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Video Presentations on Lipids and the Low Carb Diet

"Why LDL Cholesterol Goes Up with Low Carb Diet and Is It Bad for Health?" - Dr. Nadir Ali

"What is Fat Toxicity? Lipotoxicity? - Nadir Ali Explains

Do Statins Prevent of Cause Heart Disease? Should LDL Be Called 'Bad' Cholesterol?" - Dr. Nadir Ali

Dr. Nadir Ali is an interventional cardiologist with over 25 years of experience. He is also the chairman of the Department of Cardiology at Clear Lake Regional Medical Center. Before working as a cardiologist, he served as an assistant professor of medicine for eight years at Baylor College of Medicine in Houston, where he also received his medical training.

Dr. Ali has championed many aspects of the science and practice of a low-carb lifestyle in the local Clear Lake area since 2013. He organises a monthly nutritional seminar in the Searcy Auditorium of the Clear Lake Hospital that receives more than 100 visitors every month from the local community. Dr Ali’s focus is on managing heart disease, obesity, metabolic syndrome and diabetes.

"Statins - Emperor Has No Clothes" - Dr. Nadir Ali

Cardiology, Statins and Low Carb Diets - with Dr. Nadir Ali

"An Assessment of the Cardiovascular Risks of a Low Carbohydrate, High Fat Diet" - Dr. David Diamond, PhD

David. M. Diamond received his Ph.D. in Biology in 1985, with a specialization in Behavioral Neuroscience, from the Center for the Neurobiology of Learning and Memory at the University of California, Irvine. He is a professor in the Departments of Psychology and Molecular Pharmacology and Physiology at the University of South Florida, where he has directed his research program on post-traumatic stress disorder (PTSD).

Dr. Diamond has served on federal government study sections and committees evaluating research on the neurobiology of stress and memory, and has over 100 publications, reviews and book chapters on the brain and memory. He has served on the editorial boards of numerous medical journals and has received 30 years of federally funded support for his research.

In the past decade, Dr. Diamond has expanded his research program to include cardiovascular disease and nutrition. His controversial research is an extension of an advanced seminar he directs at the University of South Florida entitled “Myths and Deception in Medical Research”, which emphasizes the critical evaluation of methods and conflicts of interest in health-related research.

In recent years he added to his list of publications controversial papers on diet, cholesterol and statins, including one paper published in the peer- reviewed medical journal “Expert Review of Clinical Pharmacology”, which described the deceptive practices employed by researchers promoting statins for the treatment of cardiovascular disease. Dr. Diamond has been invited to present his myth-busting views on nutrition and cholesterol to lay people and physicians at nutrition, cardiology, obesity and diabetes conferences all over the world.

"Statins, Cholesterol and Low Carb Diets" - Low Carb Conferences Podcast with Dr. David Diamond, PhD

LDL and Statins on Low Carb - with Dr. David Diamond, PhD

Professor David Diamond says you have been misled and deceived when it comes to LDL cholesterol and statins. But he isn't just going to tell you his opinion. He wants to show you the science. In his quest to set the record straight, he has been compared to "anti vaxers" and been called "dangerous." But the fascinating thing is that he is pointing out data that is in published, respected, peer-reviewed journals and showing a vastly different perspective than what we "know" about cholesterol and statins. 

In a world of pharma industry influence and a medical culture that isn't good at reevaluating its beliefs, it's important to have voices like Dr. Diamond's to help us realize the science is far from settled. Please remember, this is meant for educational purposes only and in no way constitutes medical advice. Please contact your physician before making any changes or medical decisions.

"Cholesterol, LDL and Statins" - Dr. David Diamond, PhD at Low Carb Houston (2019)

Low Carb Houston 2019 was held in Clear Lake at the University of Houston Clear Lake in October.

"Should You Be Concerned About High LDL-Cholesterol on a Low Carb Diet?" - Dr. David Diamond, PhD

David M. Diamond received his Ph.D. in Biology in 1985, with a specialization in Behavioral Neuroscience, from the Center for the Neurobiology of Learning and Memory at the University of California, Irvine. He is a professor in the Departments of Psychology and Molecular Pharmacology and Physiology at the University of South Florida, where he has directed his research program on post-traumatic stress disorder (PTSD).

