Sunday, January 13, 2013

Well, Hyperlipid is on going within the limits of the time I have. At the moment I am busy fabricating the data which were recorded but not reported in this fat mouse paper.

All takes time.

Plus there were some interesting comments over on Sidereal's blog about why some people start off feeling great on ketogenic diets, then it all goes pear shaped. I've pulled out a couple of rat studies that might shed some light on this, for some people anyway.

And I still want to look at iron and PUFA in the liver. Or at least in yeasts cells (!!!! might not be quite the same but...).

And needs some serious thought (thanks Purposelessness, espec for the full text).

All of these need looking at from the Protons thread point of view.

Nick Lane has a new paper out on the origins of the electron transport chain precursor as life made the move away from the freebie energy gradients of the White Non Smokers to the wide ocean.

And then there is the triggering of apoptosis by blocking fat uptake in to mitochondria.

There is just so much going on and after the fantastic two weeks off of work over the Christmas period the case load is quite high at the moment. But when I get the chance...



karl said...

I think this is the Nick Lane link

RE: Sidereal's blog and low-carb diet end game stalling.

I've noticed the same deal with low-carb diets - often the last 10-15% of weight loss everything appears to stall. I've dug into possible explanations.

There is a thyroid bit - where the T4 => T3 pathway seems to get blocked. You can add T4, but T3 stays low. This pathway is mediated by iodothyronine deiodinase and needs selenium. It seemed like possibly adding selenium might make a difference - it did for me, but only for a few days. I've resorted to taking T3 until it was in the upper half of the normal range ( which may well be important for heart disease).

This led me to trying to understand what is known about the thyroid system and I came up with this
which is still quite incomplete (besides not knowing the relative magnitudes of these control loop signals) and it became apparent that there is much left for man to learn. ( more notes ..

It could be that this lack of T4 to T3 conversion is an indirect result of other systems. Thus right now I'm suspecting PUFA consumption. If the adipose set point is controlled by insulin sensitivity, as long as we eat too many PUFAs, we will remain some level over our set point.

This could easily be tested by avoiding PUFA, but that is more difficult than just avoiding carbs - the PUFAs are in most meats via corn feed.

I have noticed that If I eat mostly fish I tend to lose a little more. Could wild caught fish, grass and bug fed chickens, (and eggs) and grass fed dairy, pork, and beef make a difference in that last 10-15 lbs?

Stan Bleszynski said...

I was trying to follow that paper with other similar studies, for example this (begin with Discussion chapter):

- but find the amount of information a bit confusing and results contradictory, as if they/we were missing some other very important factor.


karl said...

One more note - notice that the homeostasis control of biological systems typically have a maze of over-lapping feed back loops ( as is the case for both BG and thyroid regulation).

A clear understanding of how and feedbacks work - ( the inputs can be summed, multiplied, difference, integrated, differentiated (in space and in time) is a bit complex ( familiar to some EEs ). If you get a basic understanding of these control loops it becomes clear that modulating the absolute level of one feedback (let's say the insulin level ) can cause non intuitive changes in other inputs levels (via their feed back sources )( the other loops can even over compensate inverting the expected result! ).

The differences of levels, also depend where they are sampled ( portal vein vs other veins ) which has to be taken into account. The tendency to over simplify and make assumptions is human, but must be overcome if a clear understanding is to be achieved.

(I posted this thinking of someone who I won't name (it is easy if you try) and that eliminates the distracting tit-for-tat of insults.)

Puddleg said...

Low carb stalling? Itsthewoo has just posted a great series about this, with much good sense not available elsewhere:

karl said...

Stan (Heretic)

re: High-fat diets cause insulin resistance despite
an increase in muscle mitochondria

Once again it looks like they consider sugar a form of fat - ( there was this deal I literally learned in grade school, that in an experiment we only change one variable at a time ......).
I don't think we can ignore the known effects of fructose.

Stargazey said...

Just a purely practical thought on losing those last few pounds. In my own case, I had to realize that once you near your ideal weight, calories count. You have to be willing to be a little bit hungry, if necessary. And maintenance doesn't improve that. You won't be starving, but you can't eat until you're full, either.

