Adding carbohydrate to a high-fat meal

dkm1987

New Member
Appl Physiol Nutr Metab. 2008 Apr;33(2):315-25.

Adding carbohydrate to a high-fat meal blunts postprandial lipemia in women and reduces meal-derived fatty acids in systemic circulation.

Knuth ND, Remias DB, Horowitz JF.

The lipemic response to a meal is an important independent risk factor for the development of cardiovascular disease. The purpose of this study was to determine the effect of adding carbohydrate (CHO) to a fat meal on the bioavailability of ingested fat in different blood lipid fractions in men and women. On two separate occasions, 18 healthy adults (9 women, 9 men) ate either a high-fat meal (0.7 grams fat per kilogram) (FAT), or the same meal with added CHO (1 gram CHO per kilogram) (FAT+CHO) in the morning after a 12 h fast. Both meals were supplemented with [13C]-palmitate (25 mg.kg-1). Plasma concentrations of triglyceride (TG), fatty acids, insulin, and glucose were measured in blood samples taken hourly from 0 to 8 h after the meal. In addition, we measured TG concentrations in chylomicron (CHYLO-TG) and in very-low-density lipoprotein (VLDL-TG) fractions. The addition of CHO to the fat meal increased plasma glucose and insulin concentrations identically in men and women. In contrast, adding CHO to the fat meal reduced the plasma TG concentration in the 5 h after the meal in women (average 5 h [TG]: 1.27 +/- 0.11 and 1.01 +/- 0.09 mmol.L-1; p <0.05), but not in men (1.25 +/- 0.23 and 1.24 +/- 0.20 mmol.L-1). Despite differences in the lipemic response to the meals between men and women, we found that adding carbohydrate to a fat meal decreased the bioavailability of meal-derived [13C]-palmitate in the systemic fatty acid pool, and decreased the incorporation of [13C]-palmitate into VLDL-TG in both men and women. In summary, adding CHO to a fat meal markedly blunted the plasma TG response in women, but not in men, which may augment the atherogenic potential after each meal in men.
 
<div>
(Dan Moore @ Apr. 29 2008,8:33)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">In summary, adding CHO to a fat meal markedly blunted the plasma TG response in women, but not in men, which may augment the atherogenic potential after each meal in men.</div>
I can never read these damn studies!

Can I get an interpreter?
 
<div>
(jwbond @ Apr. 29 2008,3:18)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"><div>
(Dan Moore @ Apr. 29 2008,8:33)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">In summary, adding CHO to a fat meal markedly blunted the plasma TG response in women, but not in men, which may augment the atherogenic potential after each meal in men.</div>
I can never read these damn studies!

Can I get an interpreter?</div>
Atherogenic means to cause atherosclerosis. Insulin is known to cause atherosclerosis already so that paper is nothing new.
 
<div>
(quadancer @ Apr. 29 2008,6:45)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Was new to me.</div>
What did you think was the cause of atherosclerosis?
 
<div>
(quadancer @ Apr. 29 2008,9:35)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">I didn't. I try not to eat great amounts of fat and carbs together.</div>
I see. Do you know about the glycemic index? It's a scale of glycemic load foods. Glycemic means to cause blood glucose to rise. For instance, ice cream has a low glycemic load yet is full of sugar. If it weren't for the fat it contains, ice cream would be just as high on the scale as pure sugar. The point is, fat will slow down carb absorption so if you must eat carbs, it's a good idea to eat fat with it too. At least, if you believe the glycemic index principles.

Yeah, I know. It goes against the hypothesis that we use the glucose and store the fat. But what can you do, ice cream does what it does.
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">I see. Do you know about the glycemic index? It's a scale of glycemic load foods. Glycemic means to cause blood glucose to rise. For instance, ice cream has a low glycemic load yet is full of sugar. If it weren't for the fat it contains, ice cream would be just as high on the scale as pure sugar. The point is, fat will slow down carb absorption so if you must eat carbs, it's a good idea to eat fat with it too. At least, if you believe the glycemic index principles.</div>

That is a very good point Martin.
 
Dan, should I refrain here from quoting from K&amp;N? I'm not sure if I can legally post quotes directly from it. Anyway, regarding the index, it can be virtually ignored for our purposes.
My point in avoiding meals high in fat and carbs together is that the body won't use up both for fuel, storing more fat due to that.
I know that's kind of simple, but it works for me. I know what happens when I mess up. Still, the average meal has carbs and fat together; I'm just referring to mass amounts with low protein macro. I believe that one or the other has to be greater; depending upon what mode the body is in, and most of us are in carb burning mode.
Have I missed something? Always ready to learn.
 
