Re: Re: Starch, Monounsaturated Fats and Prostate Cancer

[Guest guest]

There are many variables but it seems to me that there is an essential need for

some poly, so we need some omega 6 and 3. And we need them in a certain ratio.

In addition, we dont want to overdo the fat of any kind, nor the omega 6s.

So, perhaps that is the confusion. Poly is essential and at some level is good.

But too much omega 6 and/or too much above and beyond the need is not good.

Jeff

________________________________

From: on behalf of citpeks

Sent: Mon 04/17/06 9:35 AM

Subject: [ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

Once again, we seem to be faced with making dietary decisions from

partial or contradictory information. The bulk of the information

seems to suggest that:

1) linoleic acid, a polyunsaturated omega-6 fatty acid, is an

essential fatty acid that reduces cholesterol, among other

things.(PMID: 8503356)

2) ratios of omega-6:omega-3 of 4:1 have been associated with reduced

mortality from cardiovascular disease, suppressed inflammation in

patients with rheumatoid arthritis, and decreased risk of breast

cancer.(PMID: 12442909)

One BIG variable is the amount of fat in the diet. Anybody who

consumes animal fats, which are high in saturated fats, should

probably balance their diet by adding sources of omega-6 like walnuts

or sunflower seeds to avoid high cholesterol levels. At the same

time, sources of omega-3 (flaxseed, fish oil) should be consumed in

enough quantity to achieve the 4:1 ratio. All this has to be done

while restricting calories to avoid becoming overweight or obese, of

course.

Optimum Nutrition = Perfect Balance.

Tony

> >

> > Hi folks:

> >

> > Males should find this of interest:

> >

> > " CONCLUSIONS: Starch and monounsaturated fatty acids were directly

> > associated with prostate cancer risk and polyunsaturated fatty acids

> > were inversely associated. "

> >

> > PMID: 15598953

> >

> > Free full text is available.

> >

> > Rodney.

> >

>

[Guest guest]

There are many variables but it seems to me that there is an essential need for

some poly, so we need some omega 6 and 3. And we need them in a certain ratio.

In addition, we dont want to overdo the fat of any kind, nor the omega 6s.

So, perhaps that is the confusion. Poly is essential and at some level is good.

But too much omega 6 and/or too much above and beyond the need is not good.

Jeff

________________________________

From: on behalf of citpeks

Sent: Mon 04/17/06 9:35 AM

Subject: [ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

Once again, we seem to be faced with making dietary decisions from

partial or contradictory information. The bulk of the information

seems to suggest that:

1) linoleic acid, a polyunsaturated omega-6 fatty acid, is an

essential fatty acid that reduces cholesterol, among other

things.(PMID: 8503356)

2) ratios of omega-6:omega-3 of 4:1 have been associated with reduced

mortality from cardiovascular disease, suppressed inflammation in

patients with rheumatoid arthritis, and decreased risk of breast

cancer.(PMID: 12442909)

One BIG variable is the amount of fat in the diet. Anybody who

consumes animal fats, which are high in saturated fats, should

probably balance their diet by adding sources of omega-6 like walnuts

or sunflower seeds to avoid high cholesterol levels. At the same

time, sources of omega-3 (flaxseed, fish oil) should be consumed in

enough quantity to achieve the 4:1 ratio. All this has to be done

while restricting calories to avoid becoming overweight or obese, of

course.

Optimum Nutrition = Perfect Balance.

Tony

> >

> > Hi folks:

> >

> > Males should find this of interest:

> >

> > " CONCLUSIONS: Starch and monounsaturated fatty acids were directly

> > associated with prostate cancer risk and polyunsaturated fatty acids

> > were inversely associated. "

> >

> > PMID: 15598953

> >

> > Free full text is available.

> >

> > Rodney.

> >

>

[Guest guest]

I think LA would be associated with all cancers because that's the arachidonic acid pathway to inflammatory eicosanoids. Mediated by EPA perhaps - maybe not in everyone. Also mediated by ASA.

LA is a true essential fatty acid:

http://www.merck.com/mrkshared/mmanual/section1/chapter2/2e.jsp

"EFAs are needed for many physiologic processes, including maintaining the integrity of the skin and the structure of cell membranes and synthesizing prostaglandins and leukotrienes. Eicosapentaenoic acid and docosahexaenoic acid are important components of the brain and retina."

Without the full text, I can't understand the article. I think the data may be skewed by the weight of the patients and the fact that PCa is highly associated with choosing relatives. Also age.

Look at:

http://www.benbest.com/health/essfat.html#chem

pgdn about 12

It leaves out the AA metabolite, eicosatetraynoic acid which mediates the AA production.

Here's what I suggested to another guy:

I think there's a possibility that aging effects theconversion of ALA to EPA and that's why my EPA/DHAsupplement. And I seriously doubt EPA regulates the AA(ARA) pathway in the main.I started my review with: (get the full texts)Calder PC, Yaqoob P, Thies F, Wallace FA, Miles EA. Fatty acids and lymphocyte functions.Br J Nutr. 2002 Jan;87 Suppl 1:S31-48. Review.PMID: 11895154"A high fat diet can impair lymphocyte function.""Amongst the fatty acids it is the n-3 PUFA which possessthe most potent immunomodulatory activities, and amongst then-3 PUFA those from fish oil (EPA and DHA) are morebiologically potent than ALNA."While you're there get:Calder PC. N-3 polyunsaturated fatty acids and immune cell function.Adv Enzyme Regul. 1997;37:197-237. Review.PMID: 9381972AND:Belury MA, KE, Locniskar M, Fischer SM. Eicosapentaenoic and arachidonic acid: comparison ofmetabolism and activity in murine epidermal cells.Lipids. 1989 May;24(5):423-9.PMID: 2547133AND:Calder PC. n-3 polyunsaturated fatty acids and cytokine production inhealth and disease.Ann Nutr Metab. 1997;41(4):203-34. Review.PMID: 9363294 At that point I decided this was way over my head but itwas obvious the regulation of the AA pathway by EPA was notnearly as important to me as the antitumor benefitsindicated by the competition of EPA with AA in tumours.

previously posted:

http://www.osti.gov/energycitations/product.biblio.jsp?osti_id=5267213

5,8,11,14-Eicosatetraynoic acid, a competitive inhibitor of arachidonic acid metabolism, rapidly and reversibly inhibited DNA synthesis in U937 cells.^

PMID: 12837767

Arachidonic acid or 5,8,11,14-eicosatetraynoic acid (ETYA), a non-metabolized analog of arachidonic acid, induced a time-dependent inhibition of Na+ transport.