Dr. Diamond has served on federal government study sections and committees evaluating research on the neurobiology of stress and memory, and has over 100 publications, reviews and book chapters on the brain and memory. He has served on the editorial boards of numerous medical journals and has received 30 years of federally funded support for his research.

In the past decade, Dr. Diamond has expanded his research program to include cardiovascular disease and nutrition. His controversial research is an extension of an advanced seminar he directs at the University of South Florida entitled “Myths and Deception in Medical Research”, which emphasizes the critical evaluation of methods and conflicts of interest in health-related research.

In recent years he added to his list of publications controversial papers on diet, cholesterol and statins, including one paper published in the peer- reviewed medical journal “Expert Review of Clinical Pharmacology”, which described the deceptive practices employed by researchers promoting statins for the treatment of cardiovascular disease. Dr. Diamond has been invited to present his myth-busting views on nutrition and cholesterol to lay people and physicians at nutrition, cardiology, obesity and diabetes conferences all over the world. 

"New Data on Energy, Exercise and Cholesterol" - Dave Feldman

Dave Feldman is a senior software engineer, business developer and entrepreneur. He began a Low Carb, High Fat diet in April 2015 and after experiencing a significant rise in his total cholesterol he committed himself to learning everything he could about cholesterol and the lipid system.

As an engineer, Dave spotted a pattern in the lipid system that’s very similar to distributed objects in networks. Through research and N=1 experimentation he has revealed some very powerful data which he continues to share in this presentation and in further detail on his website www.CholesterolCode.com.

"Interpreting Common Low Carb Lipid Profiles" - Dave Feldman

"It's About Energy, Not Cholesterol" - Dave Feldman

"A Very Brief Review of the Lipid Energy Model & Top Secret" - Dave Feldman

"Low Carb LDL - Passenger or Killer?" - with Dave Feldman

Dave Feldman has done more to call into question the lipid hypothesis of heart disease than practically anyone over the past few decades. His self experimentation and his theories on an energy model for lipids question the foundation of the theory that LDL is "bad" and we should all strive for a low level. He recently had his model "stress tested" on the Peter Attia podcast which for some created more questions than answers. 

In this episode, we review his energy model and inversion pattern, and we explore what this means for low carb individuals with elevated LDL levels. Since there are no clear answers, it helps to explore the possibilities so that we can try to make sense of this unique and unstudied area of lipidology.

"Low-Carb and High LDL Hyper-responders: New Evidence" - with Dave Feldman

A new study scientifically defines the group of people whose LDL cholesterol rises dramatically after starting a low-carb diet — so-called lean mass hyper-responders. But what does this mean if you are in this group, and what does it mean for the broader topic of cholesterol?

"Cholesterol and Low-Carb: What's the 'Skinny' on High LDL?" - with Dave Feldman

Does an elevated LDL cholesterol on a low-carb diet confer the same risk as an elevated LDL on a standard American diet? We don’t know the answer for certain. But thanks to Dave Feldman and his colleagues, we may learn the answer sooner rather than later.

"Keto Diet and High LDL Study" - Dave Feldman

Dave Feldman released preliminary data from a lean mass hyper-responder study that investigates elevated LDL while on a keto diet. He presented the baseline data at the Symposium for Metabolic Health in San Diego, and the reaction was notable — both supportive and critical.

The results of the study have the potential to change how we view elevated LDL cholesterol. But for now, we have to be patient for the end results and cautiously take away the lessons we can from the preliminary data.

"The Truth About High Cholesterol" - Dr. Paul Mason

This lecture is part 1 of 4 delivered by Dr Paul Mason at the Low Carb Down Under Gold Coast conference in October 2022. Dr Mason demolishes the weak science that LDL cholesterol is inherently harmful, and brings nuance to the conversation in a way that can be easily understood.

"The Shady Truth About Statins" - Dr. Paul Mason

This lecture is part 2 of 3 delivered by Dr Mason at the Low Carb Down Under Gold Coast conference in October 2022. Dr Mason exposes the catastrophic harms caused by the first cholesterol lowering drug, Triparanol, and the guilty verdict that followed. 

This is followed by a brief history of statins, including the high rates of cancer in test animals seen with the first statin to come to market, and the massive (+$1,000,000,000) legal payouts made to settle lawsuits from statin side effects.