<div>
(quadancer @ Apr. 30 2008,5:16)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">My point in avoiding meals high in fat and carbs together is that the body won't use up both for fuel, storing more fat due to that.</div>
Whereas I've always figured the carbs produce an insulin spike that helps to tuck the fat safely away around my waistline.
sad.gif


That's why I try to avoid fats and carbs together -- but I'm ready to learn, too.
 
If you are exercising regularly and eating like a normal person should (even when bulking) I wouldn't worry about.

Now comes the oh so familar cry from masses,
&quot;But I'll gain fat&quot;........
my reply.......
&quot;uh yup you probably will because your bulking&quot;.

Here comes the next familar cry from the masses..........
But I don't want to get fat.......
my reply........
uh yup you probably will because your bulking.

Then of course comes the obligatory question..........
So how do I not get fat?........
My reply.......
uh don't bulk up or of course you can always turn to the darkside and start pinning.

Apologising ahead of time for the soapbox moment.

I know with all the banter here lately about insulin= really really bad mojo and I'm talking really bad mojo (I mean mojo so bad it's going to track down your great grandkids and F with them too) it's easy to take a stance against carbs. It's also easy to make assumptions when you look at those who have gone low carb and lost plenty of fat. Naturally I'm not disputing that going low carb will not have some specific benefit (mostly weight loss) but there is no &quot;magic&quot; here and there never was, it's essentially a matter of energy in vs out. Please don't hate me for speaking the truth, then again who cares if I'm hated.

Anyway, back to the rant. I find it amusing that with all the talk of insulin=again, some really really bad mojo (yup you get it by now bad bad mojo) that so much information was passed over and not brought up. But such is the way of the internet I guess. For instance there is an overwhelming body of evidence that points in a completely different direction and in fact IMO is far more convincing than insulin=really bad mojo (ohhhhhhhhh scary mojo, bad mojo, evil insulin is, evil I say).

Stepping down from the soapbox now..........
 
<div>
(Dan Moore @ May 01 2008,1:31)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">...
I know with all the banter here lately about insulin= really really bad mojo and I'm talking really bad mojo (I mean mojo so bad it's going to track down your great grandkids and F with them too) it's easy to take a stance against carbs. It's also easy to make assumptions when you look at those who have gone low carb and lost plenty of fat. Naturally I'm not disputing that going low carb will not have some specific benefit (mostly weight loss) but there is no &quot;magic&quot; here and there never was, it's essentially a matter of energy in vs out. Please don't hate me for speaking the truth, then again who cares if I'm hated.

Anyway, back to the rant. I find it amusing that with all the talk of insulin=again, some really really bad mojo (yup you get it by now bad bad mojo) that so much information was passed over and not brought up. But such is the way of the internet I guess. For instance there is an overwhelming body of evidence that points in a completely different direction and in fact IMO is far more convincing than insulin=really bad mojo (ohhhhhhhhh scary mojo, bad mojo, evil insulin is, evil I say).
...</div>
That is very telling of your own views on the matter. Your opinion seems to dismiss everything that is known about insulin. Which in turn brings doubt to your objectivity and ultimately your credibility.

Do you mean to say that a high carb diet does not cause hyperinsulinemia? Do you mean to say that hyperinsulinemia does not cause insulin resistance? Do you mean to say that insulin resistance does not cause obesity or Metabolic Syndrome? Do you mean to say that Metabolic Syndrome does not cause a chronic and acute hunger which, if fed carbs, simply exacerbates the entire hyperinsulinemia/insulin resistance/obesity/hunger loop? Or do you mean to say that it's all true but prefer not to take it too seriously?

This is a bodybuilding forum and we would be the first to argue that eating carbohydrate, because of its effect on insulin and because of the effect of insulin on protein uptake, would be a good thing. After all, we want an increased protein uptake so why should we not indulge in eating sugar just for its effect on insulin? I supposed this mechanism works for a while. But insulin resistance builds up over time. And hyperinsulinemia builds up over time. And eventually, the pancreas can't keep up. It can't overcome insulin resistance anymore. That's when things go really bad really quickly.

The alternative is that 66% of US adults overeat because they all have the same weak will. The same psychological problem. The same behavior. Somehow, they decided to eat more as if there was some overeating epidemic. Some psychological problem epidemic that, coincidentally, also caused the same behavioral character flaw: Overeating.