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

PUFA inversely associated with prostate cancer? Isn't the evidencebeing strongly established that exactly the opposite is the case whenit comes to consumption of omega-6 FA? More than enough to make anyonesuspicious?Conclusions drawn by the authors of a famous study published a coupleof months ago:Taken together, the data suggest that arachidonic acid via conversionto PGE2 plays an important role in stimulation of growth-related genesand proliferation via PI3K signaling and NF-{kappa}B translocation tothe nucleus. (Cancer Res 2006; 66(3): 1427-33)http://cancerres.aacrjournals.org/cgi/content/abstract/66/3/1427Introducing another abtract to the same research:For the past 60 years, dietary intake of essential fatty acids hasincreased. Moreover, the omega-6 fatty acids have recently been foundto play an important role in regulation of gene expression.Proliferation of human prostate cells was significantly increased 48 hafter arachidonic acid (AA) addition. http://carcin.oxfordjournals.org/cgi/content/abstract/26/9/1520--- In , "Rodney" <perspect1111@...> wrote:>> Hi folks:> > Males should find this of interest:> > "CONCLUSIONS: Starch and monounsaturated fatty acids were directly > associated with prostate cancer risk and polyunsaturated fatty acids > were inversely associated."> > PMID: 15598953> > Free full text is available.> > Rodney.>

[Guest guest]

I think LA would be associated with all cancers because that's the arachidonic acid pathway to inflammatory eicosanoids. Mediated by EPA perhaps - maybe not in everyone. Also mediated by ASA.

LA is a true essential fatty acid:

http://www.merck.com/mrkshared/mmanual/section1/chapter2/2e.jsp

"EFAs are needed for many physiologic processes, including maintaining the integrity of the skin and the structure of cell membranes and synthesizing prostaglandins and leukotrienes. Eicosapentaenoic acid and docosahexaenoic acid are important components of the brain and retina."

Without the full text, I can't understand the article. I think the data may be skewed by the weight of the patients and the fact that PCa is highly associated with choosing relatives. Also age.

Look at:

http://www.benbest.com/health/essfat.html#chem

pgdn about 12

It leaves out the AA metabolite, eicosatetraynoic acid which mediates the AA production.

Here's what I suggested to another guy:

I think there's a possibility that aging effects theconversion of ALA to EPA and that's why my EPA/DHAsupplement. And I seriously doubt EPA regulates the AA(ARA) pathway in the main.I started my review with: (get the full texts)Calder PC, Yaqoob P, Thies F, Wallace FA, Miles EA. Fatty acids and lymphocyte functions.Br J Nutr. 2002 Jan;87 Suppl 1:S31-48. Review.PMID: 11895154"A high fat diet can impair lymphocyte function.""Amongst the fatty acids it is the n-3 PUFA which possessthe most potent immunomodulatory activities, and amongst then-3 PUFA those from fish oil (EPA and DHA) are morebiologically potent than ALNA."While you're there get:Calder PC. N-3 polyunsaturated fatty acids and immune cell function.Adv Enzyme Regul. 1997;37:197-237. Review.PMID: 9381972AND:Belury MA, KE, Locniskar M, Fischer SM. Eicosapentaenoic and arachidonic acid: comparison ofmetabolism and activity in murine epidermal cells.Lipids. 1989 May;24(5):423-9.PMID: 2547133AND:Calder PC. n-3 polyunsaturated fatty acids and cytokine production inhealth and disease.Ann Nutr Metab. 1997;41(4):203-34. Review.PMID: 9363294 At that point I decided this was way over my head but itwas obvious the regulation of the AA pathway by EPA was notnearly as important to me as the antitumor benefitsindicated by the competition of EPA with AA in tumours.

previously posted:

http://www.osti.gov/energycitations/product.biblio.jsp?osti_id=5267213

5,8,11,14-Eicosatetraynoic acid, a competitive inhibitor of arachidonic acid metabolism, rapidly and reversibly inhibited DNA synthesis in U937 cells.^

PMID: 12837767

Arachidonic acid or 5,8,11,14-eicosatetraynoic acid (ETYA), a non-metabolized analog of arachidonic acid, induced a time-dependent inhibition of Na+ transport.

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

PUFA inversely associated with prostate cancer? Isn't the evidencebeing strongly established that exactly the opposite is the case whenit comes to consumption of omega-6 FA? More than enough to make anyonesuspicious?Conclusions drawn by the authors of a famous study published a coupleof months ago:Taken together, the data suggest that arachidonic acid via conversionto PGE2 plays an important role in stimulation of growth-related genesand proliferation via PI3K signaling and NF-{kappa}B translocation tothe nucleus. (Cancer Res 2006; 66(3): 1427-33)http://cancerres.aacrjournals.org/cgi/content/abstract/66/3/1427Introducing another abtract to the same research:For the past 60 years, dietary intake of essential fatty acids hasincreased. Moreover, the omega-6 fatty acids have recently been foundto play an important role in regulation of gene expression.Proliferation of human prostate cells was significantly increased 48 hafter arachidonic acid (AA) addition. http://carcin.oxfordjournals.org/cgi/content/abstract/26/9/1520--- In , "Rodney" <perspect1111@...> wrote:>> Hi folks:> > Males should find this of interest:> > "CONCLUSIONS: Starch and monounsaturated fatty acids were directly > associated with prostate cancer risk and polyunsaturated fatty acids > were inversely associated."> > PMID: 15598953> > Free full text is available.> > Rodney.>

[Guest guest]

perhaps a better diagram:

http://circ.ahajournals.org/cgi/content/full/108/2/155

perhaps the explanation:

"However, the present results are in contrast to the customary assumption that high intake of n-6 fatty acids antagonizes the antiinflammatory effects of n-3 fatty acids. One possible explanation for our observation is that n-6 fatty acids lower soluble TNF receptor levels by indirectly reducing insulin resistance.20,27 Furthermore, the activities of the 6 and 5-desaturase (which are the rate-limiting steps for arachidonic acid and EPA synthesis in humans) and the activity of the cyclooxygenase are inhibited by both n-3 and n-6 PUFAs.28–30 Through this mechanism, high intake of both types of fatty acids could reduce inflammatory mediators."

Regards

[Guest guest]

perhaps a better diagram:

http://circ.ahajournals.org/cgi/content/full/108/2/155

perhaps the explanation:

"However, the present results are in contrast to the customary assumption that high intake of n-6 fatty acids antagonizes the antiinflammatory effects of n-3 fatty acids. One possible explanation for our observation is that n-6 fatty acids lower soluble TNF receptor levels by indirectly reducing insulin resistance.20,27 Furthermore, the activities of the 6 and 5-desaturase (which are the rate-limiting steps for arachidonic acid and EPA synthesis in humans) and the activity of the cyclooxygenase are inhibited by both n-3 and n-6 PUFAs.28–30 Through this mechanism, high intake of both types of fatty acids could reduce inflammatory mediators."

Regards

[Guest guest]

Not enough info there and I cannot get the PDF to download.

