Moderators: JeffN, carolve, Heather McDougall
grammie2nic wrote:What about Dr. Michael Greger's assertion that we need to eat our vegetables with some fat source in order to absorb and utilize the nutrients? To the best of my recollection, he cited research in his latest nutrition dvd that showed people were not absorbing much of the beneficial phytonutrients from their food when they ate it without some source of fat. When eaten WITH fat, the absorbed phytonutrient levels increased hugely. He said it doesn't take much fat but that you should add some.
grammie2nic wrote:The other issue about fat is simply palatability. I find it very unsatisfying to eat salads with most of the fat-free dressings I have bought or made so I end up blending spinach and kale into green or fruit smoothies. I find it hard to enjoy plain boiled or steamed vegetables but I can use them in soups. I am finding I am caving in on adding a little olive oil to vegetables or salad just because I can't face another bare kale leaf. I realize this is less than optimal and I continue to search for recipes/ideas that will make the food more palatable and satisfying while staying within the McDougall guidelines.
grammie2nic wrote:Thank you for the link and the information, Jeff. I tend to forget that this is a starch-based diet, not a vegetable based diet. I appreciate the link also...very enlightening. The books I have been reading lately on health and disease prevention all come with the assumption that more is better when it comes to phytonutrients... it hadn't occurred to me that maybe that whole approach is wrong.
JeffN wrote:Quoting from
Was Dr Atkins right? Dean Ornish, MD
JADA, Issue 4, Pages 537-542 (April 2004)
What about HDL?
The reduction in HDL-C that may occur on a low-fat diet is another example of a half-truth that is confusing to many people. HDL returns cholesterol to the liver for metabolism, a pathway known as reverse cholesterol transport. Most Americans consume a diet high in saturated fat and cholesterol, so those who are able to increase HDL-C in response to this diet are at lower risk than those who cannot, since they will be more efficient at metabolizing excessive dietary fat and cholesterol. In simple terms, those with higher HDL-C levels have more “garbage trucks” (HDL) to get rid of the “garbage” (excessive fat and cholesterol).
However, reducing dietary fat and cholesterol may cause a decrease in HDL-C because there is less need for it. This does not confer the same risk of atherosclerosis as in Americans with low HDL levels who are consuming a high-fat diet (41). In other words, when you have less garbage, you need fewer garbage trucks to remove it, so a reduction in HDL on a low-fat diet is not harmful.
There are no data showing that the physiologic reduction of HDL-C levels with a low-fat diet is detrimental, especially in that LDL-C usually decreases more than HDL-C (42). In locations such as Asia, where a low-fat diet has been the norm, HDL-C levels are low, yet the incidence of CVD is among the lowest in the world (43). In rural China, for example, the average LDL is less than 95 mg/dL.
In contrast, someone who increases the amount of fat and cholesterol in their diet (eg, an Atkins diet) may increase their HDL-C because their body is trying to get rid of the extra garbage (fat and cholesterol) by increasing the number of available garbage trucks (HDL). Eating a stick of butter will raise HDL-C in those who are able to do so, but that does not mean that butter is good for the heart. HDL-C is predictive of relative heart disease risk only in populations in which everyone is eating a similar high-fat diet, such as the Framingham population.
To understand better the mechanism of this phenomenon, Breslow and colleagues studied the turnover of HDL apolipoproteins (apo) A-I and A-II in 13 subjects on two contrasting metabolic diets. Upon changing from high to low intake of saturated fat and cholesterol, the mean HDL-C decreased 29%, whereas apo A-I levels fell 23%. Mean apo A-II levels did not change. The fractional catabolic rate (FCR) of apo A-I increased 11%, whereas its absolute transport rate decreased 14%. The decrease in HDL-C and apo A-I levels correlated with the decrease in apo A-I transport rate but not with the increase in apo A-I FCR. In contrast, within each diet, the HDL-C and apo A-I levels were inversely correlated with apo A-I FCR both on the high- and low-fat diets but not with apo A-I transport rate (44).