Alright, I'm done with the soapbox too.
 
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Some psychological problem epidemic that, coincidentally, also caused the same behavioral character flaw</div>
You said psychological. I believe social epidemics would be a closer description, and not at all hard to believe, as we have so many others. Even if psychological is apt, it still rings true; sheep tend to follow the herd and 66% isn't unbelievable. If you don't believe me, to to any church social and watch 'em eat. Lovable people, but disgusting habits.
 
<div>
(quadancer @ May 01 2008,5:42)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"> <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Some psychological problem epidemic that, coincidentally, also caused the same behavioral character flaw</div>
You said psychological. I believe social epidemics would be a closer description, and not at all hard to believe, as we have so many others. Even if psychological is apt, it still rings true; sheep tend to follow the herd and 66% isn't unbelievable. If you don't believe me, to to any church social and watch 'em eat. Lovable people, but disgusting habits.</div>
Right. So it's a character flaw. Is it innate or acquired? Is it affected by other agents or does it follow its own programmed course? Is there another character flaw that can cause us to act compulsively in a similar manner? Does this other character flaw somehow appear in the same epidemic fashion as this one does? Is there a historic reference to a common character flaw where a whole population did the same thing during the same period and that brought about the same consequences?

These are all reasonable questions once we delve into the psychological realm. We have to make a whole bunch of assumptions to get to this point but let's say we did and here we are, dealing with a psychological problem. So what's the therapy, the cure? Is there a therapy or cure to this epidemic? Some will immediately say that there is: Control calorie intake. To which I reply, it doesn't work for everybody so it's not an actual cure or even a therapy that can be applied to everybody. What about a drug, is there a drug that somehow fixes this character flaw? Remember, this is a psychological problem so the cure surely must be one that directly affects our brain. If we come up with a drug that somehow inhibits fat accumulation directly, then it's not a cure of the disease but only deals with the symptom. Remember, the character flaw is overeating. Excessive fat accumulation is a symptom of this disorder.

At least, that's what we end up with when we think of it as a simple caloric equation.
 
<div>
(Martin Levac @ May 02 2008,8:17)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Do you mean to say that a high carb diet does not cause hyperinsulinemia? Do you mean to say that hyperinsulinemia does not cause insulin resistance? Do you mean to say that insulin resistance does not cause obesity or Metabolic Syndrome? Do you mean to say that Metabolic Syndrome does not cause a chronic and acute hunger which, if fed carbs, simply exacerbates the entire hyperinsulinemia/insulin resistance/obesity/hunger loop? Or do you mean to say that it's all true but prefer not to take it too seriously?</div>
That is very telling of your own views on the matter. Your opinion seems to dismiss everything that is known about high carbohydrate diets. Which in turn brings doubt to your objectivity and ultimately your credibility.
 
<div>
(quadancer @ May 01 2008,5:42)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">...
sheep tend to follow the herd and 66% isn't unbelievable.
...</div>
Let's take a closer look at this proposition.

You pay taxes, I pay taxes, everybody pays taxes. We do so according to a system with a bunch of rules to determine how much taxes to pay. So we do that math and come up with a number at the end of the year and pay that amount for that year. The success rate, i.e. the number of people who pay their taxes, in this system is fairly high. I'd say it's about 90% or more. In other words, it works well.

We have a system in place for dietary recommendations. This system is intended to prevent all kinds of things. One of which is obesity. In the US, 66% of adults are overweight. In other words, the success rate of this system is no more than 34%. And it's growing worse every year. Quite a contrast to the taxes system, don't you think?

Do you know what this dietary system is based on? The Positive Caloric Balance hypothesis. The diet/heart hypothesis. The saturated fat/heart hypothesis. The cholesterol/atherosclerosis hypothesis. The dietary fat/obesity hypothesis. It really looks bad for all these hypotheses.
 
<div>
(Martin Levac @ May 01 2008,2:17)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Do you mean to say that a high carb diet does not cause hyperinsulinemia? Do you mean to say that hyperinsulinemia does not cause insulin resistance? Do you mean to say that insulin resistance does not cause obesity or Metabolic Syndrome? Do you mean to say that Metabolic Syndrome does not cause a chronic and acute hunger which, if fed carbs, simply exacerbates the entire hyperinsulinemia/insulin resistance/obesity/hunger loop? Or do you mean to say that it's all true but prefer not to take it too seriously?