You also have to be willing to tweak your eating plan. In my own case, I finally realized that although mayonnaise and pork rinds are essentially zero carb, I don't have an off switch for either one. I had to eliminate both of them. For other people, the trigger foods may be completely different, but if you have one, you have to be willing to put it on your forbidden list. I also had to eliminate fake low-carb foods. In my body, there are no net carbs. Just carbs.

Long story short, if you're serious about reaching goal, you have to do an ongoing series of n=1 experiments. And keep doing them until you figure it out. And when the pounds sneak back on, go back to doing them again until you figure it out. It's lots of work. It requires lots of commitment. But it can be done if you choose to.

karl said...


The problem is that some of us - if we cut down on calories - end up getting cold and hypothyroid.

A look at thyroid tests will show high T4 and low T3. T3 is the active form of the thyroid hormone - it is what makes things happen. TSH can even go high in spite of elevated T4 if there is not enought T4 +>T3 conversion.

This is the body doing all it can to conserve calories - ( and pretty good proof that it isn't food reward that makes folks retain weight ).

I don't think anyone has a definitive understanding of this - Some possibilities:

* PUFA's are causing inappropriate insulin sensitivity.

* Selenium is washing out ( less retention of water - some folks lose potassium on low-carb) reducing deiodinase ( doubtful - supplementation does not seem to help )

Of course there could be something else going on that we don't understand yet.

There was a low-carb cruise that my report of was that the low-carbers tended to not lose that last 10-15 lbs..

Our bodies have really complex and robust homeostasis control - yet there appears that something beyond just dietary carbohydrates that also effects the body mass set point. I wish I knew what it was - I suspect we are seeing the effect of PUFA.

I can look at pictures I took during high-school in the early '70s - there just were very few kids that had a few extra pounds - compare that with my sons high-school - As I waited for him in the car - there was close to a third of the kids that were visibly overweight.

Several things have changed over the years - one of them is - a huge increase in PUFA consumption

The problem is many other things have changed as well, so we need quality research to see if PUFA is a factor in human diets.

It is also possible that the problem is due to permanent damage from eating excess carbs/transfats/CIAB/insert-your favorite-junkfood-here for long years.

Stargazey said...


I know about T3 and T4, and some people do have that problem. Solving it is a very important thing.

But the majority of the low-carbers I know who can't make it to goal simply will not give up the low-carb fake food, the rolls with dinner, or the mass quantities. They can discuss theory with you in great detail, but when it comes to the nitty gritty of actually doing what it takes, they simply will not put it into practice. I've sat with them at dinner. I've seen it.

Which is not to dicount the effects of PUFAs and leptin. But for many low-carbers the answer to losing those last few pounds is right there on their plate.

Gabriella Kadar said...

Karl: ' As I waited for him in the car - there was close to a third of the kids that were visibly overweight.'

That might be the problem right there: kids are not active at all. It might not take a lot of calories to walk but it sure reduces the amount of time a person can sit and snack.

I'm not discounting the additive effect of junk food. But the kids I went to school with ate junk too, mostly sweets and crisps. But back in those days a bag of crisps was tiny compared to what is for sale today. Sweets were purchased for pennies from the shop where different treats were measured out from big jars. No one could buy bags of stuff like what's available today. (1960s Putney, London, UK). We also got really decent hot school lunches with dessert, usually white cake and custard (hot or cold).

The quantity of snackfoods today is orders of magnitude larger than what was available when I was a child. People have no concept of 'serving size'. Go to any Costco or Walmart. The bags of snackfood are large enough to feed an army.

John said...

Ah, yes -- eat less, move more. How gratifying that in the end it turned out to be so simple!

And here's poor Peter, worrying his pretty little head over this proton nonsense. Potatoes, Pete! That's the ticket! Potatoes, and move that cute little butt of yours!

(And best to put your tinfoil hat back on, lest the Great and Powerful Wooo try to reprogram your brain again.)

Makro said...

"Ah, yes -- eat less, move more. How gratifying that in the end it turned out to be so simple!"

I wouldn´t discount the importance of "reward", I.e. making the human crapinabag that messes with dem protons palatable enough to chew down, sometimes in a compulsive fashion.

Nor would I discount the role of moving around for mitigating the metabolically negative effects of chewing down said crapinabag.

That´s why I appreciate Lustig´s efforts to create some kind of overarching framework that integrates reward, activity and metabolism into a coherent framework, despite disagreeing with a lot of what he says.

