Great Cholesterol Numbers After 4 Years on an Ultra-Strict LCHF Diet

Is a strict LCHF diet with unlimited amounts of saturated fat bad for cholesterol levels?

Tommy Runesson has had his blood lipid levels checked four times, including just recently, during his four years on an ultra-strict LCHF diet. The major part of his 200 lb-weight loss (!) occurred before his first blood test, and we don’t know what the numbers were before his weight loss.

The numbers look great. We’re not seeing the significantly elevated total-cholesterol number that a small percentage of individuals show on a strict LCHF diet.

I’d say Runesson’s numbers represent the typical result of a long-term strict LCHF: a normal total cholesterol and LDL, excellent HDL and triglycerides, and a very nice apo-B/apo-A1 ratio. This is what I typically see in most patients that I follow.

Runesson’s results also contradict the strange idea that an LCHF diet may produce good lipid numbers because of ongoing weight loss, but that they would suddenly turn disastrous when weight stabilizes, for some obscure reason. This idea has been put forward by some LCHF skeptics. As far as I know there’s no science to support this idea.

In any case: Runesson has been eating an extremely strict LCHF diet for four years, and has maintained stable weight for the last 2.5 years. And his cholesterol profile is far better than most people’s.

Eat Low Carb High Fat: Cholesterol after 4 years on LCHF

PS: I’m planning another cholesterol checkup myself this fall, after 7 years on an LCHF diet.

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86 Comments

  1. charles grashow
    http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase...

    “I went low-carb/higher fat paleo (with dairy) about 1.5 yrs ago. I've struggled with weight all my life.  Even though I've exercised religiously since high school and tried to eat healthy foods--even eating vegetarian for a couple of years--I still couldn't get lean. I'm 5'4" and my teenage/adult weight was always around 145-160, though my body fat wasn't (and isn't) particularly high due to a lifetime of exercise.  I have not had diabetes, metabolic syndrome or hypertension, and am very active.  I've been interested in nutrition/fitness since my teens and try to keep up with the latest to do whatever I can to live a long and healthy life. I started reading about paleo, low-carb and the benefits of eating whole-foods in early 2011 and thought it made sense. I thought it might help me get lean and it did. Over the last year I started thyroid hormone (levothyroxine 50 mcg) to correct hypothyroidism and use MHT (menopausal hormone therapy: Estrogel 0.06% plus Prometrium brand of progesterone 100 mg). I take vitamin D3 (1 000 u daily) and get Omega-3 FA from dietary sources.”

    “My family does have a tendency toward higher cholesterol--three brothers (maybe all four, but I couldn't confirm one) and my mother are on statins. My mother, who will be 76 in May, was recently diagnosed diabetic and has some indications of heart disease but I'm not clear on what heart tests she's had. No other family members with heart disease that I'm aware of. Most in my family are not big exercisers or overly concerned with their diet.”

    “I started eating paleo/low-carb (with dairy) in Apr 2011. I should add that my diet has never been ultra low-carb -- just lower-carb than most people. My last blood test before going paleo was in Nov 2010 and my past numbers have always been similar:”
    Total cholesterol = 196, LDL-C =105, HDL-C = 75, TG = 78 (all in mg/dL)   
    TSH = 2.15

    “I lost 30 pounds in about 3 months and have kept it off ever since. Today I weigh 124 and maintain my weight easily eating this way, even though I am menopausal.” The lipid panel was repeated on the new diet:
    TC = 323, LDL-C = 230 , HDL-C 83, TG 49   (all in mg/dL)
    Total LDL-P = 2643 nmol/L (99th percentile population cut point)
    TG/HDL-C = 0.59 (poor man’s marker of insulin sensitivity) Under 2.0 is excellent

    My goodness! If a new healthy looking, normal weight patient showed up with an LDL-C ~ 230 mg/dL, we are all presuming that familial hypercholesterolemia is present. At the age of 54 we would be searching for arcus senilis, a sternotomy scar or xanthomata. Although there is no premature CHD, there are certainly cholesterol issues in her family. Although we do not have a baseline LDL-P or apoB, how can one go from a perfect lipid profile to a seeming very high risk one in a very short period of time? Can CV lipid/lipoprotein-related risk be worsened by the weight loss? Or perhaps the question is - does it matter what one consumes to lose weight? Is there a danger too low carbs/high fat in some people? Or how about this absurd question - can an LDL-P of ~2600 nmol/L not be associated with atherothrombotic risk? It has been reported for years that diets high in saturated fat raise TC and LDL-C and diets with reduced saturated fat lowers them (Evidence Level IA in NCEP ATP-III). MUFA and PUFA can be neutral or lower LDL-C. MUFA may raise HDL-C. Of course we now know what any therapy does to CV outcomes likely has little if any relationship to what that therapy does to HDL-C but the story that raising LDL-C is associated with or causal of atherosclerosis is widely accepted.

    I, other lipidologists, and many patients themselves, are starting to see that the above lipid response to a high fat diet as not being very rare response in people who abandon carbs and replace it with saturated fat, especially in those doing extreme carb restriction to achieve nutritional ketosis. Many of the patients who pursue this lifestyle did so because they were overweight and exhibited many phenotypic and metabolic markers of insulin resistance and were at risk for the associated morbidities. Carbohydrate intake reduction or avoidance in IR patients, regardless of how much fat is consumed, tends to tremendously improve insulin sensitivity: as measured by weight, waist size, IR-related lipid parameters (TG, HDL-C), IR-related lipoprotein parameters (large VLDL-P, reduced large HDL-P, HDL size, LDL size, VLDL size, LP-IR score) inflammation biomarkers, metabolic (UA, homocysteine), and platelet coagulation biomarkers (urine 11-dehydrothromboxane B2). In many (including the patient being discussed) but certainly not all (the true incidence remains to be determined but experienced colleagues who have a lot of patients on low carb diets advise it is about 1/3 of patients), despite all of the above biomarker and waist size and BMI improvements there is a drastic worsening of TC, LDL-C and most worrisome of all apoB and LDL-P. There is little doubt after a review of the literature that the most important CHD risk factor apart from age and smoking is having too many atherogenic lipoproteins as measured by elevated apoB (LDL-P). In the US there are now 5 major CV subspecialty organizations that have signed on to use of apoB and LDL-P (via NMR) specifically the ADA, ACC, AACC, AACE, and NLA in appropriate patients (mostly the IR patients who are typically at high cardiometabolic risk). Of course for years nutritionists have been, and still are telling us, to avoid dietary fat and cholesterol or else LDL-C will go up and we all know how bad that is with respect to CHD risk – right? As always in medicine, there is more to the story.

    Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL's? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB and an inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation: please see Ira Tabas, Kevin Jon Williams, Jan Borén. Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis Update and Therapeutic Implications Circulation. 2007;116:1832-44.

     So is a low carber with high LDL-C and not high LDL-P is likely safe from CVD risk. But what about a low carber with both high LDL-P and LDL-C – check the Kaplan Meir survival plot above (blue line) in that group – Oh Oh lights out – dead men walking? The answer I often get from advocates of that lifestyle is that Framingham offspring is not a study of those on a low carb or paleo diet and thus does not necessarily apply to them and that is true and that is the dilemma.

    Numerous studies have shown that high risk (80th percentile population cut points) LDL biomarker levels are:
                LDL-C > 160 mg/dL
                LDL-P > 1600 nmol/L
                ApoB > 120 mg/dl

    For those new to that terminology- having a lab value at the 80th percentile cut point of a reference population means that 80% of the patients had a lower value and 20% had a higher value – With respect to LDL-C, LDL-P or apoB that would be associated with CHD high risk.

    So, should the people who have this increased LDL-C and LDL-P response to a low carb or ketotic diet be worried? Have they simply gone from one type of CV risk to another. Usually the diet drives weight loss and improves many markers of insulin resistance (TG, glucose, insulin, etc). Some have proposed based on anecdotal experience that rise in LDL-P may be transient and take several months to return to normal theorizing there is confusion on the part of the body as to where and from what substrate to generate ATP. The big question right now really is: Are there persons who do not get atherosclerosis with apoB-cholesterol/lipoprotein levels greater than the above posted concentrations who do not get atherosclerosis? Can a human last long with atherogenic lipid concentrations above the 80th percentile population cut point? It seems for a small percentage of people that is true, but using existing trial evidence (which looked at folks on no specific diets or standard AHA low fat, low cholesterol type diets) they are rare exceptions, not the rule. Maybe one day someone will do a mega trial enrolling tens of thousands of low-carbers or paleo diet enthusiasts and follow them over many years to determine what happens to morbidity and mortality. But let’s not hold our breath on that one? Could some sort of atherosclerosis trial utilizing imaging be done – i.e. carotid intimal thickening or coronary calcium? Before we use in them to advise a therapy is working or not working a trial relating positive or negative changes in those images to CV events has to be done. As of 2013, neither of those imaging techniques has shown in an empowered clinical trial that changes (good or bad) in response related to a given therapy are related to CV outcomes and no national CV guideline advices them to be used in that fashion. Right now CAC and IMT should only be used for risk assessment and even there coronary calcium is especially poor in risk assessment in women unless they are rather elderly and CIMT is only of value for screening when done by very competent professionals.

    The patient was informed of all of the above and was given the option of altering the diet without returning to carbohydrates or using an LDL-P lowering medication, specifically a statin. The dietary advice was to cut back on saturated fat and use more MUFA and PUFA without increasing carbs. After doing just that for a few months the patient reports: “The only modifications I've made because of my high lipids are eating steel cut oats regularly, adding chia seeds to my diet, and eating apples regularly (to increase fiber levels); cutting out most dairy; and watching my saturated fat intake a little more closely--all aimed at getting my high LDL-P down.” Weight has remained stable.

    Here are the follow up labs:
    TC = 178, LDL-C = 92 (was 230), HDL-C = 82, TG = 21, Non-HDL-C = 96 (all in mg/dL)
    Total LDL-P:  948 nmol/L (recall it was grossly elevated at 2643) < 1000 nmol/L (20th percentile population cut point) is desirable
    Small LDL-P: < 90 nmol/L (normal)
    LDL Size: 21.4 nm (quite large)
    CRP was near 0.
    Metabolic #s are all great.
    Patient also notes: “Testing confirmed I am a hyper absorber of cholesterol and plant sterols.”
    Synthesis marker: Lathosterol/TC: 31   (low)
    Absorption marker: Campesterol/TC: 217 (normal)
    Absorption marker: Beta-sitosterol/TC: 231 (high)

    Couple of key points: Note those sterol markers are adjusted for cholesterol and are not absolute levels. Many believe especially in drug naïve patients, the absolute levels not adjusted for cholesterol are best suited to estimate risk in individual patients. In this case, I wish we had had absorption/synthesis markers prior to reducing the saturated fat as it is very likely in view of the very high LDL-C and LDL-P that the cholesterol synthesis was very high. The reduction of saturated fat certainly normalized cholesterol synthesis and elevated LDL-P. It is not at all unusual that when a person reduces cholesterol hypersynthesis that some increase in absorption occurs and that is what we are seeing here. However because the overall CV risk is now low, and the LDL-P is perfect the mild hyperabsorption likely has little if any consequences.

    Another key point regarding absorption synthesis markers is that these change in response to nutrition, drugs, aging, other morbidities and they are not ever too be used as a onetime assessment. In at risk persons, like lipid and lipoprotein and other biomarkers, they need to be repeated with each and every blood draw.