Perhaps the important point:

"Energy deprivation results in the greatest decline in synthesis, likely accounting for the beneficial decline in circulating cholesterol concentrations observed with weight loss. "

One apparent contradiction may be the fact that some have very high TC and others not.

Is the question:

What causes the liver to make more that we would think necessary? dunno.

Similarly:

What causes the system to recover that put into the gut as waste? dunno.

Can a person diet to the point of starvation (fast) and get the cholesterol down and KEEP it down. Not likely, IMO, by observation.

Grizzlies have a very high TC (600) (recalling TV program), starting hibernation and come out low and quickly add it back with food intake. Of course, they have a short period to get it back for the next winter survival.

So we have to do CR as long as we can.

Did you look at the cited articles?

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

Yes, it's hard to get around the fact that despite the disadvantangesbrought about by PUFA consumption, there is long standing scientificevidence regarding benefits when it comes to cadio-vascular health.PUFAs lower plasma cholesterol. But -curiously- (according to thefollowing reviewer) it does seem to increase cholesterol biosynthesis.Why??? Regulation of cholesterol biosynthesis by diet in humansPJ School of Dietetics and Human Nutrition, Faculty of Agricultural andEnvironmental Sciences, McGill University, Ste-Anne-de-Bellevue,Quebec, Canada. jonesp@...Biosynthesis of cholesterol represents a major input into whole-bodypools; however, its regulation has been difficult to study in humansbecause of limitations in methodologies. The present objectives are tocompare available techniques for measuring this process and examinehow dietary factors alter human cholesterol biosynthesis. Review ofexisting techniques suggests that mass isotopomer distributionanalysis and deuterium incorporation approaches offer advantages overother methods. Dietary factors influencing human cholesterol synthesisinclude energy restriction, meal frequency, dietary fat type, andcholesterol and phytosterol content. Food deprivation for as short as24 h results in almost complete cessation of cholesterol biosynthesis.Similarly, increased meal frequency patterns are associated with asubstantial depression in synthesis. In contrast, consumption of oilsrich in polyunsaturated fatty acids, despite reducing circulatingconcentrations, increases the cholesterol synthesis rate compared withother fats. Stepwise addition of dietary cholesterol is associatedwith only a modest decline in cholesterogenesis while raising plasmaconcentrations slightly. It can be concluded that synthesis, as acontributor to circulating cholesterol concentrations, is sensitive tomany dietary factors. Energy deprivation results in the greatestdecline in synthesis, likely accounting for the beneficial decline incirculating cholesterol concentrations observed with weight loss.Does anyone have any input? Studies on cholesterol biosynthesis arehard to come across but would seem more promising in furnishingessential clues to bring us out of these apparent contradictions. Ifthe body makes more cholesterol following consumption of PUFA, butpresents lower plasma levels of the stuff, doesn't that mean that itis somehow using it up because a need for it has been created? Is thatgood? A protective reaction offsetting the effects of some deleteriousfactor???http://www.ajcn.org/cgi/content/abstract/66/2/438Way out at sea on this one...

[Guest guest]

Not enough info there and I cannot get the PDF to download.

Perhaps the important point:

"Energy deprivation results in the greatest decline in synthesis, likely accounting for the beneficial decline in circulating cholesterol concentrations observed with weight loss. "

One apparent contradiction may be the fact that some have very high TC and others not.

Is the question:

What causes the liver to make more that we would think necessary? dunno.

Similarly:

What causes the system to recover that put into the gut as waste? dunno.

Can a person diet to the point of starvation (fast) and get the cholesterol down and KEEP it down. Not likely, IMO, by observation.

Grizzlies have a very high TC (600) (recalling TV program), starting hibernation and come out low and quickly add it back with food intake. Of course, they have a short period to get it back for the next winter survival.

So we have to do CR as long as we can.

Did you look at the cited articles?

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

Yes, it's hard to get around the fact that despite the disadvantangesbrought about by PUFA consumption, there is long standing scientificevidence regarding benefits when it comes to cadio-vascular health.PUFAs lower plasma cholesterol. But -curiously- (according to thefollowing reviewer) it does seem to increase cholesterol biosynthesis.Why??? Regulation of cholesterol biosynthesis by diet in humansPJ School of Dietetics and Human Nutrition, Faculty of Agricultural andEnvironmental Sciences, McGill University, Ste-Anne-de-Bellevue,Quebec, Canada. jonesp@...Biosynthesis of cholesterol represents a major input into whole-bodypools; however, its regulation has been difficult to study in humansbecause of limitations in methodologies. The present objectives are tocompare available techniques for measuring this process and examinehow dietary factors alter human cholesterol biosynthesis. Review ofexisting techniques suggests that mass isotopomer distributionanalysis and deuterium incorporation approaches offer advantages overother methods. Dietary factors influencing human cholesterol synthesisinclude energy restriction, meal frequency, dietary fat type, andcholesterol and phytosterol content. Food deprivation for as short as24 h results in almost complete cessation of cholesterol biosynthesis.Similarly, increased meal frequency patterns are associated with asubstantial depression in synthesis. In contrast, consumption of oilsrich in polyunsaturated fatty acids, despite reducing circulatingconcentrations, increases the cholesterol synthesis rate compared withother fats. Stepwise addition of dietary cholesterol is associatedwith only a modest decline in cholesterogenesis while raising plasmaconcentrations slightly. It can be concluded that synthesis, as acontributor to circulating cholesterol concentrations, is sensitive tomany dietary factors. Energy deprivation results in the greatestdecline in synthesis, likely accounting for the beneficial decline incirculating cholesterol concentrations observed with weight loss.Does anyone have any input? Studies on cholesterol biosynthesis arehard to come across but would seem more promising in furnishingessential clues to bring us out of these apparent contradictions. Ifthe body makes more cholesterol following consumption of PUFA, butpresents lower plasma levels of the stuff, doesn't that mean that itis somehow using it up because a need for it has been created? Is thatgood? A protective reaction offsetting the effects of some deleteriousfactor???http://www.ajcn.org/cgi/content/abstract/66/2/438Way out at sea on this one...

[Guest guest]

Well, my take is that comparing cancer risk to high cholesterol - using more PUFA's is not a good tradeoff.

Got the full text thanks to a friend, and it looks to me like CR is the big factor.

Interesting that "extrahepatic" tissues are 80% of synthesis. Of course that's what they thought in 1997.

Gotta look deeper.

BTW, verapamil, indomethacin are also 6-desaturase inhibitors. To both AA and EPA pathways.

