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Medical Forum / General / Cardiology / October 2007Cardiovascular event risk in relation to dietary fat intake in middle-aged individuals: data from The Malmo Diet and Cancer Study.
Cardiovascular event risk in relation to dietary fat intake in middle- aged individuals: data from The Malmo Diet and Cancer Study. Original Scientific Papers European Journal of Cardiovascular Prevention & Rehabilitation. 14(5): 701-706, October 2007. Leosdottir, Margret a b; Nilsson, Peter M. b; Nilsson, Jan-Ake b; Berglund, Goran b Abstract: Background and design: The hypothesis that diets rich in total and saturated fat and poor in unsaturated fats increase the risk for cardiovascular disease is still vividly debated. The aim of this study was to examine whether total fat, saturated fat, or unsaturated fat intakes are independent risk factors for cardiovascular events in a large population-based cohort. Methods: 28 098 middle-aged individuals (61% women) participated in the Malmo Diet and Cancer Study between 1991 and 1996. In this analysis, individuals with an earlier history of cardiovascular disease were excluded. With adjustments made for confounding by age and various anthropometric, social, dietary, and life-style factors, hazard ratios (HR) were estimated for individuals categorized by quartiles of fat intake [HR (95% confidence interval, CI), Cox's regression model]. Results: No trend towards higher cardiovascular event risk for women or men with higher total or saturated fat intakes, was observed. Total fat: HR (95% CI) for fourth quartile was 0.98 (0.77-1.25) for women, 1.02 (0.84-1.23) for men; saturated fat: 0.98 (0.71-1.33) for women and 1.05 (0.83-1.34) for men. Inverse associations between unsaturated fat intake and cardiovascular event risk were not observed. Conclusions: In relation to risks of cardiovascular events, our results do not suggest any benefit from a limited total or saturated fat intake, nor from relatively high intake of unsaturated fat. MarilynMann <mannm@comcast.net> wrote in part: >Cardiovascular event risk in relation to dietary fat intake in middle- >aged individuals: data from The Malmo Diet and Cancer Study. [quoted text clipped - 32 lines] >results do not suggest any benefit from a limited total or saturated >fat intake, nor from relatively high intake of unsaturated fat. I've never seen convincing evidence for deleterious effects of % fats of any type (with the exception of partially-hydrogenated fats). It's pretty amazing that most people believe, and are still told by their doctors, to reduce the fat % of their diets. I got a haircut from a new barber yesterday. She talked and talked about how her doctor wanted to put her on Lipitor because of high cholesterol. She told him she could bring it down with diet. So she is having almost no fat. She has gained two pounds and I suspect her cholesterol will be higher at her next visit. As to the above study, the confidence intervals are awfully large despite the fact that over 28,000 people participated. It probably didn't last long enough to shed much light on the questions addressed. -- Jim Chinnis Warrenton, Virginia, USA > I got a haircut from a new barber yesterday. She talked and talked about how > her doctor wanted to put her on Lipitor because of high cholesterol. She > told him she could bring it down with diet. So she is having almost no fat. > She has gained two pounds and I suspect her cholesterol will be higher at > her next visit. > Jim Chinnis Warrenton, Virginia, USA You should invite her over to dinner and have Susan there too. Dreaming...I'd wait on the table. Some how I think of the movie "My dinner with Andre" only dealing with food and health issues and misc. Then the warmth and love in Babbetts feast. http://preview.tinyurl.com/28kvtf Pricey!!!! http://preview.tinyurl.com/25uk2e Bill  SignatureS Jersey USA Zone 5 Shade This article is posted under fair use rules in accordance with Title 17 U.S.C. Section 107, and is strictly for the educational and informative purposes. This material is distributed without profit. http://www.ocutech.com/ High tech Vison aid > I've never seen convincing evidence for deleterious effects of % fats of any > type (with the exception of partially-hydrogenated fats). It's pretty > amazing that most people believe, and are still told by their doctors, to > reduce the fat % of their diets. Even if there is an effect with respect to saturated fat or unsaturated fat, the effect may not be very large. It's very hard to provide convincing evidence of a small effect. > I got a haircut from a new barber yesterday. She talked and talked about how > her doctor wanted to put her on Lipitor because of high cholesterol. She > told him she could bring it down with diet. So she is having almost no fat. > She has gained two pounds and I suspect her cholesterol will be higher at > her next visit. How old is she? Few women are at high cardiovascular risk prior to menopause, unless diabetic, obese or other extreme risk factors. If she is following a diet that is making her *gain* weight, that clearly makes no sense. Marilyn MarilynMann <mannm@comcast.net> wrote