LCHF on the Front Cover of US Magazine

WW

Who’s that handsome doctor? Well, it’s Dr. Eric Westman, president of the American Society of Bariatric Physicians (weight loss doctors).

According to the magazine he is “the world’s number-one expert on low-carb diets” – and they may be right. I spent a few days with him at his Duke University clinic back in 2010. I’ve also interviewed him on video a couple of times, here’s the latest interview.

The “last-chance diet” is a strict Atkins diet, virtually identical to LCHF.

Obviously the text on the front cover contains a few too-big promises. In the article Dr. Westman says he often sees 20 pounds of weight loss in two weeks and 100 pounds in a year, not that it happens to everybody. And when it comes to heart disease he only says that risk factors typically improve (that’s all we know for sure).

Woman’s World apparently has a circulation of almost 7 million copies. Not a bad way to spread the message.

More details on Jimmy Moore’s blog

How to Lose Weight

LCHF for beginners

93 comments

Top comment

  1. I've never come across the results of studies such as this:

    http://www.ncbi.nlm.nih.gov/pubmed/24380692

    mentioned by DickK earlier.

    On the surface it sounds disconcerting. Afterall, biomarkers are very often dismissed as not being relevant, eg increase in LDL in some on a LCHF diet with the argument being that there's an increase in the better sub type. However, a physical change such as that mentioned in the study of the vessels in the neck can't really be dismissed.

    Thoughts anyone?

    It's not a randomized controlled trial, it's observational data, meaning the groups are potentially different in X number of ways.

    Apples and oranges.

    In a real RCT on adults the effect was the opposite:
    http://circ.ahajournals.org/content/121/10/1200.full

    Read more →
1 2

All comments

  1. murray
    "The new trials with PCSK9 inhibitors are soon on the markets and allow doctors to reduce LDL in the 20s on high risk people."

    Good to see Big Pharma has a new panacea in the works to flog now that the patents on statins have started to expire. What could possibly go wrong?

    I eagerly await something convincing that it is the lowering of LDL that makes a difference and not other factors. At the risk of being insulted by Dickk as a "denialist" or "creationist" or whatever, I am simply not convinced at this point. Other explanations seem much more credible the more I look into the matter of the mechanisms of artery health, damage and response. Why, for example, would consumption of oxidized vegetable oils make a difference if the gradient of LDL concentration were the only factor. Perhaps a new universal drug solution is a fantastic wet dream for the Pharma Dickks seeking the next patentable cash cow they can sell as a magic bullet paid for by health insurance, but the rest of us want a long healthspan without drugs.

  2. Z.M.
    Sill waiting for Dr. Ridker to properly explain the points raised by the critics. So far he has provided no substance. Dr. de Lorgeril created a nice slide for everyone to see (could not post the link because it is being marked as spam, so search his website).

    Why are you even trying you defend a trial which provided no cardiovascular mortality benefit and a possible chance mortality finding driven by fewer cancer deaths? Dr. Ridker himself acknowledged that "There was a small reduction in fatal cancers, but the steering committee believes that was likely the play of chance". Even the FDA officers found it unclear stating "Further inspection of the data shows that the Kaplan-Meier curves converge toward the end of the trial. At approximately 1600 days (4.4 years), the Kaplan-Meier estimate of the absolute difference in risk of death is 0.7% in favor of rouvastain with a 95% confidence interval (-0.4%, 1.8%). Thus, it is not clear whether or not rosuvastatin confers a total mortality advantage compared to placebo even though the logrank test appears to detect the separation of the survival curves up to over 4 years."

    The Jupiter data set is simply unreliable no matter how you spin it.

  3. FrankG
    I guess what loses the most credibility for Dik Dik, is his seeming need to constantly defend his apparently insurmountable position!

    He claims to have the "preponderance of evidence", to have the backing of the best minds in science and medicine, the support of "every single health organization dealing with public health on the face of this planet" and yet he evidently feels threatened by a family Doctor and a few comments on a blog?!?

    Seriously?!?

    One can only assume that his position is not quite so rock solid, nor unassailable, as he would try to have us believe.