    So what conclusions do I have regarding patients on low-carb and paleo regimens who show the response of drastically aggravating LDL-C and LDL-P (apoB) together? Every trial, many of them quite large has associated those markers with atherogenesis and CV morbidity and mortality. But some folks are “outliers” and defy that rule. Could the low carb crowd be outliers and in them we can ignore LDL-C and LDL-P? The advocates of those diets say there is no study showing harm of elevated LDL-P and LDL-C in patients who have eliminated or drastically reduced their insulin resistance and inflammatory markers by low carbing. That is true, but what they want to ignore is, that there is no data anywhere that shows they are an exception. Their belief is that by reducing all other atherosclerotic risk factors and normalizing their arterial wall and endothelial biology that, apoB-containing lipoproteins, like LDL, cannot enter the arterial wall. Although LDL-C and LDL-P in plasma are high, none of the cholesterol content of the apoB-particles gains entry into the arterial wall. Is that plausible???? Sure! But is that also erroneous or wishful thinking? Sure? Does one want to bet their CV health or life on a plausible theory? Some do and some do not. Seems to me the first step is to do what this woman did: adjust the nutritional regimen. Now for those who want to live in a ketotic state – ketosis will not happen on this patients regimen, the options are then threefold – (1) stop repeating these measurements, keep your fingers crossed and go about life or (2) reduce saturated fat in the diet to whatever level does not cause cholesterogenesis or (3) start apoB-lowering therapy, specifically statins or statin/ezetimibe depending on absorption/synthesis markers. Sometimes options (2) and (3) are needed together. Statins are not only among the most effective drugs ever created (have saved more lives than anything but antibiotics and vaccines) but are also among the safest. I sometimes get a laugh out of those condemning drugs, especially statins, in favor of some therapy that has little outcome or safety evidence like supplements or various diets. Even diets may have adverse consequences!

    So what conclusions do I have regarding patients on low-carb and paleo regimens who show the response of drastically aggravating LDL-C and LDL-P (apoB) together? Every trial, many of them quite large has associated those markers with atherogenesis and CV morbidity and mortality. But some folks are “outliers” and defy that rule. Could the low carb crowd be outliers and in them we can ignore LDL-C and LDL-P? The advocates of those diets say there is no study showing harm of elevated LDL-P and LDL-C in patients who have eliminated or drastically reduced their insulin resistance and inflammatory markers by low carbing. That is true, but what they want to ignore is, that there is no data anywhere that shows they are an exception. Their belief is that by reducing all other atherosclerotic risk factors and normalizing their arterial wall and endothelial biology that, apoB-containing lipoproteins, like LDL, cannot enter the arterial wall. Although LDL-C and LDL-P in plasma are high, none of the cholesterol content of the apoB-particles gains entry into the arterial wall. Is that plausible???? Sure! But is that also erroneous or wishful thinking? Sure? Does one want to bet their CV health or life on a plausible theory? Some do and some do not. Seems to me the first step is to do what this woman did: adjust the nutritional regimen. Now for those who want to live in a ketotic state – ketosis will not happen on this patients regimen, the options are then threefold – (1) stop repeating these measurements, keep your fingers crossed and go about life or (2) reduce saturated fat in the diet to whatever level does not cause cholesterogenesis or (3) start apoB-lowering therapy, specifically statins or statin/ezetimibe depending on absorption/synthesis markers. Sometimes options (2) and (3) are needed together. Statins are not only among the most effective drugs ever created (have saved more lives than anything but antibiotics and vaccines) but are also among the safest. I sometimes get a laugh out of those condemning drugs, especially statins, in favor of some therapy that has little outcome or safety evidence like supplements or various diets. Even diets may have adverse consequences!

  2. Zepp
    Nice try.. but everyone knows that carbs is the major elevator of APOb!

    And that high blodd sugar and hyperinsulinemia is the major cause to CVD!

    And its strange.. now that SBU going thru the best sciens.. find that Low carb diets improve those risk factors moste!

    I say.. he dont know what he is talking about, trying to look like he is updated and in level with best knowledge.

    Did you know that 90% of those in CVD emergency have elevated blood sugar!

    Strange.. very strange, that best sciense show that one get better risk values of a low carb diet.. and then he tryes to make it look like one get worse!

    Let my put it in this way.. how could better risk values be a higher risk.. he have some advanced explanations to do!

  3. charles garshow
    "he dont know what he is talking about"

    SO - Dr Thomas Dayspring doesn't know what he's talking about??

    And your qualifications are??

    Your resume is ??

  4. Zepp
    Well if he not knowing about sciens.. hes not knowing what he talks about!

    Did you know that our top scientists did get thru all the available sciens in the area.. and they find the opposite!

    He draws the wrong conclutions.. and if one dont know how to draw firm conclutions on data one dont know what one is talking about.. thats a fact!

    To be a lipidologist.. and he dont know differens betwen familiar hyperkolesterolemia.. and low carb eating!

    You know.. saturated fat dont rise ones cholesterol.. not even ones APOb.. its carbs and metabolic syndrome that does this!

    It rises ones APOa1.. HDL.. well known.. and make ones LDL bigger and more boyant.

    He should ask doctors on CVD emergency rooms.. about blood sugar levels!

    Nice try of the old paradigm to make a new start for the lipid hypotesis.. that never was proved.. how much they event tryed!

    Heres an cardiologist!

    What Did the Greenland Eskimos Teach Us About Fats and Heart Disease?

    http://www.docsopinion.com/

  5. charles grashow
    http://www.indiana.edu/~k536/articles/diet/popular%20diet%20JAMA.pdf
    Comparison of the Atkins, Ornish, Weight Watchers, and Zone Diets for Weight Loss and Heart Disease Risk Reduction
    A Randomized Trial

    Look at Table 2 (page 5 of 12) and compare the saturated fat amounts between the Atkins dieters and the Ornish dieters (after 12 months)

    Atkins = 13% of daily calories, Ornish = 10.14%

    Carbs
    Atkins = 40.3%, Ornish = 47.9%

    Cholesterol
    Atkins = 321 mg/day, Ornish = 280 mg/day

    http://www.webmd.com/heart-disease/news/20090401/how-the-atkins-diet-...

    In an email exchange with WebMD, Atkins Vice President of Nutrition and Education Colette Heimowitz, MSc, says that on the maintenance phase of the Atkins diet, fat should make up no more than 40% of total calories, and no more than 10% of calories should come from saturated fat.

