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Friday, February 8, 2013

Quick commentary on Dr. Lustig’s take on fructose




I’ve recently had the opportunity to skim through Dr. Robert Lustig’s book, Fat Chance.  I haven’t watched his YouTube lecture (and I don’t plan to), which people have used to justify the avoidance of fructose (and sugar) on, but I’m assuming that the main arguments in the lecture are summarized in his book.    I’m planning on addressing the entire book, bit by bit, but first, herein, I will provide commentary on each of Dr. Lustig’s conclusions about fructose, which can be found on pages 120 to 121.  Dr. Lustig’s comments are in red.


1. Triple the dose mean the liver needs triple the energy to metabolize this combo versus glucose alone, depleting the liver cell of adenosine triphosphate (or ATP, the vital chemical that conveys energy within cells).  ATP depletion leads to the generation of the waste product uric acid.  Uric acid causes gout and increases blood pressure.

This supposition was addressed briefly here.  

In short, there is no evidence that fructose, in the way that it’s consumed in the US now (i.e., with glucose), increases blood uric acid levels or causes gout.

Large doses of liquid fructose, unreflective of the consumption habits of the majority of the US population, does, in fact, raise uric acid levels, but this rise is only transient, no where near the levels seen in gout, and not necessarily harmful.


2. The fructose does not go to glycogen.  It goes straight to the mitochondria.  Excess acetyl-CoA if formed, exceeding the mitochondria’s ability to metabolize it.

Although the conversion of fructose to glycogen is a minor pathway, fructose results in more glycogen storage than glucose does.  In one of the few studies available, the infusion of fructose resulted in about 360 percent more liver glycogen than glucose infusion did, as measured by biopsy (Nilsson & Hultman, 1974).

Isotope tracer studies show that fructose is predominantly converted to glucose and lactate, supplying fuel to cells in the periphery.  In comparison, the conversion of fructose to fat–via acetyl-CoA–is a minor, and highly energy-consuming, pathway, as is its conversion to glycogen (Tappy & Lê, 2010).

The proportion of each pathway used by fructose is further fine-tuned by (1) the type of sugar co-ingested with fructose, (2) the amount of fructose ingested, and (3) the body’s energy needs at the moment.  Ingesting fructose with glucose, for instance, increases the oxidation rate of each sugar far more than if each sugar were ingested alone.  

As an aside, Dr. Lustig’s assertion here is especially hard to stomach because fructose, in a non-insulin dependent manner, (1) stimulates the trapping of glucose inside cells, which is the first step in synthesizing glycogen (e.g., McGuinness & Cherrington, 2003) and (2) increases the flux of glucose through the enzyme called glycogen synthase, which catalyzes the conversion of glucose to glycogen (Petersen, Laurent, Yu, Cline, & Shulman, 2001).  These processes are impaired in diabetics, who have been shown to have lower amounts of glycogen in their muscle and liver.

So although fructose doesn’t itself convert to glycogen in significant quantities, it does in fact stimulate the conversion of glucose to glycogen.  Moreover, fructose is unlikely to lead to the accumulation of acetyl CoA. (Nonetheless, much like alcohol, extra protein and nutrients provide further insurance against the accumulation of fat in the liver by high doses of pure fructose.)


3. The excess acetyl-CoA leaves the mitochondria and gets metabolized into fat, which can promote heart disease.

This is unfortunately wishful thinking.  The idea that fructose leads to the excessive accumulation of acetyl CoA and fat in the liver relies on (1) theoretical explorations of biochemical pathways and mechanisms and (2) studies in which fructose is given alone and in doses unreflective of the consumption habits of the population at large. 

In short, experimental evidence does not bear out the supposition here.  Fructose is predominantly converted to glucose and lactate, and oxidized to carbon dioxide.


4. Fructose activates a liver enzyme, which is the bridge between liver metabolism and inflammation.  This inactivates a key messenger of insulin action, leading to liver insulin resistance.

I think Dr. Lusting is alluding to protein kinase C (the epsilon [ϵ] isoform), which is an enzyme activated by diacylglycerol (though diacylglycerol is not unconditionally required for this activation).  In turn, the activation of protein kinase C impairs insulin signaling  (Samuel et al., 2007).