    Oh dear... poor little Dick :-P

  4. Z.M.
    BTW loss of function mutations in PCSK9 promote increased LDLR activity, allowing more LDL particles to be cleared from plasma, which reduces particle residence time. This is important because if LDL receptor expression is increased, this leads to an increase in the turnover of LDL and a decreased chance of LDL modification. Same can be said of other genetic disorders. Therefore even IF these studies could be extrapolated to the normal population it still does not prove that lowering cholesterol will reduce risk. In fact, research throughout the decades have shown that lowering cholesterol is a waste of time (http://diettrialclaims.blogspot.com/2013/06/animal-studies.html) so there is no reason to suspect that PCSK9 inhibitors will work.
  5. charles grashow
    http://circ.ahajournals.org/content/118/6/672.full
    Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia

    One important line of evidence comes from a consideration of the Japanese experience. In 1952, mortality from CHD among Japanese men 55 to 64 years of age was <10% of what it was in the United States.15,16 Their total cholesterol levels at the time averaged ≈160 mg/dL (estimated LDL, ≈80 mg/dL). It is noteworthy that the Japanese enjoyed this relative immunity to CHD despite the fact that the prevalence of one of the major risk factors—cigarette smoking—was much higher in Japan than in Western countries,17 and another—-hypertension—was just as high.18 Even the diabetic population in Japan fares better than the diabetic population in Western countries. In 1985, almost 30% of British male diabetics but only ≈15% of the Japanese male diabetics had CHD.19 The implication is that if blood cholesterol levels are sufficiently low, the other dominant risk factors, including cigarette smoking, hypertension, and diabetes mellitus, constitute much less of a threat.

    Are these large differences in incidence between Japan and Western countries based primarily on genetic factors? No. Two cleverly designed epidemiological studies showed that the Japanese who had migrated and taken up permanent residence in Hawaii had higher blood cholesterol levels and a higher incidence of CHD than those who remained on the home island. For those who migrated even further, on to California, the differences were even more striking.20,21 This and other migration studies22 showed that the differences in CHD risk among different populations are certainly not entirely genetic. Which environmental factors are at play? A number of factors could be involved, but there is reason to believe that the major factors are changes in diet and exercise patterns that predispose to elevated blood cholesterol and obesity. Keys23 reported as early as 1957 that the fat content of the diet, as a percentage of total calories, rose from 10% to 15% in Japanese on the home island to ≈30% in Japanese migrants to Hawaii and to almost 40% in migrants to Los Angeles.

    A crucially important point needs to be noted here: For whatever reasons, the Japanese have their lower cholesterol levels for their entire lifetimes. Lowering the cholesterol level of a 50-year-old American for just 5 years, even if his cholesterol is successfully brought down to a Japanese-like level, is unlikely to convert his risk to a Japanese-like risk. At 50 years of age, he most likely enters the study with well-established, extensive arterial disease.24,25 It would be unreasonable to expect that all that damage could be reversed in just 5 years. The canonical 5-year trials have given us a minimum estimate of the impact of preventive management. Only after longer trials with younger subjects will we have some estimate of the maximum potential. We will return later to this key issue, the need for earlier treatment.

    Is lowering LDL levels intrinsically dangerous? That possibility has been suggested in the past, but no hard evidence exists for such a concern, and a number of considerations make such an effect quite improbable.

    First, levels of intracellular cholesterol are jealously guarded by the wonderfully efficient LDL receptor homeostatic mechanism elucidated by Brown and Goldstein. Consequently, lowering plasma cholesterol levels does not decrease intracellular cholesterol levels. The LDL receptor has a very high affinity for its ligand, so much so that even at plasma LDL cholesterol concentrations of 10 mg/dL, the LDL receptors in peripheral tissues would still be 50% saturated and uptake would continue unabated.

    Second, we know that most mammalian species have LDL levels well below those reached in humans during even the most aggressive treatment of hypercholesterolemia (mean value, 42 mg/dL).38 Obviously, these animals’ cells do just fine. In addition, cord-blood LDL levels in humans are <20% of adult levels,39 showing that growth and development of the fetus are just fine at LDL cholesterol levels <40 mg/dL.

    Third, in some kindreds with hypobetalipoproteinemia, LDL cholesterol levels can be <15 mg/dL throughout life, yet the affected members show perfectly normal growth and development and actually have increased longevity.40,41

    We know now from the large-scale statin trials that lowering LDL values to well below 100 mg/dL not only is safe but actually decreases overall mortality significantly.4,11,29,42–46 Thus, there should be no hesitation at all about lowering LDL levels through attention to lifestyle changes (ie, diet and exercise), in which the intervention itself carries no risks. Here, the only rule necessary is “the lower, the better.”