Specific statin side effects, including dementia are covered, followed by a close analysis of the measurable benefits that may be attributed to statins. This includes a review of a recent paper co-authored by David Diamond, Ben Bikman and Paul Mason that discusses how to identify who is likely and not likely to benefit from statin therapy using triglyceride and LDL levels.

"Saturated Fat Is Not Dangerous" - Dr. Paul Mason

"High Cholesterol on a Ketogenic Diet (Plus Do Statins Work?)" - Dr. Paul Mason

"The Truth About Statins" - Dr. Paul Mason

"Blood Tests on a Ketogenic Diet: What Your Cholesterol Results Mean" - Dr. Paul Mason

Scholarly Articles on Lipids and the Low Carb Diet

A short history of saturated fat: the making and unmaking... : Current Opinion in Endocrinology, Diabetes and Obesitya potential conflict of interest for the American Heart Association; a number of crucial details regarding studies considered influential to the hypothesis; irregularities in the scientific reviews on saturated fats, for both the 2015 and 2020 Dietary Guidelines for Americans; and possible conflicts of interest on the relevant subcommittee reviewing saturated fats for the 2020 Dietary Guidelines Advisory Committee. Information obtained via the Freedom of Information Act (FOIA) on emails from the 2015 process is published here for the first time. These findings are highly relevant to the 2025–2030 Dietary Guidelines process, now underway, which has plans for a new review on saturated fats. Recent findings Recent findings include shortcomings in the scientific review processes on saturated fats, for both the current 2020–2025 Dietary Guidelines for Americans and the previous edition (2015–2020). Revelations include the fact the 2015 Advisory Committee acknowledged, in an e-mail, the lack of scientific justification for any specific numeric cap on these fats. Other, previously unpublished findings include significant potential financial conflicts on the relevant 2020 guidelines subcommittee, including the participation of plant-based advocates, an expert who promotes a plant-based diet for religious reasons, experts who had received extensive funding from industries, such as tree nuts and soy, whose products benefit from continued policy recommendations favoring polyunsaturated fats, and one expert who had spent more than 50 years of her career dedicated to ‘proving’ the diet-heart hypothesis. Summary The idea that saturated fats cause heart disease, called the diet-heart hypothesis, was introduced in the 1950s, based on weak, associational evidence. Subsequent clinical trials attempting to substantiate this hypothesis could never establish a causal link. However, these clinical-trial data were largely ignored for decades, until journalists brought them to light about a decade ago. Subsequent reexaminations of this evidence by nutrition experts have now been published in >20 review papers, which have largely concluded that saturated fats have no effect on cardiovascular disease, cardiovascular mortality or total mortality. The current challenge is for this new consensus on saturated fats to be recognized by policy makers, who, in the United States, have shown marked resistance to the introduction of the new evidence. In the case of the 2020 Dietary Guidelines, experts have been found even to deny their own evidence. The global re-evaluation of saturated fats that has occurred over the past decade implies that caps on these fats are not warranted and should no longer be part of national dietary guidelines. Conflicts of interest and longstanding biases stand in the way of updating dietary policy to reflect the current evidence....