in part: >> I've never seen convincing evidence for deleterious effects of % fats of any >> type (with the exception of partially-hydrogenated fats). It's pretty [quoted text clipped - 4 lines] >unsaturated fat, the effect may not be very large. It's very hard to >provide convincing evidence of a small effect. Unless there is a large effect of % sat vs % unsat fat, no studies are going to find it. That's because not all sat or unsat fats have the same effects anyway. It would take a large class effect to overcome the variable contributions of the varying fatty acid components in actual diets. I think we are just looking at noise in these studies. >> I got a haircut from a new barber yesterday. She talked and talked about how >> her doctor wanted to put her on Lipitor because of high cholesterol. She [quoted text clipped - 4 lines] >How old is she? Few women are at high cardiovascular risk prior to >menopause, unless diabetic, obese or other extreme risk factors. I'd guess 45. Maybe 30 lb overweight. >If she is following a diet that is making her *gain* weight, that >clearly makes no sense. It makes sense to her because she thinks she will reduce her "cholesterol" by being on a very low % fat diet. But, no, it doesn't make any sense. -- Jim Chinnis Warrenton, Virginia, USA > I got a haircut from a new barber yesterday. She talked and talked about how > her doctor wanted to put her on Lipitor because of high cholesterol. She > told him she could bring it down with diet. So she is having almost no fat. > She has gained two pounds and I suspect her cholesterol will be higher at > her next visit. My wife's sister is being put on a statin because of her cholesterol levels despite being thin, active, and no history of CVD. I think some doctors are just overly aggressive with the statin drugs. -- Ron > My wife's sister is being put on a statin because of her cholesterol > levels despite being thin, active, and no history of CVD. I think some > doctors are just overly aggressive with the statin drugs. Hard to comment without more information, but I agree that some doctors are too quick to prescribe statins. I'm not on one myself. However, I recently allowed my 14-year-old daughter to be put on lovastatin 20 mg. Her LDL was 246. That's off the charts, to put it mildly. Marilyn >>My wife's sister is being put on a statin because of her cholesterol >>levels despite being thin, active, and no history of CVD. I think some [quoted text clipped - 5 lines] > lovastatin 20 mg. Her LDL was 246. That's off the charts, to put it > mildly. Except in Askenazi Jews with little CVD, who are often even higher, but with large, fluffy LDL that does no harm. Did you have hers directly measured before allowing her to take the drug? Susan > x-no-archive: yes > [quoted text clipped - 14 lines] > > Susan Yes. > Yes. Did she have a high percentage of VLDL? Susan > x-no-archive: yes > [quoted text clipped - 3 lines] > > Susan Here are some of her lab results: LDL 246 HDL 71 VLDL 28 TC 346 Triglycerides 112 Lp(a) 25 mg/dL Real-LDL size pattern: large buoyant LDL Remnant lipoproteins 35 mg/dL HDL-2 24 mg/dL HDL-3 47 mg/dL VLDL-3 15 mg/dL Total ApoB100 Calc 168 mg/dL Apo A1 184 mg/dL Apo B 150 mg/dL Apo B/A1 ratio 0.92 Cardio Crp <0.2 Marilyn > Here are some of her lab results: > [quoted text clipped - 14 lines] > Apo B/A1 ratio 0.92 > Cardio Crp <0.2 What part of this caused you to believe that she needed treatment with a statin? Her high HDL and low TGLs put her at very low CVD risk categorization and are a marker for her large, undamaging type LDL. Susan I'm just replying to Susan's post to try to get it to Marilyn. Susan <nevermind@nomail.com> wrote in part: >x-no-archive: yes > [quoted text clipped - 24 lines] > >Susan -- Jim Chinnis Warrenton, Virginia, USA > x-no-archive: yes > [quoted text clipped - 26 lines] > > - Show quoted text - Susan, In spite of what you say, there are very early heart attacks in my husband's family and my husband is at high risk of a heart attack as well. I know nothing about the Ashkenazi Jews you refer to, but I have done quite a bit of reading on familial hypercholesterolemia. Some people with FH have high HDL and low TG but have early heart disease anyway (there is no link between FH and high TG, so far as I know). Anyway, the bottom line is that I made my decision. Marilyn > Susan, > [quoted text clipped - 7 lines] > > Anyway, the bottom line is that I made my decision. Marilyn, I understand that you've made what you think is the wisest decision for your child, that's understood. You've mentioned in the past that your husband's family eat an extremely atherogenic, pro oxidation type diet. I believe you said they never eat non starchy veggies. That alone would explain a tendency to early heart attack. It's not as if statins are benign. Susan > You've mentioned in the past that your husband's family eat an extremely > atherogenic, pro oxidation type diet. I believe you said they never eat > non starchy veggies. That alone would explain a tendency to early heart > attack. I don't think you can explain fatal heart attacks at 35 or 40 based on diet. > It's not as if statins are benign. I agree. Do you