    http://www.nobelprize.org/nobel_prizes/medicine/laureates/1985/brown-...
    When LDL-cholesterol levels are below 100 mg/dl (equivalent to a total plasma cholesterol level of 170 mg/dl), heart attacks are rare. When LDL-cholesterol levels are above 200 mg/dl (equivalent to a total plasma cholesterol level of -280 mg/dl),heart attacks are frequent. Controversy arises over the middle ground, i.e.,individuals with plasma LDL-cholesterol levels between 100 and 200 mg/dl (total plasma cholesterol of 170 to 280mg/dl). This is the, range in which the vast bulk of heart attacks occur. Somewhere within this range there is a threshold value of cholesterol at which heart attacks begin to become more frequent. In this middle ground how much of the heart attack burden is attributable to plasma cholesterol? There is no definitive answer. In addition to cholesterol, heart attacks in this group are aggravated by smoking, hypertension, stress, diabetes mellitus, and poorly understood genetic factors. However, it seems reasonable to propose that plasma cholesterol does have something to do with heart attacks in these subjects, and that the incidence of heart attacks would be reduced if plasma cholesterol could be lowered

    The LDL receptor studies lend experimental support to the epidemiologists’ suggestion that the levels of plasma cholesterol usually seen’ in Western industrialized societies are inappropriately high (9). This support derives from knowledge of the affinity of the LDL receptor for LDL. The receptor binds LDL optimally when the lipoprotein is present at a cholesterol concentration of 2.5 mg/dl (28). In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol (118). This is roughly one-fifth of the level usually seen in Western societies (Fig. 16 and ref.119). Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl (Fig. 16 and ref. 120). In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels (9,119). Second, the LDL level in newborn humans is approximately 30 mg/dl (121), well within the range that seems to be appropriate for receptor binding (Fig. 16). Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies (116)

    http://truthcentral.wordpress.com/2013/06/26/119/
    Rebuttal to Main Cholesterol Skeptic

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1312295/
    Of the various atherosclerotic risk factors, which one is an absolute prerequisite for development of atherosclerosis?

    The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop?

    Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL (8). If the LDL cholesterol level is <100— and possibly it needs to be 150 mg/dL and the LDL cholesterol is >100 mg/dL, the other risk factors clearly accelerate atherosclerosis.

    Reply: #56
  6. FrankG
    Seriously Charles.. trying to drown everyone out with an avalanche of words? You really expect others to wade through all that? Haven't you been told before about how pointless it is to simply copy and paste vast swathes from other sites... especially when, as in this case, you have made no attempt to differentiate between what is a direct quote, what is opinion, what is your own words etc.. etc.. etc... an absolutely pointless waste of time!
    Reply: #58
  7. Z.M.
    Charles, have you even read my review on cholesterol? - http://diettrialclaims.blogspot.com/2013/06/animal-studies.html

    You have a tendency of not communicating with others, so it would be nice if you can answer my question directly.

    Reply: #59
  8. charles grashow
    I'll try to dumb down my answers so you can more readily understand them.
    Reply: #61
  9. charles grashow
    Yes I have - you just post studies that support your POV. BTW what are your academic qualifications?
  10. FrankG
    Given that Dick Dick likes to claim that only a "denialist" would suggest that "every single health organization dealing with public health on the face of this planet has been wrong about diet-heart and lipid theory"...

    ...along with an emphasis (shared by others apparently) that "LDL" is the major culprit -- even allowing for this gross oversimplification of a complex and nuanced topic...

    Here is the link to a table showing the World Health Organisation's Clinical Criteria for [the diagnosis of] Metabolic Syndrome...

    http://circ.ahajournals.org/content/109/3/433/T2.expansion.html

    Please read it and relay back to the class what upper level they set for "LDL" in these criteria.

    I'll save you the bother... they include Plasma triglycerides and HDL cholesterol but LDL does not even get a mention!

    Weird eh? Especially given the "preponderance of evidence". Or perhaps we are to take it that those with Metabolic Syndrome are not seen as high risk for CVD?

    ---

    Here again we can wonder about the agenda when we only currently have drugs which effectively lower "LDL" levels... no drugs for trigs or HDL-C (although I know a dietary intervention which helps.. but where's the money in that? LOL)

    Have a look at the NCEP Adult Treatment Panel III Update 2004: Financial Disclosure statement for the 9 member (self-selected) working group... and do bear in mind that these guidelines are adopted and used by many countries, not just the US of A

    http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3upd04_disclose.htm

    72 (SEVENTY TWO) Financial Conflicts of interest across 8 of the 9 panel... 72!!!