This is a bodybuilding forum and we would be the first to argue that eating carbohydrate, because of its effect on insulin and because of the effect of insulin on protein uptake, would be a good thing. After all, we want an increased protein uptake so why should we not indulge in eating sugar just for its effect on insulin? I supposed this mechanism works for a while. But insulin resistance builds up over time. And hyperinsulinemia builds up over time. And eventually, the pancreas can't keep up. It can't overcome insulin resistance anymore. That's when things go really bad really quickly.

The alternative is that 66% of US adults overeat because they all have the same weak will. The same psychological problem. The same behavior. Somehow, they decided to eat more as if there was some overeating epidemic. Some psychological problem epidemic that, coincidentally, also caused the same behavioral character flaw: Overeating.

Alright, I'm done with the soapbox too.</div>
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Your opinion seems to dismiss everything that is known about insulin. </div>No this is obviously how you are taking my statement and not what I have said. Read what is written and do not read &quot;into&quot; what is written. My opinion is that insulin is not this evil substance that some fanatics tend to rave on about. Neither are carbohydrates.

If you would read the research instead of keeping this close minded approach to insulin you may see that hyperinsulinemia may not be the only cause of IR. You may even see that insulin may not be the only cause of obesity or Metabolic syndrome. Here is but a sample of the wealth of knowledge that is available if you ever decide to reach beyond Gary Taubes.

1: Maassen JA, Romijn JA, Heine RJ.
Fatty acid-induced mitochondrial uncoupling in adipocytes as a key protective
factor against insulin resistance and beta cell dysfunction: do adipocytes
consume sufficient amounts of oxygen to oxidise fatty acids?
Diabetologia. 2008 May;51(5):907-8. Epub 2008 Mar 4. No abstract available.
PMID: 18317722 [PubMed - in process]

2: Chess DJ, Stanley WC.
Role of diet and fuel overabundance in the development and progression of heart
failure.
Cardiovasc Res. 2008 Apr 10. [Epub ahead of print]
PMID: 18343896 [PubMed - as supplied by publisher]

3: Carpentier AC.
Postprandial fatty acid metabolism in the development of lipotoxicity and type 2
diabetes.
Diabetes Metab. 2008 Apr;34(2):97-107. Epub 2008 Mar 18.
PMID: 18353699 [PubMed - in process]

4: Wells GD, Noseworthy MD, Hamilton J, Tarnopolski M, Tein I.
Skeletal muscle metabolic dysfunction in obesity and metabolic syndrome.
Can J Neurol Sci. 2008 Mar;35(1):31-40. Review.
PMID: 18380275 [PubMed - indexed for MEDLINE]

5: Mittra S, Bansal VS, Bhatnagar PK.
From a glucocentric to a lipocentric approach towards metabolic syndrome.
Drug Discov Today. 2008 Mar;13(5-6):211-8. Epub 2008 Mar 7.
PMID: 18342796 [PubMed - in process]

6: Civitarese AE, Ravussin E.
Mitochondrial energetics and insulin resistance.
Endocrinology. 2008 Mar;149(3):950-4. Epub 2008 Jan 17. Review.
PMID: 18202132 [PubMed - indexed for MEDLINE]

7: Kim JA, Wei Y, Sowers JR.
Role of mitochondrial dysfunction in insulin resistance.
Circ Res. 2008 Feb 29;102(4):401-14. Review.
PMID: 18309108 [PubMed - indexed for MEDLINE]

8: Phielix E, Mensink M.
Type 2 Diabetes Mellitus and Skeletal Muscle Metabolic Function.
Physiol Behav. 2008 Jan 31. [Epub ahead of print]
PMID: 18342897 [PubMed - as supplied by publisher]

9: Guo Z.
Intramyocellular lipids: maker vs. marker of insulin resistance.
Med Hypotheses. 2008;70(3):625-9. Epub 2007 Sep 4.
PMID: 17766054 [PubMed - in process]

10: van Herpen NA, Schrauwen-Hinderling VB.
Lipid accumulation in non-adipose tissue and lipotoxicity.
Physiol Behav. 2007 Dec 5. [Epub ahead of print]
PMID: 18222498 [PubMed - as supplied by publisher]

11: Nabben M, Hoeks J.
Mitochondrial uncoupling protein 3 and its role in cardiac- and skeletal muscle
metabolism.
Physiol Behav. 2007 Nov 28. [Epub ahead of print]
PMID: 18191161 [PubMed - as supplied by publisher]

