Sunday, August 25, 2013

17 Low-Carbohydrate Diet studies and All-Cause Mortality

Low-Carbohydrate Diets and All-Cause Mortality: A Systematic Review and Meta-Analysis of 17 Observational Studies (Published: January 25, 2013)

Results

"We included 17 studies for a systematic review, followed by a meta-analysis using pertinent data. Of the 272,216 people in 4 cohort studies using the low-carbohydrate score, 15,981 (5.9%) cases of death from all-cause were reported. The risk of all-cause mortality among those with high low-carbohydrate score was significantly elevated: the pooled RR (95% CI) was 1.31 (1.07-1.59)."

Conclusions

"Our meta-analysis supported long-term harm and no cardiovascular protection with low-carbohydrate diets. However, the observational studies were limited and moderately heterogeneous. Our findings underscore the imminent need for large-scale trials on the complex interactions between low-carbohydrate diets and long-term outcomes."

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0055030#authcontrib

This is one of many red flags that indicate the general public should be very cautious about adopting a long term low carbohydrate diet.

Saturday, May 4, 2013

Why a diet very high in red meat and saturated fat is dangerous for the average person during weight maintenance.

1. Lowering LDL-C has been shown by a meta-analysis of 108 RCTs (the strongest possible evidence) to lower the risk of heart disease. The Atkins diet does not lower LDL-C during weight loss and raises LDL-C during weight maintenance in the average person. (1)
    2. Raising HDL has been shown by a meta-analysis of 108 RCTs (the strongest possible evidence) to provide no significant protection against heart disease. (1)
      3. Each LDL particle is just as atherogenic as the next whether it's fluffy or dense because each particle contains one ApoB. "Fluffy" LDL is much smaller than VLDL which carries most of the triglycerides and no one claims that VLDL is harmless.
        4. This kind of diet increases the risk of heart disease, cancer, Alzheimer`s disease and all-cause mortality.
          5. Short term studies during weight loss tell us very little about the long term effects of a diet because any diet will give relatively good lipid values during weight loss.
            6. Studies during weight maintenance give the most useful information. And during weight maintenance very high saturated fat diets increase LDL-C, ApoB and CRP in the average person. (2)
              7. Another study by Dr. Ronald Krauss showed during weight maintenance that a high beef, high saturated fat diet increased LDL particle number. (3)
                8. All prospective cohort studies of very high saturated fat diets show increased heart disease and all-cause mortality.
                  To summarize (during weight maintenance), very high saturated fat diets increase LDL particle number and inflammation in the average person. And they increase the risk of mortality from a variety of illnesses in the average person.


                    References
                      1. Briel M, Ferreira-Gonzalez I, You JJ, Karanicolas PJ, Akl EA, Wu P, Blechacz B, Bassler D, Wei X, Sharman A, Whitt I, Alves da Silva S, Khalid Z, Nordmann AJ,Zhou Q, Walter SD, Vale N, Bhatnagar N, O'Regan C, Mills EJ, Bucher HC, Montori VM, Guyatt GH. Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis. BMJ. 2009 Feb 16;338:b92. doi: 10.1136/bmj.b92. (http://www.ncbi.nlm.nih.gov/pubmed/19221140)
                        2. Miller M, Beach V, Sorkin JD, Mangano C, Dobmeier C, Novacic D, Rhyne J, Vogel RA. Comparative effects of three popular diets on lipids, endothelial function, and C-reactive protein during weight maintenance. J Am Diet Assoc. 2009 Apr;109(4):713-7. doi: 10.1016/j.jada.2008.12.023. (http://www.ncbi.nlm.nih.gov/pubmed/19328268)
                          3. Mangravite LM, Chiu S, Wojnoonski K, Rawlings RS, Bergeron N, Krauss RM. Changes in atherogenic dyslipidemia induced by carbohydrate restriction in men are dependent on dietary protein source. J Nutr. 2011 Dec;141(12):2180-5. doi: 10.3945/jn.111.139477. Epub 2011 Oct 26. (http://www.ncbi.nlm.nih.gov/pubmed/22031660)

                          Saturday, April 20, 2013

                          Why the Atkins/Paleo crowd is wrong about Ancel Keys.


                          Connor WE, Connor SL. The key role of nutritional factors in the prevention of coronary heart disease. Prev Med. 1972 Mar;1(1):49-83.