Importance of Coagulation Factors as Critical Components of Premature Cardiovascular Disease in Familial HypercholesterolemiaFor almost a century, familial hypercholesterolemia (FH) has been considered a serious disease, causing atherosclerosis, cardiovascular disease, and ischemic stroke. Closely related to this is the widespread acceptance that its cause is greatly increased low-density-lipoprotein cholesterol (LDL-C). However, numerous observations and experiments in this field are in conflict with Bradford Hill’s criteria for causality. For instance, those with FH demonstrate no association between LDL-C and the degree of atherosclerosis; coronary artery calcium (CAC) shows no or an inverse association with LDL-C, and on average, the life span of those with FH is about the same as the surrounding population. Furthermore, no controlled, randomized cholesterol-lowering trial restricted to those with FH has demonstrated a positive outcome. On the other hand, a number of studies suggest that increased thrombogenic factors—either procoagulant or those that lead to high platelet reactivity—may be the primary risk factors in FH. Those individuals who die prematurely have either higher lipoprotein (a) (Lp(a)), higher factor VIII and/or higher fibrinogen compared with those with a normal lifespan, whereas their LDL-C does not differ. Conclusions: Many observational and experimental studies have demonstrated that high LDL-C cannot be the cause of premature cardiovascular mortality among people with FH. The number who die early is also much smaller than expected. Apparently, some individuals with FH may have inherited other, more important risk factors than a high LDL-C. In accordance with this, our review has shown that increased coagulation factors are the commonest cause, but there may be other ones as well.
Dietary Recommendations for Familial Hypercholesterolaemia: an Evidence-Free ZoneWe have evaluated dietary recommendations for people diagnosed with familial hypercholesterolaemia (FH), a genetic condition in which increased low-density lipoprotein cholesterol (LDL-C) is associated with an increased risk for coronary heart disease (CHD). Recommendations for FH individuals have emphasised a low saturated fat, low cholesterol diet to reduce their LDL-C levels. The basis of this recommendation is the ‘diet-heart hypothesis’, which postulates that consumption of food rich in saturated fat increases serum cholesterol levels, which increases risk of CHD. We have challenged the rationale for FH dietary recommendations based on the absence of support for the diet-heart hypothesis, and the lack of evidence that a low saturated fat, low cholesterol diet reduces coronary events in FH individuals. As an alternative approach, we have summarised research which has shown that the subset of FH individuals that develop CHD exhibit risk factors associated with an insulin-resistant phenotype (elevated triglycerides, blood glucose, haemoglobin A1c ( HbA1c), obesity, hyperinsulinaemia, high‐sensitivity C reactive protein, hypertension) or increased susceptibility to develop coagulopathy. The insulin-resistant phenotype, also referred to as the metabolic syndrome, manifests as carbohydrate intolerance, which is most effectively managed by a low carbohydrate diet (LCD). Therefore, we propose that FH individuals with signs of insulin resistance should be made aware of the benefits of an LCD. Our assessment of the literature provides the rationale for clinical trials to be conducted to determine if an LCD would prove to be effective in reducing the incidence of coronary events in FH individuals which exhibit an insulin-resistant phenotype or hypercoagulation risk.