I for instance suspect tht Lustig is not entirely forthcoming on some topics, for instance low-carb and fat, in order to make his writings more... erm, palatable to the CICO crowd. (I base this assessment on the contrast between his earlier musings on the topic and what´s in his new book).

In the end though, I do believe that metabolism is indeed king. That´s why it´s not enough that something is "palatable" for it to cause metabolic dysfunction, and it´s also why it´s so hard to nail down exactly what is "hyperrewarding" if one discounts the importance of metabolism.

It´s also why exercise is most likely far more effective as a preventative measure rather than as a treatment once metabolic problems have already manifested themselveds.

karl said...

@Gabriella Kadar

While sedentary life styles are not healthy, they have tried repeatably to come up with a study where people lose weight via exercise - only one problem, it just doesn't work. Study after study have failed.

I see people at the gym that go on treadmills an hour a day - day-in day-out and they just don't lose weight. (They are quite strong (yet sadly remain obese ) )

I've seen sedentary life style blamed again and again - it just isn't supported by science. ( I can think of other health issues it might explain ). I'm also not willing to bite on the lack of morals (resistance to food reward) as the cause.

We have seen increased fructose containing sugar consumption, consumption of oxChol, changes in wheat strains, exposure to estrogen-mimic plastics, and several other factors change in the same time period.

I think the two most likely explanations are:

Sucrose (or HFCS) - the glucose bumps BG up - fructose kicks DNL into high gear - pumping trygly to amazing levels - causing leaks of FFA - the combination of FFA and glucose may damage (permanently?) BG control. ( If DNL is in high gear - is the production of long-chain FA increased? ) Trygly may block the transport of leptin across the blood-brain barrier - appetite fails to get modulated by Leptin. ( There are studies that show a sugar drink appetizer increases the amount eaten during the meal - but I'm not sure that leptin responds that fast?)

#2 Increases in PUFA causes inappropriately high adipose insulin sensitivity - effectively changing the set-point of adipose tissue. There is also evidence of O-6 PUFAs causing inflammation that may damage BG control.

Anyone that says they have a definitive answer, obviously does not understand the question.

Anonymous said...

Well, Peter, I never thought I'd utter these words, but I look forward to hearing what your rat studies have to say!

With regard to getting out of "the last 20 lbs syndrome" stall situation, I agree with Stargazey. I don't think there's any great mystery here. As you approach your ideal weight (asymptotically), calories start to count. Personally, I lost all my weight never counting or measuring anything, just eating VLC real foods to satiety, but there comes a point where this stops working and you just have to go a bit hungry at times if you are to lose the remaining weight. I know how to get out of my stall but for health, sanity and ideological reasons, I refuse to count calories and starve myself. Although socially desirable, I'm not really sure one needs to be BMI 20, medically speaking, but I do greatly respect those who get there.

Scott Russell said...
This comment has been removed by the author.
Scott Russell said...

RE: stalls,
I wonder exactly where our bodies want to be. Our subjective determination of "the last 15 lbs" might be exactly where our bodies want to be. I also have found that cyclic bursts of carbs are very useful in keeping metabolic rate high, especially post workout.

RE: activity,
Little kids tend to be active on their own accord. I have relatives with little ones, and they are unstoppable bundles of energy. Also amusing is watching the parents barter with them to get them to eat. Certainly throws a wrench in the ELMM philosophy, especially with regard to small children.

However, I think the uselessness of exercise is overstated. Strength training definitely carries numerous metabolic benefits. (Metformin actually is very similar to strength training in some regards.)

I definitely agree with karl re: PUFA, although I am wondering more and more about the role of antibiotics on our gut flora, or even just more generally how modern diets have shifted the flora in a negative manner.

nancan said...

I think the moving more simply gets one doing something positive rather than eating, and helps bolster the good eating habits, etc. When you feel less stress which is a super benefit of exercise like long walks, then you are less likely to feel hunger that stress also stimulates. Plus, if most low carb blogs are any clue, people get very good at finding less than good substitutions for old comfort foods, which means calories begin to go up after some time on a lc diet.

Galina L. said...

