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High Cholesterol Message Board


High Cholesterol Board Index


How many carbohydrates does it take to produce an insulin response?
 To answer this, keep in mind that 5 grams of carbohydrate equals approximately 1 teaspoon of sugar, which is close to the normal amount of sugar found in the blood.
 Now, a single can of one of the more well-known brands of soft drinks lists 39 grams of carbohydrates in the nutrition information panel printed on the can.
 Divide 39 total carbohydrate grams by 5 grams per teaspoon and you quickly discover that this single can of soda water contains nearly 8 teaspoons of sugar that will actually enter your blood stream.
 Since 1 teaspoon of sugar is the normal healthy amount contained in the blood, 8 times that amount is clearly too much, which means if you drink that soft drink a quick rise in blood sugar and a quick insulin response to lower the rising blood sugar is absolutely guaranteed.
How high do insulin levels climb in order to reduce rising blood sugar?
According to the Textbook of Medical Physiology, insulin secreted to bring down rising blood sugar rises dramatically within 15 minutes and peaks 2-3 hours later in ranges that are from 10 to 25 times above normal, and insulin levels remain elevated for hours.
 Now that you understand that once stimulated, insulin levels stay elevated for several hours, its easy to understand how eating sugary foods or high carbohydrate meals and snacks throughout the day essentially insures that insulin stays abnormally high all day long and that glucagon is left entirely out of the metabolic picture.
 The key to activating glucagon and putting it in the metabolic driver's seat is to eat meals with plenty of protein and, ideally, carbohydrates that come almost entirely from fresh vegetables. Like cholesterol, as long as you avoid the chemically altered fats that produce dangerous transfatty acids, dietary fat consumption is essentially a non issue because, much like protein, natural fat is turned into structural raw material needed for cell growth and maintenance.
Keep in mind that your body contains something on the order of a hundred trillion cells and each and every one of them is made from and contains both protein and fat.
 Not one single cell in your body is made from carbohydrates. Protein and fat consumption is essential to life, carbohydrate consumption is not.
 There is not a single disease state associated with a lack of carbohydrates in the diet. The reason for this is that dietary consumption of carbohydrates is simply not that important because your body can make all the glucose it needs directly from protein and fat.
The important point is that in order to keep excess insulin to a minimum and insure you have enough glucagon in your system, you need meals that contain protein and that are pointedly low in processed and starchy carbohydrates like bread, pasta, rice, potatoes, corn and so on.
Eating in a way that avoids the production of excess insulin is, without question, the single most important thing you can do to lose weight easily, keep it off permanently and improve your health literally in every way measurable.
 Excess insulin is a serious threat to your health.
 Excess insulin is your enemy and excess insulin is produced in your body primarily as a direct result of your food choices.
 Excess insulin leads to higher triglycerides, higher cholesterol, poor HDL to LDL ratios, higher blood pressure, excess fat production and storage, obesity, insulin resistance, and dramatically increased risk for diabetes, heart disease, and stroke.
Glucagon is your friend and enjoying protein meals with a minimum of processed carbohydrates activates glucagon in your system.
Glucagon is the hormone that causes you to burn stored body fat for energy. When glucagon is in the metabolic driver's seat it is amazingly easy to establish and maintain your ideal healthy body weight.
There is an increasing awareness in the medical community that total cholesterol levels are not as significant a predictor of heart disease as they once believed to be as long as HDL and LDL are in proper relationship.
 There is a significant and growing amount of research that shows that cholesterol does not cause heart disease and the dietary consumption of foods containing cholesterol has only a minor effect in determining total cholesterol levels.
[QUOTE=ARIZONA73]Of course, too high of an LDL can potentially be detrimental, but you can't just go by number values. All LDL is not the same. It is quite possible for someone with an LDL of 150 to be at less risk than someone with an LDL of 100. You need to look at other factors, such as LDL particle size and HDL levels. If your LDL is predominately Pattern B, that certainly renders the LDL more dangerous. Also, since most people are given only a calculated LDL, the amount of lipoprotein(a) is likely included in that lump-sum figure, but most of us have no idea what our Lp(a) is. But this number is important, especially since an elevated Lp(a) can carry as much as 10 times the danger of ordinary LDL. So, it really isn't fair to simply say that a person is at a higher or lower risk based on a single value if you don't take these other factors into consideration. That would be far too simplistic. You simply cannot judge a book by its cover. But that's exactly what you're doing if all you're looking at is a number.[/QUOTE]

[B]Lipoprotein (a)[/B]
Several studies274-277 report a strong association between Lp(a) levels and CHD risk. Indeed, a recent meta-analysis of reported prospective studies supports an independent predictive power for elevated Lp(a).278 In addition, concomitant elevations of Lp(a) and LDL cholesterol have been reported to have synergy in elevating risk in both men and women with hypercholesterolemia. On the basis of these studies, some authorities hold that an elevation of Lp(a) is an independent risk factor for CHD. [B]It must be noted nonetheless that several prospective studies279,280 do not confirm independent prediction.[/B] Of note, Lp(a) levels are higher in African Americans than in Caucasians, but an increased risk for CHD associated with higher Lp(a) levels in African Americans has not been documented.279 [B]Thus, the quantitative contribution of elevated Lp(a) to CHD risk beyond the major risk factors is uncertain[/B]. This uncertainty extends both to individuals and populations; in the latter, the frequency of elevated Lp(a) is not as high as for the major risk factors.