Scholarly Articles on Lipids, the Ketogenic Diet and the Lean Mass Hyper Responder (LMHR) Phenotype

The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted DietsWhen lean people adopt carbohydrate-restricted diets (CRDs), they may develop a lipid profile consisting of elevated LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) with low triglycerides (TGs). The magnitude of this lipid profile correlates with BMI such that those with lower BMI exhibit larger increases in both LDL-C and HDL-C. The inverse association between BMI and LDL-C and HDL-C change on CRD contributed to the discovery of a subset of individuals—termed Lean Mass Hyper-Responders (LMHR)—who, despite normal pre-diet LDL-C, as compared to non-LMHR (mean levels of 148 and 145 mg/dL, respectively), exhibited a pronounced hyperlipidemic response to a CRD, with mean LDL-C and HDL-C levels increasing to 320 and 99 mg/dL, respectively, in the context of mean TG of 47 mg/dL. In some LMHR, LDL-C levels may be in excess of 500 mg/dL, again, with relatively normal pre-diet LDL-C and absent of genetic findings indicative of familial hypercholesterolemia in those who have been tested. The Lipid Energy Model (LEM) attempts to explain this metabolic phenomenon by positing that, with carbohydrate restriction in lean persons, the increased dependence on fat as a metabolic substrate drives increased hepatic secretion and peripheral uptake of TG contained within very low-density lipoproteins (VLDL) by lipoprotein lipase, resulting in marked elevations of LDL-C and HDL-C, and low TG. Herein, we review the core features of the LEM. We review several existing lines of evidence supporting the model and suggest ways to test the model’s predictions.
Thyroid markers and body composition predict LDL-cholesterol change in lean healthy women on a ketogenic diet: experimental support for the lipid energy modelIntroductionThere is a large heterogeneity in LDL-cholesterol change among individuals adopting ketogenic diets. Interestingly, lean metabolically healthy individuals seem to be particularly susceptible, with an inverse association between body mass index and LDL-cholesterol change. The lipid energy model proposes that, in lean healthy individuals, carbohydrate restriction upregulates systemic lipid trafficking to meet energy demands. To test if anthropometric and energy metabolism markers predict LDL-cholesterol change during carbohydrate restriction.MethodsTen lean, healthy, premenopausal women who habitually consumed a ketogenic diet for ≥6 months were engaged in a three-phase crossover study consisting of continued nutritional ketosis, suppression of ketosis with carbohydrate reintroduction, and return to nutritional ketosis. Each phase lasted 21 days. The predictive performance of all available relevant variables was evaluated with the linear mixed-effects models.ResultsAll body composition metrics, free T3 and total T4, were significantly associated with LDL-cholesterol change. In an interaction model with BMI and free T3, both markers were significant independent and interacting predictors of LDL-cholesterol change. Neither saturated fat, HOMA-IR, leptin, adiponectin, TSH, nor rT3 was associated with LDL-cholesterol changes.DiscussionAmong lean, healthy women undergoing carbohydrate restriction, body composition and energy metabolism markers are major drivers of LDL...
Oreo Cookie Treatment Lowers LDL Cholesterol More Than High-Intensity Statin therapy in a Lean Mass Hyper-Responder on a Ketogenic Diet: A Curious Crossover ExperimentRecent research has identified a unique population of ‘Lean Mass Hyper-Responders’ (LMHR) who exhibit increases in LDL cholesterol (LDL-C) in response to carbohydrate-restricted diets to levels ≥ 200 mg/dL, in association with HDL cholesterol ≥ 80 mg/dL and triglycerides ≤ 70 mg/dL. This triad of markers occurs primarily in lean metabolically healthy subjects, with the magnitude of increase in LDL-C inversely associated with body mass index. The lipid energy model has been proposed as one explanation for LMHR phenotype and posits that there is increased export and subsequent turnover of VLDL to LDL particles to meet systemic energy needs in the setting of hepatic glycogen depletion and low body fat. This single subject crossover experiment aimed to test the hypothesis that adding carbohydrates, in the form of Oreo cookies, to an LMHR subject on a ketogenic diet would reduce LDL-C levels by a similar, or greater, magnitude than high-intensity statin therapy. The study was designed as follows: after a 2-week run-in period on a standardized ketogenic diet, study arm 1 consisted of supplementation with 12 regular Oreo cookies, providing 100 g/d of additional carbohydrates for 16 days. Throughout this arm, ketosis was monitored and maintained at levels similar to the subject’s standard ketogenic diet using supplemental exogenous d-β-hydroxybutyrate supplementation four times daily. Following the discontinuation of Oreo supplementation, the subject maintained a stable ketogenic diet for 3 months and documented a return to baseline weight and hypercholesterolemic status. During study arm 2, the subject received rosuvastatin 20 mg daily for 6 weeks. Lipid panels were drawn water-only fasted and weekly throughout the study. Baseline LDL-C was 384 mg/dL and reduced to 111 mg/dL (71% reduction) after Oreo supplementation. Following the washout period, LDL-C returned to 421 mg/dL, and was reduced to a nadir of 284 mg/dL with 20 mg rosuvastatin therapy (32.5% reduction). In conclusion, in this case study experiment, short-term Oreo supplementation lowered LDL-C more than 6 weeks of high-intensity statin therapy in an LMHR subject on a ketogenic diet. This dramatic metabolic demonstration, consistent with the lipid energy model, should provoke further research and not be seen as health advice.

Scholarly Articles on Triglycerides, HDL and Atherosclerotic Cardiovascular Disease (ASCVD)

Scholarly Articles on Plant-Based Sterols

Scholarly Articles on Lipids and the Nuclear Magnetic Resonance (NMR) LipoProfile