Recall that the excessive delivery of fatty acids to the liver leads to the accumulation of lipids therein–one of which is diacylglycerol (Samuel et al., 2004). Experimentally, because it doesn’t stimulate the secretion of insulin, fructose does not activate LPL on fat cells or HSL inside fat cells, thereby leading to an intense mobilization and delivery of fatty acids to the liver and other organs.

However, once again, because fructose is always present with glucose, and because glucose stimulates the secretion of insulin, fatty acid mobilization, free fatty acids, and the flux of fat to the liver (and subsequent inactivation of the insulin receptor) are kept in check.

Fructose in the liver could convert to fat more efficiently than glucose, but quantitatively the amount of fat synthesized is inconsequential (Chong, Fielding, & Frayn, 2007). 

Fructose increases energy expenditure, more than any other carbohydrate does, and so is least likely to result in an accumulation of fat in organs not designed to store much fat, and thus, to activate protein kinase C.  Inflammation, it turns out, although present in most cases of diabetes, is secondary to this accumulation of fat in organs and tissues as it relates to causing insulin resistance (Mayerson et al., 2002; Kitt Falk Petersen et al., 2005).


5. The lack of insulin effect in the liver means that there is no method to keep the glucose down, so the blood glucose rises, which can eventually lead to diabetes.

Earlier in his book, Dr. Lustig makes the point that fructose is always present with glucose.  High fructose corn syrup, for instance, contains either (1) 53 percent glucose and 42 percent fructose or (2) 42 percent glucose and 55 percent fructose.

So you can’t have it both ways, because with glucose, the dangerous increase in blood glucose levels is buffered against, as glucose stimulates the secretion of insulin (fructose, to a small extent, does as well).

Nonetheless, even the ingestion of pure fructose of upwards of 200 grams per day leads only to a modest decrease in hepatic and peripheral insulin sensitivity.  The hypercaloric feeding of pure fructose can increase the deposition of fat in the liver in humans, but, fortunately, no where near the levels seen, for instance, in NAFLD (Faeh et al., 2005; Lê et al., 2006, 2009).


6. The liver insulin resistance means the pancreas has to release extra insulin, which can force energy into fat cells, leading to obesity.  And the fat cells that fill up most are in the visceral fat, the bad kind associated with metabolic disease.

The faulty premise here, that fructose causes hepatic insulin resistance effectively nullifies Dr. Lustig’s deduction that fructose leads to hyperinsulinemia, obesity, etc.

(Note that carbohydrates suppress cortisol, which promotes fat storage in visceral storage sites more than any other single factor.)


7. The high insulin can drive the growth of many cancers.10

Fructose alone decreases blood insulin and glucose levels.


8. The high insulin blocks leptin signaling, giving the hypothalamus the false sense of “starvation,” and causing you to eat more.

See the answer to the above question.


9. Fructose may also contribute to breakdown of the intestinal barrier.  Normally the intestine prevents bacteria from entering the bloodstream.  The intestinal breakdown may lead to a breach in the walls of the intestines.  The result is a “leaky gut,”11 which could increase the body’s exposure to inflammation and more ROS.  This worsens insulin resistance and drives the insulin levels even higher.12

The conclusion drawn here, that fructose leads to “leaky gut," is based entirely on evidence that is circumstantial.

In the study that is linked to, subjects with NAFLD were compared with healthy subjects with respect to blood lipopolysaccharide (LPS) levels (an indirect measure of intestinal permeability) and fructose intake.

Although subjects with NAFLD had higher blood LPS levels that coincided with, on average, higher intakes of fructose as compared to healthy subjects, data of this type can’t provide causal information.  There are a myriad of reasons, aside from the differences in fructose intake, that could explain the differences in LPS levels observed. (Offhand the subjects with NAFLD, on average, were fatter, older and ate more calories.)  

Fructose alone could increase the generation of LPS because of its malabsorption in the intestines, thereby providing fodder for certain intestinal bacteria to proliferate.  But as I keep laboring the point, the co-ingestion of glucose greatly increases the efficiency of fructose absorption.  Because fructose is typically co-ingested with glucose, the LPS raising effect of fructose in this study is probably overblown and irrelevant.

(Unsaturated fats, starches, hypothyroidism and poor cardiovascular functioning [by diminishing circulation to the bowels] I think are greater contributors to intestinal permeability and the subsequent increase in LPS levels.)


10. Fructose undergoes the Maillard (browning) reaction 7 times faster than glucose, which can damage cells directly.  Although the experiments are in their infancy, preliminary results suggest that in a susceptible environment, fructose can accelerate aging and the development of cancer.