    The study participants typically ate about three times as much saturated fat as they should have if they were following Atkins for weight maintenance, she says.

    http://www.webmd.com/diet/news/20111104/best-diets?page=2

    Colette Heimowitz, MSc, vice president of nutrition and education for Atkins, the diet that got the lowest score, said in a statement that the program ''teaches individuals to find their personal ideal carb balance. The Atkins Diet does not overly restrict vegetables fruits, or whole grains."

    The plan does restrict high-sugar fruits at the beginning, but reintroduces them, she says. The fats in the diet plan are a balance of types, including heart-healthy ones.

    Zepp - what are your qualifications - your educational background - your curriculum vitae

  6. Z.M.
    "SO - Dr Thomas Dayspring doesn't know what he's talking about??"

    I'd say he doesn't. He has been part of some dubious papers with some very misleading interpretations and conclusions. e.g. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402055/

    "Statins are not only among the most effective drugs ever created (have saved more lives than anything but antibiotics and vaccines) but are also among the safest."

    Yes, statins may be the most effective drugs but they still suck as they fail to prevent the majority of events. Furthermore, there is no evidence that the benefits seen with statins are due to their cholesterol lowering effect. My guess is that without the pleiotropic effects, statins would have been just another failed cholesterol lowering drug. The effectiveness of statins are probably overestimated and its harmful effects are probably underestimated.

    Dayspring supports the "response to retention hypothesis". The evidence for it is mostly based on animal models. However, animal models also strongly support the "oxidative modification hypothesis", they also strongly support the idea that the pleiotropic effects of statins are relevant and strongly support the idea that inflammation is very important independently of cholesterol.

    "And your qualifications are??"

    Trained in the art of BS detection.

  7. charles grashow
    A RECEPTOR-MEDIATED PATHWAY FOR CHOLESTEROL HOMEOSTASIS
    Nobel lecture, 9 December, 1985
    by
    MICHAEL S. BROWN AND JOSEPH L. GOLDSTEIN
    Department of Molecular Genetics,
    University of Texas Health Science
    Center, Southwestern Medical School, 5323 Harry Hines Blvd. Dallas, Texas,
    U.S.A.

    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)

    Once LDL receptors become saturated, the removal rate of LDL is proportional to the number of receptors. Whenever the number of receptors is reduced, plasma LDL levels must rise. Experiments in animals indicate that the consumption of a high fat diet decreases the number of LDL receptors in the liver (123, 124). We believe that this mechanism operates through feedback suppression as described above. That is, when excess dietary cholesterol accumulates in the liver, the liver responds by decreasing the production of LDL receptors (Fig. 13C). The entry of dietary cholesterol into the liver is mediated by a receptor, termed the chylomicron remnant receptor, whose activity is genetically distinct from the LDL receptor (125). The chylomicron remnant receptor is unaffected by cholesterol accumulation (126), and it causes cholesterol to accumulate to high levels in liver when the diet contains excess fat. The combination of saturation and suppression of hepatic LDL receptors contributes in a major way to the buildup of LDL in plasma when a diet rich in saturated fats and cholesterol is ingested. Insofar as such a diet also may increase production of LDL in the face of a fixed or declining removal capacity, the LDL level would rise even higher If the LDL receptor does limit the removal of LDL from plasma, then maneuvers that increase LDL receptor activity might be effective in individuals who have high plasma LDL-cholesterol levels, but who do not have defective LDL receptor genes. Such therapy seems feasible with the development of HMG CoA reductase inhibitors. However, it is still too early to tell whether such therapy would decrease the incidence of myocardial infarctions in individuals with moderately elevated plasma LDL-cholesterol levels in the range of 100 to 200 mg/dl. There is much circumstantial evidence to expect such improvement (127), but unequivocal data are simply not there. Hopefully, with the availability of powerful receptor-stimulating drugs, the hypothesis should be susceptible to testing in the near future. In considering the role of diet and drugs in treatment of high cholesterol levels, physicians and public health authorities must bear in mind the genetic variability between individuals. This variability exists at three levels: 1) The degree of increase in plasma cholesterol upon ingestion of a high cholesterol diet is variable. Not all people develop hypercholesterolemia. Some people, such as the Pima Indians, maintain low plasma cholesterol levels despite ingestion of a high fat diet (10). 2) Even when the plasma cholesterol level becomes elevated, the propensity for atherosclerosis varies. For example, a substantial proportion of FH heterozygotes (10 to 20%) escape myocardial infarction until the 8th or 9th decade despite pronounced hypercholesterolemia from birth (14). 3) Genetic susceptibility to contributory risk factors is variable. Some people can withstand hypertension and cigarette smoking for decades without developing atherosclerotic complications; others are highly sensitive.

    http://legacy.library.ucsf.edu/tid/xsa38c00/pdf;jsessionid=76799A30E7...

  8. Z.M.
    Ah, the favorite ldl receptor argument. Since saturated fat decreases LDL receptor activity and increases LDL cholesterol, we should have ample evidence of the harms of saturated fat, right? Unfortunately for Brown and Goldstein surrogate markers do not always pan out. Over 50 years of research from observational and clinical studies and we have yet to see any harmful effects of these fats. The real question is: when are they going to stop flogging a dead horse?
    Reply: #85
  9. murray
    It seems from my reading of the Dayspring manuscript (the entirety of which is tediously quoted above) that he concedes there is no epidemiological data yet to show whether highly elevated LDL-C and LDL-P from LCHF in the subset of individuals who have this response to ketosis and saturated fats is a risk for cardiovascular disease and that it is "plausible" that there is no problem. His point, it seems, is that this is new territory (among the subset of individuals with this measured response) and that such individuals are taking a risk until it is demonstrated safe by epidemiological studies.

