Why NO OIL?

A place to get your questions answered from McDougall staff dietitian, Jeff Novick, MS, RDN.

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Postby JeffN » Sun Oct 04, 2009 4:37 pm

Even the so called "good" aspects of Olive Oil is not "good" enough to offset the bad aspects of it over the long term.

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Dietary extra-virgin olive oil rich in phenolic antioxidants and the aging process: long-term effects in the rat.
J Nutr Biochem. 2009 Apr 13. [Epub ahead of print]
PMID: 19369055

The aim of the present work was to verify whether extra-virgin olive oil, a food naturally containing phenolic antioxidants, has the potential to protect from the pro-aging effects of a high-calorie diet.

Male rats were fed from age 12 months to senescence a high-calorie diet containing either corn oil (CO), or extra-virgin olive oil with high (H-EVOO) or low (L-EVOO) amounts of phenols.

The prolonged high fat intake led to obesity, liver lipid degeneration and insulin resistance, which were not counteracted by high phenol intake. No difference in overall survival was found at the end of the experiment in the animals treated with H-EVOO compared to the other groups. However, we did detect a protective effect of olive oil on some age-related pathologies and on blood pressure, of which the former was associated with the antioxidant content. Concomitantly, a decrease in DNA oxidative damage in blood cells and plasma TBARS and an increase in liver superoxide dismutase were detected following H-EVOO consumption.

Thus, although olive oil phenols cannot reverse the detrimental effects of a prolonged intake of high amounts of fat, improving the quality of olive oil in terms of antioxidant content can be beneficial.

In conclusion, these data suggest that improving the quality of olive oil in terms of antioxidant content can have some beneficial effects, but it is not sufficient by itself to counteract the detrimental effects of a high-calorie diet containing large amounts of fat. Future experiments will elucidate whether the protective effects of olive oil phenols on age-related dysfunctions would be more evident using a lower-calorie and lipid intake regimen.
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Postby rijman » Mon Oct 05, 2009 6:29 pm

Thank you very much Jeff.

From Dr. McDougall I was aware that oils were bad but your comments provide a great refresher on this topic and much more than I previously knew.

As a result of Dr. McDougall I stopped sateing onion and veggies in oil, I use water, and my family no longer cooks taco shells in oil, we steam them.

Thanks again Jeff, your information is greatly appreciated!
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Postby grammie2nic » Wed Oct 21, 2009 3:28 pm

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.

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 understand the whole not letting pleasure dictate your choices idea, especially when your health is at stake, but I have been doing this diet for probably four months now and 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.
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Re: fats

Postby JeffN » Wed Oct 21, 2009 3:44 pm

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.


This is not accurate and discussed here...

http://www.drmcdougall.com/forums/viewtopic.php?t=5939

There is also absolutely no evidence that absorbing "more" is "better" in regard to morbidity and mortality. The long lived Okinawans actually had a few nutrient deficiencies in their diet but still became centenarians.

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.


This is not a vegetable based diet and you are not required to eat kale, let alone plain raw or steamed kale, or even salads. While they can be healthy, and are good for you, they are not required nor is any one food. :)


http://www.drmcdougall.com/forums/viewtopic.php?t=11028

Also, no one is recommending you consume plain or boiled steamed vegetables. If you check my favorite threads above for the Basic Recipes, each one of them contains several pounds of vegetables in a starch based meal that is delicious. :)

Oil is not palatable nor does it taste good. A food that tastes good is one we enjoy to consume on its own. Yet, no one, pours themselves a "shot" glass full of oil to consume and relax with. In regard to palatability , lets remember that oil is a relatively new addition to the human diet so the human diet was extremely palatable before any oil was added to it. It may also be valuable to know that virtually everyone who gives up oil for any period of time will tell you that adding oil to food makes it taste and feel greasy not palatable, even to plain vegetables and salad.

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Postby grammie2nic » Wed Oct 21, 2009 4:06 pm

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.
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Re: fats

Postby JeffN » Wed Oct 21, 2009 4:41 pm

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.