    As Dr Kendrick succinctly puts it... " the mere fact that there were seventy two financial conflicts of interest does not mean that the guidelines themselves were biased. But you know what, I don’t believe it. Imagine if eight Supreme Court judges, ruling on any issue, had seventy two direct financial conflicts of interest to do with that issue…..Well, the outcry would never end"

    Oh and he has a few telling words about the good Dr Ridker in the same article :-P

    http://drmalcolmkendrick.org/2013/08/02/who-shall-guard-the-guardians/

    ---

    Bottom line for me is that there IS controversy, it is NOT a done deal and there are HIGHLY questionable agendas relating to billion$ of dollar$ of profits... this makes me highly skeptical of ANYTHING which is presented supporting the lipid hypothesis and widespread use of statins.

    All of which is to say that you would really have your work cut out to try and convince me that my current choice of diet is somehow killing me, despite all my personal evidence to the contrary.

  11. FrankG
    That whole spiel was an "answer"??? What the heck was the question?!?

    And if you want to start insulting my intelligence, then do expect me, going forward, to treat you with all the respect that you deserve :-P

  12. Z.M.
    Charles: "Yes I have - you just post studies that support your POV. BTW what are your academic qualifications?"

    Then you haven't read it because I include studies that allegedly support the lipid hypothesis contrary to your claim. In other words my review includes almost all of the relevant evidence available. In fact, I take into consideration a bunch of studies in the links that you provide which is why I presented the question to you.

    Charles: "BTW what are your academic qualifications?"

    You asking me this question is problematic because it confirms that you are unable to review the evidence on your own, which explains why you hold the position that you do. You know, following the principles of science and logic goes a long way to filtering the BS propagated against cholesterol.

  13. murray
    Gentlemen, is this supposed to be a productive discussion or an argument?

    It is not productive to cherry pick studies, especially when there is so much evidence of manipulation of studies to suit pharmaceuticals and withholding of negative studies and blocking funding for the types of studies that might prove negative.

    Further, when a renowned lipidologist such as Dr. Tom "Just take the damn statins!" Dayspring (i.e., not hostile to statins) concludes the evidence does not show elevated cardiovascular risk when the number of LDL particles is in normal range despite much higher level of LDL-C, it is difficult to ascribe much credibility to cherry-picked studies.

    And arguments from cholesterol levels in other animals are utterly unpersuasive. Humans have a much bigger brain in proportion, which is to a large degree cholesterol. So anything that relates to brain will likely be different in humans because the proportionate quantum human brain needs are so different. Indeed, low cholesterol correlates to earlier onset of senility in Framington analysis: Elias, et al, "Serum Cholesterol and Cognitive Performance in the Framington Heart Study, " Psychosomatic Medicine 67, No. 1 (2005): 24-30. Dr. Perlmutter in Grain Brain cites other studies along the same lines, so something must be going on metabolically.

    Where does this all leave me in terms of which side of the debate seems more credible? Going home to have some duck liver gently cooked rare in butter from grass-fed cow milk.

    I have found in my personal experience that eating in this manner has raised my HDL and LDL, without putting LDL-P or apoB/apoA out of normal, has left my arteries perfectly clear, blood pressure decent (95/65), triglycerides very low, CRP below measured range and my skin and other tissues in noticeably better condition, especially during times I up my consumption of coconut oil. So absent any evidence of personal health detriment, I simply don't find the cherry-picked hysterics of Dickk convincing. Charles, at least, is human in his demeanor. But I still don't think it addresses the reasons so many people are skeptical of the gradient LDL hypothesis.

  14. Z.M.
    FrankG: "Oh and he has a few telling words about the good Dr Ridker in the same article"

    Exactly. If anyone has the motivation to propagate nonsense about statins and CRP Dr. Ridker would be the man!

  15. DickK
    @ZM;

    if statins would work mainly through some other unknown mechanism, it would be hard to explain why people with inherited mutation that lower cholesterol throughout the life via the statin targeted HMG-CoA gene have 55% reduced risk for CHD for every mmol/l (39mg/dl) lower cholesterol. The same magnitude of decreased risk for CHD is seen in people with genetic mutation that lower life-time cholesterol through a very different pathway, through the PCSKY9, in fact the result are identical with all the 9 genetic polymorphism studied so far. Tough times for being a cholesterol denialist.

    Nearly all free-ranging mammalians have very low levels of cholesterol, LDL way under 70s.

    Ridker explained himself in the article published in Medscape that I linked to as well as in separate the article published in American Journal of Cardiology.