On paper, because it linearizes more readily than glucose does, fructose is postulated to glycate amine groups of molecules at a very high rate, which is the initial step of advanced glycation end product (AGE) formation (i.e., the Maillard reaction). 

It’s conceivable that in uncontrolled diabetes, the saturation of the polyol pathway, which leads to the accumulation of fructose and sorbitol, could lead to the uncontrolled generation of reactive aldehydes, namely methylglyoxal and 3-deoxoglucosone.  Methylglyoxal and 3-deoxoglucosone, in turn, form a myriad of AGE.

In reality, on absorption, fructose is cleared rapidly such that blood fructose levels hardly rise by more than 10 milligrams per deciliter in the blood.  Fructose also provides pyruvate, which is postulated to, via competition, prevent glycation reactions.  And, fructose, to some extent, curtails the flux of glucose through the polyol pathway, thereby preventing the accumulation of the reducing cofactor NADH, so the conditions that favor lipid peroxidation processes are thusly staved off.

Lipid peroxidation processes provide many of reactive aldehydes as well.  Some in vitro studies have shown that AGE are produced faster, and more abundantly, in the presence of unsaturated fat than sugar.  

It’s difficult to determine where AGE originate from  because glycation reactions happen quickly, there is great overlap in the AGE produced from glucose and fatty acids, and in vivo isotope tracer studies have not been conducted.  Nonetheless, the idea that sugar leads to the pathological accumulation of AGE is poorly substantiated.


11. The data on fructose and dementia in humans are currently correlative and indirect.  However, the data on insulin resistance and dementia show clear causation.  African Americans and Latinos are the biggest fructose consumers and those with the highest waist circumference (a marker for insulin resistance).  Coincidentally, they also have the highest risk for dementia.

I concur with Dr. Lustig about the relationship among insulin resistance, waist circumference (an indirect measure of visceral fat), and dementia.  As to how that happens, on the other hand, when more data becomes available, we will have ample opportunity to judge better.
                                                              

References

Chong, M. F.-F., Fielding, B. A., & Frayn, K. N. (2007). Mechanisms for the acute effect of fructose on postprandial lipemia. The American journal of clinical nutrition, 85(6), 1511–20. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/17556686
Faeh, D., Minehira, K., Schwarz, J.-M., Periasamy, R., Periasami, R., Park, S., Seongsu, P., et al. (2005). Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men. Diabetes, 54(7), 1907–13. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15983189
Lê, K.-A., Faeh, D., Stettler, R., Ith, M., Kreis, R., Vermathen, P., Boesch, C., et al. (2006). A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans. The American journal of clinical nutrition, 84(6), 1374–9. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/17158419
Lê, K.-A., Ith, M., Kreis, R., Faeh, D., Bortolotti, M., Tran, C., Boesch, C., et al. (2009). Fructose overconsumption causes dyslipidemia and ectopic lipid deposition in healthy subjects with and without a family history of type 2 diabetes. The American journal of clinical nutrition, 89(6), 1760–5. doi:10.3945/ajcn.2008.27336
Mayerson, A. B., Hundal, R. S., Dufour, S., Lebon, V., Befroy, D., Cline, G. W., Enocksson, S., et al. (2002). The effects of rosiglitazone on insulin sensitivity, lipolysis, and hepatic and skeletal muscle triglyceride content in patients with type 2 diabetes. Diabetes, 51(3), 797–802. Retrieved from http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2995527&tool=pmcentrez&rendertype=abstract
McGuinness, O. P., & Cherrington, A. D. (2003). Effects of fructose on hepatic glucose metabolism. Current opinion in clinical nutrition and metabolic care, 6(4), 441–8. doi:10.1097/01.mco.0000078990.96795.cd
Nilsson, L. H., & Hultman, E. (1974). Liver and muscle glycogen in man after glucose and fructose infusion. Scandinavian journal of clinical and laboratory investigation, 33(1), 5–10. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/4827760
Petersen, K F, Laurent, D., Yu, C., Cline, G. W., & Shulman, G. I. (2001). Stimulating effects of low-dose fructose on insulin-stimulated hepatic glycogen synthesis in humans. Diabetes, 50(6), 1263–8. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11375325
Petersen, Kitt Falk, Dufour, S., Befroy, D., Lehrke, M., Hendler, R. E., & Shulman, G. I. (2005). Reversal of nonalcoholic hepatic steatosis, hepatic insulin resistance, and hyperglycemia by moderate weight reduction in patients with type 2 diabetes. Diabetes, 54(3), 603–8. Retrieved from http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2995496&tool=pmcentrez&rendertype=abstract
Samuel, V. T., Liu, Z.-X., Qu, X., Elder, B. D., Bilz, S., Befroy, D., Romanelli, A. J., et al. (2004). Mechanism of hepatic insulin resistance in non-alcoholic fatty liver disease. The Journal of biological chemistry, 279(31), 32345–53. doi:10.1074/jbc.M313478200
Samuel, V. T., Liu, Z.-X., Wang, A., Beddow, S. A., Geisler, J. G., Kahn, M., Zhang, X., et al. (2007). Inhibition of protein kinase Cepsilon prevents hepatic insulin resistance in nonalcoholic fatty liver disease. The Journal of clinical investigation, 117(3), 739–45. doi:10.1172/JCI30400
Tappy, L., & Lê, K.-A. (2010). Metabolic effects of fructose and the worldwide increase in obesity. Physiological reviews, 90(1), 23–46. doi:10.1152/physrev.00019.2009