You are welcome,

You may want to read the third point I make it this thread..

http://www.drmcdougall.com/forums/viewtopic.php?t=11112

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fats

Postby grammie2nic » Thu Oct 22, 2009 7:23 am

As to palatability, no one would eat a spoonful of dill weed or oregano or mustard (or salt or sugar, for that matter) because they don't taste good straight either, but mixed with food they can add a lot of flavor and make the food more enjoyable. But I definitely understand that oil is in a whole other category being a highly refined and caloric item which my body certainly doesn't need...just need to get used to no oil I guess..I have been doing this for a quite a while now and I was very strict for many months and still miss the flavor/texture oil adds to food...if there is very much oil, I have the same reaction...it's too oily but without it at all many times food seems to be missing something. It is kind of freeing to just think I can relax and not worry about eating salads if I don't like them without an oily dressing. It is interesting how locked-in to certain viewpoints I can get without realizing it. Thank you for helping me change my point of view, Jeff.
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Re: Why NO OIL?

Postby Mike Crosby » Tue Dec 13, 2011 12:26 pm

Just to respond and add absolutely nothing to the topic:

Wow, has this been a great thread! Talk about Jeff giving some great information.

From why one needs no oil to the mechanisms of how heart disease is reversed to the Fuhrman/McDougall diet disagreement.

Wonderful info, thank you Jeff, Jim and Devil's Advocate;)
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Re: HDL

Postby JeffN » Thu May 28, 2015 5:42 am

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




Study links better 'good cholesterol' function with lower risk of later heart disease
May 26, 2015
University of Pennsylvania School of Medicine

http://www.sciencedaily.com/releases/20 ... 0526215036.

Summary:
HDL, the 'good cholesterol' helps remove fat from artery walls, reversing the process that leads to heart disease. Yet recent drug trials and genetic studies suggest that pushing HDL levels higher doesn't reduce the risk of heart disease. Now, an epidemiological study shows that a person's HDL function -- the efficiency of HDL molecules at removing cholesterol -- may be a better measure of coronary heart disease risk and target for heart-protecting drugs.



Daniel J Rader, MD et al. Association of HDL cholesterol efflux capacity with incident coronary heart disease events: a prospective case-control study. Lancet Diabetes & Endocrinology, May 2015 DOI: 10.1016/S2213-8587(15)00126-6

http://www.thelancet.com/journals/landi ... 13-8587(15)00126-6/abstract

Summary
Background
Although HDL cholesterol concentrations are strongly and inversely associated with risk of coronary heart disease, interventions that raise HDL cholesterol do not reduce risk of coronary heart disease. HDL cholesterol efflux capacity—a prototypical measure of HDL function—has been associated with coronary heart disease after adjusting for HDL cholesterol, but its effect on incident coronary heart disease risk is uncertain.

Methods
We measured cholesterol efflux capacity and assessed its relation with vascular risk factors and incident coronary heart disease events in a nested case-control sample from the prospective EPIC-Norfolk study of 25 639 individuals aged 40–79 years, assessed in 1993–97 and followed up to 2009. We quantified cholesterol efflux capacity in 1745 patients with incident coronary heart disease and 1749 control participants free of any cardiovascular disorders by use of a validated ex-vivo radiotracer assay that involved incubation of cholesterol-labelled J774 macrophages with apoB-depleted serum from study participants.

Findings
Cholesterol efflux capacity was positively correlated with HDL cholesterol concentration (r=0·40; p<0·0001) and apoA-I concentration (r=0·22; p<0·0001). It was also inversely correlated with type 2 diabetes (r=–0·18; p<0·0001) and positively correlated with alcohol consumption (r=0·12; p<0·0001). In analyses comparing the top and bottom tertiles, cholesterol efflux capacity was significantly and inversely associated with incident coronary heart disease events, independent of age, sex, diabetes, hypertension, smoking and alcohol use, waist:hip ratio, BMI, LDL cholesterol concentration, log-triglycerides, and HDL cholesterol or apoA-I concentrations (odds ratio 0·64, 95% CI 0·51–0·80). After a similar multivariable adjustment the risk of incident coronary heart disease was 0·80 (95% CI 0·70–0·90) for a per-SD change in cholesterol efflux capacity.