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

> Perhaps the important point:> "Energy deprivation results in the greatest decline in synthesis,likely accounting for the beneficial decline in circulatingcholesterol concentrations observed with weight loss. "An important point to be sure. But what this effect brought about insuch a short time can mean on overall health status I am not qualifiedto guess as long as high cholesterol is in itself considered (byassociation) a risk factor and not just a marker for artherosclerosisor for anything else for that matter. If considered a marker such adecrease would mean nothing as we know for sure that scleroticartheries are not made well in 24 hours. All that would be proven isthat plama cholesterol levels are sensitive to dietary factors. Howfar does this get us?> What causes the liver to make more that we would think necessary? dunno.Neither do I. But I am mightily tempted to be consequential. There arenumerous studies out there which establish the peroxidative effects ofPUFAs on different tissues. Here's one:The effect of increased intakes of polyunsaturated fatty acids andvitamin E on DNA damage in human lymphocytesA. McE. JENKINSON1, A. R. COLLINS, S. J. DUTHIE, K. W. J. WAHLE and G.G. DUTHIERowett Research Institute, Bucksburn, Aberdeen, Scotland, U.K. AB21 9SB1Correspondence: Rowett Research Institute, Greenburn Rd., Bucksburn,Aberdeen, Scotland, U.K. AB21 9SB. E-mail: aj@... ABSTRACTThe effect of increasing dietary intakes of polyunsaturated fattyacids (PUFAs) and vitamin E on indices of oxidative DNA damage wasinvestigated. Twenty-one healthy male, nonsmokers aged 28.9 ± 1.3years participated in a free-living, split plot/change over trial inwhich half the volunteers consumed diets containing 5% PUFA as foodenergy for 4 wk and, after a 10 wk washout period, consumed a 15% PUFAdiet for another 4 wk. The other volunteers followed an identicalprotocol, except that they consumed the 15% PUFA diet first. The dietswere provided to volunteers either with or without an additional 80 mgd{alpha}-tocopherol acetate/day; otherwise total fat, carbohydrates,protein, and basal vitamin E contents remained unchanged. DNA damageinduced by 200 µM H2O2 in lymphocytes from volunteers as well asendogenous DNA damage in the form of oxidized pyrimidines, measured byalkaline single-cell gel electrophoresis (the comet assay),significantly decreased after consumption of the 5% PUFA diet (P<0.001and P=0.01, respectively), but significantly increased afterconsumption of the 15% PUFA diet when {alpha}-tocopherol levels werein the range of 5–7 mg/day (P=0.008 and P=0.03, respectively). Thesechanges were abolished by an additional 80 mg d{alpha}-tocopherol/day.This study indicates that increasing dietary levels of PUFA to 15% mayadversely affect some indices of DNA stability. However, increasingthe dietary intake of vitamin E by 80 mg/day ameliorates the damagingeffects of PUFA.—on, A. McE., , A. R., Duthie, S. J.,Wahle, K. W. J., Duthie, G. G. The effect of increased intakes ofpolyunsaturated fatty acids and vitamin E on DNA damage in humanlymphocytes.Here's another:Polyunsaturated fatty acids partially reproduce the role ofmelanocytes in the epidermal melanin unit.Cario-Andre M, Briganti S, Picardo M, Nikaido O, de Verneuil H, Taieb A.INSERM E0217, Universite Victor Segalen Bordeaux II, 146 rue LeoSaignat, 33076 Bordeaux cedex, France.The incidence rate of melanoma is higher in fair-skinned than indark-skinned individuals. In negroid skin there is more eumelaninwhich is present in all skin layers and fewer polyunsaturated fattyacids (PUFA) than in caucasoid skin. The western diet, which is richin omega-6 polyunsaturated fatty acids, is associated with moreproneness to cancer including cutaneous melanoma. To study therespective influence of omega-6 PUFA and low phototype melanocytes onredox status -basal and following UV irradiation-, we used epidermalreconstructs. The addition of polyunsaturated fatty acids as well asthe presence of low phototype melanocytes affected basal statussimilarly except for catalase activity, which decreased significantlyin polyunsaturated fatty acid-supplemented reconstructs. Following UV,polyunsaturated fatty acids and low phototype melanocytes increasedlipid and protein oxidative damage without affecting direct DNAdamage. However, polyunsaturated fatty acids increased epidermalapoptosis whereas low phototype melanocytes decreased it. Since ourdata suggest that an omega-6 PUFA rich-diet may increase oxidativedamage in melanocytes without inducing apoptosis, the long-term netoutcome could be cumulated mutations and an increased risk of skincancer, especially melanoma.PMID: 15740592 [PubMed - indexed for MEDLINE]So that if PUFA intake increases cholesterol production whiledecreasing plasma levels, could we not venture to guess that the needfor increased cholelesterol migh not be, as a reaction to rapidperoxidation (since PUFAs are so damaging), antioxidative? How else dowe explain it?

[Guest guest]

Well, my take is that comparing cancer risk to high cholesterol - using more PUFA's is not a good tradeoff.

Got the full text thanks to a friend, and it looks to me like CR is the big factor.

Interesting that "extrahepatic" tissues are 80% of synthesis. Of course that's what they thought in 1997.

Gotta look deeper.

BTW, verapamil, indomethacin are also 6-desaturase inhibitors. To both AA and EPA pathways.

