How LOW Cholesterol Can Harm Your Health Grain-Wheat-Chronic Poison Nutritional Supplement Offers Promise in Treatment of Unique Form of Autism Myocardial infarction in relation to mercury and fatty acids from fish Supplement Your Stem Cells—how to look at this study ************************************************************************** How LOW Cholesterol Can Harm Your Health You’ve heard for decades about the dangers of high cholesterol, but did you know that LOW cholesterol can lead to violence towards self and other, and has been linked to premature aging, death and other adverse health effects?–In a world gone mad with anti-cholesterol anxiety, and where gobbling down pharmaceuticals designed to poison the body into no longer synthesizing it is somehow considered sane behavior, it is refreshing to look at some of the research on the health benefits of cholesterol, or conversely, the dangers of low cholesterol. Benefits of Cholesterol Cholesterol Is Needed To Prevent Aggression It has been known for almost 30 years that low serum cholesterol levels are associated with habitually violent tendencies of homicidal offenders under the influence of alcohol.[i] Since then, there are at least 8 other studies that have either confirmed or explored the cholesterol-violence link, including both violence towards self and other. One of the possible explanations for this association was discussed in an article published in the British Journal of Psychiatry in 1993: “One of the functions of serotonin in the central nervous system is the suppression of harmful behaviour impulses…Low membrane cholesterol decreases the number of serotonin receptors. Since membrane cholesterol exchanges freely with cholesterol in the surrounding medium, a lowered serum cholesterol concentration may contribute to a decrease in brain serotonin, with poorer suppression of aggressive behaviour”.[ii] Not surprisingly, several reports have now surfaced on cholesterol-lowering statin drugs contributing to irritability and/or aggression. Cholesterol Is Needed To Fight Cancer The inverse relationship between cholesterol levels and the risk for a variety of cancers, and mortality associated with cancer, has been known about since the late 80′s.[iii] Since then, the cholesterol-cancer connection has been confirmed over and over again. It is to be expected, therefore, that statin drug use would be linked with increased cancer incidence, which indeed it is.[iv] Even when you take so-called “bad” LDL-cholesterol and administer it to a culture of highly malignant, multi-drug resistant leukemia cells, the cells lose their resistance to chemotherapy. Cholesterol Is Needed To Prevent Hemorrhagic Stroke There are two types of stroke: 1) Ischemic, associated with lack of blood flow and oxygen to the brain 2) Hemorrhagic, associated with the rupture of a blood vessel in the brain, and bleeding. The risk for the former, in theory, could be raised in the presence of excessive oxidized cholesterol. However, it is the risk for the second, hemorrhagic stroke, which is increased when cholesterol levels are low. Noted as far back as 1994 in the British Medical Journal, in an article titled, “Assessing possible hazards of reducing serum cholesterol,” researchers found “The only cause of death attributable to low serum cholesterol concentration was haemorrhagic stroke.”[vi] Other studies can be viewed that confirm this association on our stroke-cholesterol link page. Cholesterol Is Needed for Memory Low HDL cholesterol has been identified as a risk factor for deficit and decline in memory in midlife. [vii] Even in Parkinson’s disease, higher total serum cholesterol concentrations are associated with slower clinical progression of the disease.[viii]Statin drugs, which inhibit the production of cholesterol, hence severely affecting the brain, are now required by the FDA to display the black box warning that they may adversely affect the memory.[ix] We have indexed over 50 studies from the National Library of Medicine’s bibliographic database, Medline, on the neurotoxicity of statin drugs, with six of these specifically addressing statin-induced memory impairment. Cholesterol is Needed for Longevity In a fascinating study published in PLoS in 2011, telomere length – the shoestring cap-like ends of the chromosomes which prevent DNA damage associated with cellular aging – was linked to higher LDL and total cholesterol levels. The longer the length of these protective caps, the higher the cholesterol.[x] Indeed, several studies indicate that lower cholesterol is associated with increased mortality. Cholesterol Helps Us Fight Infection It has been observed that a cholesterol-rich diet improves patients with tuberculosis, leading researchers to suggest “cholesterol should be used as a complementary measure in antitubercular treatment.”[xi] Cholesterol-lowering drugs, incidentally, exhibit immunosuppressive and potent immunotoxic properties, likely in part due to their cholesterol depleting effects. Given that cholesterol is essential for all animal life and that each cell is capable of synthesizing it from simpler molecules, we should not be surprised by examples provided above of cholesterol’s significant health benefits. Nor should it be surprising that cholesterol-lowering drugs have over 300 adverse health effects. For now, suffice it to say, that conventional medical practice would do well to receive instruction from basic principles of biology, rather than simply the drug-company marketing copy it increasingly falls prey to. Article Sources
- [i] M Virkkunen. Serum cholesterol levels in homicidal offenders. A low cholesterol level is connected with a habitually violent tendency under the influence of alcohol. Neuropsychobiology. 1983 ;10(2-3):65-9. PMID: 6674827
- [ii] K Hawthon, P Cowen, D Owens, A Bond, M Elliott. Low serum cholesterol and suicide. Br J Psychiatry. 1993 Jun ;162:818-25. PMID: 7980726
- [iii] P Knekt, A Reunanen, A Aromaa, M Heliövaara, T Hakulinen, M Hakama. Serum cholesterol and risk of cancer in a cohort of 39,000 men and women. J Clin Epidemiol. 1988;41(6):519-30. PMID: 3290396
- [iv] GreenMedInfo.com, Focused Articles: Cancer-Statin Drug Link.