  16. FrankG
    Did Dr Ridker perhaps go on to explain (in the Medscape article) why it took JAMA to expose his...

    "Unreported Financial Disclosures in: ‘Association of LDL Cholesterol, Non–HDL Cholesterol, and Apolipoprotein B Levels With Risk of Cardiovascular Events Among Patients Treated With Statins: A Meta-analysis.’"

    The fact that he had board membership with Merck Sharp and Dohme…… a company that has made billions from selling statins.

    This just slipped his mind perhaps? Maybe short-term memory loss and confusion as a result of taking statins..? Although it sure would be interesting to see exactly how many of these statinators are actually risking taking their own drugs. Eh Dick? :-P

    http://jama.jamanetwork.com/article.aspx?articleid=1148176

  17. Liam
    Doc. It's comical you tried to counter a weight maintenance study in children with an extremely low calorie weight loss study with adults which are using drugs.
    Apples and oranges?

    "if statins would work mainly through some other unknown mechanism, it would be hard to explain why people with inherited mutation that lower cholesterol throughout the life via the statin targeted HMG-CoA gene have 55% reduced risk for CHD for every mmol/l (39mg/dl) lower cholesterol. The same magnitude of decreased risk for CHD is seen in people with genetic mutation that lower life-time cholesterol through a very different pathway, through the PCSKY9, in fact the result are identical with all the 9 genetic polymorphism studied so far. Tough times for being a cholesterol denialist."

    I suspect this statement will attempted to be refuted by distractions like irrational hatred of "Big Pharma" and other paranoid rhetoric.

    "In scientific contexts, the denialist can deny a cause, an effect, the association between the two, the direction of the cause-and-effect relationship or the identification of the cause-and-effect relationship . Often denialists practice minimization and use misplaced skepticism to give an unwarranted veneer of scientific thinking"

    Reply: #68
  18. FrankG
    "...Often denialists practice minimization and use misplaced skepticism to give an unwarranted veneer of scientific thinking"

    ...while others try to skulk around behind the anonymity of yet another pseudonym in the mistaken belief that their style of writing will not betray them as still being a little... Dick! LOL :-P

  19. Liam
    Frankg...While others impart even more Pseudoskepticism to distract and confuse.

    LDL and LDL-p are usually discordant in people with metabolic syndrome. Which is why high LDL isn't listed as a major risk factor.

    It's funny you're linking to the website of confusionist Dr Malcomn kendrick. Do you know he says that diet has nothing to do with CVD?
    Would you agree with that statement? Or would you pass him off as some kind of crank?

    Reply: #70
  20. FrankG
    It seems we are surrounded by "confusionists" and "denaliasts" on all sides... oh dear!

    Good job that we can rely on the solid foundation of such upstanding and trustworthy people as yourself... eh Dick K K K? :-P

  21. Z.M.
    Dick: "if statins would work mainly through some other unknown mechanism, it would be hard to explain why people with inherited mutation that lower cholesterol throughout the life via the statin targeted HMG-CoA gene have 55% reduced risk for CHD for every mmol/l (39mg/dl) lower cholesterol."

    Assuming that statins actually work (I'm not convinced), the mechanism by which they are said to work is through increases in the LDLr. This is the same mechanism of loss of function mutations in PCSK9 and the many genetic disorders that you refer to. So even by the mainstream view, the data and proposed mechanism are consistent with the idea that modifications of LDL is the important factor, not LDL per se. However, since the majority of cholesterol LOWERING trials throughout the decades have failed to show any benefit, I fail to see the value in lowering cholesterol.

  22. Dickk
    ZM

    You neglect the fundamental fact that LDL injection itself causes artery disease in experimental models. Direct LDL injection results in aggregate increase in LDL-C.

    "However, since the majority of cholesterol LOWERING trials throughout the decades have failed to show any benefit, I fail to see the value in lowering cholesterol".

    LOL! Even if we accept this we ought to look things in bigger picture. Most lipid-lowering trials have been performed on high risk people with existing cardiovascular disease. The median age at the randomization in typical statin trial has been 63 and medium duration 5 years. Most of the trials have been performed using low potency statins. Drugs and moderate dietary modification can only have a very limited impact when adopted at later in midlife with pre-existing disease. Even though the plaques will be stabilized and even though high-potency statins can actually regress the plaques to some extent, still the plaques can cause a rupture and result in MI in people with pre-existing coronary artery disease.

    Anyways, the degree to which LDL is lowered with statin corresponds linearly to the decreased risk of CHD events in people with pre-existing disease at are the late stages in their mid-life.