Sometimes I wonder how much modern style of exercise
(sit or lay down for 23 hours a day, very intense cardio one hour a day) and heavy involvement into sports contribute to the obesity problem. My mom was an accomplished sportsmen (speed skater)in her early 20, before I was born. She had to be put on a diet during two last month of pregnancy because I was growing in her uterus way too fast. My mom gained about 100 lb by the time she finished breastfeeding, and managed to loose all extra weight during one year, and dieted regularly even since. She was born normal weigh without her mom going on a diet, and grandma didn't get abnormally fat after pregnancies. We all are heavy build and look alike - my mom, grandma and me, but I am 4 inches taller. My grandma always enjoyed baked goodies with her after-meal sweet tea, liked to lay down after dinner, never walked fast, while my mom always did some sport-related activities, very often dieted, avoided sugary staff. She lives on the 4-th floor apartment last 40 years without an elevator, but ate rye bread with every meal and probably way too many fruits till recently. Guess who out of two more senior women of three was fatter by the age 70 and had an abnormal appetite? To be fair toward exercises, I have to add my mom spent 4 years as a small child in a foster home for evacuated children during World War II in Siberia. It could contribute to the whole picture.

I have to eat a VLC diet in order to feel well and to keep my weight stable after a weight loss.It looks like I am more pre-disposed to obesity than mom and grandma. I grew-up without any fast food, eating traditional Russian self-cooked meals, due to my mom's obsession with a weight loss, my diet was low in sugar and wheat.

karl said...

RE " Ah, yes -- eat less, move more. How gratifying that in the end it turned out to be so simple!"

Not to pick on the author of this nonsense, but I want to hold it up as an example to look at what motivates such stuff.

I think there are folks that want to reduce the obesity pandemic to something similar to a morals crusade. "You are fat because you have weak will, morally deficient etc" I suppose if they have not struggled with losing weight, or have succeeded via calorie restriction they can feel superior to those that have failed. I just don't understand where the hatred comes from.

I see people torturing themselves on treadmills - desperate to lose weight - I know that some people despise the sight of obesity - it troubles me that they would not want to help them instead.

Having lived on a low-fat low calorie diet for close to 10 years and now having lived on low-carb for 4 or 5 years I have no doubt of the difference. I can suppose that low-carb might not work for some people that have different metabolic/neurologic problems - and they could fail on low-carb, but I don't think that is where this hatred comes from.

It is very difficult to grasp the science of this obesity pandemic - I suppose that for many they will never get past a parrot-and-preach understanding and thus we get this kind of dogmatic conversation. It is human to not want to accept how much remains unknowable - but I have little patience for the hatred.

Stargazey said...
This comment has been removed by the author.
Stargazey said...


Thanks for your support. I should have been careful to mention that for health reasons it's fine to stay well above a BMI of 20. But if that's your goal, and if you have ever been obese, it's not a trivial undertaking. Just read Wooo's blog to get an idea of the constant unremitting effort involved.

Unrelated: (1) I know your name is a real word. Are you also an amateur astronomer? (2) "asymptotically." Now there's a word I haven't heard in a long long time. So true.

Unknown said...

The last 20 lbs comes from the Pentose phosphate shunt replenishing D-ribose. When you are burning fat you must have a constant supply of D-Ribose to replenish liver glycogen. Remember that the PPP rate limiting enzyme is G6PD and it blocked by carbs. And the PPP in RBC's produces massive amounts to replenish glutathione by increasing NADPH. In fact it is the main function of the PPP. Paleo and the carb addicts dont know it and the VLC do not realize their mitochondria is deficient in it because because its recycling takes 12 -24 months.

karl said...

@ Jack Kruse

About the D-Ribose info - can you point to any papers?

Where did you hear about this?

I once tried some D-Ribose - didn't notice anything.. So I'm wondering about dosages etc.. I've seen people pushing both D-Ribose and PPP, but I've not seen any papers ( not that they don't exist ).

Puddleg said...

This one's for blogblog (where he/she?)