think I'm happy about the situation? Marilyn MarilynMann <mannm@comcast.net> wrote in part: >> You've mentioned in the past that your husband's family eat an extremely >> atherogenic, pro oxidation type diet. I believe you said they never eat [quoted text clipped - 3 lines] >I don't think you can explain fatal heart attacks at 35 or 40 based on >diet. True. >> It's not as if statins are benign. > >I agree. Do you think I'm happy about the situation? I'm not happy about taking a statin, but I take it. -- Jim Chinnis Warrenton, Virginia, USA > I'm not happy about taking a statin, but I take it. I'm not happy about taking tamoxifen, but I take it. Tamoxifen increases the risk of thromboembolic events and endometrial cancer and various other things. Women who are on tamoxifen also tend to do worse on tests of verbal memory. After 5 years of tamoxifen, the plan is for me to take an aromatase inhibitor. AIs cause osteoporosis and muscle and joint problems. They don't have long-term data on cardiovascular effects yet but I think it's safe to assume there are some. AIs work to prevent breast cancer occurrence because they suppress estrogen to very low levels (hence, the osteoporosis). We know that women have some protection against heart disease until after menopause, when hormone levels drop. I think you're catching my drift . . . There is some preliminary research indicating adverse cognitive effects as well, although not much is known on that yet. Unfortunately, there's a tradeoff between risk of heart disease and osteoporosis on the one hand and risk of breast cancer on the other. Women with more lifetime exposure to endogenous hormones (e.g., through later age of menopause) have a lower risk of heart disease and osteoporosis but a higher risk of breast cancer. More women die of cardiovascular disease than of breast cancer, of course, although many women do not know that. At one time, oncologists wanted to prescribe tamoxifen for prevention of breast cancer, but they had to give up that idea due to all the adverse effects. There are some clinical trials going on testing AIs for prevention of breast cancer. My guess is that not too many women would want to take an AI for that purpose, though. By the way, tamoxifen lowers LDL levels although it can also raise triglycerides. My impression is that the lower LDL levels from tamoxifen have not really been proven to reduce the risk of cardiac events in breast cancer survivors. Maybe the higher TGs offset the lower LDL . . . maybe the thromboembolic effects also cause cardiac effects . . . I don't think they really know. If there is a positive effect it is probably not very large. Marilyn This study illustrates some of what I was saying about endogenous hormones and heart disease. Severity of cardiovascular disease in women: Relation with exposure to endogenous estrogen Katerina Saltikia, Charalambos Doukasa, John Kanakakisa, Eleni Anastasioua, Emily Mantzoua and Maria Alevizaki, a, , aEndocrine Unit, Evgenidion Hospital and Dept Medical Therapeutics, ALEXANDRA Hospital, Athens University School of Medicine, Athens, Greece Abstract Objectives Coronary artery disease (CAD) is more common in men than in women. Endogenous sex steroids may be the main factor responsible, as long- term estrogen action appears to be protective. The aim of the study was to investigate the predisposing factors responsible for the severity of CAD in women. Methods One hundred and eight women (100 menopausal) undergoing coronary angiography were studied. Reproductive function was recorded. The severity of CAD was assessed by the number of arteries with severe stenosis, the presence of angina and myocardial infarctions (MI). Results The time since menopause (TSM) was significantly longer in women with angina and with MIs compared to those without (20.3 ? 8.7 years versus 15.8 ? 8.7 years and 22.6 ? 8.6 years versus 18.1 ? 8.9 years, p < 0.05), independently of chronological age. The age at menopause was significantly younger in women who had 2 MIs compared to those with 1 or 0 MI (41.5 ? 3.5, 47.5 ? 5.3 and 48.4 ? 5.4 years, respectively; p = 0.04); the total duration of menstrual cyclicity was inversely related to the number of MIs (35.6 ? 5.8, 34.2 ? 5.3 and 28.3 ? 3.3 years, 0, 1 and 2 MIs, respectively; p = 0.03). Conclusions The severity of CAD in women referred for coronary angiography is correlated with measures of exposure to endogenous estrogen. Both the TSM and the age at menopause are aggravating factors for MI, independently of age. There is an independent protective effect of the duration of estrogen exposure on the number of MIs; this has not been reported before and supports the protective role of the length of exposure to endogenous estrogen, especially for the occurrence of MI in this selected group of women. Corresponding author. Tel.: +30 2103381393; fax: +30 2107704143. Maturitas Volume 55, Issue 1, 20 August 2006, Pages 51-57 * * * I have not read the whole article, but I assume the way they calculate total duration of menstrual cyclicity is to take age at menopause, subtract age at menarche, and subtract time while pregnant, or something along those lines. One of the first