/Carbon, while an 18 carbon fatty acid produces 147 ATP providing a ratio of 8.2 ATP/Carbon. HOWEVER!, carbohydrate is more efficient than fat when the amount of ATP produced per unit of oxygen consumed is considered. Six oxygen molecules are required to metabolize six-carbon glucose producing 36 ATP (ratio = 6 ATP/oxygen molecule), while 26 oxygen molecules are required to produce 147 ATP from an 18 carbon fatty acid (5.7 ATP/oxygen molecule). During hypoxia that matters.
You can pack as much fat around your belly as you want, you get zero ATP if you cannot access oxygen.
Phosphocreatine could help for the first 10 seconds or so but later on you will start starving your cells from ATP. I am just answering if upregulating glucose metabolism is something that happens (could happen?) during hypoxia as well as stopping uncoupling as a cellular response to resist the threat.

Jack Kruse said...

You said, "HOWEVER!, carbohydrate is more efficient than fat when the amount of ATP produced per unit of oxygen consumed is considered. Six oxygen molecules are required to metabolize six-carbon glucose producing 36 ATP (ratio = 6 ATP/oxygen molecule), while 26 oxygen molecules are required to produce 147 ATP from an 18 carbon fatty acid (5.7 ATP/oxygen molecule). During hypoxia that matters.
You can pack as much fat around your belly as you want, you get zero ATP if you cannot access oxygen." I hope Peter realizes this is why Gilbert Ling really matters now. ATP is not the energy source. Don't believe it? Read Ling or tell my why the main reducing element in biochemistry is made from the PPP and uses no ATP or makes any? Ling gave us the answer 60 years ago and we have ignored it. Light release from the mitochondria also has a massive effect on cells. This is why mitochondria in demyelinating plaques are all hypoxic. Their mitochondria are leaking massive amounts of IR heat and that is why we see it as white matter plaques on MRI. You know the machine that Ling's science created. Somebody has to begin to put it together.

Jack Kruse said...

Electrons are used to create di-molecular oxygen in our Electron Chain Transporters in mitochondria.

As electrons flow faster they reduce more oxygen and create larger electric and magnetic fields in mitochondria. When oxygen is reduced by food electrons, it is in is molecular state, called O2.

Most people do not know molecular oxygen (O2) has two unpaired electrons.

It is the only gas on the periodic table that is naturally paramagnetic.

This means that it reacts more to the magnetic field strength it is found within. This is why O2 is coupled to a mitochondria’s magnetic strength.

When mitochondria have a large current of electron flow on the inner mitochondria membrane it induces mitochondria to become strong electro-magnets in our tissues; this system is designed to raise oxygen levels in our tissues with a lot of mitochondrial density.

As electrons flow faster on our inner mitochondrial membrane, the associated magnetic field strength also increases. The only other way to induce a stronger magnetic sense in mitochondria is by introducing cold. This is why all mammals uncouple in cold. It is magnetic effect. This is why O2 is the only paramagnetic gas on the periodic table. Paramagnetism means it is drawn to local magnetic fields. Guess what else is paramagnetic? DHA when it is only in the SN-2 position. The only way to deliver O2 and DHA to things like the brain and heart is to have a large current flowing on the inner mito membrane. This also points out why RBC's have no nuclei or mitochondria. It they did they would never offload their DHA or O2 to tissues who have a ton of mitochondria. Gilbert Ling 101. Maxwell's laws of magnetism 101. This is why the ATPase is located 90 degrees to the inner mitochondrial membrane.

Jack Kruse said...

And when DHA cant get into the brain heart or immune cells they can't turn the excess light from mitochondria released (infra red) back into the signal it needs to. DHA takes sunlight and changes it to an electrical signal. That signal travels on the piezo electronic collagen/water system (Ling and Becker) worked out. At the inner mito membrane the electric signal must be changed back to IR light to be contained in the inner mitochondrial matrix. The only things that can contain light is strong consistent. electric and magnetic fields. This is why it takes photons from the sun 100,000 −1,000, 000 million years to release photons created in the sun's core. The mitochondria uses the effects to contain its IR heat in the matrix and releases its when it needs too. Too much release occurs in hypoxia states. This is also why all neuro-degenerative disorder have low voltage and MEG data from brain because the brain has no DHA in it because the neurons have lost their ability to draw DHA or O2 into it because of a lack of charge and magnetic ability from the loss of electron flow.