12: Jucker BM, Yang D, Casey WM, Olzinski AR, Williams C, Lenhard SC, Legos JJ,
Hawk CT, Sarkar SK, Newsholme SJ.
Selective PPARdelta agonist treatment increases skeletal muscle lipid metabolism
without altering mitochondrial energy coupling: an in vivo magnetic resonance
spectroscopy study.
Am J Physiol Endocrinol Metab. 2007 Nov;293(5):E1256-64. Epub 2007 Aug 28.
PMID: 17726146 [PubMed - indexed for MEDLINE]

13: Guldstrand MC, Simberg CL.
High-fat diets: healthy or unhealthy?
Clin Sci (Lond). 2007 Nov;113(10):397-9.
PMID: 17714072 [PubMed - indexed for MEDLINE]

14: Sinitskaya N, Gourmelen S, Schuster-Klein C, Guardiola-Lemaitre B, Pévet P,
Challet E.
Increasing the fat-to-carbohydrate ratio in a high-fat diet prevents the
development of obesity but not a prediabetic state in rats.
Clin Sci (Lond). 2007 Nov;113(10):417-25.
PMID: 17608620 [PubMed - indexed for MEDLINE]

15: Schrauwen-Hinderling VB, Roden M, Kooi ME, Hesselink MK, Schrauwen P.
Muscular mitochondrial dysfunction and type 2 diabetes mellitus.
Curr Opin Clin Nutr Metab Care. 2007 Nov;10(6):698-703. Review.
PMID: 18089950 [PubMed - indexed for MEDLINE]

16: Civitarese AE, Smith SR, Ravussin E.
Diet, energy metabolism and mitochondrial biogenesis.
Curr Opin Clin Nutr Metab Care. 2007 Nov;10(6):679-87. Review.
PMID: 18089947 [PubMed - indexed for MEDLINE]

17: Saris WH, Heymsfield SB.
All metabolic roads lead to mitochondrial (dys)-function.
Curr Opin Clin Nutr Metab Care. 2007 Nov;10(6):661-3. No abstract available.
PMID: 18089944 [PubMed - indexed for MEDLINE]

18: Yaspelkis BB 3rd, Lessard SJ, Reeder DW, Limon JJ, Saito M, Rivas DA, Kvasha
I, Hawley JA.
Exercise reverses high-fat diet-induced impairments on compartmentalization and
activation of components of the insulin-signaling cascade in skeletal muscle.
Am J Physiol Endocrinol Metab. 2007 Oct;293(4):E941-9. Epub 2007 Jul 10.
PMID: 17623749 [PubMed - indexed for MEDLINE]

19: Boudina S, Sena S, Theobald H, Sheng X, Wright JJ, Hu XX, Aziz S, Johnson JI,
Bugger H, Zaha VG, Abel ED.
Mitochondrial energetics in the heart in obesity-related diabetes: direct
evidence for increased uncoupled respiration and activation of uncoupling
proteins.
Diabetes. 2007 Oct;56(10):2457-66. Epub 2007 Jul 10.
PMID: 17623815 [PubMed - indexed for MEDLINE]

20: Medina-Gomez G, Gray S, Vidal-Puig A.
Adipogenesis and lipotoxicity: role of peroxisome proliferator-activated receptor
gamma (PPARgamma) and PPARgammacoactivator-1 (PGC1).
Public Health Nutr. 2007 Oct;10(10A):1132-7. Review.
PMID: 17903321 [PubMed - indexed for MEDLINE]

21: Helge JW, Bentley D, Schjerling P, Willer M, Gibala MJ, Franch J,
Tapia-Laliena MA, Daugaard JR, Andersen JL.
Four weeks one-leg training and high fat diet does not alter PPARalpha protein or
mRNA expression in human skeletal muscle.
Eur J Appl Physiol. 2007 Sep;101(1):105-14. Epub 2007 May 26.
PMID: 17530276 [PubMed - indexed for MEDLINE]

22: Dube JJ, Bhatt BA, Dedousis N, Bonen A, O'Doherty RM.
Leptin, skeletal muscle lipids, and lipid-induced insulin resistance.
Am J Physiol Regul Integr Comp Physiol. 2007 Aug;293(2):R642-50. Epub 2007 May 9.
PMID: 17491114 [PubMed - indexed for MEDLINE]

23: Toledo FG, Menshikova EV, Ritov VB, Azuma K, Radikova Z, DeLany J, Kelley DE.
Effects of physical activity and weight loss on skeletal muscle mitochondria and
relationship with glucose control in type 2 diabetes.
Diabetes. 2007 Aug;56(8):2142-7. Epub 2007 May 29.
PMID: 17536063 [PubMed - indexed for MEDLINE]

