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Re: Triglycerides Formula

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At 07:08 AM 1/24/2006, you wrote:

It is well established that

carbohydrates can be

converted into triglycerides. I was curious if there

was a formula for triglycerides akin to the Hegsted

formula for cholesterol. Fortunately, Mensink and

Katan (PMID: 1386252) have provided a formula for

triglycerides, as well as HDL and LDL cholesterol

specific formulas.

Logan

--To wit (worthy of spelling out here, imo):

Effect of dietary fatty acids on serum lipids and

lipoproteins. A meta-analysis of 27 trials.

Mensink RP,

Katan MB.

Department of Human Biology, Limburg University, Maastricht, The

Netherlands.

To calculate the effect of changes in carbohydrate and fatty acid intake

on serum lipid and lipoprotein levels, we reviewed 27 controlled trials

published between 1970 and 1991 that met specific inclusion criteria.

These studies yielded 65 data points, which were analyzed by multiple

regression analysis using isocaloric exchanges of saturated (sat),

monounsaturated (mono), and polyunsaturated (poly) fatty acids versus

carbohydrates (carb) as the independent variables. For high density

lipoprotein (HDL) we found the following equation: delta HDL cholesterol

(mmol/l) = 0.012 x (carb----sat) + 0.009 x (carb----mono) + 0.007 x

(carb---- poly) or, in milligrams per deciliter, 0.47 x (carb----sat) +

0.34 x (carb----mono) + 0.28 x (carb----poly). Expressions in parentheses

denote the percentage of daily energy intake from carbohydrates that is

replaced by saturated, cis-monounsaturated, or polyunsaturated fatty

acids. All fatty acids elevated HDL cholesterol when substituted for

carbohydrates, but the effect diminished with increasing unsaturation of

the fatty acids. For low density lipoprotein (LDL) the equation was delta

LDL cholesterol (mmol/l) = 0.033 x (carb----sat) - 0.006 x (carb----mono)

- 0.014 x (carb----poly) or, in milligrams per deciliter, 1.28 x

(carb----sat) - 0.24 x (carb----mono) - 0.55 x (carb---- poly). The

coefficient for polyunsaturates was significantly different from zero,

but that for monounsaturates was not. For triglycerides the equation was

delta triglycerides (mmol/l) = -0.025 x (carb----sat) - 0.022 x

(carb----mono) - 0.028 x (carb---- poly) or, in milligrams per deciliter,

-2.22 x (carb----sat) - 1.99 x (carb----mono) - 2.47 x

(carb----poly).(ABSTRACT TRUNCATED AT 250 WORDS)

Maco

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At 07:08 AM 1/24/2006, you wrote:

It is well established that

carbohydrates can be

converted into triglycerides. I was curious if there

was a formula for triglycerides akin to the Hegsted

formula for cholesterol. Fortunately, Mensink and

Katan (PMID: 1386252) have provided a formula for

triglycerides, as well as HDL and LDL cholesterol

specific formulas.

Logan

--To wit (worthy of spelling out here, imo):

Effect of dietary fatty acids on serum lipids and

lipoproteins. A meta-analysis of 27 trials.

Mensink RP,

Katan MB.

Department of Human Biology, Limburg University, Maastricht, The

Netherlands.

To calculate the effect of changes in carbohydrate and fatty acid intake

on serum lipid and lipoprotein levels, we reviewed 27 controlled trials

published between 1970 and 1991 that met specific inclusion criteria.

These studies yielded 65 data points, which were analyzed by multiple

regression analysis using isocaloric exchanges of saturated (sat),

monounsaturated (mono), and polyunsaturated (poly) fatty acids versus

carbohydrates (carb) as the independent variables. For high density

lipoprotein (HDL) we found the following equation: delta HDL cholesterol

(mmol/l) = 0.012 x (carb----sat) + 0.009 x (carb----mono) + 0.007 x

(carb---- poly) or, in milligrams per deciliter, 0.47 x (carb----sat) +

0.34 x (carb----mono) + 0.28 x (carb----poly). Expressions in parentheses

denote the percentage of daily energy intake from carbohydrates that is

replaced by saturated, cis-monounsaturated, or polyunsaturated fatty

acids. All fatty acids elevated HDL cholesterol when substituted for

carbohydrates, but the effect diminished with increasing unsaturation of

the fatty acids. For low density lipoprotein (LDL) the equation was delta

LDL cholesterol (mmol/l) = 0.033 x (carb----sat) - 0.006 x (carb----mono)

- 0.014 x (carb----poly) or, in milligrams per deciliter, 1.28 x

(carb----sat) - 0.24 x (carb----mono) - 0.55 x (carb---- poly). The

coefficient for polyunsaturates was significantly different from zero,

but that for monounsaturates was not. For triglycerides the equation was

delta triglycerides (mmol/l) = -0.025 x (carb----sat) - 0.022 x

(carb----mono) - 0.028 x (carb---- poly) or, in milligrams per deciliter,

-2.22 x (carb----sat) - 1.99 x (carb----mono) - 2.47 x

(carb----poly).(ABSTRACT TRUNCATED AT 250 WORDS)

Maco

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Thanks, Logan,

Just to keep things in perspective, my HDL has averaged 31.27 +/- 5.5 since 1992, regardless of diet or weight (235 to 180)(diet from 3000 kcals to 1800). Maybe it works for people with high cholesterol?