Jack Kruse said...

When a magnetic field is applied to a moving electric charge, such as a moving proton or the electrical current in a wire, the force on the charge is called a Lorentz force. Protons move 90 degrees to the electron flow in mitochondria by magnetic flux lines. 4 Protons make ATP. The ATPase has an umbrella like Fo rotating head that can spin both ways depending upon the direction of the current. Peter has been hinting at reverse flow in his proton series. Reverse flow is tied to low ATP, chronic hypoxia and many neurologic diseases. This is also why they all have low EEG voltages and low MEG data. The change in proton precession is what radiologists are picking up in MS. And this is all tied to this mechanism.

dr j said...

hi Jack
seeing that you are on about IR, I wrote to Gerald Pollack to introduce Danielle Goodspeed's work on salicylate levels in circadian entrained plant tissues being at a zenith, at about midnight, in preparation for the attack of pathogens at dawn when plant surfaces are at dew point with water condensation and IR coming on stream as the earth rotates into the solar flux ( my interest lies in the fermentation of "entrained" green plant tissue in the hindgut). An example of Goodspeed's work -

Qori Mayu said...

Jack, Peter or anyone else that cares to provide insight; what are your opinions on eating LC/VLC/HF/Ketogenically and regularly exercising/training in a very anaerobically demanding manner?

I do this and have no problem sustaining my performance in these endeavours (although I'm aware that my performance/endurance in some of the more glycolytically demanding activities may be improved hypothetically by increased carb intake -Jack you may not agree with this based on what you've written about this).

My training consists of weight training and sprintwork. Both being phosphogenic in nature I imagine but becoming more glycolytic during repeated bouts with minimal rest between sets.

Essentially i'm interested in how training and eating this way pertains to the type of long-term health so often addressed here. -Mitochondria, Insulin, Cardiac events, Growth factors, DNA damage etc.

I have no interest in aerobic endurance as so many in the keto/LC/HF world seem to have and I've not really read much relating to this way of eating with these types of activities and the impact on health

Any input on such a matter?


raphi said...

Hi Peter,

This is the "TestDiet 5TSY AIN-93G Atkins/Rodent" used by Wang et al. (

It's terrible. So terrible that the the TestDiet website doesn't seem to make it easy to find, except via an email request.

Also, love the "NOT for human consumption" disclaimer. Damn right. Except that pretty much the worst of what's in it makes it into all processed foods.

It seems the premise of uncoupling per se being an issue doesn't is based on subjects with poorly built mitochondrial machinery incapable of sustaining sufficient mitochondrial ATP levels.

J. Stanton surmised that High Intensity exercises could jump-start the mitochondrial adaptations that are often uncomfortable for people suddenly switching to a HF diet. Could this have to do with better uncoupling dynamics?


john said...


I lift 4 days per week and have about 7 dance classes per week. I've never noticed any "glucose deficiency" symptoms like Jaminet and am usually <100g carbohydrate. There have been periods of time where I was having ~50g/day. I'm not sure why some people have issues and some don't.

Passthecream said...

An interesting post as usual.

Care to comment on this?

It seems a bit worriesome to me!

raphi said...

An extract of the article linked to by "Passthecream":

<< What we're doing inside cells is like putting the car's transmission into neutral by uncoupling it from the transmission. Then you step on the gas so the engine runs full throttle but the car doesn't move. If too much of the fuel in the cell is fat, you keep burning it until the fuel gauge reaches empty. Without the interference of fat, you hope that sugar will then enter the cell normally .>>

<< "We wanted a safe and practical compound to deplete fat inside cells," says Jin. "We went to the literature and found an approved drug that does in parasitic worms what we wanted to do in liver cells." >>

Galina L. said...

Some people don't have issues with glucose deficiency while doing intense exercises because they adapted to working out in a fasted state or ketosis. You just can't jump into keto-adaptation after years of carbo-loading.

Jack Kruse said...

You can once you institute auptophagy to recycle all the bad mitochondria.........considering how many mitochondria the brain and heart alone have that is why 18-36 months is the window most people find for adaptation.

john said...