Monosodium glutamate (MSG) intake is associated with the prevalence of metabolic syndrome in a rural Thai population.
Insawang T, Selmi C, Cha'on U, Pethlert S, Yongvanit P, Areejitranusorn P, Boonsiri P, Khampitak T, Tangrassameeprasert R, Pinitsoontorn C, Prasongwattana V, Gershwin ME, Hammock BD.
Department of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
Epidemiology and animal models suggest that dietary monosodium glutamate (MSG) may contribute to the onset of obesity and the metabolic syndrome.
Families (n = 324) from a rural area of Thailand were selected and provided MSG as the sole source for the use in meal preparation for 10 days. Three hundred forty-nine subjects aged 35-55 years completed the study and were evaluated for energy and nutrient intake, physical activity, and tobacco smoking. The prevalence of overweight and obesity (BMI ≥ 25 kg/m2), insulin resistance (HOMA-IR >3), and the metabolic syndrome (ATP III criteria) were evaluated according to the daily MSG intake.
The prevalence of the metabolic syndrome was significantly higher in the tertile with the highest MSG intake. Further, every 1 g increase in MSG intake significantly increased the risk of having the metabolic syndrome (odds ratio 1.14, 95% confidence interval-CI- 1.12 - 1.28) or being overweight (odds ratio 1.16, 95% CI 1.04 - 1.29), independent of the total energy intake and the level of physical activity.
Higher amounts of individual MSG consumption are associated with the risk of having the metabolic syndrome and being overweight independent of other major determinants.


(reply to letter about above study.)

"It is well-established that
obesity can be induced by an injection of MSG to new born rodents"

blogblog said...

@George Hendersen:
"This one's for blogblog (where he/she?)"

The paper you mention is an absolute farce. There wan't even a control group for comparison.

The Thai diet already contains huge amounts of MSG via the use of salty fermented foods such as fish sauce. Ading a tiny bit of MSG isn't going to make any difference.

blogblog said...

@George Hendersen,

you will also find that the MSG paper was pretty much torn to shreds by Dr Rogers after publication.

Anonymous said...


My goal isn't BMI 20. Having once been at BMI 36, I don't think it's realistic to aim that low. However, I do know that for some obese people that is their goal and anything short of it is considered a "stall" and a disappointment. Some people in our LC community also expect to get there while eating to satiety every time. It's important to manage people's expectations and point out that these are unrealistic expectations for most formerly obese people. What it takes to get rid of the last 20 is infinitely more than what it takes to get rid of the first 20 or even the first 40. Needless to say, the answer doesn't lie in d-ribose supplementation but in the kind of unrelenting dedication Woo describes as you mentioned.

(Hehe, I am not an amateur astronomer, though I take it you are? The explanation behind my screen name is much weirder (not astrology!). I don't wish to clutter up the place here but I am happy to tell you off-blog.)

Jane said...

Peter, I think you ought to ask Jack Kruse to explain himself. His latest comment is completely unintelligible. I have never heard of half the things he says, which doesn't necessarily mean they don't exist, but at the very least he should give references. You may remember that last time I asked him for references the very first one he gave completely contradicted what he'd said. It was astonishing, but at least we knew where we were.

Anonymous said...

Yes, I agree with Jane. This is an extraordinary claim, even for Kruse. Citations, por favor.

ItsTheWooo said...

Jack Kruse:

How do you think of these new gimmicks? It's like you are the most creative story telling 6 year old child I have ever seen.

When I read a Kruse comment, it makes me think of what it must be like to be doing an intake/admission assessment at the state ward.

karl said...


Busy - just a quick couple of links
D-ribose induces cellular protein glycation and impairs mouse spatial cognition.

Also -
"In summary, 20 grams of oral D-ribose/day for 14-days in healthy subjects did not elicit significant adverse hematological or biochemical abnormalities. However, a mild state of hypoglycemia and hyperuricemia can be observed after oral consumption."

On the TYP forum - several people tried it and found it lacking.

I have not found any studies showing that it does great things - and I don't like the idea that it might induce AGE production.

Things that drop BG, may do so in ways that are good for us - or bad - I'll wait for someone to come up with some research papers. lowcarb controls my BG..

Unknown said...

1. Benson, E. S., G. T. Evans, and B. E. Hallaway. Myocardial creatine phosphate and nucleotides in anoxic cardiac arrest and recovery. Am. J. Physiol. 201: 687, 1961.

2. Foker, J. E., S. Einzig, and T. Wang. Adenosine metabolism and myocardial preservation. J. Thorac. Cardiovasc. Surg. 80: 506-516, 1980.

3. Pasque, M. K. and A. Wechsler. Metabolic intervention to affect myocardial recovery following ischemia. Annals of Surgery 200: 1-10, 1984.