things they ask you when you are diagnosed with breast cancer is your age at menarche, age at menopause (if applicable), number of pregnancies and number of births. They even ask whether you breastfed your kids and if you had a miscarriage they want to know what trimester it occurred in. It's the same concept, but longer duration of menstrual cyclicity *increases* breast cancer risk. I should note that androgens also decrease at menopause and there is some evidence that androgens lower risk of CVD in women. This is controversial, however. Women with higher BMI tend to have higher androgen levels. If you don't correct for BMI you will come up with an association between higher androgens and higher CVD risk. If you correct for BMI, that association tends to disappear or go the other way. Marilyn >>You've mentioned in the past that your husband's family eat an extremely >>atherogenic, pro oxidation type diet. I believe you said they never eat [quoted text clipped - 7 lines] > > I agree. Do you think I'm happy about the situation? No, I understand that you're hoping to have chosen the lesser of two evils and that you did a lot of questioning first. I'm wondering if your husband's relations who died of heart attacks died of atherogenesis or of some other cardiac cause, and if their lipid profiles leaned toward the low risk profile your daughter has? Susan > x-no-archive: yes > [quoted text clipped - 20 lines] > > - Show quoted text - We have no info on my husband's grandfather and uncle with respect to their lipid profiles because they died too long ago. They were smokers, and the grandfather was overweight. Still, 35 and 40 are awfully young ages to die of a heart attack. My husband's mother had a heart attack at 58. Unfortunately, I don't have exact info on her lipid profile because she is one of those people who gets confused about the difference between LDL and HDL. My general impression is that her LDL is very high and I think her HDL is probably in the good range, based on what she has said. She has never smoked or been overweight. She has hypertension now but I have no idea how long she has had it. Marilyn > We have no info on my husband's grandfather and uncle with respect to > their lipid profiles because they died too long ago. They were > smokers, and the grandfather was overweight. Still, 35 and 40 are > awfully young ages to die of a heart attack. Yeah, it happened on my father's side, too. They weren't smokers, but they were poor and likely ate highly atherogenic diets. Both my father's parents died around that age of heart failure of some sort, and his brothers closer to 50. > My husband's mother had a heart attack at 58. Unfortunately, I don't > have exact info on her lipid profile because she is one of those [quoted text clipped - 3 lines] > smoked or been overweight. She has hypertension now but I have no > idea how long she has had it. You mentioned her diet as being of a very highly atherogenic type, IIRC? I wonder if your husband's living relations would consent to your getting copies of their serology, or even to having the direct measurement tests run? Susan > You mentioned her diet as being of a very highly atherogenic type, IIRC? > I wonder if your husband's living relations would consent to your > getting copies of their serology, or even to having the direct > measurement tests run? Not likely, in the case of my mother-in-law. She is basically in denial about this stuff. For one thing, she feels we blame her for Monica having FH (this is not true). My husband has a brother, but it is not likely that he has FH, because his LDL is not that high and was actually normal when he was younger (and thinner). I wanted to call her niece, the daughter of the guy who died at 40, to explain that he probably died of FH. My mother-in-law is totally against this, because she does not want to "interfere in her life." I feel that this niece has the right to this information and might benefit from it, in that she might choose to share the information with her doctors (this would be up to her, of course). If it were me, I would want to know why my father died so young. Her mother had already died of cancer, so she was left an orphan. Marilyn > Not likely, in the case of my mother-in-law. She is basically in > denial about this stuff. For one thing, she feels we blame her for [quoted text clipped - 3 lines] > his LDL is not that high and was actually normal when he was younger > (and thinner). Your MIL sounds like a real prize, but you know that. :-) > I wanted to call her niece, the daughter of the guy who died at 40, to > explain that he probably died of FH. My mother-in-law is totally [quoted text clipped - 4 lines] > I would want to know why my father died so young. Her mother had > already died of cancer, so she was left an orphan. I'm with you; giving her the info isn't interference, it's just information for her to ignore or act upon. I'm walking a similar line with family over the likely partial/selective glucocorticoid resistance I've accidentally discovered in pursuing my own health issues. Susan .... > My husband has a brother, but it is not likely that he has FH, because > his LDL is not