41 comments:

  1. Great to see you weighing in. This isn't my area of expertise, but he does address anthropology, economics, food politics (he's a wannabe food police), and history in his book and those chapters are incredibly wrong in almost every single way. I'll have to post a review later.

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  2. Hi Melissa, I'm just getting started. Look forward to reading the review.

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  3. 1) fructose metabolism varies between individuals more than glucose metabolism does (or can). (The same is true for galactose.) As well as studying large groups for statistical purposes, we should look at what happens in the outliers in those studies. Short term studies of healthy volunteers don't say much.
    Studying the effects on ATP or uric acid using the average amount consumed is missing the point that some people consume much less, some much more, than this amount. Are any clinical trials being done to determine how fructose is metabolized in young children? I doubt it.
    You rightly say that glucose and fructose should be considered together, I'd like to see what happens when we add galactose to the mix.

    4) I believe Lustig is talking about the transcription factor Fox-01. Fox-01 promotes gluconeogenesis in liver and, I think, decreases insulin output.

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    Replies
    1. HI George, By in the way it's consumed, I mean with glucose. Some people do indeed ingest more fructose than others, but even at the extreme ends of ingestion (i.e., in the 95+ percentile) fructose isn't consumed in quantities needed to produce the toxic, uric acid increasing effect.

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    2. I'm fairly confident that there's a genetic variation that produces this effect. I mean, for gout we are only talking 62.3 cases per 100,000 in 1995-1996 (Rochester Minn. http://ccjm.org/content/75/Suppl_5/S9.full.pdf). Only a tiny fraction of the people who consume fructose. But for many of them, it may be the factor driving the high uric acid, with other factors, perhaps higher carb intake overall or food sensitivities, leading to deposition.

      Individual variation in fructose metabolism in man
      http://journals.cambridge.org/download.php?file=%2FBJN%2FBJN26_02%2FS0007114571000801a.pdf&code=97fdce26d8b3ff9b417e3dfa463249ff

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    3. This comment has been removed by the author.

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  4. This extra-canonical Gary Taubes work has some of the fructose-uric acid research history.
    http://www.fourhourworkweek.com/blog/2009/10/05/gout/

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  5. I did my dissertation on methylglyoxal. In my opinion, you can get a reasonable glimpse into the predominant sources of AGEs by using LC-MS/MS to identify specific AGEs and compare them to in vitro AGE production from different sources. I realize it would be nice to have tracer studies mapping everything out, though I think definitive studies like that are probably unreasonably complicated. In any case, I do not think that lipid peroxidation is the main source of AGEs in vivo because it generates glyoxal much more effectively than methylglyoxal, whereas AGEs derived from methylglyoxal are found much more abundantly than those formed by glyoxal in vivo. That said, it's common to attribute methylglyoxal primarily to glycolysis, but I think there's better in vivo evidence for its derivation from acetone. I suspect both are sources, but I highly suspect acetone is a more significant source, especially in diabetes.

    I've blogged about this here:

    http://blog.cholesterol-and-health.com/2011/10/where-do-most-ages-come-from-o.html

    Chris

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    Replies
    1. Thanks for the detailed response Dr. Masterjohn. I think I'll address the points you've made here in a future post.