4. Lee, H. T., R. J. LaFaro, and G. E. Reed. Pretreatment of human myocardium with adenosine during open heart surgery. J Card. Surg. 10: 665-676, 1995.

5. Jennings, R. B. and C. Stanbergen, Jr. Nucleotide metabolism and cellular damage in myocardial ischemia. Annual Rev. Physiol. 47: 727 - 749, 1985.

6. Ward, H. B., J. A. St. Cyr, J. A. Cogordan, D. Alyono, R. W. Bianco, J. M. Kriett, & J. E. Foker. Recovery of adenine nucleotide levels after global myocardial ischemia in dogs, Surgery 96(2): 248-255, 1984.

7. Stathis, C. G., M. A. Febbraio, M. F. Carey, and R. J. Snow. Influence of sprint training on human muscle purine nucleotide metabolism. J. of Appl. Physiol. 76(4): 1802-1809, 1994.

8. Hellsten-Westing, Y., P. D. Balsom, B. Norman, and B. Sjodin. The effect of high-intensity training on purine metabolism in man. Acta Physiol. Scand. 149: 405-412, 1993.

9. Hellsten-Westing, Y., B. Norman, P. D. Balsom, and B. Sjodin. Decreased resting levels of adenine nucleotides in human skeletal muscle after high-intensity training. J. Appl. Physiol. 74(5): 2523-2528, 1993.

10. Tullson, P. C. and R. L. Terjung. Adenine nucleotide synthesis in exercising and endurance-trained skeletal muscle. Am. J. Physiol. 261: C342-C347, 1991.

11. Tullson, P. C., J. Bangsbo, Y. Hellsten, and E. A. Richter. IMP metabolism in human skeletal muscle after exhaustive exercise. J. Appl. Physiol. 78: 146-152, 1995.

12. Zimmer, H.-G. and E. Gerlach. Stimulation of myocardial adenine nucleotide biosynthesis by pentoses and pentitols. Pflugers Arch. 376: 223 - 227, 1978.

13. Zimmer, H.-G. Restitution of myocardial adenine nucleotides: acceleration be administration of ribose. J. Physiol., Paris 76(7): 769 - 775, 1980.

14. Zimmer, H.-G. and J. Schad. Ribose intervention in the cardiac pentose phosphate pathway is not species-specific. Science 223: 712 - 713, 1984.

15. Zimmer, H.-G. Regulation of and intervention into the oxidative pentose phosphate pathway and adenine nucleotide metabolism in the heart. Molec. Cell. Biochem. 160/161: 101 - 109, 1996.

Unknown said...

16. Pasque, M. K., T. L. Spray, G. L. Pellom, P. Van Trigt, R. B. Peyton, W. D. Currie, and A. S. Wechsler. Ribose-enhanced myocardial recovery following ischemia in the isolated working rat heart, J. Thorac. Cardiovasc. Surg. 83(3): 390-398, 1982.

17. St. Cyr, J. A., H. Ward, J. Kriett, D. Alyono, S. Einzig, R. Bianco, R. Andersoon, and J. Foker. Long term model for evaluation of myocardial metabolic recovery following global ischemia. In: N. Bratbar (ed.) Myocardial and Skeletal Muscle Bioenergetics pp. 401 -414, Plenum, New York, 1986.

18. St. Cyr, J. A., R. W. Bianco, J. R. Schneider, J. R. Mahoney, K. Tveter, S. Einzig, and J. E. Foker. Enhanced high energy phosphate recovery with ribose infusion after global myocardial ischemia in a canine model. J. Surg. Res. 46, 157 - 162, 1989.

19. Chatham, J. C., R. A. J. Challiss, G. K. Radda, and A-M. L. Seymour. Studies of the protective effect of ribose in myocardial ischaemia by using 31P-nuclear-magnetic-resonance spectroscopy. Biochem. Soc. Trans. 13: 885 - 886, 1985.

20. Hiatt, H. H. Glycogen formation via the pentose phosphate pathway in mice in vivo. J. Biol. Chem. 224: 851 - 859, 1957.

21. Segal, S. and J. Foley. The metabolism of D-ribose in man. J. Clinical Invest. 37: 719 - 735, 1958.

22. Bloom, B., F. J. Eisenberg, and D. J. Stetten. Glucose catabolism in liver slices via the phospho-gluconate oxidation pathway, J. Biol., Chem. 215: 461 - 466, 1954.