    The issue is joined, I think, on how plausible it is that elevated LDL-P from high sat-fat ketosis is not a genuine cardiovascular risk. As a lipidologist, Dayspring plainly leans to risk factors and statistics, as opposed to clinical observation. When one sees a low LDL-P vegan getting coronary by-pass surgery for a totally blocked heart artery with all the other heart arteries entirely clear, the plausibility of the gradient hypothesis (more LDL-P per se implies more LDL-C depositing) seems shaky. Rather, any correlation between LDL-P and LDL-C buildup in arteries may turn on why LDL-P is higher. Is it to deliver more cholesterol to repair artery wall damage? Then it is indicative of artery damage, not causative.

    Dayspring plainly seems unaware of statin side effects, which are coming out of the woodwork now that patents on statins are expiring.

  10. FrankG
    In terms of risk assessment and these vague threats that we don't really know yet how safe these cholesterol levels (based off a population of carb addicts) are for someone eating LCHF:

    what we DO know are the risks attendant with raised blood glucose and insulin levels over the long term... hypertension, nerve damage, CVD, blindness, renal failure, chronic foot/leg ulcers, lower limb amputations, followed by an early, painful (needless) death. Not just suffering and cost to the individual but to their whole family and the economy of the country where they live. These are NOT some vague threats but well known, well documented and uncontroversial facts of life.

    To me the choice is easy.

    Reply: #61
  11. sten
    Agree. The lower the blood sugar the lower the risk, yet within reason like maybe over 3, unless ketones are elevated? Anyone with tables of both for at least a week ?

    According to the cardiologist William Davies (Yes, he used to stent people before he realized the only only long term beneficiaries were his own wallet and the bypass team.), ...plaque can regress with blood sugar around/below 5 and minimum postprandial spikes. Low BS means low insulin. Just like pennies and pounds.
    Looking forward to more detailed research in the area of BS and plaque growth/regression!

  12. charles grashow
    Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH) Vitamin D on Coronary Calcium Scores in Asymptomatic Adults

    Davis, William MD, FACC1*; Rockway, Susie PhD, CNS2; Kwasny, Mary ScD3

    Abstract

    The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS).

    Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of ≥ 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides ≤60 mg/dL; high-density lipoprotein ≥60 mg/dL; and vitamin D3 supplementation to achieve serum levels of ≥50 ng/mL 25(OH) vitamin D, in addition to diet advice.

    Lipid profiles of subjects were significantly changed as follows: total cholesterol −24%, low-density lipoprotein −41%; triglycerides −42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%.

    After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of −14.5% (range 0% to −64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progressionexceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

  13. FrankG
    @sten -- for sure BG has an established normal range. 3mmol/L I would say is pushing it a bit out beyond the low end.. I start feeling faint at around 4.5 but some of that is to do with how quickly it changes. Yet again, the stable BGs LCHF gives me, has saved me from that very unpleasant roller-coaster ride.

    And to add to the above list of complications, some which may not be quite as well established but I suspect will very soon be: Alzheimer's and several forms of Cancer.

    So I daresay it will take a great deal more that Dr Dayspring and CG's vague scare tactics to have me running back to the waiting arms of a conventional wisdom practitioner with his pen (sponsored by LIPITOR®) poised over a prescription pad (thoughtfully provided by Crestor of course). :-P

  14. charles grashow
    http://www.trackyourplaque.com/library/fl_06-027faseb.asp

    Progression and Regression of Coronary Calcium Score

    William R. Davis1 and Susie W. Rockway2

    1 Medical Director, Milwaukee Heart Scan, Wauwatosa, WI
    2 Clinical Nutrition, Rush University Medical Center, Chicago, IL

    ABSTRACT

    Serial calcium scoring obtained by CT scanning has been proposed as a means of following progression or regression of coronary atherosclerotic plaque. In an open-label study, we combined pharmaceutical lipid treatment with dietary supplementation in patients presenting with coronary calcium (Agatston) scores ≥ 50 to test the impact on progression or regression of annual plaque growth as measured by serial coronary calcium scoring in a cohort of 45 men and women. Treatment included statin therapy, niacin, the American Heart Association Therapeutic Lifestyle Changes (TLC) diet, omega-3 fatty acids and vitamin D-3 supplementation at levels to achieve target fasting lipid values of: LDL cholesterol ≤ 60 mg/dl, HDL ≥ 60 mg/dl and triglycerides of 60 ≤ mg/dl and a serum level of 25-OH-vitamin D3 of ≥ 50 ng/ml. All atherogenic lipids were significantly reduced when tested 1 to 2 years after treatment (p<0.001). Total cholesterol dropped by 23%, LDL-c by 37%, TG by 29% while HDL significantly (p<0.001) increased by 18%. Unexpectedly, 21 subjects demonstrated reduced calcium plaque burden as evidenced by a percent decrease in coronary calcium scores (ranges from 0 to –64%), while 21 experienced slowing of progression (mean 12%), defined as less than 30% increase in calcium score (ranges 0.95% to 29%), while only 3 subjects continued to progress at a rate greater than 30%. In conclusion, though wide variation in response following this approach is seen, substantial regression of atherosclerotic coronary plaque using a CT calcium scoring approach is achievable with treatment efforts that extend beyond LDL cholesterol reduction.

  15. FrankG
    Do you think CG actual is trying to make a point, or is even a real person. or maybe just a bot who copies and pastes random abstracts? :-P
  16. Zepp
    Must be a bot.. he/she never express any inteligent thougts!
  17. sten
    CG, thanks for posting. That study is just over 5 years old. Later Davies seem to have realized that blood sugar (BS) variations are also very important tools. Please read this article:

    http://www.trackyourplaque.com/library/fl_04-022postprandialcarbs.asp

    He advises the use of blood sugar meter and to measure BS only one (!) hour after each meal (instead of 2) and trial/error remove foods suspect to increase BS very much, which in part can be individual. (The scientific way to arrive at LCHF ?)

    Standard morning cereal with plenty of light milk (5% sugar (lactose)) would cause a significant BS peak as he writes, while I think old-fashioned porridge with a small amount of cream (!) instead of such milk could pass, then satisfying many low carbers that once in a while would long for something like that. (In effect with cream any cravings for sweet sugar on top of porridge may well vanish!)