                          Using data from 29 countries this study found the following correlations between the mortality rate from coronary heart disease and certain nutrients in the diet:

                          positive correlations (risk factors)
                          -------------------
                          animal protein 0.782
                          cholesterol 0.762
                          meat 0.697
                          total fat 0.676
                          eggs 0.666
                          sugar 0.638
                          total calories 0.633
                          animal fat 0.632

                          no correlation
                          -------------
                          plant sterols 0.144
                          fish 0.013
                          vegetable fat 0.011
                          vegetables 0.009

                          negative correlations (protective)
                          --------------------
                          starch -0.463
                          vegetable protein -0.403

                          ------------------

                          The Mediterranean diet is considered to have to most evidence of being a healthy diet, and it is near vegetarian, low in saturated fat, low in animal protein and higher in starch than the SAD. And in clinical trials by Dr. Ornish and Dr. Esselstyn ---- high starch, high fiber, low saturated fat diets consistently reduce cardiac events and all-cause mortality in severely ill heart patients. All of this is consistent with this study that included 29 countries, not just six.

                          --------

                          Furthermore Ancel Keys is accused of making us fat, however the American public never adopted the Mediterranean diet the Dr. Keys recommended. At that time Italy with it's Mediterranean diet had one of the lowest obesity rates in the world. And in general populations with the lowest obesity rates eat the most starch and fiber and the least meat.


                          COUNTRY/% OBESITY/YEAR/REGION

                          United States/34/2006/US
                          Thailand/8/2003/SE Asia
                          Singapore/7/2004/SE Asia
                          Philippines/4/2003/SE Asia
                          Eritrea/3/2004/Africa
                          Korea, South/3/2001/SE Asia
                          Japan/3/2000/SE Asia
                          China/3/2002/SE Asia
                          Indonesia/2/2001/SE Asia
                          Madagascar/2/2005/Africa
                          Laos/1/2000/SE Asia
                          Vietnam/1/2000/SE Asia


                          http://www.drmcdougall.com/misc/2013nl/mar/med.htm

                          New study reveals mechanism of how LDL cholesterol damages the brain to promote Alzheimer's and the blood vessels to promote atherosclerosis


                          "Cholesterol increases risk of Alzheimer's and heart disease

                          High levels of blood cholesterol increase the risk of both Alzheimer's disease and heart disease, but it has been unclear exactly how cholesterol damages the brain to promote Alzheimer's disease and blood vessels to promote atherosclerosis.

                          Using insights gained from studying two much rarer disorders, Down Syndrome and Niemann Pick-C disease, researchers at the Linda Crnic Institute for Down Syndrome and the Department of Neurology of the University of Colorado School of Medicine found that cholesterol wreaks havoc on the orderly process of cell division, leading to defective daughter cells throughout the body.

                          In the new study published this week in the on-line journal PLOS ONE, Antoneta Granic, PhD, and Huntington Potter, PhD, show that cholesterol, particularly in the LDL form, called 'bad cholesterol', causes cells in both humans and mice to divide incorrectly and distribute their already-duplicated chromosomes unequally to the next generation. The result is an accumulation of defective daughter cells with the wrong number of chromosomes and therefore the wrong number of genes. Instead of the correct two copies of each chromosome, and thus two copies of each gene, some cells acquired three copies and some only one.

                          Granic and Potter's study of the effects of cholesterol on cell division included a prominent finding of cells carrying three copies of the chromosome (#21 in humans and #16 in mice) that encodes the amyloid peptide that is the key component of the neurotoxic amyloid filaments that accumulate in the brains of Alzheimer patients.

                          Human trisomy 21 cells are significant because people with Down syndrome have trisomy 21 in all of their cells from the moment of conception, and they all develop the brain pathology and many develop the dementia of Alzheimer's disease by age 50. Earlier studies by Granic, Potter and others have shown that as many as 10% of cells in an Alzheimer patient, including neurons in the brain, have three copies of chromosome 21 instead of the usual two. Thus, Alzheimer's disease is, in some ways, a form of acquired Down syndrome. Furthermore, mutant genes that cause inherited Alzheimer's disease cause the same defect in chromosome segregation as does cholesterol, thus indicating the presence of a common cell division problem in both familial and 'sporadic' (non-familial) Alzheimer's disease."

                          http://medicalxpress.com/news/2013-04-cholesterol-alzheimer-heart-disease.html#jCp

                          Sunday, March 3, 2013

                          Low LDL probably does not cause cancer.


                          Low-Density Lipoprotein Cholesterol and the Risk of Cancer: A Mendelian Randomization Study

                          Marianne Benn, Anne Tybjærg-Hansen, Stefan Stender, Ruth Frikke-Schmidt, Børge G. Nordestgaard
                          Manuscript received August 19, 2010; revised December 15, 2010; accepted January 4, 2011.