23. Coffey, R.G., Morse H., and Newburgh R.W. The synthesis of nucleic acid constituents in the early chick embryo, Biochim. Biophys. Acta 114: 547-558, 1965.

24. Zimmer, H.-G., H. Ibel, and G. Steinkopff. Studies on the hexose monophosphate shunt in the myocardium during development of hypertrophy. In: Advances in Myocardiology Volume 1 (eds. M Tajuddin, P. K. Das, M. Tariq, and N. S. Dhalla) pp. 487 - 492, University Park Press, Baltimore, 1980.

25. Zimmer, H.-G. and H. Ibel. Effects of ribose on cardiac metabolism and function in isoproterenol-treated rats. Am. J. Physiol. 245: H880 - H886, 1983.

26. Pliml, W, T. von Arnim, A. Stablein, H. Hofmann, H.-G. Zimmer, and E. Erdmann. Effects of ribose on exercise-induced ischaemia in stable coronary artery disease. Lancet 340: 507 - 510, 1992.

27. Angello, D. A., R. A. Wilson, D. Gee, and N. Perlmutter. Recovery of myocardial function and thallium-201 redistribution using ribose. Am. J. Card. Imaging 3(4): 256 - 265, 1989.

28. Angello, D. A., R. A. Wilson, and D. Gee. Effect of ribose on thallium-201 myocardial redistribution. J. Nucl. Med 29: 1943 - 1950, 1988.

29. Perlmutter, N. S., R. A. Wilson, D. A. Angello, R. T. Palac, J. Lin, and B. G. Brown. Ribose facilitates thallium-201 redistribution in patients with coronary artery disease. J. Nucl. Med. 32: 193- 200, 1991.

Unknown said...

30. Hegewald, M. G., R. T. Palac, D. A. Angello, N. S. Perlmutter, and R. A. Wilson. Ribose infusion accelerates thallium redistribution with early imaging compared with late 24-hour imaging without ribose. J. Am. Coll. Cardiol. 18: 1671 - 1681, 1991.

31. Gradus-Pizlo, I., S. Sawada, S. Lewis, S. Khouri, D. Segar, R. Kovacs, and H. Feigenbaum. Effect of D-ribose on the detection of the hibernating myocardium during the low dose dobutamine stress echocardiography. Circulation Suppl. 100(18):3394, 1999.

32. Pauli, D.F. and C.J. Pepine. D-ribose as a supplement for cardiac energy metabolism. J. Cardiovasc. Pharmacol. Therapeut. 5:249-258, 2000.

33. Brault, J.J. and R.L. Terjung. Purine salvage rates differ among skeletal muscle fiber types and are limited by ribose supply. Med. Sci. Sports Exer. Suppl. 31(5): 1365, 1999.

34. Zarzeczny, R., J. Brault, K. Abraham, C. Hancock, and R.L. Terjung. Purine salvage is not reduced during recovery following intense contractions. Med. Sci. Sports Exer. Suppl. 32(5): 214, 2000.

35. Brault, J.J., R.L. Terjung. Attempted expansion of resting muscle ATP content by a prolonged period of adenine salvage Med. Sci. Sports Exer. Suppl. 32(5): 213, 2000.

36. Witter, J., P. Gallagher, D. Williamson, M. Godard, and S. Trappe. Effects of ribose supplementation on performance during repeated high-intensity cycle sprints. Midwest Regional Chapter of the ACSM, October 2000.

37. Gallagher, P.M., D.L. Williamson, M.P. Godard, J. Witter, S.W. Trappe. Effects of ribose supplementation on adenine nucleotide concentration in skeletal muscle following high-intensity exercise. Midwest Regional Chapter of the ACSM, October 2000.

38. Antonio, J. D. Van Gammeren, and D. Falk. The effects of ribose supplementation of exercise performance in recreational male bodybuilders. Data on file at Bioenergy, Inc., 13840 Johnson Street N.E., Ham Lake, Minnesota 55304 USA.

And After my next blog post you might begin to see why you need to pay attention to the Pentose phosphate pathway a bit more Jane and Woo. Pity how bright people can be so closed.

LeonRover said...