24: Heilbronn LK, Gregersen S, Shirkhedkar D, Hu D, Campbell LV.
Impaired fat oxidation after a single high-fat meal in insulin-sensitive
nondiabetic individuals with a family history of type 2 diabetes.
Diabetes. 2007 Aug;56(8):2046-53. Epub 2007 Apr 24.
PMID: 17456847 [PubMed - indexed for MEDLINE]

25: Guo ZK.
Intramyocellular lipid kinetics and insulin resistance.
Lipids Health Dis. 2007 Jul 24;6:18. Review.
PMID: 17650308 [PubMed - indexed for MEDLINE]

26: Noland RC, Thyfault JP, Henes ST, Whitfield BR, Woodlief TL, Evans JR, Lust
JA, Britton SL, Koch LG, Dudek RW, Dohm GL, Cortright RN, Lust RM.
Artificial selection for high-capacity endurance running is protective against
high-fat diet-induced insulin resistance.
Am J Physiol Endocrinol Metab. 2007 Jul;293(1):E31-41. Epub 2007 Mar 6.
PMID: 17341547 [PubMed - indexed for MEDLINE]

27: Alevizos I, Misra J, Bullen J, Basso G, Kelleher J, Mantzoros C,
Stephanopoulos G.
Linking hepatic transcriptional changes to high-fat diet induced physiology for
diabetes-prone and obese-resistant mice.
Cell Cycle. 2007 Jul 1;6(13):1631-8. Epub 2007 May 1.
PMID: 17603298 [PubMed - indexed for MEDLINE]

28: Berndt J, Kovacs P, Ruschke K, Klöting N, Fasshauer M, Schön MR, Körner A,
Stumvoll M, Blüher M.
Fatty acid synthase gene expression in human adipose tissue: association with
obesity and type 2 diabetes.
Diabetologia. 2007 Jul;50(7):1472-80. Epub 2007 May 11.
PMID: 17492427 [PubMed - indexed for MEDLINE]

29: Menshikova EV, Ritov VB, Ferrell RE, Azuma K, Goodpaster BH, Kelley DE.
Characteristics of skeletal muscle mitochondrial biogenesis induced by
moderate-intensity exercise and weight loss in obesity.
J Appl Physiol. 2007 Jul;103(1):21-7. Epub 2007 Mar 1.
PMID: 17332268 [PubMed - indexed for MEDLINE]

30: Choi CS, Fillmore JJ, Kim JK, Liu ZX, Kim S, Collier EF, Kulkarni A,
Distefano A, Hwang YJ, Kahn M, Chen Y, Yu C, Moore IK, Reznick RM, Higashimori T,
Shulman GI.
Overexpression of uncoupling protein 3 in skeletal muscle protects against
fat-induced insulin resistance.
J Clin Invest. 2007 Jul;117(7):1995-2003.
PMID: 17571165 [PubMed - indexed for MEDLINE]

31: Qatanani M, Lazar MA.
Mechanisms of obesity-associated insulin resistance: many choices on the menu.
Genes Dev. 2007 Jun 15;21(12):1443-55. Review.
PMID: 17575046 [PubMed - indexed for MEDLINE]

32: Østergård T, Jessen N, Schmitz O, Mandarino LJ.
The effect of exercise, training, and inactivity on insulin sensitivity in
diabetics and their relatives: what is new?
Appl Physiol Nutr Metab. 2007 Jun;32(3):541-8. Review.
PMID: 17510695 [PubMed - indexed for MEDLINE]

33: Schenk S, Horowitz JF.
Acute exercise increases triglyceride synthesis in skeletal muscle and prevents
fatty acid-induced insulin resistance.
J Clin Invest. 2007 Jun;117(6):1690-8. Epub 2007 May 17.
PMID: 17510709 [PubMed - indexed for MEDLINE]

34: Caldwell SH, Ikura Y, Iezzoni JC, Liu Z.
Has natural selection in human populations produced two types of metabolic
syndrome (with and without fatty liver)?
J Gastroenterol Hepatol. 2007 Jun;22 Suppl 1:S11-9. Review.
PMID: 17567458 [PubMed - indexed for MEDLINE]

35: Maffeis C, Castellani M.
Physical activity: an effective way to control weight in children?
Nutr Metab Cardiovasc Dis. 2007 Jun;17(5):394-408. Epub 2007 Mar 2. Review.
PMID: 17336508 [PubMed - indexed for MEDLINE]