    There are actually 3 such trials that I am aware of the tested the hypothesis that smoking cessation would lower the risk of lung cancer mortality. All 3 trials failed to produce statistically significant findings despite reporting significant reductions in smoking prevalence in the group that received counselling on smoking cessation. These trials include the Whitehall Study, the Lung Health Study, and MRFIT, which included in total over 20,000 participants and up to 20 years of follow-up. This makes these trials considerably larger in both in terms of participant size and length of follow-up than the trials that focused on replacing primarily saturated fats with polyunsaturated fats. The largest of these 3 trials found that the number of lung cancer deaths were actually 15% greater, albeit not statistically significant in the group that received counselling on smoking cessation.
    http://onlinelibrary.wiley.com/doi/10.1002/1097-0142(20001201)89:11+%3C2422::AID-CNCR16%3E3.0.CO;2-E/full

    The relative failure of these smoking cessations trials can be considered a very good example of why all forms of evidence need to be considered when evaluating a hypothesis, not just a few data points from a few randomized controlled trials. The lack of statistically significant favourable findings in the group that received counselling on smoking cessation has been explained by a lack of follow-up time sufficient to achieve the maximum benefits of smoking cessation (which is believed to be more than 2 decades), lack of participant size, a smaller than anticipated number of participants in the group that received counselling that quit smoking, and a greater than anticipated number in the group that did not receive counselling that quit smoking. These limitations are very similar to those that plague the trails that attempted to test the diet-heart hypothesis.

  23. FrankG
    Genesis Land of Confusion...

    http://www.youtube.com/watch?v=zU9lv_WqK6k

    It's your stock in trade eh Dick? :-P

  24. Z.M.
    Ah the false analogy of smoking. The lipid hypothesis is in really bad shape if it needs to create all sorts of ad hoc hypotheses for its failures which it has been doing for decades! In any case, there are actually common factors to familial hypercholesterolemia and smoking which may explain the increased risk in both - oxidative stress.
  25. FrankG
    What's really comical is the way you will simultaneously try to offer a trial as incontrovertible evidence (there is no such thing in science, by the way) in support of your position, while in the exact same breath, point out why so many of these same "trails" have been plagued (plaqued?) with limitations! ROFLOL

    In much the same way as your tactic above "LOL! Even if we accept this we ought to look things in bigger picture." ...where the reader is left confused (bemused?) as to whether you do accept the point as potentially valid, or if you are simply LOL'ing at it.

    It's all just fun and games to you... eh Dick? :-P

  26. Dickk
    Saturated fat and dietary cholesterol both oxidizes LDL cholesterol, moreover, it has been demonstrated that macrophages are able to take up LDL particles even in their unmodified form.
    http://www.ncbi.nlm.nih.gov/pubmed/20634472?dopt=Abstract&holdin...
    http://www.youtube.com/watch?v=FXV4MEO5s_E&list=PLDBBB98ACA18EF67C

    1) "The amount of LDL oxidized and the subsequent risk of CAD can also be affected by dietary factors other than antioxidants. Reducing saturated fat intake (Figure 1) lowers the plasma con- centration of LDL and thus the amount of LDL available for oxidative modification. Parks et al (1) achieved this by replacing fat in the diet with carbohydrates."
    http://ajcn.nutrition.org/content/68/4/759.full.pdf

    2) Dietary cholesterol increases the susceptibility of low density lipoprotein to oxidative modification.
    http://www.ncbi.nlm.nih.gov/pubmed/10704618

    3) Lowering dietary saturated fat and total fat reduces the oxidative susceptibility of LDL in healthy men and women.
    http://www.ncbi.nlm.nih.gov/pubmed/10958817

    Moreover, the results from the new study on children fed ketogenic diet are on par with other studies that have looked fatty acids and carotid thickness.

    1) Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study

    “Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT. The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs"

    http://www.ncbi.nlm.nih.gov/pubmed/18054937

    2) Dietary fat intake and carotid artery wall thickness: the Atherosclerosis Risk in Communities (ARIC) Study.