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

> Perhaps the important point:> "Energy deprivation results in the greatest decline in synthesis,likely accounting for the beneficial decline in circulatingcholesterol concentrations observed with weight loss. "An important point to be sure. But what this effect brought about insuch a short time can mean on overall health status I am not qualifiedto guess as long as high cholesterol is in itself considered (byassociation) a risk factor and not just a marker for artherosclerosisor for anything else for that matter. If considered a marker such adecrease would mean nothing as we know for sure that scleroticartheries are not made well in 24 hours. All that would be proven isthat plama cholesterol levels are sensitive to dietary factors. Howfar does this get us?> What causes the liver to make more that we would think necessary? dunno.Neither do I. But I am mightily tempted to be consequential. There arenumerous studies out there which establish the peroxidative effects ofPUFAs on different tissues. Here's one:The effect of increased intakes of polyunsaturated fatty acids andvitamin E on DNA damage in human lymphocytesA. McE. JENKINSON1, A. R. COLLINS, S. J. DUTHIE, K. W. J. WAHLE and G.G. DUTHIERowett Research Institute, Bucksburn, Aberdeen, Scotland, U.K. AB21 9SB1Correspondence: Rowett Research Institute, Greenburn Rd., Bucksburn,Aberdeen, Scotland, U.K. AB21 9SB. E-mail: aj@... ABSTRACTThe effect of increasing dietary intakes of polyunsaturated fattyacids (PUFAs) and vitamin E on indices of oxidative DNA damage wasinvestigated. Twenty-one healthy male, nonsmokers aged 28.9 ± 1.3years participated in a free-living, split plot/change over trial inwhich half the volunteers consumed diets containing 5% PUFA as foodenergy for 4 wk and, after a 10 wk washout period, consumed a 15% PUFAdiet for another 4 wk. The other volunteers followed an identicalprotocol, except that they consumed the 15% PUFA diet first. The dietswere provided to volunteers either with or without an additional 80 mgd{alpha}-tocopherol acetate/day; otherwise total fat, carbohydrates,protein, and basal vitamin E contents remained unchanged. DNA damageinduced by 200 µM H2O2 in lymphocytes from volunteers as well asendogenous DNA damage in the form of oxidized pyrimidines, measured byalkaline single-cell gel electrophoresis (the comet assay),significantly decreased after consumption of the 5% PUFA diet (P<0.001and P=0.01, respectively), but significantly increased afterconsumption of the 15% PUFA diet when {alpha}-tocopherol levels werein the range of 5–7 mg/day (P=0.008 and P=0.03, respectively). Thesechanges were abolished by an additional 80 mg d{alpha}-tocopherol/day.This study indicates that increasing dietary levels of PUFA to 15% mayadversely affect some indices of DNA stability. However, increasingthe dietary intake of vitamin E by 80 mg/day ameliorates the damagingeffects of PUFA.—on, A. McE., , A. R., Duthie, S. J.,Wahle, K. W. J., Duthie, G. G. The effect of increased intakes ofpolyunsaturated fatty acids and vitamin E on DNA damage in humanlymphocytes.Here's another:Polyunsaturated fatty acids partially reproduce the role ofmelanocytes in the epidermal melanin unit.Cario-Andre M, Briganti S, Picardo M, Nikaido O, de Verneuil H, Taieb A.INSERM E0217, Universite Victor Segalen Bordeaux II, 146 rue LeoSaignat, 33076 Bordeaux cedex, France.The incidence rate of melanoma is higher in fair-skinned than indark-skinned individuals. In negroid skin there is more eumelaninwhich is present in all skin layers and fewer polyunsaturated fattyacids (PUFA) than in caucasoid skin. The western diet, which is richin omega-6 polyunsaturated fatty acids, is associated with moreproneness to cancer including cutaneous melanoma. To study therespective influence of omega-6 PUFA and low phototype melanocytes onredox status -basal and following UV irradiation-, we used epidermalreconstructs. The addition of polyunsaturated fatty acids as well asthe presence of low phototype melanocytes affected basal statussimilarly except for catalase activity, which decreased significantlyin polyunsaturated fatty acid-supplemented reconstructs. Following UV,polyunsaturated fatty acids and low phototype melanocytes increasedlipid and protein oxidative damage without affecting direct DNAdamage. However, polyunsaturated fatty acids increased epidermalapoptosis whereas low phototype melanocytes decreased it. Since ourdata suggest that an omega-6 PUFA rich-diet may increase oxidativedamage in melanocytes without inducing apoptosis, the long-term netoutcome could be cumulated mutations and an increased risk of skincancer, especially melanoma.PMID: 15740592 [PubMed - indexed for MEDLINE]So that if PUFA intake increases cholesterol production whiledecreasing plasma levels, could we not venture to guess that the needfor increased cholelesterol migh not be, as a reaction to rapidperoxidation (since PUFAs are so damaging), antioxidative? How else dowe explain it?

[Guest guest]

Here's an interesting treatise on cholesterol tests.

http://library.usask.ca/theses/available/etd-01232006-123919/unrestricted/g_woo.pdf

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

> Perhaps the important point:> "Energy deprivation results in the greatest decline in synthesis,likely accounting for the beneficial decline in circulatingcholesterol concentrations observed with weight loss. "An important point to be sure. But what this effect brought about insuch a short time can mean on overall health status I am not qualifiedto guess as long as high cholesterol is in itself considered (byassociation) a risk factor and not just a marker for artherosclerosisor for anything else for that matter. If considered a marker such adecrease would mean nothing as we know for sure that scleroticartheries are not made well in 24 hours. All that would be proven isthat plama cholesterol levels are sensitive to dietary factors. Howfar does this get us?> What causes the liver to make more that we would think necessary? dunno.Neither do I. But I am mightily tempted to be consequential. There arenumerous studies out there which establish the peroxidative effects ofPUFAs on different tissues. Here's one:

[Guest guest]

Here's an interesting treatise on cholesterol tests.

http://library.usask.ca/theses/available/etd-01232006-123919/unrestricted/g_woo.pdf

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

> Perhaps the important point:> "Energy deprivation results in the greatest decline in synthesis,likely accounting for the beneficial decline in circulatingcholesterol concentrations observed with weight loss. "An important point to be sure. But what this effect brought about insuch a short time can mean on overall health status I am not qualifiedto guess as long as high cholesterol is in itself considered (byassociation) a risk factor and not just a marker for artherosclerosisor for anything else for that matter. If considered a marker such adecrease would mean nothing as we know for sure that scleroticartheries are not made well in 24 hours. All that would be proven isthat plama cholesterol levels are sensitive to dietary factors. Howfar does this get us?> What causes the liver to make more that we would think necessary? dunno.Neither do I. But I am mightily tempted to be consequential. There arenumerous studies out there which establish the peroxidative effects ofPUFAs on different tissues. Here's one:

[Guest guest]

I've wondered if the fructose in fruit is the same high fructose corn syrup that is used almost exclusively for sweetening. I eat perhaps more fruit than others but no corn syrup, just because it's processed and fructose is already "digested" and the number of calories in anything is very high.

Compare a coke to 2 tsps of sugar I used to use in coffee. I might have used 200 kcals of 3000 kcals years ago. Colas would be 600. That a lot of sweetener to overcome the acids taste.

Fructose goes directly to fat, but in her tests she was unable to get some rats hypertriged. Interesting hypotheses there.

This treatise is not necessarily in agreement with other articles, BTW. I liked the simplified flow diagram. The HDL flow in Endocrinology is more specific. A lot of the process is effected by genetics.

Cells give up excess cholesterol to HDL particles, so I wonder if my genetically low is due to lack of excess in cells (good) or lack of the right amount of Apo.

A cupla interesting things:

All cells can synthesize cholesterol de novo. (not agreed how much is done by liver versus extrahepatic).

So effectiveness of drugs acting on the liver might be limited. I mean, slowing the liver's production may have no effect on the cell's capacity to grow cholesterol which is not measured in serum.

Cells can burn triglycerides but not cholesterols. (that means that exercise may effect TC only by using up TG)

That makes it hard for me to understand how exercise can be touted to raise HDL. (a hole)

What exercise might do, I'm GUESSing, is break cholesterol loose from the cell in the muscle rebuilding activity. I question if that is athero buildup or not.