36: Befroy DE, Petersen KF, Dufour S, Mason GF, de Graaf RA, Rothman DL, Shulman
GI.
Impaired mitochondrial substrate oxidation in muscle of insulin-resistant
offspring of type 2 diabetic patients.
Diabetes. 2007 May;56(5):1376-81. Epub 2007 Feb 7.
PMID: 17287462 [PubMed - indexed for MEDLINE]

37: Shoelson SE, Herrero L, Naaz A.
Obesity, inflammation, and insulin resistance.
Gastroenterology. 2007 May;132(6):2169-80. Review.
PMID: 17498510 [PubMed - indexed for MEDLINE]

38: Steinberg GR.
Inflammation in obesity is the common link between defects in fatty acid
metabolism and insulin resistance.
Cell Cycle. 2007 Apr 15;6(8):888-94. Epub 2007 Apr 11. Review.
PMID: 17438370 [PubMed - indexed for MEDLINE]

39: Guo W, Pirtskhalava T, Tchkonia T, Xie W, Thomou T, Han J, Wang T, Wong S,
Cartwright A, Hegardt FG, Corkey BE, Kirkland JL.
Aging results in paradoxical susceptibility of fat cell progenitors to
lipotoxicity.
Am J Physiol Endocrinol Metab. 2007 Apr;292(4):E1041-51. Epub 2006 Dec 5.
PMID: 17148751 [PubMed - indexed for MEDLINE]

40: Boushel R, Gnaiger E, Schjerling P, Skovbro M, Kraunsøe R, Dela F.
Patients with type 2 diabetes have normal mitochondrial function in skeletal
muscle.
Diabetologia. 2007 Apr;50(4):790-6. Epub 2007 Feb 15.
PMID: 17334651 [PubMed - indexed for MEDLINE]

41: Hawley JA, Lessard SJ.
Mitochondrial function: use it or lose it.
Diabetologia. 2007 Apr;50(4):699-702. No abstract available.
PMID: 17279353 [PubMed - indexed for MEDLINE]

42: Heilbronn LK, Gan SK, Turner N, Campbell LV, Chisholm DJ.
Markers of mitochondrial biogenesis and metabolism are lower in overweight and
obese insulin-resistant subjects.
J Clin Endocrinol Metab. 2007 Apr;92(4):1467-73. Epub 2007 Jan 23.
PMID: 17244782 [PubMed - indexed for MEDLINE]

43: Corcoran MP, Lamon-Fava S, Fielding RA.
Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty
acids and exercise.
Am J Clin Nutr. 2007 Mar;85(3):662-77. Review.
PMID: 17344486 [PubMed - indexed for MEDLINE]

44: Nishikawa T, Araki E.
Impact of mitochondrial ROS production in the pathogenesis of diabetes mellitus
and its complications.
Antioxid Redox Signal. 2007 Mar;9(3):343-53. Review.
PMID: 17184177 [PubMed - indexed for MEDLINE]

45: Delarue J, Magnan C.
Free fatty acids and insulin resistance.
Curr Opin Clin Nutr Metab Care. 2007 Mar;10(2):142-8. Review.
PMID: 17285001 [PubMed - indexed for MEDLINE]

46: Conley KE, Amara CE, Jubrias SA, Marcinek DJ.
Mitochondrial function, fibre types and ageing: new insights from human muscle <u>in
vivo.</u>Exp Physiol. 2007 Mar;92(2):333-9. Epub 2006 Dec 14. Review.
PMID: 17170059 [PubMed - indexed for MEDLINE]

47: Sreekumar R, Nair KS.
Skeletal muscle mitochondrial dysfunction &amp; diabetes.
Indian J Med Res. 2007 Mar;125(3):399-410. Review.
PMID: 17496364 [PubMed - indexed for MEDLINE]

48: Civitarese AE, Carling S, Heilbronn LK, Hulver MH, Ukropcova B, Deutsch WA,
Smith SR, Ravussin E; CALERIE Pennington Team.
Calorie restriction increases muscle mitochondrial biogenesis in healthy humans.
PLoS Med. 2007 Mar;4(3):e76.
PMID: 17341128 [PubMed - indexed for MEDLINE]

49: Thyfault JP, Cree MG, Zheng D, Zwetsloot JJ, Tapscott EB, Koves TR, Ilkayeva
O, Wolfe RR, Muoio DM, Dohm GL.
Contraction of insulin-resistant muscle normalizes insulin action in association
with increased mitochondrial activity and fatty acid catabolism.
Am J Physiol Cell Physiol. 2007 Feb;292(2):C729-39. Epub 2006 Oct 18.
PMID: 17050616 [PubMed - indexed for MEDLINE]