    "Wall thickness was measured with B-mode ultrasound. After adjustment for age and energy intake, animal fat, saturated fat, monounsaturated fat, cholesterol, and Keys’ score were positively related to wall thickness, while vegetable fat and polyunsaturated fat were inversely related to wall thickness. These associations persisted after further adjustment for smoking and hypertension and were consistent across the four race and sex groups. Thus, elements of habitual dietary intake were consistently associated with carotid artery wall thickness, compatible with their putatively atherogenic and antiatherogenic properties”.,

    http://www.ncbi.nlm.nih.gov/pubmed/8178786

    Bonus:

    Reducing saturated fat intake is associated with increased levels of LDL receptors on mononuclear cells in healthy men and women.
    http://www.ncbi.nlm.nih.gov/pubmed/9101427

  27. Z.M.
    Lowering LDL does not do anything beneficial for the umpteenth time, so any explanation invoking lowering LDL is a poor one. It follows that IF oxldl is indeed the cause of disease then lowering LDL to achieve lowered oxldl seems like a poor strategy. Futhermore, oxldl and oxidative stress are not necessarily correlated with LDL and you're confusing oxldl with oxidative stress which is much broader in connotation.

    I've already done a review on saturated fat - http://diettrialclaims.blogspot.com/2013/08/saturated-fat-and-inflamm...

  28. DickK
    ZM;

    it's rather clear that you are ideologically opposed to any strategy that involves lowering LDL. The online is full ideologically motivated denialists like you who will tell you that Darwin manipulated his data or the climate change is a hoax created by Al Gore to suppress American global domination, etc. You are on par with these people! Often we get to read about these people when they are trying to blow up abortion clinics or detonate their local tax bureau.

    "The State makes war on cholesterol because it is your best defense against that State: Cholesterol empowers independent thought by strengthening mental capabilities. In truth, to be anti-cholesterol is to be pro-State; to be anti-State – that, dear reader, is to be pro-cholesterol."

    --Chris Masterjohn

    Reply: #79
  29. FrankG
    Surely you must realise by now DICK that you are wasting your time here? You are not impressing, nor convincing anyone with your games. You have zero credibility with the intelligent, skeptical, reasonable, free-thinkers who read this blog... and a great many other blogs besides; where it seems you elicit the same negative response and often end up banned -- just as you did recently at Denise Minger's blog, despite your attempts to reappear under another pseudonym. How pitiful is that?!?

    Every time you try to detract from another's post, as you just did above, by suggesting that ZM is a closet bomber (hah!) you actually reveal more about your OWN tactics than anything else... you are showing us how YOU think and it is really not pretty, nor reasonable at all. You are a nasty, vile, obnoxious, dangerous, slimy, contemptuous waste of an individual.

    I don't bother trying to engage you in reasonable discussion because with you it is JUST like trying to reason with a new-earth creationist, or a vegan zealot... there is NO room for reasonable discussion with people like you. You are either an ideologue yourself OR you are paid to pollute these blogs with your verbal diarrhoea.

    It is just so obvious and so transparent, yet even when called out on trying to hide behind yet another pseudonym like "liam", you just plow right on regardless. People here are not idiots and yet you seem to think you can ride rough-shod over as if we are. YOU ARE WRONG.

  30. Z.M.
    charles grashow: "Masterjohn has lost his mind."

    Hmm, do you realize that he has a comment section on that very Alzheimer's post? Why comment here that he has "lost his mind" when you can do so on his website?

    Reply: #82
  31. charles grashow
    Because the article was published in 2005 - I think it's a little too late for comments.
  32. Z.M.
    It's irrelevant when the article was published because the comment section is open. In fact, the comment section was opened recently: "Comments were enabled on June 17, 2013 - http://www.cholesterol-and-health.com/Cause-Of-Alzheimers.html"

    So please, take the time to enlighten him.

  33. charles grashow
    http://shop.pomwonderful.com/pdf/clinical_nutrition.pdf
    Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation

    "Ten patients were supplemented with PJ for 1 year and five of them continued for up to 3 years. Blood samples were collected before treatment and during PJ consumption. In the control group that did not consume PJ, common carotid intima-media thickness (IMT) increased by 9% during 1 year, whereas, PJ consumption resulted in a significant IMTreduction, by up to 30%, after 1 year."

  34. Z.M.
    A very small study which showed benefits in the carotid arteries and in oxidative status despite no changes in LDL? Supports what I said before.
  35. Roxanne W
    Here is a link to a 38-minute video on YouTube of Dr. Westman speaking to a group of patients at the Duke Lifestyle Medicine Clinic in Durham, North Carolina, USA, about his "No Sugar, No Starch" program.
  36. Roxanne W
    Here is a link to a 38-minute video on YouTube of Dr. Westman speaking to a group of patients at the Duke Lifestyle Medicine Clinic in Durham, North Carolina, USA, about his "No Sugar, No Starch" program:

    http://www.youtube.com/watch?v=dSLf4bzAyOM

    Replies: #88, #90
  37. robert
    "And if you lose page 4, I will send you another one. I have many page 4s."
  38. charles grashow
    http://onlinelibrary.wiley.com/doi/10.1111/j.1520-037X.2002.01231.x/full