[B]Moreover, issues related to measurement of Lp(a) in clinical practice have not been fully resolved.281,282 Measurement of Lp(a) is made by immunological methods, and standardized methods are available only in a few reference laboratories[/B]. Population reference levels are available from these laboratories, but they are not widely available in clinical practice. Accurate methodology has not yet been established in most clinical chemistry laboratories; samples generally must be sent to special laboratories for measurement. As a result, extra expense in measurement is required. [B]Serum Lp(a) is relatively resistant to therapeutic lowering. Statin drugs are ineffective. Among currently available drugs, only nicotinic acid reduces Lp(a) concentrations, and only moderately.[/B]283,284 In postmenopausal women, estrogen therapy also causes some reduction in Lp(a) concentrations.285 Although these therapies typically lower elevated Lp(a) levels, they have not been widely adopted. [B]At present no clinical trial evidence supports a benefit from lowering Lp(a) levels with particular agents[/B].

Despite limitations in measurement and therapy, some authorities believe that Lp(a) measurement is a useful addition to the major risk factors for identifying persons at still higher risk than revealed by those factors. According to advocates for Lp(a), the option of measurement is best reserved for persons with a strong family history of premature CHD or those with genetic causes of hypercholesterolemia, such as familial hypercholesterolemia.281,282 An elevated Lp(a) thus presents the option to raise a person's risk to a higher level. [B]For example, if a person has a high LDL cholesterol and only one other risk factor, the finding of a high Lp(a) could count as a second risk factor to justify a lower goal for LDL cholesterol. ATP III did not find strong evidence to support this approach, but accepts it as an option for selected persons. [/B]

[B]Small LDL particles[/B]
One component of atherogenic dyslipidemia is small LDL particles. They are formed in large part, although not exclusively, as a response to elevations of triglycerides. Their presence is associated with an increased risk for CHD;125,286,287 however, [B]the extent to which they predict CHD independently of other risk factors is unresolved.288 Moreover, standard and inexpensive methodologies are not available for their measurement. For these reasons, ATP III does not recommend measurement of small LDL particles in routine practice[/B]. If the clinical decision is made to detect and measure small LDL, their presence is best used as an indicator for atherogenic dyslipidemia and the metabolic syndrome. Their elevation also supports intensified therapeutic lifestyle changes. If small LDL particles accompany elevated triglycerides or low HDL cholesterol in high-risk persons, consideration can be given to using nicotinic acid or fibric acid as components of lipid-lowering therapy. [B]Nonetheless, LDL cholesterol remains the primary target of treatment in persons with small LDL particles. [/B]
[QUOTE=hunter44]Good referral Rahod -
Pretty much says it all. Triglycerides are directly related to high carb intakes/scientifically proven. I have never seen anyone not succeed reducing trigs with a reduction of carb intake. Saturated fats help.
http://www.enc-online.org/ncu1503.htm#results[/QUOTE]

On that link you gave...did you read the NEXT article?


[B]Exercise Combined with a Low-fat Diet Lowers LDL Cholesterol [/B]

Stefanick et al. investigated the effects of the [B]NCEP Step 2 diet [/B] plus exercise on plasma lipids of overweight middle-aged men and postmenopausal women with atherogenic lipoprotein profiles. The average baseline plasma LDL and HDL cholesterol concentrations in 180 women were 16118 and 477 mg/dl, respectively, and in 197 males 15614 and 364 mg/dl. Initially, the baseline dietary patterns of all subjects were within the NCEP Step 1 diet guideline. In order to test the individual effects which exercise and diet have on plasma lipoprotein levels, as well as their combined effects, subjects were divided into control (n=91), exercise only (n=90), diet only (n=95), and diet plus exercise (n=91) groups. Activity levels required in the exercise group were equivalent to 10 miles of brisk walking or jogging per week.

The change in plasma lipoprotein levels following a 1 year follow-up period showed that the diet plus exercise group achieved the greatest plasma LDL cholesterol reduction followed by the diet only, exercise only, and control groups. The table below presents the changes in plasma lipoprotein values for each group. Results from this study indicate that there is a wide heterogeneity associated with the plasma cholesterol response to diet therapy. However, exercise combined with the NCEP Step 2 diet can result in significantly greater plasma LDL cholesterol reductions. Dr. Ronald Krauss with the American Heart Association's Nutrition Committee was quoted in an AHA press release stating "Individuals should not be discouraged from trying to reduce levels of LDL cholesterol with diet, since many people can achieve a beneficial response. This study suggests the diet may be more effective when combined with increased physical activity," in response to the findings that reiterate the importance of physical activity in treating elevated LDL cholesterol.

% Change Cholesterol (Sex) Control Exercise Diet Diet & Exercise
LDL (M/F) -4.6/-2.5 -3.6/-5.6 -10.8/-7.3 -20.0/-14.5
HDL (M/F) -0.2/+1.0 +1.2/+2.3 -0.8/+0.3 +0.4/-1.1
Total (M/F) -3.9/-1.0 -5.2/-5.7 -13.2/-7.9 -20.6/-17.5


Stefanick, M.L., Mackey, S., Sheehan, M., et al. Effects of diet and exercise





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