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

Hi JW:Interesting that they induce hypertriglyceridemia by feeding a 10% solution of fructose to the rats. Do we know if it has the same effect on humans? If so then it does cast doubt on the health properties of some fruits. Rodney.>> Here's an interesting treatise on cholesterol tests.> http://library.usask.ca/theses/available/etd-01232006-123919/unrestricted/g_woo.pdf> >

[Guest guest]

I've wondered if the fructose in fruit is the same high fructose corn syrup that is used almost exclusively for sweetening. I eat perhaps more fruit than others but no corn syrup, just because it's processed and fructose is already "digested" and the number of calories in anything is very high.

Compare a coke to 2 tsps of sugar I used to use in coffee. I might have used 200 kcals of 3000 kcals years ago. Colas would be 600. That a lot of sweetener to overcome the acids taste.

Fructose goes directly to fat, but in her tests she was unable to get some rats hypertriged. Interesting hypotheses there.

This treatise is not necessarily in agreement with other articles, BTW. I liked the simplified flow diagram. The HDL flow in Endocrinology is more specific. A lot of the process is effected by genetics.

Cells give up excess cholesterol to HDL particles, so I wonder if my genetically low is due to lack of excess in cells (good) or lack of the right amount of Apo.

A cupla interesting things:

All cells can synthesize cholesterol de novo. (not agreed how much is done by liver versus extrahepatic).

So effectiveness of drugs acting on the liver might be limited. I mean, slowing the liver's production may have no effect on the cell's capacity to grow cholesterol which is not measured in serum.

Cells can burn triglycerides but not cholesterols. (that means that exercise may effect TC only by using up TG)

That makes it hard for me to understand how exercise can be touted to raise HDL. (a hole)

What exercise might do, I'm GUESSing, is break cholesterol loose from the cell in the muscle rebuilding activity. I question if that is athero buildup or not.

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

Hi JW:Interesting that they induce hypertriglyceridemia by feeding a 10% solution of fructose to the rats. Do we know if it has the same effect on humans? If so then it does cast doubt on the health properties of some fruits. Rodney.>> Here's an interesting treatise on cholesterol tests.> http://library.usask.ca/theses/available/etd-01232006-123919/unrestricted/g_woo.pdf> >

[Guest guest]

HFCS and the amount and type of fructose in fruit are

very different.

http://www.westonaprice.org/motherlinda/cornsyrup.html

Also, the glycemic load in fruit is much lower than in

foods with HFCS.

--- jwwright <jwwright@...> wrote:

> I've wondered if the fructose in fruit is the same

> high fructose corn syrup that is used almost

> exclusively for sweetening. I eat perhaps more fruit

> than others but no corn syrup, just because it's

> processed and fructose is already " digested " and the

> number of calories in anything is very high.

> Compare a coke to 2 tsps of sugar I used to use in

> coffee. I might have used 200 kcals of 3000 kcals

> years ago. Colas would be 600. That a lot of

> sweetener to overcome the acids taste.

> Fructose goes directly to fat, but in her tests she

> was unable to get some rats hypertriged. Interesting

> hypotheses there.

>

> This treatise is not necessarily in agreement with

> other articles, BTW. I liked the simplified flow

> diagram. The HDL flow in Endocrinology is

> more specific. A lot of the process is effected by

> genetics.

> Cells give up excess cholesterol to HDL particles,

> so I wonder if my genetically low is due to lack of

> excess in cells (good) or lack of the right amount

> of Apo.

>

> A cupla interesting things:

> All cells can synthesize cholesterol de novo. (not

> agreed how much is done by liver versus

> extrahepatic).

> So effectiveness of drugs acting on the liver might

> be limited. I mean, slowing the liver's production

> may have no effect on the cell's capacity to grow

> cholesterol which is not measured in serum.

>

> Cells can burn triglycerides but not cholesterols.

> (that means that exercise may effect TC only by

> using up TG)

> That makes it hard for me to understand how exercise

> can be touted to raise HDL. (a hole)

> What exercise might do, I'm GUESSing, is break

> cholesterol loose from the cell in the muscle

> rebuilding activity. I question if that is athero

> buildup or not.

>

> Regards.

>

> [ ] Re: Starch,

> Monounsaturated Fats and Prostate Cancer

>

>

> Hi JW:

>

> Interesting that they induce hypertriglyceridemia

> by feeding a 10%

> solution of fructose to the rats. Do we know if

> it has the same

> effect on humans? If so then it does cast doubt

> on the health

> properties of some fruits.

>

> Rodney.

>

>

>

> >

> > Here's an interesting treatise on cholesterol

> tests.

> >

>

http://library.usask.ca/theses/available/etd-01232006-

> 123919/unrestricted/g_woo.pdf

> >

> >

>

------------------------------------------------

c_bonanno@...

http://calorierestrictionexperiment.blogspot.com/

__________________________________________________

[Guest guest]

HFCS and the amount and type of fructose in fruit are

very different.

http://www.westonaprice.org/motherlinda/cornsyrup.html

Also, the glycemic load in fruit is much lower than in

foods with HFCS.

--- jwwright <jwwright@...> wrote:

> I've wondered if the fructose in fruit is the same

> high fructose corn syrup that is used almost

> exclusively for sweetening. I eat perhaps more fruit

> than others but no corn syrup, just because it's

> processed and fructose is already " digested " and the

> number of calories in anything is very high.

> Compare a coke to 2 tsps of sugar I used to use in

> coffee. I might have used 200 kcals of 3000 kcals

> years ago. Colas would be 600. That a lot of

> sweetener to overcome the acids taste.

> Fructose goes directly to fat, but in her tests she

> was unable to get some rats hypertriged. Interesting

> hypotheses there.

>

> This treatise is not necessarily in agreement with

> other articles, BTW. I liked the simplified flow

> diagram. The HDL flow in Endocrinology is

> more specific. A lot of the process is effected by

> genetics.

> Cells give up excess cholesterol to HDL particles,

> so I wonder if my genetically low is due to lack of

> excess in cells (good) or lack of the right amount

> of Apo.

>

> A cupla interesting things:

> All cells can synthesize cholesterol de novo. (not

> agreed how much is done by liver versus

> extrahepatic).

> So effectiveness of drugs acting on the liver might

> be limited. I mean, slowing the liver's production

> may have no effect on the cell's capacity to grow

> cholesterol which is not measured in serum.

>

> Cells can burn triglycerides but not cholesterols.

> (that means that exercise may effect TC only by

> using up TG)

> That makes it hard for me to understand how exercise

> can be touted to raise HDL. (a hole)

> What exercise might do, I'm GUESSing, is break

> cholesterol loose from the cell in the muscle

> rebuilding activity. I question if that is athero

> buildup or not.

>

> Regards.

>

> [ ] Re: Starch,

> Monounsaturated Fats and Prostate Cancer

>

>

> Hi JW:

>

> Interesting that they induce hypertriglyceridemia

> by feeding a 10%

> solution of fructose to the rats. Do we know if

> it has the same

> effect on humans? If so then it does cast doubt

> on the health

> properties of some fruits.