                          Background: Low plasma levels of low-density lipoprotein (LDL) cholesterol are associated with an increased risk of cancer, but whether this association is causal is unclear.

                          Methods: We studied 10613 participants in the Copenhagen City Heart Study (CCHS) and 59566 participants in the Copenhagen General Population Study, 6816 of whom had developed cancer by May 2009. Individuals were genotyped for PCSK9 R46L (rs11591147), ABCG8 D19H (rs11887534), and APOE R112C (rs429358) and R158C (rs7412) polymorphisms, all of which are associated with lifelong reduced plasma LDL cholesterol levels. Plasma LDL cholesterol was calculated using the Friedewald equation in samples in which the triglyceride level was less than 354 mg/dL and measured directly by colorimetry for samples with higher triglyceride levels. Risk of cancer was estimated prospectively using Cox proportional hazards regression analyses and cross-sectionally by logistic regression analyses. Causality was studied using instrumental variable analysis. All statistical tests were two-sided.

                          Results: In the CCHS, compared with plasma LDL cholesterol levels greater than the 66th percentile (>158 mg/dL), those lower than the 10th percentile (<87 mg/dL) were associated with a 43% increase (95% confidence interval [CI] = 15% to 79% increase) in the risk of cancer. The polymorphisms were associated with up to a 38% reduction (95% CI = 36% to 41% reduction) in LDL cholesterol levels but not with increased risk of cancer. The causal odds ratio for cancer for a 50% reduction in plasma LDL cholesterol level due to all the genotypes in both studies combined was 0.96 (95% CI = 0.87 to 1.05), whereas the hazard ratio of cancer for a 50% reduction in plasma LDL cholesterol level in the CCHS was 1.10 (95% CI = 1.01 to 1.21) (P for causal odds ratio vs observed hazard ratio = .03).

                          Conclusion: Low plasma LDL cholesterol levels were robustly associated with an increased risk of cancer, but genetically decreased LDL cholesterol was not. This finding suggests that low LDL cholesterol levels per se do not cause cancer.

                          J Natl Cancer Inst 2011;103:508-519

                          http://jnci.oxfordjournals.org/content/103/6/508.full.pdf

                          --------

                          This study provides powerful evidence that low LDL does not cause cancer. And there is other evidence as well. Calorie restriction lowers serum cholesterol and reduces the risk of cancer and heart disease at the same time. Meta-analysis of statin trials show no increase in the overall risk of cancer even after 5 to 10 years of use. Countries with lower serum cholesterol like China have lower rates of prostate, breast and colon cancer than the U.S. Hunter gatherers with their low LDL levels are known for the near-absence of cancer. In clinical trials, the cholesterol lowering Ornish diet slows the growth of prostate cancer. And finally people with stable low cholesterol levels don't have higher cancer rates, just people whose cholesterol level has fallen recently. (1,2,3)

                          References 

                          1. Iribarren C, Reed DM, Chen R, Yano K, Dwyer JH. Low serum cholesterol and mortality. Which is the cause and which is the effect? Circulation. 1995 Nov 1;92(9):2396-403
                          2. Jacobs EJ, Newton CC, Thun MJ, Gapstur SM. Long-term use of cholesterol-lowering drugs and cancer incidence in a large United States cohort. Cancer Res. 2011 Mar 1;71(5):1763-71.
                          3. Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO, Crutchfield L, Yglecias L, Carroll PR, Ornish D. Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology. 2008 Dec;72(6):1319-23.

                          Friday, February 1, 2013

                          LARGE LDL PARTICLES ARE JUST AS ATHEROGENIC AS SMALL LDLS

                          According to a meta-analysis of 24 studies by Ip et al in 2009, higher LDL particle number was consistently associated with increased risk for cardiovascular disease, independent of size or density.

                          Ip S, Lichtenstein AH, Chung M, Lau J, Balk EM. Systematic review: association of low-density lipoprotein subfractions with cardiovascular outcomes. Ann Intern Med. 2009 Apr 7;150(7):474-84.

                          -------

                          LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA).

                          Mora S, Szklo M, Otvos JD, Greenland P, Psaty BM, Goff DC Jr, O'Leary DH, Saad MF, Tsai MY, Sharrett AR.