that high and was actually normal when he was younger [quoted text clipped - 6 lines] > benefit from it, in that she might choose to share the information > with her doctors (this would be up to her, of course). .... Is this the MIL's decision to make? If she's not niece's legal guardian I'd run it by whoever is, and if niece is 18 or over, I'd consider telling her directly. Given that you have this information, you have a moral dilemma whether to inform or not, and it's arguably not resolved simply by acquiescing to the MIL's wishes (which are probably unreasonable). BTW, what is FH? > Is this the MIL's decision to make? If she's not niece's legal guardian I'd > run it by whoever is, and if niece is 18 or over, I'd consider telling her > directly. Given that you have this information, you have a moral dilemma > whether to inform or not, and it's arguably not resolved simply by > acquiescing to the MIL's wishes (which are probably unreasonable). The niece is in her fifties, but I don't have her contact information because my MIL refuses to give it to me. I have had two arguments with her about this and I finally told my husband and his brother that it was up to them to deal with the issue. After all, it's their family, not mine. My husband does not have his cousin's contact information. > BTW, what is FH? Sorry, familial hypercholesterolemia. There are two types, homozygous FH and heterozygous FH. The former is very rare. My daughter has heterozygous familial hypercholesterolemia. I use "FH" to refer to the heterozygous type, which occurs in approximately 1/500 people. FH is caused by a mutation, usually in the genes relating to the LDL receptor, although there are other types of mutations that cause it as well. It is characterized by very high LDL and TC levels. Marilyn >> Is this the MIL's decision to make? If she's not niece's legal guardian >> I'd [quoted text clipped - 10 lines] > family, not mine. My husband does not have his cousin's contact > information. It's a shame that MIL is keeping potentially lifesaving info from her own flesh and blood for such a poor reason. FWIW, there are some pretty powerful search engines for finding people. One is publicdata.com, which is a pay service but fairly powerful. Another even more powerful one is autotrack. I think you need a subscription to use it but I have a friend who has it (last time I checked). If you'd like me to have him run your niece's info, please contact me privately with what you know about her (full name and DOB may be enough) and I'll see what I can do. >> BTW, what is FH? > [quoted text clipped - 5 lines] > receptor, although there are other types of mutations that cause it as > well. It is characterized by very high LDL and TC levels. Thanks for the info and best of luck to you and your family in beating these medical problems. > It's a shame that MIL is keeping potentially lifesaving info from her own > flesh and blood for such a poor reason. FWIW, there are some pretty powerful [quoted text clipped - 4 lines] > contact me privately with what you know about her (full name and DOB may be > enough) and I'll see what I can do. I'll have to ask my husband what information he has. I'm sure he does not have her DOB, though. > Thanks for the info and best of luck to you and your family in beating these > medical problems. Thanks. Marilyn > > x-no-archive: yes > [quoted text clipped - 24 lines] > > Marilyn Susan, Did you reply to this post? The main page seems to indicate that you did, but no post appears. Marilyn >>>x-no-archive: yes >> [quoted text clipped - 31 lines] > > Marilyn Yes, I did. I was wondering what part of those labs made you or her doctor think her lipids needed treating. Her HDL, TGLs and LDL pattern are indicative of a very low risk for CVD. Susan Some citations: LDL Size: Does it Matter: http://www.endokrinologie-dim.usz.ch/NR/rdonlyres/A43C7A0B-BF9C-408D-B01E-B9DBF1 7B39D9/0/LDLsize.pdf The Ashkenazi phenotype: I know about this group because the author of www.phlaunt.com/diabetes was in the study with her family. Her father died at 95 or so, having had LDL of well over 300 for most of his life. I'm kind of surprised that you've not encountered a zillion references to this group if you were researching FH; there seem to be no papers that don't cite their high LDL and longevity. Unique lipoprotein phenotype and genotype associated with exceptional longevity. CONTEXT: Individuals with exceptional longevity have a lower incidence and/or significant delay in the onset of age-related disease, and their family members may inherit biological factors that modulate aging processes and disease susceptibility. OBJECTIVE: To identify specific biological and genetic factors that are associated with or reliably define a human longevity phenotype. DESIGN, SETTING, AND PARTICIPANTS: In a case-control design, 213 Ashkenazi Jewish probands with exceptional longevity (mean [SD] age, 98.2 [5.3] years) and their offspring (n = 216; mean [SD] age, 68.3 [6.7] years) were recruited from 1998 to 2002, while an age-matched control group of Ashkenazi Jews (n = 258) and participants from the Framingham Offspring Study (n = 589) were accepted as control