Lipoprotein subclass measurements by nuclear magnetic resonance spectroscopy improve the prediction of coronary artery disease in Type 1 Diabetes. A prospective report from the Pittsburgh Epidemiology of Diabetes Complications Study - DiabetologiaAim/hypothesis To examine whether nuclear magnetic resonance lipoprotein spectroscopy improves the prediction of coronary artery disease in patients with Type 1 diabetes, independently of conventional lipid and other risk factors. Methods A prospective nested case-control design of subjects with childhood onset Type 1 diabetes from the Pittsburgh Epidemiology of Diabetes Complications Study was used. 59 controls were age-, sex- and duration-matched to 59 incident cases of coronary artery disease (fatal or non-fatal myocardial infarction, angina, coronary stenosis >50%) occurring during 10 years of follow-up. Lipid mass and particle concentrations of VLDL, LDL, and HDL subclasses, grouped into three size categories (large, medium, and small), were assessed prior to event with nuclear magnetic resonance spectroscopy. Results Univariate analyses showed that both lipid mass and particle concentrations of all three VLDL subclasses, small LDL, medium LDL, and medium HDL were increased in CAD cases compared to controls, while large HDL was decreased. Mean LDL and HDL particle sizes were lower in cases. In multivariate models using conventional lipid and non-lipid risk factors, triglycerides and overt nephropathy were the strongest predictors of CAD. Nuclear magnetic resonance measures further improved the prediction, i.e. large HDL particle concentration (OR=0.43, p=0.030), medium HDL mass (OR=3.79, p=0.026) and total VLDL particle concentration (OR=2.33, p=0.033). Conclusion/interpretation While these results underscore the importance of triglycerides and overt nephropathy in CAD risk in Type 1 diabetic patients, they also suggest that nuclear magnetic resonance lipoprotein spectroscopy could further refine its prediction and show novel findings concerning HDL subclasses.
Toward Reliable Lipoprotein Particle Predictions from NMR Spectra of Human Blood: An Interlaboratory Ring TestLipoprotein profiling of human blood by 1H nuclear magnetic resonance (NMR) spectroscopy is a rapid and promising approach to monitor health and disease states in medicine and nutrition. However, lack of standardization of measurement protocols has prevented the use of NMR-based lipoprotein profiling in metastudies. In this study, a standardized NMR measurement protocol was applied in a ring test performed across three different laboratories in Europe on plasma and serum samples from 28 individuals. Data was evaluated in terms of (i) spectral differences, (ii) differences in LPD predictions obtained using an existing prediction model, and (iii) agreement of predictions with cholesterol concentrations in high- and low-density lipoproteins (HDL and LDL) particles measured by standardized clinical assays. ANOVA-simultaneous component analysis (ASCA) of the ring test spectral ensemble that contains methylene and methyl peaks (1.4–0.6 ppm) showed that 97.99% of the variance in the data is related to subject, 1.62% to sample type (serum or plasma), and 0.39% to laboratory. This interlaboratory variation is in fact smaller than the maximum acceptable intralaboratory variation on quality control samples. It is also shown that the reproducibility between laboratories is good enough for the LPD predictions to be exchangeable when the standardized NMR measurement protocol is followed. With the successful implementation of this protocol, which results in reproducible prediction of lipoprotein distributions across laboratories, a step is taken toward bringing NMR more into scope of prognostic and diagnostic biomarkers, reducing the need for less efficient methods such as ultracentrifugation or high-performance liquid chromatography (HPLC).
Characterization of lipid profile by nuclear magnetic... : Medicinerestriction and physical exercise. A total of 115 nondiabetic women (aged 35–55 years) with a body mass index (BMI) of 30 to 40 kg/m2 and ≤1 of the following criteria: blood pressure ≤135/85 mm Hg, fasting plasma glucose ≤100 mg/dL, HDL-cholesterol ≤50 mg/dL, and triglycerides ≤150 mg/dL were included. After 3 months of intensive lifestyle modification (Mediterranean diet and physical exercise), they were classified according to their weight loss: <5%, ≥5% to <10%, and ≥10%. Lipoprotein size, particle, and subclass concentrations were measured using 1H NMR. The final sample, after dropouts, comprised 104 women (age: 44.4 ± 3.7 years, BMI: 36.3 ± 4.7 kg/m2), of whom 47 (45.2%), 27 (26%), and 30 (28.8%) lost <5%, ≥5% to <10%, and ≥10% of baseline body weight, respectively. All participants experienced significant weight loss and decreases in BMI. The lipid profiles showed an increase in small, medium, and large very low density lipoprotein (VLDL) particles in all groups of study with the exception of small VLDL particles in women with ≥10% of weight loss, in which it decreased. The number of VLDL particles decreased in women who had ≥10% weight loss. On the other hand, we detected a decrease in all low density lipoprotein (cLDL) and high density lipoprotein (cHDL) concentrations. These results indicate that intensive lifestyle modification alters lipid profiles. In particular, it decreases small LDL and HDL particle numbers and does not increase medium or large HDL particles numbers....