One of the reasons to doubt the article I just found this morning:

From HSTAT PMC:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search & db=books & doptcmdl=GenBookHL & term=hdl+low+AND+hstat%5Bbook%5D+AND+297774%5Buid%5D & rid=hstat4.section.10760

"Will Reduction of High Triglyceride and/or Elevation of HDL Cholesterol Help Prevent Coronary Heart Disease?

The evidence most relevant to answer this question would consist of intervention trials with clinical or vascular imaging endpoints that demonstrated that reduction in very low density lipoproteins and/or elevations of HDL-C were associated with reduced clinical CHD events. These include fatal and nonfatal MI, angina, sudden death, need for coronary artery bypass graft surgery, angioplasty and other cardiovascular endpoints, or favorable changes in coronary lesions as evaluated by serial quantitative imaging of the coronary artery. Ideally, there would be quantitative correlations between the lipid-lipoprotein parameters and the study endpoints, and it would be shown that the lipoprotein alterations completely account for the favorable study endpoints. The data would be particularly convincing if total mortality also were favorably affected, and drug toxicity and drug side effects were acceptably low. Supporting data from appropriate experiments in animals would also be valuable.

Several large-scale clinical trials involving both primary and secondary prevention have assessed the effects of lipid lowering on clinical coronary endpoints and have also measured total cholesterol, triglyceride, or HDL-C throughout the study. None of these trials was designed specifically to test the hypothesis that altering triglyceride or HDL-C concentrations would reduce coronary risk. Hence, none of the studies selected patients based solely on elevated triglyceride or low HDL-C. Instead, most studies sought to test the efficacy of lowering the LDL-C, and most subjects were chosen based on elevations of total cholesterol, LDL-C, or apolipoprotein B concentrations. Each of the interventions affected total cholesterol and/or LDL-C and one or more of the other components of the lipid profile. However, in only one of these studies, the Stockholm Ischaemic Heart Disease Secondary Prevention Study, was there a clear relationship between triglyceride levels in the treated group and beneficial change in CHD event rates. Since this study did not measure HDL levels, no conclusions could be drawn with regard to HDL. "

30 yrs ago I was eliminated from an early cholesterol study because my cholesterol was too low.

Regards.

[ ] Triglycerides Formula

It is well established that carbohydrates can beconverted into triglycerides. I was curious if therewas a formula for triglycerides akin to the Hegstedformula for cholesterol. Fortunately, Mensink andKatan (PMID: 1386252) have provided a formula fortriglycerides, as well as HDL and LDL cholesterolspecific formulas.Logan

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Share on other sites

Thanks, Logan,

Just to keep things in perspective, my HDL has averaged 31.27 +/- 5.5 since 1992, regardless of diet or weight (235 to 180)(diet from 3000 kcals to 1800). Maybe it works for people with high cholesterol?

One of the reasons to doubt the article I just found this morning:

From HSTAT PMC:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search & db=books & doptcmdl=GenBookHL & term=hdl+low+AND+hstat%5Bbook%5D+AND+297774%5Buid%5D & rid=hstat4.section.10760

"Will Reduction of High Triglyceride and/or Elevation of HDL Cholesterol Help Prevent Coronary Heart Disease?

The evidence most relevant to answer this question would consist of intervention trials with clinical or vascular imaging endpoints that demonstrated that reduction in very low density lipoproteins and/or elevations of HDL-C were associated with reduced clinical CHD events. These include fatal and nonfatal MI, angina, sudden death, need for coronary artery bypass graft surgery, angioplasty and other cardiovascular endpoints, or favorable changes in coronary lesions as evaluated by serial quantitative imaging of the coronary artery. Ideally, there would be quantitative correlations between the lipid-lipoprotein parameters and the study endpoints, and it would be shown that the lipoprotein alterations completely account for the favorable study endpoints. The data would be particularly convincing if total mortality also were favorably affected, and drug toxicity and drug side effects were acceptably low. Supporting data from appropriate experiments in animals would also be valuable.

Several large-scale clinical trials involving both primary and secondary prevention have assessed the effects of lipid lowering on clinical coronary endpoints and have also measured total cholesterol, triglyceride, or HDL-C throughout the study. None of these trials was designed specifically to test the hypothesis that altering triglyceride or HDL-C concentrations would reduce coronary risk. Hence, none of the studies selected patients based solely on elevated triglyceride or low HDL-C. Instead, most studies sought to test the efficacy of lowering the LDL-C, and most subjects were chosen based on elevations of total cholesterol, LDL-C, or apolipoprotein B concentrations. Each of the interventions affected total cholesterol and/or LDL-C and one or more of the other components of the lipid profile. However, in only one of these studies, the Stockholm Ischaemic Heart Disease Secondary Prevention Study, was there a clear relationship between triglyceride levels in the treated group and beneficial change in CHD event rates. Since this study did not measure HDL levels, no conclusions could be drawn with regard to HDL. "

30 yrs ago I was eliminated from an early cholesterol study because my cholesterol was too low.

Regards.

[ ] Triglycerides Formula

It is well established that carbohydrates can beconverted into triglycerides. I was curious if therewas a formula for triglycerides akin to the Hegstedformula for cholesterol. Fortunately, Mensink andKatan (PMID: 1386252) have provided a formula fortriglycerides, as well as HDL and LDL cholesterolspecific formulas.Logan

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