Interpretation
HDL cholesterol efflux capacity might provide an alternative mechanism for therapeutic modulation of the HDL pathway beyond HDL cholesterol concentration to help reduce risk of coronary heart disease.
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Re: Why NO OIL?

Postby JeffN » Thu Jul 16, 2015 5:01 am

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Re: Why NO OIL?

Postby JeffN » Thu May 12, 2016 5:47 am

Abstract

Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor? New Insights From the Framingham Offspring Study. Circulation: Cardiovascular Quality and Outcomes. Online: May 10, 2016. doi: 10.1161/CIRCOUTCOMES.115.002436

http://m.circoutcomes.ahajournals.org/c ... 115.002436

Background—Although the inverse association between high-density lipoprotein cholesterol (HDL-C) and risk of cardiovascular disease (CVD) has been long established, it remains unclear whether low HDL-C remains a CVD risk factor when levels of low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG) are not elevated. This is a timely issue because recent studies have questioned whether HDL-C is truly an independent predictor of CVD.

Methods and Results—3590 men and women from the Framingham Heart Study offspring cohort without known CVD were followed between 1987 and 2011. Low HDL-C (<40 mg/dL in men and <50 mg/dL in women) was defined as isolated if TG and LDL-C were both low (<100 mg/dL). We also examined higher thresholds for TG (150 mg/dL) and LDL-C (130 mg/dL) and compared low versus high HDL-C phenotypes using logistic regression analysis to assess association with CVD. Compared with isolated low HDL-C, CVD risks were higher when low HDL-C was accompanied by LDL-C ≥100 mg/dL and TG <100 mg/dL (odds ratio 1.3 [1.0, 1.6]), TG ≥100 mg/dL and LDL-C <100 mg/dL (odds ratio 1.3 [1.1, 1.5]), or TG and LDL-C ≥100 mg/dL (odds ratio 1.6, [1.2, 2.2]), after adjustment for covariates. When low HDL-C was analyzed with higher thresholds for TG (≥150 mg/dL) and LDL-C (≥130 mg/dL), results were essentially the same. In contrast, compared with isolated low HDL-C, high HDL-C was associated with 20% to 40% lower CVD risk except when TG and LDL-C were elevated.

Conclusions—CVD risk as a function of HDL-C phenotypes is modulated by other components of the lipid panel.



Press Release

New study: Has HDL, the 'good' cholesterol, been hyped?
UNIVERSITY OF MARYLAND MEDICAL CENTER
PUBLIC RELEASE: 10-MAY-2016
http://www.eurekalert.org/pub_releases/ ... 051016.php

Baltimore, Md. - May 10, 2016 - For years, physicians have told patients that HDL (high-density lipoprotein cholesterol) helps protect them from cardiovascular disease (CVD). And the higher the number, the more the protection. HDL, often considered an independent predictor of heart disease, has been dubbed the "good" cholesterol, thanks to its protective effects. But a new study shows for the first time that HDL's protection depends on the levels of two other blood fats or lipids associated with heart disease. If these fats are not within normal ranges, even a high HDL may not be protective.

The new research analyzes nearly 25 years of data from the Framingham Heart Study's Offspring Cohort. It focuses on the roles HDL, LDL (low-density lipoprotein cholesterol) and triglycerides (TG) play in increasing or decreasing the risk of heart disease. The study, published online in Circulation: Cardiovascular Quality and Outcomes, followed 3,590 men and women without known cardiovascular disease between 1987 and 2011.

"There's no question that HDL does have a protective role, as we also confirm in the study, but HDL has been hyped-up," says senior author Michael Miller, MD, professor of cardiovascular medicine at the University of Maryland School of Medicine and preventive cardiologist at the University of Maryland Medical Center. "HDL really should be viewed as a third priority, with LDL on top and TG second."