I think I just happened to decrease carb intake slowly over the course of a couple years, and now I've been pretty low for another 2-3 years. I used to have a sweet potato binge per week because of cravings, but I haven't done that in about a year either. Perhaps people need longer to adapt or are eating the wrong foods. It's also possible I could have been performing suboptimally all along, but my strength has increased, and my dance endurance is better than most.

Jack Kruse said...

Guillermo would benefit from reading Ling and my current blog on protons (Tensegrity #6). It might open your eyes to something biology has missed but Ling has been saying for 60 years now.

JohnN said...

It's a Catch-22 situation. The body (start with mitochondria) can't remodel unless given a need to do so and with appropriate environmental conditions.

It probably starts this way:
Need to remodel (getting rid of damaged complex1 from years of glucose burning) --> (restrict glucose-ketogenic-high intensity exercise - endurance exercise - induce uncoupling) --> Apoptosis --> autophagy --> fusion --> fission --> mitobiogenesis.

End result: rejuvenation of whatever body parts the demands are placed on.

Processing glucose occasionally may be the equivalent of fire-drill to teach mitochondria to handle ROS better, I think.

JohnN said...

It's a Catch-22 situation. The body (start with mitochondria) can't remodel unless given a need to do so and with appropriate environmental conditions.

It probably starts this way:
Need to remodel (getting rid of damaged complex1 from years of glucose burning) --> (restrict glucose-ketogenic-high intensity exercise - endurance exercise - induce uncoupling) --> Apoptosis --> autophagy --> fusion --> fission --> mitobiogenesis.

End result: rejuvenation of whatever body parts the demands are placed on.

Processing glucose occasionally may be the equivalent of fire-drill to teach mitochondria to handle ROS better, I think.

Peter said...

Hi Guillermo, going back to Veech’s paper on ketones and metabolism in cardiac muscle, the gain with ketones was an increase in energy yield from ATP hydrolysis rather than increased ATP production. Table 1 has the basic data.

Qori, not much help from me, I don’t really exercise deliberately nowadays. I walk miles and will surf when I can (not much at the moment but this will eventually change as the children grow up).

Raphi, I’d guess HIT activates AMKP and almost certainly generates superoxide, although it’s not an area I’ve read in to very much.

Passthecream, they are looking for a drug which mimics palmitic acid in its free acid form. Simply skipping carbs will be asking for far less in the way of unintended consequences…

Jack, under Crabtree there is extensive mtDNA damage. All you need is for a subgroup of badly damaged mitochondria which happen to reproduce more rapidly than healthy mitochondria and you might well be looking at a single cell converting all of its mitochondria to rapidly replicating duds. I’m guessing autophagy should be “aware” of this but it speaks of why some people may have long term issues with adaptation to a fat based diet.And the issues could be quite loclaised.


Stan Bleszynski said...

Regarding supposedly detrimental effects of FFA claimed by some researchers, this paper was mentioned in the course of a debate with some high-carbers on Twitter (I am not posting the link because of the spam cop rule, but you can google the title):

"Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet", by Teri L Hernandez et al., Am J Clin Nutr. 2010 Mar; 91(3): 578–585.

Appart form being short (6 weeks) the study shows some unusually high peaks of serum FFA, for patients on Atkins eating 20g of carbohydrates. Not sure if (1) this is problematic (though there are some other papers indicating that the high level of FFA seems to be damaging for pancreatic beta cells (is it really?).(2) not sure if that study is representative for normal people on a low carb diet. What do you think?
Stan (Heretic)

Peter said...

Hi Stan, the biggest problem with the paper is that the authors appear to consider that LDLc is the cause of CVD. As such there is no common ground for any sort of discussion, If, as I do, you consider that one of the core drivers of CVD is chronic hyperinsulinaemia, there is no way of dropping to the level of stupidity that describes eu-insulinaemia in these terms: “As expected, patterns of 24-h insulin concentrations in the High Fat group lacked a physiologic pattern, remaining low and blunted (Figure 1A), which assumedly contributed to the lack of FFA suppression”. Words fail me. They have no concept of normal physiology.

