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The Triglyceride/HDL Cholesterol Ratio


In 1961, a group of investigators from the Rockefeller Institute, led by Pete Ahrens published a paper entitled “Carbohydrate-induced and fat-induced lipemia”.

The authors pointed out that fat-induced increase in TG following a meal is a postprandial phenomenon (we all have high TG for a few hours following a fatty meal) caused by chylomicrons is different from the carbohydrate-induced rise in TG (later found to be caused by elevation of VLDL).

These findings have been confirmed in several more recent studies. Despite this, low fat, high carbohydrate diets are still being recommended as a primary option to reduce the risk of heart disease.

Although low-fat diets may help lowering LDL-C, low carbohydrate diets are more effective in improving the TG/HDL-C ratio.

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he he ...""intelligent" fiber" :D ...good business idea ...diabetic friendly intelligent fiber :)

what are other things ...Anup and how fiber affects the absorption of other things ??

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My opinion: Cholesterol doesn't cause heart disease.

I think moderate fat/moderate carbs/moderate proteins may be more helpful in keeping TG/HDL ratio lower in long run. High fat diet may increase TC levels and high carb diet will increase LDL levels (as per this article). Either fat has to be replaced by carbs in low fat diet (high carbs increases TG and decrease HDL) or carbs to be replaced by fat in low carbs diet (high fat diet may increase total cholesterol), both of which may not be beneficial in long run.

One has to check homocysteine levels also which may be corrected by taking folic acid supplement. Nutritional deficiencies are the key to any diseases, may be it a heart disease, CAD or atherosclerosis. Homocysteine levels can rise for alternate reasons. In otherwise healthy people elevated levels of homocysteine arise due to stress or to a deficiency of methyl donating antioxidants. Stress raises the demand for methyl donations. If supply cannot match overall demand methyl deficiency occurs with a corresponding rise in homocysteine. Methyl deficiency permits levels of oxidation and oxidative stress to rise above that which could be considered merely basal and normal.

Excerpts from comments section of above article:

It is my understanding/novel research that CHD/CVD is precipitated by inflammation.

(1) Hyperglycaemia oxidises LDL

(2) This oxidised LDL works it's way under the endothelium and forms plaque.

(3) The plaque will gradually build up and eventually rupture causing an infarct.

So! a Heart attack will primarily occur with

(a) Electrical current causing V Fib. Causing the heart to go spasmodically s**thouse and end in cardiac arrest (low survival rate)

(b) Heart attack (infarct) where heart muscle dies, leaving a % of the heart depleted. This % of damage is expressed as a 'Ejection Fraction' which determines the blood flow that the heart can pump in and out through the ventricles.

To be plain then discussion of HDL/triglyceride ratios doesn't impress me much. They do not inform much about how epiphysiological risk factors result in atherogenicity. On the other hand come at this from an endocrinological perspective and there is a strong indication that hormonal alterations that accompany stress increased demand for methyl groups and could result in methyl deficiency and a rise in oxidative stress. And while this last statement may still rest upon conjectural basis there is a lot about the statement that is in accord accord with evidence that has been established but ignored by the mainstream who remain insistent that cholesterol and dyslipidemia cause heart disease, which is contrary to the evidence on cholesterol and cholesterol oxides entirely.

Peng and Morin, 'Biological effects of cholesterol oxides' (book) is a good source doubters could visit.

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My TG/HDL ratio is 1.24.Is it OK?




Thanks a lot for your quick reply!


yes very Good alwaysoptimistic

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Thank you,cure!


And what about LIPOPROTIEN ASSOCIATED PHOSPHOLIPASE A2(lp-pLA20 Test? ADA has approved it recently. Yes Thyrocare has facilities for this test

Lp-PLA2 is a specific marker of vascular inflammation and found to be up regulated in atherosclerotic lesions especially in complex plaque prone to rupture.A meta- analysis found that Lp-PLA2 levels are positively correlated with increased risk of developing coronary heart disease and stroke.Lp-PLA2 is not acute phase reactant and thus is unaffected by systemic inflammatory process.

Lp-PLA2activity should be interpreted in conjunction with clinical evaluation and other risk factor assessment.


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