    Would there be anything like a simple ultrasonic method to measure blood vessel plaque?
    In my own case I am more or less convinced that the blood sugar -inflammation- partial healing - high BS again - renewed inflammation year in year out with no or little "purging" like involuntary fasts is the mechanism building of blood vessel plaque formation.
    Yet it would be nice to see some accurate data, not just blood pressure reduction and resting heart beat reduction, apart from yearly blood data. My calcium score scan was 6 in 2007 and had then dropped from 7 the year before. The 2nd year I managed to get the images which showed that all the plaque was localized in one spot. Today it is probably 1 or 2 meaning something else is needed. My blood pressure averages were up in the 150's but is now down at 130, which indicates something is changing with good blood sugar control, LCHF and 18:6 fasting. (skipping breakfast..)

  18. Z.M.
    FrankG: "Do you think CG actual is trying to make a point, or is even a real person. or maybe just a bot who copies and pastes random abstracts?"

    Possibly just playing devil's advocate. This is what he does on many blogs.

    Charles, where do you stand on the diet and cholesterol issues?

    Reply: #69
  19. FrankG
    Possibly Z.M. but I'm not about to speculate or guess based on his penchant for simply pasting swathes of text from other sites. If he has a point to make then why not state it?

    As for those who do claim they are playing devil's advocate or are just offering "balance": sorry but I'm not interested.. so far as I am concerned there is already an heavy bias towards the conventional wisdom and I don't see why I should have to read it all again here.

    Frankly it is insulting and more than a little irritating to come on here and think that I must have mistakenly typed in the URL for Dr Dayspring's blog instead. Personally I like to exercise my own choice as to what I read on the interweb and not have others try to force their opinions on me.

  20. charles grashow
    Here are the results of my last complete blood work

    blood drawn on 10/18/12

    TC 242 mg/dL
    LDL-C 158 mg/dL
    HDL-C 76 mg/dL
    Triglycerides 41 mg/dL
    Ap- B 104 mg/dL Reference Range <115 mg/dL
    LP(a) <2 mg/dL Reference Range 0-30 mg/dL

    Lipid SubClass Detail
    Berkeley Lab analyzes LDL for 7 sub classes from large buoyant to small dense

    LDL I, IIa and IIb are considered large buoyant - As a % these 3 totalled 82.5% - LDL I=51.1%, LDL IIa=16.2% and LDL IIb=15.2%
    LDL IIIa+b, LDL IVa and LDL IVb are considered small dense with IVb being the smallest. As a % these totalled 17.5% - LDL IIIa=11.2%, LDL IIIb=3.8%, LDL IVa=1.8% and LDL IVb=0.7%
    LDL IIIa+b=15% Reference Range=13.6-43%
    LDL IVb=0.7% Reference Range=1.7-9.8%
    LDL IIIa=B = 17.9 mg/dL Reference Range=12.0-32.1 mg/dL
    LDL IVb=1.0 mg/dL Reference Range=1.5-11.2 mg/dL

    HDL is analyzed for 5 subclasses

    HDL2b=34%, HDH2a=24%, HDL3a=20%, HDL3b=14% and HDL3c=8%
    HDL2b Reference Range 7-30%

    HA1C - 5.6
    Fasting Glucose - 100mg/dL Ref Range 65-99 mg/dL
    Estimated Average Glucose - 114.5 mg/dL

    LDL-P 1430 nmol/L
    Small LDL-P 132 nmol/L

    Thyroid Panel
    Thyroxine (T4) - 10.9 ug/dL Ref Range 4.5 - 10.9 ug/dL
    T3-Uptake - 34.0% Ref Range 22.5 - 37%
    TSH - 3rd Generation Ultra - 1.47 uIU/mL Ref Range 0.40 - 4.50 uIU/mL
    Reverse T3, LC/MS/MS - 34ng/dL Ref Range 9 - 28 ng/dL
    T3, Total 81 ng/dL - Ref Range 60 - 181 ng/dL
    T4, Free 1.43 ng/d/L - Ref Range 0.80 - 1.80 ng/dL

    Vitamin D (25 hydroxy) - 74 ng/dL Ref Range 30 - 100 ng/dL
    Cardiac Homocysteine - 10.0 umol/L Ref Range <11.4 umol/L
    PSA - 0.42 ng/d/L Ref Range <4.00 ng/dL

    The high LDL-C and LDL-P are of a concern to me so on 7/19/13 I started on a low dose statin (10mgs/day Atorvastatin) and started to reduce the amount of dietary saturated fat to appx 13%

    My current diet is appx 50% fat, 25% carb and 25% protein

    I do eat grass fed ground beef and low fat greek yogurt

    I/m going for some blood work on 10/18 to have TC, Non-HDL-C and ApoB measured and we will see what the results are

    Reply: #71
  21. sten
    Hi Charles,
    Apolipoproteins measure takes the allimportant LDL particle size in account.
    The quotient ApoB/ApoA has been shown to direct correlate to Heart attack risk. (Google Inter Heart study). I only see the Apo- B above !

    And what is your 1 hour after meal blood sugar ?
    Resting Blood pressure ?
    Resting Heart Rate. (Also what was the lowest RHR you ever had ?)

    Above are key markers when it comes to health and heart attack risk, as I see it.