>

> Rodney.

>

>

>

> >

> > Here's an interesting treatise on cholesterol

> tests.

> >

>

http://library.usask.ca/theses/available/etd-01232006-

> 123919/unrestricted/g_woo.pdf

> >

> >

>

------------------------------------------------

c_bonanno@...

http://calorierestrictionexperiment.blogspot.com/

__________________________________________________

[Guest guest]

There are at east 4 genotypes, so I think it's difficult to generalize.

Certainly none of the rules seem to apply to my wife, or if they do they are not significant.

People who have the very high TC, >350, eg, do not respond well even to drugs, and the drugs they get used to. So, eg, they might start at 10 mg Zocor, alternate days, then daily, then 20 mg, then 40, then 80. Add another, and the body responds.

It's not elucidated yet for those people.

After the patient finds out that exercise is "wearing" out the joints, they tend to give up. And believe me the joints actually wear out for one reason or another. As in, knee replacements.

The statins, etc, all seem to attack HMG reductase. Zetia attacks absorbed cholesterol from food or recycled. But I haven't looked at all of them yet.

IMO, a nutritional solution is not clear. Even dropping weight 25 % doesn't solve the problem. TC comes down but not enough. I've seen this in four people now, the best they can do is 250 without drugs. None of the four were what you'd call obese, in fact 2 were quite trim guys.

The cholesterol thing is not simple.

In 10 years my wife had 1 data point at 150, and we figure now that was a testing error.

She had an aunt at 350 never treated, lived to 96. Two I know have suffered dementia, not CVD.

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer> >

[Guest guest]

There are at east 4 genotypes, so I think it's difficult to generalize.

Certainly none of the rules seem to apply to my wife, or if they do they are not significant.

People who have the very high TC, >350, eg, do not respond well even to drugs, and the drugs they get used to. So, eg, they might start at 10 mg Zocor, alternate days, then daily, then 20 mg, then 40, then 80. Add another, and the body responds.

It's not elucidated yet for those people.

After the patient finds out that exercise is "wearing" out the joints, they tend to give up. And believe me the joints actually wear out for one reason or another. As in, knee replacements.

The statins, etc, all seem to attack HMG reductase. Zetia attacks absorbed cholesterol from food or recycled. But I haven't looked at all of them yet.

IMO, a nutritional solution is not clear. Even dropping weight 25 % doesn't solve the problem. TC comes down but not enough. I've seen this in four people now, the best they can do is 250 without drugs. None of the four were what you'd call obese, in fact 2 were quite trim guys.

The cholesterol thing is not simple.

In 10 years my wife had 1 data point at 150, and we figure now that was a testing error.

She had an aunt at 350 never treated, lived to 96. Two I know have suffered dementia, not CVD.

Regards.

[ ] Re: Starch, Monounsaturated Fats and Prostate Cancer> >

[Guest guest]

Fructose and High Fructose Corn Syrup (HFCS) are not

the same.

High fructose corn syrup is made by treating corn

(which is usually genetically modified corn) with a

variety of enzymes, some of which are also genetically

modified, to first extract the sugar glucose and then

convert some of it into fructose, since fructose

tastes sweeter than glucose. The end result is a

mixture of 55% fructose and 45% glucose, that is

called " high fructose corn syrup. "

http://ezinearticles.com/?The-Dangers-of-High-Fructose-Corn-Syrup & id=28535

Contrary to its name, HFCS is not high?in fructose. At

the time HFCS was developed, the only sweetener in all

other corn syrups was glucose; none contained

fructose. So the name " high " fructose corn syrup, in

comparative terms, makes sense and is entirely

appropriate. But when compared to table sugar

(sucrose), HFCS is not at all " high " in fructose. In

fact, HFCS is nearly identical in composition to table

sugar (sucrose), which is composed of 50 percent

fructose and 50 percent glucose.

http://www.hfcsfacts.com/WhatIsHFCS.html

Also, fructose has a GI of 22 and HFCS has a GI of 62.

http://www.snac.ucla.edu/pages/Resources/Handouts/HOGlycemic.pdf

Also see:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=2\

695593 & dopt=Abstract

List of al sugars:

http://www.everydiet.org/articles/sugars.htm

--- Rodney <perspect1111@...> wrote:

> Hi Christian:

>

> Also worth noting that fructose has a **low**

> glycemic index -

> between 11 and 25 - according to this site which

> appears

> authoritative:

>

> http://www.glycemicindex.com/

>

> Rodney.

>

>

> > > >

> > > > Here's an interesting treatise on

> cholesterol

> > > tests.

> > > >

> > >

> >

>

http://library.usask.ca/theses/available/etd-01232006-

> > > 123919/unrestricted/g_woo.pdf

> > > >

> > > >

> > >

> >

> >

> > ------------------------------------------------

> > c_bonanno@...

> > http://calorierestrictionexperiment.blogspot.com/

> >

> > __________________________________________________

> >

[Guest guest]

Fructose and High Fructose Corn Syrup (HFCS) are not

the same.

High fructose corn syrup is made by treating corn

(which is usually genetically modified corn) with a

variety of enzymes, some of which are also genetically

modified, to first extract the sugar glucose and then

convert some of it into fructose, since fructose

tastes sweeter than glucose. The end result is a

mixture of 55% fructose and 45% glucose, that is

called " high fructose corn syrup. "

http://ezinearticles.com/?The-Dangers-of-High-Fructose-Corn-Syrup & id=28535

Contrary to its name, HFCS is not high?in fructose. At

the time HFCS was developed, the only sweetener in all

other corn syrups was glucose; none contained

fructose. So the name " high " fructose corn syrup, in

comparative terms, makes sense and is entirely

appropriate. But when compared to table sugar

(sucrose), HFCS is not at all " high " in fructose. In

fact, HFCS is nearly identical in composition to table

sugar (sucrose), which is composed of 50 percent

fructose and 50 percent glucose.

http://www.hfcsfacts.com/WhatIsHFCS.html

Also, fructose has a GI of 22 and HFCS has a GI of 62.

http://www.snac.ucla.edu/pages/Resources/Handouts/HOGlycemic.pdf

Also see:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=2\

695593 & dopt=Abstract

List of al sugars:

http://www.everydiet.org/articles/sugars.htm

--- Rodney <perspect1111@...> wrote:

> Hi Christian:

>

> Also worth noting that fructose has a **low**

> glycemic index -

> between 11 and 25 - according to this site which

> appears

> authoritative:

>

> http://www.glycemicindex.com/

>

> Rodney.

>

>

> > > >

> > > > Here's an interesting treatise on

> cholesterol

> > > tests.