groups. MAIN OUTCOME MEASURES: Detailed questionnaires, physical examination, and blood samples were taken, including assessment of lipids and lipoprotein subclass levels and particle sizes by proton nuclear magnetic resonance. Samples were also genotyped for the codon 405 isoleucine to valine (I405V) variation in the cholesteryl ester transfer protein (CETP) gene, which is involved in regulation of lipoprotein and its particle sizes. RESULTS: High-density lipoprotein (HDL) and low-density lipoprotein (LDL) particle sizes were significantly higher in probands compared with both control groups (P =.001 for both), independent of plasma levels of HDL and LDL cholesterol and apolipoprotein A1 and B. This phenotype was also typical of the proband's offspring but not of the age-matched controls. The HDL and LDL particle sizes were significantly larger in offspring and controls without hypertension or cardiovascular disease, (P =.001 and P =.008, respectively). Furthermore, lipoprotein particle sizes, but not plasma LDL levels, were significantly higher in offspring and controls without the metabolic syndrome (P<.001). Probands and offspring had a 2.9- and 3.6-fold (in men) and 2.7- and 1.5-fold (in women) increased frequency, respectively, of homozygosity for the 405 valine allele of CETP (VV genotype), respectively, compared with controls (P<.001 for both). Those probands with the VV genotype had increased lipoprotein sizes and lower serum CETP concentrations. CONCLUSIONS: Individuals with exceptional longevity and their offspring have significantly larger HDL and LDL particle sizes. This phenotype is associated with a lower prevalence of hypertension, cardiovascular disease, the metabolic syndrome, and increased homozygosity for the I405V variant in CETP. These findings suggest that lipoprotein particle sizes are heritable and promote a healthy aging phenotype. PMID:14559957 > LDL Size: Does it Matter: > [quoted text clipped - 51 lines] > healthy aging phenotype. > PMID:14559957 I'm not saying lipoprotein subfractions don't have any significance. I just don't think Monica's high HDL cancels out the risk associated with her exceptionally high LDL. Or at least we can't be confident that it does. That's the whole problem with heart disease. It's very hard to predict. Anyway, these particular Ashkenazi Jews they're talking about do not have FH. They have some other genetic variations that my daughter probably does not have. Marilyn > I'm not saying lipoprotein subfractions don't have any significance. > I just don't think Monica's high HDL cancels out the risk associated > with her exceptionally high LDL. Or at least we can't be confident > that it does. That's the whole problem with heart disease. It's very > hard to predict. And LDL is the worst predictor. Look, I understand how much it's possible to worry about one's child and to want to protect her, believe me. > Anyway, these particular Ashkenazi Jews they're talking about do not > have FH. They have some other genetic variations that my daughter > probably does not have. I understand that they may not be the same, but they're very instructive about how high LDL, for example, can be part of a very low risk profile. Susan Susan <nevermind@nomail.com> wrote in part: >x-no-archive: yes > [quoted text clipped - 5 lines] > >And LDL is the worst predictor. FWIW, it's a stronger predictor with Lp(a). > Look, I understand how much it's >possible to worry about one's child and to want to protect her, believe me. [quoted text clipped - 5 lines] >I understand that they may not be the same, but they're very instructive >about how high LDL, for example, can be part of a very low risk profile. True. I think the difficulty here is that, in some cases, we really don't know what the risk is. This seems to me to be one of those. -- Jim Chinnis Warrenton, Virginia, USA > >And LDL is the worst predictor. It's definitely a poor predictor for people whose LDL is only slightly elevated. It becomes a better predictor for people whose LDL is very low or very high. I agree, and I've said before, that some people with very high LDL live a normal lifespan even without treatment. It's just hard to predict who those people will be. > FWIW, it's a stronger predictor with Lp(a). Yes, and her Lp(a) is elevated. > I think the difficulty here is that, in some cases, we really don't know > what the risk is. This seems to me to be one of those. > -- I generally agree with this. We know that on average the risk of early heart disease with FH is high, so high that few people would choose not to treat an adult with FH. What we don't know is the ideal age to start treatment. The studies that have been done on treating kids with statins have necessarily used surrogate endpoints such as lipid levels and IMT. We also don't know the effect of someone taking a statin over long periods of time. Another thing we don't know is whether people with FH should be treated with nonstatins like ezetimibe in addition to statins. When I took Monica to the Johns Hopkins lipid clinic, Dr. Kwiterovich wanted to put her on Vytorin so he could reduce her LDL by at least 50%. I told him I didn't want her on ezetimibe