The questions:

- Can the level of HDL by itself determine the risk of a person developing heart disease?
- What happens to the risk if LDL and TG are abnormal?

The method:

- The researchers looked at study participants with both low and high HDL levels, and
- Those who also had normal and high levels of LDL and TG

"Nobody has really looked at an isolated low and isolated high HDL, and whether or not other factors, such as triglycerides and LDL, make a difference in the risk of cardiovascular disease," says Dr. Miller.

The conclusions:

- HDL was not uniformly predictive of cardiovascular risk

- TG and LDL modified the incidence of CVD in both low- and high-level HDL

- Compared with isolated low HDL, the CVD risk was 30-60 percent higher in the presence of high levels of LDL, TG or both.

- High HDL was not associated with reduced CVD risk if TG and LDL were above 100 mg/dL
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Re: Why NO OIL?

Postby JeffN » Tue Aug 28, 2018 8:02 am

Not published yet

Could Too Much 'Good' HDL Cholesterol Be Bad for Your Heart?
blood specimen By Alan Mozes
HealthDay Reporter

MONDAY, Aug. 27, 2018 (HealthDay News) -- When it comes to protecting one's heart, high-density lipoprotein cholesterol -- or HDL -- has long had a reputation of being the "good" cholesterol, compared to the "bad" cholesterol -- LDL (low-density lipoprotein).

But new research suggests that there could be too much of a "good" thing. Very high blood levels of HDL cholesterol may actually be bad for you. The research linked it to a higher risk for heart attack, and even death, among patients who already had heart problems or who faced a higher risk of developing heart disease.

The findings are based on a roughly four-year tracking of cholesterol levels and heart disease among nearly 6,000 men and women.

"Historically, HDL cholesterol, or 'good' cholesterol, is thought to be protective at high levels for cardiovascular disease and death," said study lead author Dr. Marc Allard-Ratick, who's with Emory University School of Medicine in Atlanta. "However, our study demonstrates that this may not be the case and, in fact, higher levels may be harmful."

The study was done as part of the Emory Cardiovascular Biobank. On average, the participants were 63 years old and about one-third were women. Their HDL levels ranged from a low of less than 30 mg/dL to a high of greater than 60 mg/dL of blood.

Over the course of the study, 13 percent of the patients had a heart attack or died from a cardiovascular cause.

At the study's end, the researchers concluded that patients with HDL levels in the middle-range of the spectrum -- meaning between 41 to 60 mg/dL of blood -- fared the best, having the lowest risk for heart attack or death from heart disease.

In contrast, those with HDL readings below 41 or above 60 faced a markedly increased risk for both health outcomes, demonstrating what the researchers called a "U-shaped" risk pattern.

Specifically, patients with HDL levels exceeding 60 were found to have a 50 percent greater risk of heart disease death or heart attack, compared with those in the middle-range, the investigators reported.

The findings held up even after accounting for a patient's history of diabetes, smoking, drinking and LDL levels. Race and gender also didn't appear to affect the findings.

Dr. Gregg Fonarow is director of the Ahmanson-UCLA Cardiomyopathy Center and co-director of the UCLA Preventative Cardiology Program in Los Angeles. He said that "research from UCLA established more than two decades ago that HDL cholesterol could -- in certain individuals (including those with very high levels of HDL) and in certain circumstances -- be dysfunctional and pro-inflammatory," and contribute to narrowing of the arteries.

"In others words, the so-called 'good' cholesterol in terms of cardiovascular risk could go 'bad' and be associated with excess risk," added Fonarow, who was not part of the team behind the new study.

Allard-Ratick acknowledged that other studies have revealed a similar HDL problem among people who do not otherwise face a high risk for heart disease. But he said the new study is the first to uncover the same concern among people who are already at high-risk for cardiovascular complications, even if "the mechanism behind this finding remains unclear."