Therefore, diet-induced changes in HDL-C levels correlate with and may result from changes in apo A-I transport rate. In contrast, differences in HDL-C levels between people on a given diet correlate with and may result from differences in apo A-I FCR. The mechanism of the effects on HDL-C levels of changing from a high- to low-fat diet differs substantially from the mechanism explaining the differences in HDL-C levels between individuals who are eating a high-fat diet.
In summary, decreases in HDL-C due to a low-fat diet have a very different prognostic significance than someone who cannot raise HDL-C as much on a high-fat diet.
Raising and lowering HDL—beneficial or harmful?
An example of the half-truth of saying that anything that raises HDL-C is beneficial whereas anything that lowers it is harmful came at the November 11, 2003 annual scientific session of the American Heart Association. A paper was presented from Tufts University titled “One Year Effectiveness of the Atkins, Ornish, Weight Watchers, and Zone Diets in Decreasing Body Weight and Heart Disease Risk.” The researchers concluded “All diets resulted in significant weight loss from baseline and all but the Ornish diet resulted in significant reductions in the Framingham risk score” (45). This study was widely reported and caused many to say, “See, another study showing that the Atkins diet is good for your heart.” It sounds good, but it is not true.
The Framingham risk score is calculated from age, sex, total cholesterol, HDL, smoking, and systolic blood pressure (46). Only total cholesterol and HDL changed in this study, so these were the only factors in determining the risk score. Total cholesterol decreased much more on the Ornish diet than on any of the other diets. However, HDL increased more on the other diets, so the differences in the Framingham risk score were due primarily to changes in HDL.
The abstract did not mention that people lost the most weight on the Ornish diet, it was the only one to significantly lower LDL-C, and it was the only one to significantly lower insulin (even though one of the main premises of the Atkins and Zone diets is their purported effect on insulin). Also, C-reactive protein and creatinine clearance were significantly lowered only on the Ornish and Weight Watchers diets.
As stated earlier, a low-fat, whole foods diet has been proven to reverse heart disease using actual measures of coronary atherosclerosis and myocardial perfusion, whereas none of the other three diets has been shown to do so. It was terribly misleading when this abstract made it appear as though the Atkins diet is better for your heart. This is especially incongruous when, as mentioned earlier, the only study to examine blood flow on the Atkins diet found that it actually worsened (35).
35. 35Fleming R, Boyd LB. The effect of high-protein diets on coronary blood flow. Angiology. 2000;51:817–826. MEDLINE
41. 41Bonow RO, Eckel RH. Diet, obesity, and cardiovascular risk. N Engl J Med. 2003;348:2057. CrossRef
42. 42Connor WE, Connor SL. The case for a low-fat, high-carbohydrate diet. N Engl J Med. 1997;337:562–563. MEDLINE | CrossRef
43. 43Campbell TC, Parpia B, Chen J. Diet, lifestyle, and the etiology of coronary artery disease (The Cornell China Study). Am J Cardiol. 1998;82:18T–21T. MEDLINE
44. 44Brinton EA, Eisenberg S, Breslow JL. A low-fat diet decreases high density lipoprotein (HDL) cholesterol levels by decreasing HDL apolipoprotein transport rates. J Clin Invest. 1990;85:144–151. MEDLINE | CrossRef
45. 45Dansinger ML, Gleason JL, Griffith JL, Li W, Selker HP, Schaefer EJ. One-year effectiveness of the Atkins, Ornish, Weight Watchers, and Zone Diets in decreasing body weight and heart disease risk. 2003;Presented at the American Heart Association Scientific Sessions, Orlando, November 11, 2003.
46. 46National Institutes of Health. Risk assessment tool for estimating 10-year risk of developing hard CHD (myocardial infarction and coronary death). Available at: http://hin.nhlbi.nih.gov/atpiii/calcula ... rtype=prof. Accessed March 5, 2004
Users browsing this forum: No registered users and 59 guests