because of lack of studies with clinical endpoints. His attitude was basically "my way or the highway" so he referred Monica to a pediatric cardiologist at Children's Hospital. Marilyn >>>And LDL is the worst predictor. > [quoted text clipped - 3 lines] > with very high LDL live a normal lifespan even without treatment. > It's just hard to predict who those people will be. And some live a very extended lifespan with that pattern. >>I think the difficulty here is that, in some cases, we really don't know >>what the risk is. This seems to me to be one of those. [quoted text clipped - 16 lines] > highway" so he referred Monica to a pediatric cardiologist at > Children's Hospital. I wonder how many of the participants in studies demonstrating early CVD and mortality were eating the now known to be atherogenic low fat diet typically recommended? Susan > I wonder how many of the participants in studies demonstrating early CVD > and mortality were eating the now known to be atherogenic low fat diet > typically recommended? I don't know the answer to this, but I believe the idea that a low fat diet prevents heart disease only goes back a few decades. The main problem with a lot of these studies was that they looked at people who had been referred to lipid clinics. Obviously not a random sample of people with FH. I've posted before about a study that was done in the Netherlands where they traced back some FH families into the 19th century. In the 19th century there was no excess mortality in these families compared to the general population. Of course, the average lifespan was shorter in those days, maybe people didn't smoke as much, etc. There is some evidence that high cholesterol may provide some protection against infectious disease, which would have been more prevalent in the 19th century. So the people with FH may have had a lower rate of mortality due to infectious disease that balanced out their higher mortality due to CVD. We don't really know, of course. Marilyn > I don't know the answer to this, but I believe the idea that a low fat > diet prevents heart disease only goes back a few decades. The main > problem with a lot of these studies was that they looked at people who > had been referred to lipid clinics. Obviously not a random sample of > people with FH. Yes. And first it was cholesterol, then fats overall. > I've posted before about a study that was done in the Netherlands > where they traced back some FH families into the 19th century. In the [quoted text clipped - 6 lines] > mortality due to infectious disease that balanced out their higher > mortality due to CVD. We don't really know, of course. Higher cholesterol, specifically LDL, is very likely the body's attempt at raising adrenal hormones in a situation where the immune system or other adrenal status is in danger or not functioning properly. LDL is what all our adrenal hormones are made of. Susan Susan <nevermind@nomail.com> wrote in part: >x-no-archive: yes > [quoted text clipped - 21 lines] >other adrenal status is in danger or not functioning properly. LDL is >what all our adrenal hormones are made of. In the case of FH, this mechanism appears not to be at work. The LDL is very high due to a gene mutation tied to LDL receptors. -- Jim Chinnis Warrenton, Virginia, USA > In the case of FH, this mechanism appears not to be at work. The LDL is very > high due to a gene mutation tied to LDL receptors. Okay, but how is that necessarily not related to adrenal function? Downstream from that receptor defect, couldn't the adrenals be experiencing a deficit of building material? Susan Susan <nevermind@nomail.com> wrote in part: >x-no-archive: yes > [quoted text clipped - 4 lines] >Downstream from that receptor defect, couldn't the adrenals be >experiencing a deficit of building material? You had written: "Higher cholesterol, specifically LDL, is very likely the body's attempt at raising adrenal hormones in a situation where the immune system or other adrenal status is in danger or not functioning properly. LDL is what all our adrenal hormones are made of." I'm just saying that the gene variation that occurs in FH appears to cause more LDL to be made due to a problem with LDL receptors. That looks like sufficent cause. I'm not saying that the increased LDL may not have effects on adrenal function. I'm just suggesting that the LDL problem appears to occur due to a genetic change and not an attempt of the body to raise adrenal hormones. -- Jim Chinnis Warrenton, Virginia, USA > You had written: "Higher cholesterol, specifically LDL, is very likely the > body's attempt at raising adrenal hormones in a situation where the immune [quoted text clipped - 7 lines] > occur due to a genetic change and not an attempt of the body to raise > adrenal hormones. Okay, I see. But I still think the body has a need for a certain level of LDL to make other stuff (hormones, the brain) and lowering the LDL if the receptors don't allow for adequate delivery of LDL to the cells may cause unintended consequences. Susan MarilynMann <mannm@comcast.net> wrote in part: >> >And LDL is the worst predictor. > [quoted text clipped - 7 lines] >> >Yes, and her Lp(a) is elevated. Yes. That's