    The Effect of High-, Moderate-, and Low-Fat Diets on Weight Loss and Cardiovascular Disease Risk Factors

    "One hundred men and women followed one of four dietary programs for 1 year: a moderate-fat (MF) program without calorie restriction (28 patients); a low-fat (LF) diet (phase I) (16 patients); a MF, calorie-controlled (phase II) diet (38 patients); and a high-fat (HF) diet (38 subjects). Weight, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), homocysteine (Ho), and lipoprotein(a) [Lp(a)], were measured every 4th month. The TC/HDL-C ratio was calculated and fibrinogen levels were measured at baseline and after one year.

    Dietary Regimens

    High-Fat (HF) Diet This diet is defined as one in which patients consume 55%-65% of their daily caloric intake in the form of fat calories. Less than 100 g of carbohydrates (RCHO) were consumed daily and protein intake constituted 25%-30% of the total caloric intake. Patients ate until satiated.

    Moderate-Fat (MF) Diet Patients following this dietary program consumed 20%-30% of their calories in the form of fat. Approximately 60% of their calories were from carbohydrate sources and the remaining calories were derived from protein. Patients consumed 10–12 calories per pound per day on this diet.

    MF, Calorie-Controlled (Phase II) Diet Patients following this program were asked to consume 350–500 fewer kilocalories per day than required15,20 to maintain body weight. This was determined by multiplying their current weight in pounds by 10 kcal/lb to determine the required kcal intake per day; 350–500 was subtracted from this figure to determine the desired daily intake of calories. Of these calories, 15% were protein and 70% were carbohydrate, with an emphasis on complex carbohydrates vs. simple sugars. The remaining 15% of the calories could be consumed as fat in a 2:1 ratio of nonsaturated (polyunsaturated and monosaturated) to saturated fat, with no more than 5 g of saturated fat intake per day.

    Low-Fat (LF) (Phase I) Diet The LF diet consisted of fruits, vegetables, a limited amount of grain/cereals for breakfast and a multiple vitamin that included 100% of the US Department of Agriculture recommended daily intake of vitamins and minerals. Patients ate until satiated. Of the caloric intake, 10% was fat, 15% was protein, and 75% was carbohydrate, with an emphasis on complex vs. simple carbohydrates as shown in Table I.

    Exercise Regimen

    Each individual was instructed to exercise an average of 3–5 times per week, beginning with stretching for 15 minutes, followed by walking for 30 minutes, and then relaxing and stretching for an additional 15 minutes.
    Monitoring

    Patients returned on a monthly basis to review their progress, answer any questions regarding dietary habits, and determine if they were having any medical problems, which would require removal from the study. Weights were recorded at the beginning of the study and at the end of months 4, 8, and 12. Fasting venous blood was drawn at the beginning of the study and at the end of months 4, 8, and 12. The tests included total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDLC), triglycerides (TG), homocysteine, and Lp(a). The TC/HDL-C ratio was calculated for each of these intervals. Fibrinogen levels were measured at the beginning and end of the year.

    Reductions in TC, LDL-C, TGs, and TC/HDL ratios were significant only in patients either following a LF diet or a MF, calorically reduced diet. Only patients following HF diets showed a worsening of each cardiovascular disease risk factor (LDL-C, TG, TC, HDL-C, TC/HDL ratio, Ho, Lp(a), and fibrinogen), despite achieving statistically significant weight loss."

    Reply: #91
  39. bill
    Roxanne:

    Thank you so much for that link. I hadn't seen that
    video before.

    It is the most calm, complete explanation of how to
    go LCHF.

    Gotta get ahold of page 4!

  40. bill
    "100 g of carbohydrates...daily" is not necessarily a low
    carb diet.
  41. Linda
    Is the Ketogenic Diet good for someone who has non-alcoholic fatty liver?
    Reply: #93
  42. Zepp
    Its probably the absolutly best diet for NAFLD!

    "Curbing carbohydrates is more effective than cutting calories for individuals who want to quickly reduce the amount of fat in their liver...."

    http://www.diabetesincontrol.com/index.php?option=com_content&vi...

    “My Fatty Liver Is Gone”

    http://www.dietdoctor.com/fatty-liver-gone

1 2

Leave a reply

Reply to comment #0 by

Older posts