                          Abstract
                          BACKGROUND:
                          Previous studies showing that smaller low-density lipoprotein (LDL) size is associated with greater atherosclerotic risk did not adequately control for small and large LDL particle correlation.
                          METHODS AND RESULTS:
                          We studied the association of lipoproteins measured by proton nuclear magnetic resonance spectroscopy with carotid intima-media thickness (IMT) in apparently healthy individuals (N = 5538, 38% White, 28% African American, 22% Hispanic, 12% Chinese). Small and large LDL particle concentrations (LDL-p) were inversely correlated (r = /-0.63, P < 0.0001). Controlling for risk factors but not for LDL subclass correlation, LDL size and small LDL-p separately were associated with IMT (-20.9 and 31.7 microm change in IMT per 1-S.D., respectively, both P < 0.001), but large LDL-p was not (4.9 microm, P = 0.27). When LDL subclasses were included in the same model, large and small LDL-p were both associated with IMT (36.6 and 52.2 microm higher IMT per 1-S.D., respectively, both P < 0.001; 17.7 and 11.6 microm per 100 nmol/L, respectively). LDL size was not significant after accounting for LDL subclasses and risk factors (P = 0.10).
                          CONCLUSION:
                          Both LDL subclasses were significantly associated with subclinical atherosclerosis, with small LDL confounding the association of large LDL with atherosclerosis. Future studies of LDL size should account for the strong inverse correlation of LDL subclasses.

                          "However, after accounting for their inverse correlation, both LDL subclasses showed highly significant and independent associations with IMT, with a greater difference in IMT per large LDL particle compared with small LDL."

                          http://www.ncbi.nlm.nih.gov/pubmed/16765964

                          For more details watch this video:
                          http://plantpositive.squarespace.com/25-cholesterol-confusion-8-a-l/

                          Sunday, January 20, 2013

                          HDL probably does not protect against heart disease.

                          A meta-analysis of 108 RCTs found that HDL had little appreciable effect on the risk of heart disease or all-cause mortality after controlling for LDL."

                          http://www.bmj.com/content/338/bmj.b92

                          http://www.askdoctork.com/is-high-hdl-cholesterol-good-201212193969

                          "Posted December 19, 2012, 5:00 am

                          DEAR DOCTOR K:
                          For years my doctor has been telling me about the benefits of high levels of HDL cholesterol. Now I read that high HDL may not protect against heart disease after all. Is "good" cholesterol still good for you?

                          DEAR READER:
                          The HDL cholesterol story is a cautionary tale. It demonstrates once again that even the most persuasive theories about what should make us healthy need to be put to the test.

                          It has been solidly established that people who have high levels of LDL (bad) cholesterol have a higher risk of developing heart disease. Moreover, it has been solidly established that treatments that lower LDL cholesterol reduce the risk of developing heart disease.

                          It also has been solidly established that people with HDL levels above 60 milligrams per deciliter (mg/dL) tend to have a lower risk for heart disease. Since HDL cholesterol removes fat from the plaques in arteries, that observation made sense.

                          Not unreasonably, doctors and scientists assumed that boosting HDL with medication would lower cardiac risk even more. There are several drugs that have been around for 30 years - particularly gemfibrozil and niacin - that modestly raise levels of HDL. These drugs were tested in people with heart disease. They did lower the risk of new heart problems, but it wasn't clear if they achieved that benefit by lowering HDL cholesterol or through some other effect.

                          Then several different types of drugs were developed that could dramatically raise HDL levels. Most doctors, myself included, bet that such drugs would probably reduce the risk of heart disease. Why? Because all the evidence seemed to point in that direction.

                          Before such drugs were approved by the Food and Drug Administration, however, the agency required that studies involving large numbers of people be conducted to prove the value of the drugs. To make a long and painful story short, over the past five years these drugs have proved very disappointing. Not only have they not convincingly lowered the risk of heart trouble - in some cases, they have increased the risk.

                          In addition, a recent Harvard study pooled health information on more than 116,000 people genetically predisposed to produce higher-than-normal amounts of HDL. Surprisingly, this group did not show the predicted lower risk of heart attack.

                          How can this study be squared with previous studies that have convincingly showed that people with high levels of HDL have a lower risk of heart disease? The most likely conclusion is that it is not the high HDL levels, but rather something else about people who have high HDL levels that protects them from heart disease.

                          Many lifestyle changes raise HDL cholesterol and indisputably reduce your risk of heart disease: regular exercise, healthy weight, avoiding trans fats, quitting smoking and moderate use of alcohol. These lifestyle changes may not work through their effects on your HDL level, but they surely and powerfully do work."

                          "Dr. Anthony Komaroff is a practicing physician, Professor of Medicine at Harvard Medical School, and Editor in Chief of Harvard Health Publications."