> > > >

> > >

> >

>

http://library.usask.ca/theses/available/etd-01232006-

> > > 123919/unrestricted/g_woo.pdf

> > > >

> > > >

> > >

> >

> >

> > ------------------------------------------------

> > c_bonanno@...

> > http://calorierestrictionexperiment.blogspot.com/

> >

> > __________________________________________________

> >

[Guest guest]

Just to clarify, is HFCS a combination of a chemical fructose and mixed with glucose?

Recognize that sugar is not fructose and glucose until it's digested.

When you eat a fruit you eat fructose. When you eat sugar you eat sucrose.

I'm guessing when I eat HFCS, I'm eating a combination of fructose and glucose?

If that's true, that explains to me why HFCS might make people fatter, because fructose goes in to fat in the presence of adequate glucose.

Regards

Re: [ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

Fructose and High Fructose Corn Syrup (HFCS) are notthe same.High fructose corn syrup is made by treating corn(which is usually genetically modified corn) with avariety of enzymes, some of which are also geneticallymodified, to first extract the sugar glucose and thenconvert some of it into fructose, since fructosetastes sweeter than glucose. The end result is amixture of 55% fructose and 45% glucose, that iscalled "high fructose corn syrup."http://ezinearticles.com/?The-Dangers-of-High-Fructose-Corn-Syrup & id=28535Contrary to its name, HFCS is not high?in fructose. Atthe time HFCS was developed, the only sweetener in allother corn syrups was glucose; none containedfructose. So the name "high" fructose corn syrup, incomparative terms, makes sense and is entirelyappropriate. But when compared to table sugar(sucrose), HFCS is not at all "high" in fructose. Infact, HFCS is nearly identical in composition to tablesugar (sucrose), which is composed of 50 percentfructose and 50 percent glucose.http://www.hfcsfacts.com/WhatIsHFCS.htmlAlso, fructose has a GI of 22 and HFCS has a GI of 62.http://www.snac.ucla.edu/pages/Resources/Handouts/HOGlycemic.pdfAlso see:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=2695593 & dopt=AbstractList of al sugars:http://www.everydiet.org/articles/sugars.htm--- Rodney <perspect1111@...> wrote:> Hi Christian:> > Also worth noting that fructose has a **low**> glycemic index - > between 11 and 25 - according to this site which> appears > authoritative:> > http://www.glycemicindex.com/> > Rodney.> > > > > >> > > > Here's an interesting treatise on> cholesterol> > > tests.> > > >> > >> >>http://library.usask.ca/theses/available/etd-01232006-> > > 123919/unrestricted/g_woo.pdf> > > > > > > > > > > > > > > > > ------------------------------------------------> > c_bonanno@...> > http://calorierestrictionexperiment.blogspot.com/> > > > __________________________________________________> >

[Guest guest]

Just to clarify, is HFCS a combination of a chemical fructose and mixed with glucose?

Recognize that sugar is not fructose and glucose until it's digested.

When you eat a fruit you eat fructose. When you eat sugar you eat sucrose.

I'm guessing when I eat HFCS, I'm eating a combination of fructose and glucose?

If that's true, that explains to me why HFCS might make people fatter, because fructose goes in to fat in the presence of adequate glucose.

Regards

Re: [ ] Re: Starch, Monounsaturated Fats and Prostate Cancer

Fructose and High Fructose Corn Syrup (HFCS) are notthe same.High fructose corn syrup is made by treating corn(which is usually genetically modified corn) with avariety of enzymes, some of which are also geneticallymodified, to first extract the sugar glucose and thenconvert some of it into fructose, since fructosetastes sweeter than glucose. The end result is amixture of 55% fructose and 45% glucose, that iscalled "high fructose corn syrup."http://ezinearticles.com/?The-Dangers-of-High-Fructose-Corn-Syrup & id=28535Contrary to its name, HFCS is not high?in fructose. Atthe time HFCS was developed, the only sweetener in allother corn syrups was glucose; none containedfructose. So the name "high" fructose corn syrup, incomparative terms, makes sense and is entirelyappropriate. But when compared to table sugar(sucrose), HFCS is not at all "high" in fructose. Infact, HFCS is nearly identical in composition to tablesugar (sucrose), which is composed of 50 percentfructose and 50 percent glucose.http://www.hfcsfacts.com/WhatIsHFCS.htmlAlso, fructose has a GI of 22 and HFCS has a GI of 62.http://www.snac.ucla.edu/pages/Resources/Handouts/HOGlycemic.pdfAlso see:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=2695593 & dopt=AbstractList of al sugars:http://www.everydiet.org/articles/sugars.htm--- Rodney <perspect1111@...> wrote:> Hi Christian:> > Also worth noting that fructose has a **low**> glycemic index - > between 11 and 25 - according to this site which> appears > authoritative:> > http://www.glycemicindex.com/> > Rodney.> > > > > >> > > > Here's an interesting treatise on> cholesterol> > > tests.> > > >> > >> >>http://library.usask.ca/theses/available/etd-01232006-> > > 123919/unrestricted/g_woo.pdf> > > > > > > > > > > > > > > > > ------------------------------------------------> > c_bonanno@...> > http://calorierestrictionexperiment.blogspot.com/> > > > __________________________________________________> >

[Guest guest]

Yes, that is right, HFCS is fructose and glucose. But

it is not really mixed. The Fructose is created by

enzymatic reactions.

--- jwwright <jwwright@...> wrote:

> Just to clarify, is HFCS a combination of a chemical

> fructose and mixed with glucose?

------------------------------------------------

c_bonanno@...

http://calorierestrictionexperiment.blogspot.com/

__________________________________________________

[Guest guest]

Yes, that is right, HFCS is fructose and glucose. But

it is not really mixed. The Fructose is created by

enzymatic reactions.

--- jwwright <jwwright@...> wrote:

> Just to clarify, is HFCS a combination of a chemical

> fructose and mixed with glucose?

------------------------------------------------

c_bonanno@...

http://calorierestrictionexperiment.blogspot.com/

__________________________________________________

[Guest guest]

Fruit in general has a low to medium glycemic index,

but more importantly they have a very low glycemic

load.

It is explained well here:

http://www.mendosa.com/gilists.htm

It also has a list of fruits and their associated GI

and GL.

The one thing I do not think is too good is to drink

fruit juices.

Eat up,

C

--- Rodney <perspect1111@...> wrote:

> Hi Christian:

>

>

> Not many people here recommend avoiding fruits

> generally. Nor have I

> seen any data relating to the fructose content of

> various fruits as a

> way of deciding which fruits are preferable.

> Although I have come to

> the conclusion that berries are probably far

> preferable to the fruits

> one comes across most frequently in grocery stores.

>

> Do you see where I am coming from?

------------------------------------------------

c_bonanno@...

http://calorierestrictionexperiment.blogspot.com/

__________________________________________________