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    2. You're welcome and I look forward to your thoughts.

      I should add that there are additional complicating factors, like the specific half-lives of each AGE, but I don't think accounting for that changes the fact that methylglyoxal-derived AGEs seem to be far more abundant than glyoxal-derived AGEs, which is inconsistent with lipid peroxidation being the main source of AGEs. Also, keep in mind that a lot of experiments in this area use CML as a representative AGE, when it isn't representative of what's found in vivo at all, and a lot of papers quantify AGEs by immunoassay, often non-specifically, which is not very useful.

      Chris

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  6. Also, AGEs are constantly victimized with a bad reputation for causing disease, but there's a decent reason to consider them signaling molecules. Methylglyoxal is a substrate for gluconeogenesis, and might act as a switch to spare glucose under conditions of glucose deprivation. I've blogged about that too:

    http://blog.cholesterol-and-health.com/2012/01/we-really-can-make-glucose-from-fatty.html

    Chris

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    Replies
    1. Your point that MG could be signal molecule & a substrate of GNG is well taken but the discussion usually hinges on the excess levels of MG, either from its increased production, decreased clearance, or both. Much like ROS, which also has a physiological signaling role in cells, within a certain range, beyond which pathology kicks in.

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    2. I realize this, but the potential for a signaling role is generally not acknowledged or glossed over without being given any weight in the scientific literature, and the situation is usually much worse than that in the popular literature, so I think it is important to point that out. I don't think "signaling" and "pathology" are necessarily distinct. For example, methylglyoxal stimulating ROS in turn stimulating insulin resistance likely contributes to pathological insulin resistance, but that doesn't mean it isn't fundamentally a signaling process meant to cope with a suboptimal situation, such as cellular energy overload for example.

      Chris

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    3. Right, good point Dr. Masterjohn; I was unclear @ the distinction between the two in haste. Though even in the cases of "cellular overload" neutralizing ROS can be beneficial.

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    4. Hi Andrew,

      I think that it would be very difficult to tease apart neutralizing the signal and remedying the situation. Impairment in the mitochondrial ability to handle energy, for example, is likely to result in high production of ROS, which have the potential to exert macromolecular damage, but generally don't because they are diverted into signaling processes that decrease energy uptake (such as insulin resistance). Most treatments that would neutralize the ROS would more or less remedy or at least improve the situation justifying the ROS-induced signaling, so they're likely to result in improvements. I don't think we're really disagreeing on anything. I just don't think it's easy to tease apart the signaling roles from the pathology, or to demarcate the good amount of ROS from the bad amount of ROS.

      Chris

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    5. Right on, I WAS agreeing with you about the last part of ^ paragraph ;)

      Delete
  7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170136/

    Fructose-fed rhesus monkeys: A nonhuman primate model of insulin resistance, metabolic syndrome, and type 2 diabetes

    "In this report, we demonstrate that a high-fructose diet in rhesus monkeys produces insulin resistance and many features of the metabolic syndrome, including central obesity, dyslipidemia, and inflammation within a short period of time; moreover, a subset of monkeys developed type 2 diabetes. Given the rapidity with which the metabolic changes occur, and the ability to control for many factors that cannot be controlled for in humans, fructose feeding in rhesus monkeys represents a practical and efficient model system in which to investigate the pathogenesis, prevention, and treatment of diet-induced insulin resistance and its related co-morbidities."

    "A commercial monkey chow diet (Lab Diets 5047, Advance Protocol Old World Primate) was provided ad libitum to all the monkeys. This is a grain-based standard primate diet that provides 30% energy as protein, 11% energy as fat, and 59% energy as carbohydrate. In addition, all monkeys were provided 500 ml/day of a fruit-flavored (Kool-Aid®, Kraft Foods) 15% fructose-sweetened beverage (75 grams of fructose). Beverage intake was recorded daily and food intake was recorded for one week at baseline, and then for one-week periods at three month intervals during the 12-month study period."

    "During the course of the 12 month study, every monkey (n=29) developed components of the metabolic syndrome (principally increased body adiposity, insulin resistance, and dyslipidemia); four monkeys (~15% of the study cohort) developed frank T2DM (defined by a fasting blood glucose concentration ≥126 mg/dl)."