why I mentioned it. Though the elevation in her case isn't terribly large. >> I think the difficulty here is that, in some cases, we really don't know >> what the risk is. This seems to me to be one of those. [quoted text clipped - 16 lines] >highway" so he referred Monica to a pediatric cardiologist at >Children's Hospital. I've posted here rather negatively re people choosing drugs like ezetimibe when no clinical endpoint data have been used in randomized trials. But I can see an argument for them in a case where the concern is driven by a risk factor that the drug has been shown to control (LDL in this case). But it remains a weak argument that could very easily be shown wrong in a randomized trial with hard endpoints. My take on reducing risks of cardiovascular disease is to address all known risks. It seems to be the combinations that kill--not a single measure such as LDL. -- Jim Chinnis Warrenton, Virginia, USA > I've posted here rather negatively re people choosing drugs like ezetimibe > when no clinical endpoint data have been used in randomized trials. But I > can see an argument for them in a case where the concern is driven by a risk > factor that the drug has been shown to control (LDL in this case). But it > remains a weak argument that could very easily be shown wrong in a > randomized trial with hard endpoints. Maybe in a few years some clinical endpoint data will be available. I see no rush for her to take it at the moment. Marilyn > > My wife's sister is being put on a statin because of her cholesterol > > levels despite being thin, active, and no history of CVD. I think some [quoted text clipped - 7 lines] > > Marilyn I wonder how many 14 year olds get their blood tested for a lipid panel ? I also wonder what the average is ? I wonder who the charts address . Bill SignatureS Jersey USA Zone 5 Shade "The destiny of nations depends on how we feed ourselves." Brillat-Savarin http://www.ocutech.com/ High tech Vison aid > I wonder how many 14 year olds get their blood tested for a lipid > panel ? I don't know the answer, but some pediatricians check for total cholesterol and then send kids for a fasting lipid panel if their TC is over a certain level. Or they might do it for a kid that was overweight or had a worrisome family history. I don't think it's done routinely. I also wonder what the average is ? I wonder who the charts > address . There has been research on this. The charts are age and gender specific, just like height and weight. I can't give you averages off the top of my head, but you could find out if you are really interested. With respect to FH, you can't diagnose it reliably based simply on LDL level, because there is an overlap of LDL levels of people with FH or without. There are genetic tests, or you can look at family history and tendon xanthomas, if that info is available. As with many other tests, there is a tradeoff between sensitivity and specificity with any LDL cutoff you use. In addition, genetic testing is not 100% reliable because there are people who have clearly have FH clinically but no mutation can be identified. That doesn't mean they don't have one, just that it hasn't been identified. Marilyn > friend MarilynMann <mannm@comcast.net> wrote in part: > [quoted text clipped - 49 lines] > the fact that over 28,000 people participated. It probably didn't last long > enough to shed much light on the questions addressed. Truly, it has not been **what** we have been eating but **how much** we have been overeating that has been hurting us. Whenever we overeat (eating until full, stretching our stomachs, and killing our hunger), we have been accumulating harmful VAT. Be hungry... be healthy... be hungrier... be blessed: http://TheWellnessFoundation.com/PressRelease Prayerfully in the infinite power and might of the Holy Spirit, Andrew <>< -- Andrew B. Chung, MD/PhD Lawful steward of http://EmoryCardiology.com Bondservant to the KING of kings and LORD of lords. > Conclusions: In relation to risks of cardiovascular events, our > results do not suggest any benefit from a limited total or saturated > fat intake, nor from relatively high intake of unsaturated fat. In Journal of Internal Medicine 258 (2), 153-165. (Dietary fat intake and early mortality patterns - data from The Malm? Diet and Cancer Study.) There is shown to be an increased risk of cardiovascular mortality in the highest quartile of fat consumption. The paper also notes that trans-fats were included with unsaturated fats in doing the statistics. -- Ron >> Conclusions: In relation to risks of cardiovascular events, our >> results do not suggest any benefit from a limited total or saturated [quoted text clipped - 6 lines] > notes that trans-fats were included with unsaturated fats in doing the > statistics. Combining transfats with unsaturated fats in the study is quite obvious reason for the fact that unsaturated fat was not associated with reduced risks. It should also be noticed that in the previous Malmö study high total fat intake (~ 43 E%) was associated with higher cancer mortality in women. SignatureJuhana http://ruohikolla.blogspot.com/ |
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