    Sten

  22. Z.M.
    Charles, why not add an iron panel:

    http://www.ncbi.nlm.nih.gov/pubmed/18619522
    http://www.ncbi.nlm.nih.gov/pubmed/8970483

    From the last:

    The relationship between the iron and cholesterol hypotheses has not been clearly understood. Neither hypothesis is yet definitively confirmed. In the case of the cholesterol hypothesis, a great mass of data has been collected. Far from establishing its truth beyond question, the existing data argue more persuasively against the cholesterol hypothesis than for it.....In my view, the available data do not establish the key element of the cholesterol hypothesis, that the development of heart disease is dependent on cholesterol and lipoprotein concentrations. Several lines of evidence support this skeptical view. The following evidence uncouples cholesterol concentration from development of heart disease:

    Cumulative results of the primary prevention trials of cholesterol lowering do not support the idea that lowering cholesterol concentrations by diet or drug therapy can meaningfully decrease heart disease rates [12-151. These lengthy and costly trials were planned as a decisive test of the cholesterol hypothesis. The weak and negative results of the trials are dismissed by proponents of the cholesterol hypothesis. Now the “totality of the evidence” is said to support the hypothesis, despite the contradictory and disappointing results. The term “totality of the evidence” in this context is logically equivalent to saying the hypothesis is supported by “a point of view.” Taken together, the trials have produced important evidence that, despite the often cited statistical association between heart disease and cholesterol concentration, lowering the cholesterol concentration has no net meaningful benefit.

    Animal experiments have found that several antioxidants including probucol inhibit plaque formation, no matter whether they produce a decrease, no change, or even a large increase in plasma cholesterol [16-18]. In cholesterol-fed rabbits, butylated hydroxytoluene (BHT) dramatically increases cholesterol concentration, but equally dramatically decreases arterial plaque formation [18]. The cholesterol-fed animals given BHT had plasma cholesterol levels more than 10 times typical human levels, but had almost no atherosclerotic plaque. These results support the idea that cholesterol concentration is essentially irrelevant to plaque formation.

    The remarkably low incidence of clinically apparent heart disease in young women with familial hypercholesterolemia is further evidence that uncouples disease rates from cholesterol and lipoprotein concentrations [4,19,20]. Young women with familial hypercholesterolemia have plasma cholesterol concentrations equal to, or perhaps greater than [20], those in young men with the disorder. From childhood, affected men and women usually have plasma cholesterol levels of greater than 600 mg/dl, i.e., roughly three times the upper limit of normal as defined by the National Cholesterol Education Program. However, the young women have no more clinically evident heart disease that their unaffected female relatives, while the young men have a large excess of cardiovascular events.

    Animal experiments suggest that iron depletion has a potent antioxidant effect in vivo [21-251. There is also direct experimental evidence in humans suggesting that decreasing the level of stored iron increases the plasma concentration of HDL and the resistance of LDL to oxidation
    [26].

    The iron hypothesis is more comprehensive than the cholesterol hypothesis because it suggests a common mechanism at work in both ischemic myocardial injury and in atherogenesis. The iron hypothesis redefines the cholesterol hypothesis. Cholesterol and lipoproteins become, not culprits, but victims, targets of iron-catalyzed reactions....From the perspective of the iron hypothesis, cholesterol is not a toxic substance in itself.

    Cholesterol theorists, as well as a daily avalanche of commercial advertising, tell the public of the need to lower cholesterol levels. In my view, the available evidence suggests that even a large increase in plasma cholesterol may do no harm so long as the body’s antioxidant defenses are sufficiently enhanced.

  23. TJ
    We deal with the same troll on our US blogs. I am sorry the infection has spread overseas.
    Common knowledge says do not feed them, it only makes them stronger.
    Reply: #74
  24. sten
    Refined variants of "sceptics" that typically accept nearly everything big food and big drug say while opposing everything else ??
    Usually (?) paid by ads from drug or/and nutrition companies on their website to perpetuate the "opinions" ?
  25. NS
    "The advocates of those [LCHF] diets say there is no study showing harm of elevated LDL-P and LDL-C in patients who have eliminated or drastically reduced their insulin resistance and inflammatory markers by low carbing. That is true, but what they want to ignore is, that there is no data anywhere that shows they are an exception. Their belief is that by reducing all other atherosclerotic risk factors and normalizing their arterial wall and endothelial biology that, apoB-containing lipoproteins, like LDL, cannot enter the arterial wall. Although LDL-C and LDL-P in plasma are high, none of the cholesterol content of the apoB-particles gains entry into the arterial wall. Is that plausible???? Sure! But is that also erroneous or wishful thinking? Sure? Does one want to bet their CV health or life on a plausible theory? Some do and some do not. Seems to me the first step is to do what this woman did: adjust the nutritional regimen. Now for those who want to live in a ketotic state – ketosis will not happen on this patients regimen, the options are then threefold – (1) stop repeating these measurements, keep your fingers crossed and go about life or (2) reduce saturated fat in the diet to whatever level does not cause cholesterogenesis or (3) start apoB-lowering therapy, specifically statins or statin/ezetimibe depending on absorption/synthesis markers. Sometimes options (2) and (3) are needed together. Statins are not only among the most effective drugs ever created (have saved more lives than anything but antibiotics and vaccines) but are also among the safest. I sometimes get a laugh out of those condemning drugs, especially statins, in favor of some therapy that has little outcome or safety evidence like supplements or various diets. Even diets may have adverse consequences!"

    Charles, excellent find. Your efforts are elevating the level of the dialogue and the direction in which it is headed. This may be the most important thread on this blog, as it relates to long term LCHF safety, an issue that has had little "clarity" hitherto. Speaking of which, one wonders how on earth such information could be missing from that (very recently released) spectacularly academic and scholarly achievement, aka, "Cholesterol Clarity," where Dr. Dayspring's contribution was so narrowed, limited (i.e. purposely misrepresented, abused) to the degree to fit its author's, if one can use that word, pre-conclusions that NO such information, as you have highlighted above, was mentioned at all. How convenient......and telling.

    Reply: #76
  26. sten
    As it is mere speculation that cholesterol is the origin of CVD and people that have had heart attacks benefit from its lowering while people that have had stroke increase their risk for deadly cerebral hemorrhage and those with the highest levels live longest (nurses stydy), no known risks are being taken on by changing these numbers on a low carb high fat diet.