    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673878/

    Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans


    ReplyDelete
  8. http://ajcn.nutrition.org/content/86/5/1495.full

    Dietary glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study

    Results: Glycemic load and added sugars were not significantly associated with pancreatic cancer risk. The risk increased with higher intakes of total sugars, fructose, and sucrose, and the association with fructose was significant when the highest and lowest quartiles were compared (relative risk: 1.35; 95% CI: 1.02, 1.80; P for trend = 0.046). A significant association was found with fruit and juices intake (1.37; 1.02, 1.84; P for trend = 0.04) but not with soda intake. Statistical evidence of a significant interaction with body mass index was present only for sucrose intake (P = 0.04). A comparison of the highest and lowest quartiles of sucrose intake in overweight or obese participants gave a relative risk of 1.46 (0.95–2.25; P for trend = 0.04), but the comparison was not significant in normal-weight participants.

    Conclusions: High fructose and sucrose intakes may play a role in pancreatic cancer etiology. Conditions such as overweight or obesity in which a degree of insulin resistance may be present may also be important.

    ReplyDelete
  9. I like this. This is productive. Ever since the ideas of Ray Peat and his disciples began infiltrating the more mainstream "Paleo"-oriented health community, there has been a largely unmet need for respectful, sober, detailed discussion of the issues, instead of an exaggerated bashing of Paleo and deification of Peat, or simply parroting Peat's claims (or their counterarguments) instead of addressing their merits and flaws in detail.

    The fructose debate is centrally important. It seems that virtually no one with a modicum of intelligence currently studying these issues still believes that saturated fat is inherently dangerous, or that cereal grains are ideal human foods, or that muscle meat is entirely benign or beneficial even in ridiculously high doses, or that carbohydrate avoidance is a viable or necessary path to good health, or that a drastic reduction in metabolic rate attendant to carbohydrate restriction is a desirable condition.

    The most controversial issue still remaining--and the principal difference between sensible "Paleo" diets like Jaminet's Perfect Health Diet and the Ray Peat approach--is the question of whether to obtain carbohydrate primarily from sugars or from relatively benign starches like well-cooked tubers and white rice. Of course, the main reason for choosing potatoes and rice over sugars in the PHD approach is the presence of fructose in sugars. So if we could confidently and convincingly exonerate fructose of its supposed dangers, or firmly establish the risks of starch consumption, we could arrive at a pretty good consensus as to what constitutes the ideal human diet (with allowances made, of course, for individual differences).

    I'm still skeptical of the claim that fructose is necessary or even benign, but I may be naive. Thanks for your work, Andrew, it'll help me refine my understanding of these things over time.

    ReplyDelete
  10. http://www.alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/

    ReplyDelete
  11. Andrew

    Here is another sugar myth that is accepted as fact.

    Sugar rots your teeth. Does it?

    http://www.livescience.com/2011-truth-tooth-decay.html

    ReplyDelete
    Replies
    1. Degrading the enamel was the only negative thing I could think of about sugar. Thanks coconuts :)

      Delete
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  28. Czym tak naprawdę jest cholesterol?

    Cholesterol istnieje tak naprawdę niebezcelowym szczegółem
    cel polskiego stworu. Jest niezastąpionym budulcem cel zaœ hormonów.

    Cholesterol częściowo wyniknie w naszym systemie
    — w wątrobie, zaœ częściowo wyprowadza z pokarmu, który na co dzień konsumujemy.
    Z natur onej jest przeto niczym kiepskim.

    To co istnieje napastnicze, owe jego zbytek. A sumienniej rechocą ujmując nadmiar "złoœliwego cholesterolu" wariantu LDL.
    Przyjmuje się, że jego stężenie we farb onym winno przewyższać 100 mg/dl.
    Z drugiej stron macie "rzetelny cholesterol" rodzaju
    HDL, jakiego stężenie niego winnyœcie wykraczać 50 mg/dl u kobiety
    i 40 mg/dl obok mężczyzn. Całkowite stężenie cholesterolu w polskiej farb powinnom
    mieścić się w przedziale 114-200 mg/dl.


    Jednak jeœli te taksy zostają przekroczone natomiast ów poziom utrzymuje się przez dłuższy czas, owe zdołasz spodziewać się okazałych trudów.


    Dlatego nie zezwalajże do takiego poziomu — obstawajże cholesterol na właściwym poziomie.


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