50: Schrauwen P.
High-fat diet, muscular lipotoxicity and insulin resistance.
Proc Nutr Soc. 2007 Feb;66(1):33-41.
PMID: 17343770 [PubMed - indexed for MEDLINE]
 
WrongWrongWrong. You keep putting blame on things that apply only to your personal objective, causing you to miss the broader perspective, IMO.
Boys in the 'Hood know that joining a gang will get them dead, as in NOT BREATHING NOW or in Jail...but do they go elsewhere? No. Why? They follow the masses, believe what &quot;feels&quot; the best, and ignore the obvious consequences. Hitler led masses into obvious destruction, looking at it from an objective viewpoint. What makes people follow destructive paths? It's not from paying attention to science, common sense, morality, or any hypothesis that you can apply. It's from a basic need to belong. And if everyone else is getting careless and sloppy, there ya go.
Eventually epidemics become pandemic once they're spread or overpopularized, and it seems evident here and in Europe. Hedonism is not a new concept either; very attractive to many. I don't see the confusion here.
We can stick all the fancy names we want (I sound really ignorant here) on all the theories we come up with, scientific ideals or what have you, but people are still people and outside of direct application when it comes to usage of the mind. So we do our best with Psychology, Sociology, and Psychiatry to define mannerism and behavior. And they will still eat stupidly.
 
<div>
(quadancer @ May 01 2008,7:27)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">...
We can stick all the fancy names we want (I sound really ignorant here) on all the theories we come up with, scientific ideals or what have you, but people are still people and outside of direct application when it comes to usage of the mind. So we do our best with Psychology, Sociology, and Psychiatry to define mannerism and behavior. And they will still eat stupidly.</div>
It sounds like you're saying that if people are left to their own devices, i.e. without government or some form of leadership, they're going to choose the destructive path.

That's not what Price found. In isolated populations that hadn't yet been &quot;civilized&quot;, dental caries was extremely rare. So was the entire spectrum of chronic diseases including obesity, diabetes and cancer. As far as we know, those isolated populations were left to their own devices and were doing quite well by all accounts. It's only when they were introduced to civilized foods, i.e. refined carbs, that they started getting sick.

I could make the argument that only when they introduced an arbitrary form of leadership did things start to go bad. By leadership, I mean leadership of their everyday actions. Things like eating, sleeping, and just living. When those activities are governed by their own inherent functions, i.e. we eat for nourishment and we sleep to fulfill a basic need, then there is no other choice but to do them only to satisfy the requirements of their own inherent functions. In other words, survival drives us to do what we must. How do the national dietary recommendations fit into all this?

We eat to feed ourselves but what determines what to eat or when to eat or how much to eat? The primary regulator of food intake is hunger. It's only natural to consider that, in a situation where one overeats, this mechanism is disrupted. If it is disrupted, what's the cause? The first place I'd look is at the food itself. Is it possible that the food itself causes us to overeat? If it does, what property does that food have that makes us eat more than our share?

The obesity epidemic is growing worse. By all measures, this means the national dietary advice is a failure. People are not stupid. They'll follow advice if it looks alright and if it's easy. The dietary advice is simple: Eat less and/or be more active. We got both the 'looks alright' part and the easy part taken care of. So why does it still not work to reduce obesity? Why are people still overeating? Could it be that the food that these people eat somehow makes them eat more of it? It's a reasonable question.

Aaron_F posted one graph that showed the effect carbohydrate has on total energy intake. Shouldn't we look at that in more detail? It sure looks to me like if there's anything that would cause people to choose the destructive path in this case, then it must be the carbohydrate.

By the way, activity level has not decreased. If anything, it has increased if the number of people going to the gym is any indication. So that can't be the cause of the worsening obesity epidemic. People did not choose the destructive path on this aspect either.
 
<div>
(Dan Moore @ May 01 2008,7:23)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">...that hyperinsulinemia may not be the only cause of IR. You may even see that insulin may not be the only cause of obesity or Metabolic syndrome.
...</div>
Are you suggesting that there is something else, something common to all those millions of people that causes them to grow fat independently of carbohydrate, insulin, insulin resistance and Metabolic Syndrome? That would be easy to test: Don't eat carbohydrates and see what happens. Find the research that does just that and let's discuss the results.
 
Back
Top