    But there are numbers that have been proven to show real heart attack risk for people all over the world in the largest ever study undertaken. Based on the Inter Heart Study studying heart attcaks world wide involving over 35,000 people found the Apo-B/Apo-A quotient to be the only consistent number. Double it, and the frequency of heart attacks doubled. Totally consistent. 0.7-0.9 = normal risk. Before I suffered from angina so sometimes I could only walk 50 meters before I got totally incapacitated for 5-10 minutes. One year on a LCHF diet rendered me a "low risk" Apo-quotient of 0.63. DOn't know what it was before. The angina disappeared after 6 weeks " treatment" consisting of near zero carb intake. (My fats were and are primarily butter and fats from lamb and beef)

    But the INTER HEART study result had one BIG problem: It could not be used to sell statins, or Becel. So silence followed from the big media as they could not afford to injure their advertisers, their bread and butter. So today in our modern world we are not getting further away from the old saying "One mans bread is another ones dead", we are getting closer to it.

    Another side of the coin is that modern science points at a totally different cause for CVD: Sugar, more precisely blood sugar. As soon as blood sugar goes high inflammatory proteins (NFAT ) cause injury in a dose proportional manner; injuries that must be repaired else the blood vessels start to leak. They are repaired with LDL cholesterol. A fireman blamed for too long.

  27. Z.M.
    NS: "Charles, excellent find. Your efforts are elevating the level of the dialogue and the direction in which it is headed."

    Please explain what is so "excellent" about Dayspring's views? Go back and read my replies.

  28. Chupo
    In the DIRECT-carotid study, neither total cholesterol nor LDL was associated with regression of atherosclerosis. The regression group showed a trend toward greater increase in apoA1 levels however.

    http://circ.ahajournals.org/content/121/10/1200.long

  29. Z.M.
    Chupo: "In the DIRECT-carotid study, neither total cholesterol nor LDL was associated with regression of atherosclerosis."

    Yea, the authors attributed the benefit to weight loss and blood pressure reductions. Also, greater saturated fat intake in the low-carb group didn't prevent them from experiencing the same benefits as the other groups.

  30. London Lady
    Hi Doc. I hope you are still monitoring responses to this as I have a question. I have been following a LCHF regime for the past year with excellent results. Although my total cholesterol is up a little the ratios are very much improved and I am more than happy. However a friend of mine has adopted LCHF these past several months and her recent blood tests have scared her. Her total cholesterol is coming in at 8.6mmol/L and although she has not seen the actual breakdown her doctor says that her LDL is high and her HDL low. Prior to LCHF her total cholesterol was in the low 6mmol/L range. She is now thinking of adopting a low fat diet but surely there must be an alternative? She is already persuaded that statins are not the answer but is looking to diet to bring her numbers down. What would you advise?
    Replies: #81, #83, #84
  31. sten
    Then only thing that is dangerous with LDL is small particle size.
    Small particle size LDL is associated with high triglycerides and both come from a HIGH carb diet.
    Standard cholesterol measures weight, not number of particles or their size.

    Please ask the doctor to take blood samples and have the Apo-B/Apo-A number, see #71 and #76 above, measured. They show real risk factors. My doctor arranged the tests when I asked him!

  32. Chupo
    London Lady, That can happen if she's in the process of losing weight. Her numbers should normalize after being weight stable for a couple of months. If she's not actively losing weight she may be an ApoE4 carrier.
  33. Zepp
    The others answer is good enough.. but I have some coments anyhow.

    Take totCh/HDL= risk factor, it should be 6 or lower, better if its 5 or lower, very good if its 4 or lower!

    APOtest is the best test to predict future CVD.

    And then.. if the doctor dont take any new tests.. there are alternatives.. like more Omega-3 (EPA+DHA) and one can swith to more mono unsaturated fats.. like olive oil.

    And then.. again.. mayby your friend is one of those in danger of CVD in the future.. but then one should have a proper examination to tell!

    I can tell that I did have normal values up to my 40ties.. then it get up like a rocket.. of no perticaly reason, but heritage I think.

    When I started LCHF if get even higher.. but after some weight loss and 2 years after, it droped to nearly high normal values.. I have this genetical heritage.

    Every doctor gives me a prescription of Statins that I never use!

  34. London Lady
    I'm really grateful to you guys for taking the trouble to reply and I will pass your comments on to my friend. She is at her wits' end as she loves the LCHF lifestyle but knows that total cholesterol at the level she is currently experiencing it is probably not a good thing. She is hoping to find a way to manage it down without recourse to the low fat diet recommended by her GP and all input is appreciated, particularly if you have experienced this yourself and found a way to continue to low carb and yet bring your numbers down a notch or two. Thanks again.
  35. Maggie
    Did I read correctly - that the lady from Atkins did not recommend saturated fat (or kept it to some kind of minimum?). Very surprised about this. I have Heterozygous Familial Hyperch. (without meds - sorry can't use statins - get kidney failure very quickly on them) my numbers are 13 total cholesterol. On a highly (HIGHLY) saturated fat diet (I know I took a chance - couldn't find a single person of my ilk on this diet anywhere on the net, had to be brave) my numbers normalised for first time since birth. I reckon it's indicated for us, same as it is for some kids with epilepsy? Was a jaw dropping result for my Doctors. HAVE to stay on it - hence my surprise re the lady from Atkins. (13 in imperial I think is over 400?). My trigs came down to 0.7 . BUT, suffice to say, I fear somewhat for my sons - apparently this disease shows it's teeth with men and I have only sons. My mom is 83 with the disease, but 2 uncles died young on it. OMG!...
  36. kfd
    Dr. Eenfeldt, I recently saw some stats that said that Apoe 3/4 and 4 patients are near 20% of the population. These patients don't do well on a high fat diet. Can you comment on this? Should these patients eat low fat? This is not a small percentage of the population but is hardly mentioned in most of the LCHF popular culture. Thank you.
    Reply: #87
  37. Zepp
    APOe is of importance for fat metabolism.. and if one have problem with that one have problems with fat metabolism.

    But not everybody with that genetic predisposal have the bad outcome.. it says that there are a bigger risk.. for different bad outcomes.

    Its a part of Familare Hypercholesterolemia syndrome!

    http://en.wikipedia.org/wiki/Apolipoprotein_E

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