As regards FFA toxicity, yes, hyperglycaemia, especially post prandial, causes beta cell death in the presence of physiological fasting FFA levels. Obviously palmitic acid is the best facilitator of glucotoxicity. Also (obviously) Figure 1 lacks glucose levels, unsurprisingly for a garbage study like this. But we know from Table 2 that the HC diet increased 24h glucose (a little, despite weight loss) while LC dropped 24h glucose (a lot). And what is physiological for FFAs in the presence of low glucose? We know from

Prolonged Fasting Identifies Skeletal Muscle Mitochondrial Dysfunction as Consequence Rather Than Cause of Human Insulin Resistance

that when slim people don’t eat for 60 hours the mean physiological total FFA level is over over 2000micromol/l and palmitate is quite possibly over 1000micromol/l, this is normal (unless people think not eating for 60 hours is going to kill your pancreas!). So 800micromol in the presence of unreported but low glucose? Probably normal.


Stan Bleszynski said...

Thanks, that's what I thought too. I am surprised how few studies are available on the effects of the high serum FFA concentration alone, that's why I asked. I couldn't find any. My suspicion is that the pancreatic beta cellular damage (as reported. for example in the following study, see below) was due to glucose+FFA combination, in-vitro.

"Chronic Exposure to Free Fatty Acid Reduces Pancreatic b Cell Insulin Content by
Increasing Basal Insulin Secretion That Is Not Compensated For by a
Corresponding Increase in Proinsulin Biosynthesis", by L. Cornelius Bollheimer et al.,
Pubmed article PMC508661

Best regards,

Peter said...

Yes, I’ve got the cell death rate for beta cells with palmitic acid up to 400micromolar in either glucose 5mmol/l vs glucose 20mmol/l. Glucose 5mmol/l allows palmitate 400micromolar to be completely non toxic.

The paper is here

but the extracted graph is in this post

People will be so embarrassed when they realise how badly they have been had by the LF brigade! But for now they still believe!

All the best


Nigel Kinbrum said...

What's with you LCHF'ers & strawman fallacies?

It's not an issue of toxicity. Chronic high FFA causes an imbalance between insulin secretion & insulin synthesis, resulting in reversible loss of 1st phase insulin response. This causes very high postprandial BG when carbs are eaten.

Peter said...

Hi Nigel, nice to see you're still around!


Nigel Kinbrum said...

Hi Peter. I'm only posting here 'cos of my "debate" with Stan on Twitter. He blocked me after I dismissed your objections. Debate with Stan is futile, as he's learned nothing about how the body works.

Having fixed my IR, I can eat anything without getting adverse effects. A recent randomised crossover trial of produce-based LCHF vs HCLF I ran on myself showed that my brain works best on HCLF, so that's what I eat now. I've been maintaining a BMI of 23.9 since last September on my produce-based HCLF diet + treats. I concentrate my fat intake into 1 meal (from sardines or mackerel) to stimulate gall bladder emptying.

People who have working beta cells should try to reverse their IR, as long-term LCHF/keto impairs beta cell function. This is *not* an improvement!

If IR is irreversible &/or beta cells are damaged irreversibly, LCHF/keto is fine.

Cheers, Nige

Peter said...

There , you see, we have opposite approaches. My own plan is to eat to stimulate the minimum insulin secretion and to respond as little as possible to that signal. LC, high saturated fat.

The bottom line is minimising insulin signalling.

You have your own approach where clearly, however you have done it, systemic insulin exposure is low, ie normal BMI. This is clearly very possible. It's just not an approach I'm interested in. Equally obviously I regard decreasing insulin synthesis as a positive development, as is glucokinase down regulation and as is the deconstruction of excess complex I in the ETC. All of which happen with my approach. All of which will allow hyperglycaemia if challenged with a meal of absolute garbage. So I don't do that.

To me, the question is, what would happen to yourself given a fatty leg of lamb and nothing else to eat? Like me eating five donuts. There are lots of other "what if"s too but you realise no one convinces anyone of anything on t'internet, so let's not waste too much time on it.

Two sides (minimum) to every approach.

All the best


Nigel Kinbrum said...

Hi Peter,

You've raised some interesting points. As achieving optimum health is never a waste of time, I'd like to discuss them, if that's O.K. with you. If it isn't, this post won't pass moderation! :-D

1. My approach improves metabolic flexibility.
Your approach worsens it.
Healthy humans don't get energy from carbs or fats. They get it from carbs and fats, in ratios which vary constantly for optimum operation & glycogen storage levels. Your blog header is a false dichotomy fallacy. :-/

2. I agree that chronic hyperinsulinaemia is bad.
You keep your insulin low by minimising your exogenous carb intake, maybe insulinogenic proteins too.
I keep mine low by maximising my insulin sensitivity.