And, he said, one "surprising aspect of the study was that this association between high levels of HDL and increased risk of death or cardiovascular disease was seen more commonly in women compared to men."

As to what might constitute a dangerous HDL threshold, Allard-Ratick said that the risk association "likely occurs at (HDL) levels exceeding 80 mg/dL, and perhaps even higher in women."

Fonarow said a number of prior studies have found that when compared to those with more moderately high HDL levels, people with "very high" HDL levels -- meaning a threshold of 90 mg/dL or more -- appear to face a greater risk for heart disease.

So what should concerned patients do?

Allard-Ratick said that "as the cause of this finding remains unclear, the appropriate management is not known at this time. Patients with very high HDL cholesterol should continue to address other modifiable risk factors -- such as high blood pressure, smoking and obesity -- to reduce cardiovascular disease."

The findings were presented Saturday at the European Society of Cardiology meeting, in Munich, Germany. Research presented at meetings should be considered preliminary until it has been published in a peer-reviewed medical journal.

SOURCES: Marc Allard-Ratick, M.D., department of internal medicine, division of cardiology, Emory University School of Medicine, Atlanta; Gregg Fonarow, M.D., director, Ahmanson-UCLA Cardiomyopathy Center, and co-director, UCLA Preventative Cardiology Program, Los Angeles; European Society of Cardiology meeting, Munich, Germany, Aug. 25, 2018

Last Updated: Aug 27, 2018
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Re: Why NO OIL?

Postby JeffN » Sat Feb 15, 2020 1:50 pm

Summary: a higher, or raising of, HDL are unlikely to be of benefit.

Apolipoprotein A-I concentrations and risk of coronary artery disease: A Mendelian randomization study
DOI: https://doi.org/10.1016/j.atherosclerosis.2020.02.002
https://www.atherosclerosis-journal.com/article/S0021-9150(20)30081-2/fulltext


Abstract

Highlights
•Apolipoprotein A-I relates to lower observational risk of coronary artery disease.
•Robust evidence of atheroprotective properties of apolipoprotein A-I is lacking.
•Mendelian randomization was used to assess the causality of apolipoprotein A-I.
•Apolipoprotein A-I association with coronary artery disease is likely not causal.
•Apolipoprotein A-I increasing therapies unlikely reduce risk of heart disease.

Abstract

Background and aims
Apolipoprotein A-I (apoA-I) infusions represent a potential novel therapeutic approach for the prevention of coronary artery disease (CAD). Although circulating apoA-I concentrations inversely associate with risk of CAD, the evidence base of this representing a causal relationship is lacking. The aim was to assess the causal role of apoA-I using human genetics.

Methods
We identified a variant (rs12225230) in APOA1 locus that associated with circulating apoA-I concentrations (p < 5 × 10−8) in 20,370 Finnish participants and meta-analyzed our data with a previous GWAS of apoA-I. We obtained genetic estimates of CAD from UK Biobank and CARDIoGRAMplusC4D (totaling 122,733 CAD cases) and conducted a two-sample Mendelian randomization analysis. We compared our genetic findings to observational associations of apoA-I with risk of CAD in 918 incident CAD cases among 11,535 individuals from population-based prospective cohorts.

Results
ApoA-I was associated with a lower risk of CAD in observational analyses (HR 0.81; 95%CI: 0.75, 0.88; per 1-SD higher apoA-I), with the association showing a dose-response relationship. Rs12225230 associated with apoA-I concentrations (per-C allele beta 0.076 SD; SE: 0.013; p = 1.5 × 10−9) but not with confounders. In Mendelian randomization analyses, apoA-I was not related to risk of CAD (OR 1.13; 95%CI: 0.98,1.30 per 1-SD higher apoA-I), which was different to the observational association. Similar findings were observed using an independent ABCA1 variant in sensitivity analysis.

Conclusions
Genetic evidence fails to support a cardioprotective role for apoA-I. This is in line with the cumulative evidence showing that HDL-related phenotypes are unlikely to have a protective role in CAD.
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