Matthew 7:7

"Ask and it will be given to you."

Anonymous said...

You'd think it would have been easier for him just to point to this page...

Unknown said...

damn the link to buy RiboPure Crystals just leads to a squatted domain, can't buy :(. such a researched product too!

karl said...

I wonder how many of the links actually support the thesis? (I'm not going to sift through them)

(Reminds me of that LEF magazine - one or two links actually have something to do with the article - the rest are just a Google scholar dump - not exactly useful. And the next page is a full page add for what ever the article was hyping.)

Sadly the majority of published papers are just to fill the requirements to keep the grants coming - and then there are the ones by ex-hippies with peta/vegetarian/tree-hugger/granola/THC induced biases.

If you want to interest me in something, best to site 1-3 quality papers that aren't published in the one country selling the herb/supplement etc..

Stipetic said...

Jack, there's usually a gem somewhere in what you have to say. However, I'm no longer willing to wade through the fetid heap of excrement to get to it. If you didn't feel like you had to wrap everything relevant in bullshit, I'd listen. But if history is anything to judge by, you aren't capable of sticking to the facts(the plagiarism doesn't bother me much, though). Good luck to you. Maybe some day someone will sanitize your message for those who want the get to the sparkly bits of information. For now, I'll pass.

Anonymous said...

I'm sure Jane will let us know what's actually in those references given her ample library time.

Simon Carter said...

Don't you guys realize yet that Jack Kruse has all the answers! For only $398 a month you too can become a Gold Member with a monthly one hour consult with Jack himself. What a deal! Only $4,776 a year for all the secrets to "Optimum Health".

Jane said...

@Jack Kruse
How do those references support the idea that 'when you are burning fat you must have a constant supply of D-Ribose to replenish liver glycogen'?

How do they support the idea that G6PD is 'blocked by carbs'?

How do they support the idea that VLC people's mitochondria are deficient in the PPP? As far as I am aware the PPP is in the cytoplasm, and mitochondria use isocitrate dehydrogenase to make their NADPH.

Olga said...

Hi Peter,
Is it possible this could also be caused by a biotin deficiency? If people are eating eggs everyday for years, perhaps slightly under cooked, is it possible they could have a very slow onset marginal biotin deficiency after years of eating under cooked eggs, all the while making more demands on biotin by upregulating gluconeogenesis? The symptoms people describe are very similar to those of biotin deficiency. I would be very interested in your thoughts.

karl said...

Biotin is in a wide range of food choices - liver and green leafy vegetables - and a look at:

Would lead me to think that one would get plenty from eating meats..

From Wikipedia:
"Symptoms of biotin deficiency include:

Hair loss (alopecia)
Dermatitis in the form of a scaly, red rash around the eyes, nose, mouth, and genital area.
Neurological symptoms in adults, such as depression, lethargy, hallucination, and numbness and tingling of the extremities

I would doubt it is a problem for low-carbers - a test run with a supplement would let us know.


I'm wanting to do an experiment (n=1) on myself - trying to set up what to eat to reduce the PUFA content of my diet for a month or so. This is looking harder than I thought.

Replace olive oil with grass fed butter and/or coconut cream.. How to find chicken that isn't raised on corn? Lots of salmon..

Galina L. said...

probably, the New-Zealand lamb will suit your purpose as well, or even a very lean meat(like chicken breast or a white pork meat like pork lion) prepared with an added saturated fat.

Scott Russell said...

Biotin deficiency seems rather unlikely. Even undercooking egg whites destroys around 50%, and I think its only been experimentally induced with high-dose raw egg whites. So that's a no-go for the Rocky diet.

I'll second Galina with lean meat + fat. Also a good choice is chocolate (cocoa butter). And I'm stealing this from Wooo, but if you like things like almond butter, you can let it settle so the PUFAs rise to the top, pour them out, and replace them with something like Coconut oil.

Olga said...

Thanks for the input. It's mainly the symptoms of impaired gluconeogenisis and insomnia that I'm curious about. If pregnancy can induce a marginal deficiency, then I still wonder if it may be possible for someone who has been in ketosis for a long time.;jsessionid=5C3290E050A319400CE0747D375A14CE

Jeffrey of Troy said...

re: the last 10-20 pounds.

Chromium deficiency?

Unknown said...

Informative article, thanks for sharing!