3. You get hyperglycaemia if challenged with a meal of absolute garbage, due to 1.
I don't. I can eat whatever I want (in reasonable amounts, of course!) without getting postprandial hyperglycaemia, hyperinsulinaemia & its associated drowsiness followed by rebound ravenous hunger. Two hours after swallowing 75g of glucose, my BG was 3.7mmol/L in September 2008. Fasting BG was 5.0mmol/L.

4. I'm now metabolically flexible, so nothing would happen if I ate a fatty leg of lamb and nothing else. I have plenty of storage capacity available in liver, muscles & fat mass to clear glucose &/or TGs from circulation in good time.
Unlike you, if you ate five doughnuts.

5. "It's just not an approach I'm interested in." That's illogical.
Before October 2015, illogical statements would melt my brain figuratively speaking. Since I saw a neurodevelopmental professional who diagnosed me with Asperger's Syndrome, I've learned how to cope with life's illogicalities, so I don't care.

Cheers, Nige

Stan Bleszynski said...


You did nothing wrong, I blocked you on twitter for my own sanity sake, after you wrote that you are not going to read Peter comment that I linked. The one where he quotes this paper:

"Saturated fatty acids synergize with elevated glucose to cause pancreatic beta-cell death." by El-Assaad W. et al.

I had a bad experience once with a friend, whom I had to block after 18 years (in real life, not on-line!) who was overwhelmingly rational to the extent that his super-logical mind became his own enemy preventing him to move forward, learning new things. I wasted so much energy debating him, with nothing constructive ever coming out of it, that I developed an allergy towards people like that.

I am also borderline "Aspie", like you (scoring 28 or 29 on Baron-Cohen's scale, with the threshold being 30). I am so glad to see that you decided to post in the "enemy's" camp. I hope you have read Peters's replies which apply directly to our Twitter conversation.

I have to add that the theory that FFA or saturated fat would damage pancreas, on its own has to be incorrect for the reasons other than just the paper above. Fatty cuts of meats have been human staple diet for hundred thousands of years so it is extremely unlikely that this stuff would suddenly somehow become harmful to any of our organs. Furthermore, in my own personal observation, when I started on my high animal fat low carb nutrition in 1999, I could only consume up to ~20-30g of carbohydrates. My body was insulin resistant and glucose intolerant though not to the extent of clinical DM.If high FFA would indeed harm beta cells then this condition (IR) would have persisted or worsen. In fact the opposite happened! My IR gradually went away and was healed on eating mostly fat! After about 5-7 years (and even now) I found that I could actually eat a high carb meal (potatoes and rice for example) if I wanted to, way above the initial 20g limit!

Stan (Heretic)

Nigel Kinbrum said...

"You did nothing wrong, I blocked you on twitter for my own sanity sake, after you wrote that you are not going to read Peter comment that I linked."
You've mis-represented what I wrote yet again.

"I have no interest in Peter D's utterly biased opinions.

FFAs are CONSTANTLY HIGH on LCHF/keto. This increases insulin secretion but inhibits insulin synthesis.

Didn't you read ? This confirms that I'm right & Peter D's wrong."

I wrote that after I read Peter's reply to what you wrote. Still, a man sees what he wants to see and disregards the rest (apologies to Simon & Garfunkel).

"Saturated fatty acids synergize with elevated glucose to cause pancreatic beta-cell death." by El-Assaad W. et al."
This is irrelevant to what I wrote. The problem to which I'm referring is increased insulin secretion combined with reduced insulin synthesis, leading to depletion of insulin within beta cells, leading to loss of the 1st phase insulin response.

You repeatedly mis-represent what I write due to severe cognitive bias, which is why I've blocked you on Twitter. It's impossible to debate somebody who repeatedly uses the Strawman fallacy. Unfortunately, Peter doesn't use Disqus for the Comments section here, otherwise I would block you on here as well. This is my final reply to you. Any further comments from you to me will be ignored.


Nigel Kinbrum said...

Hi Peter,

Thank you for approving my two previous comments which are highly critical of your views on carbohydrates. I appreciate that.

Although we'll probably never agree about diet & nutrition, I like the way you moderate the comments here. Keep on keeping on!

Cheers, Nige

P.S. Hi Galina L. See, I'm not dead! :-D