- [v] Yu Shu, Hu Liu. Reversal of P-glycoprotein-mediated multidrug resistance by cholesterol derived from low density lipoprotein in a vinblastine-resistant human lymphoblastic leukemia cell line. Biochem Cell Biol. 2007 Oct;85(5):638-46. PMID: 17901905
- [vi] M R Law, S G Thompson, N J Wald. Assessing possible hazards of reducing serum cholesterol.BMJ. 1994 Feb 5;308(6925):373-9. PMID: 8124144
- [vii] Archana Singh-Manoux, David Gimeno, Mika Kivimaki, Eric Brunner, Michael G Marmot. Low HDL cholesterol is a risk factor for deficit and decline in memory in midlife: the Whitehall II study.Arterioscler Thromb Vasc Biol. 2008 Aug;28(8):1556-62. Epub 2008 Jun 30. PMID: 18591462
- [viii] Xuemei Huang, Peggy Auinger, Shirley Eberly, David Oakes, Michael Schwarzschild, Alberto Ascherio, Richard Mailman, Honglei Chen, . Serum Cholesterol and the Progression of Parkinson’s Disease: Results from DATATOP. PLoS One. 2011 ;6(8):e22854. Epub 2011 Aug 11. PMID:21853051
- [ix] Weeks MD, Black box warning changes for statin drugs, March 4th, 2012
- [x] Paul G Shiels, Liane M McGlynn, Alan Macintyre, Paul C D Johnson, G David Batty, Harry Burns, Jonathan Cavanagh, Kevin A Deans, Ian Ford, Alex McConnachie, Agnes McGinty, Jennifer S McLean, Keith Millar, Naveed Sattar, Carol Tannahill, Yoga N Velupillai, Chris J Packard. Accelerated Telomere Attrition Is Associated with Relative Household Income, Diet and Inflammation in the pSoBid Cohort. PLoS One. 2011 ;6(7):e22521. Epub 2011 Jul 27. PMID:21818333
- [xi] Carlos Pérez-Guzmán, Mario H Vargas, Francisco Quiñonez, Norma Bazavilvazo, Adriana Aguilar. A cholesterol-rich diet accelerates bacteriologic sterilization in pulmonary tuberculosis.Chest. 2005 Feb;127(2):643-51. PMID: 15706008
**************************************************************************** Grain-Wheat-Chronic Poison (CBS News) Modern wheat is a “perfect, chronic poison,” according to Dr. William Davis, a cardiologist who has published a book all about the world’s most popular grain. -Davis said that the wheat we eat these days isn’t the wheat your grandma had: “It’s an 18-inch tall plant created by genetic research in the ’60s and ’70s,” he said on “CBS This Morning.” “This thing has many new features nobody told you about, such as there’s a new protein in this thing called gliadin. It’s not gluten. I’m not addressing people with gluten sensitivities and celiac disease. I’m talking about everybody else because everybody else is susceptible to the gliadin protein that is an opiate. This thing binds into the opiate receptors in your brain and in most people stimulates appetite, such that we consume 440 more calories per day, 365 days per year.”–Asked if the farming industry could change back to the grain it formerly produced, Davis said it could, but it would not be economically feasible because it yields less per acre. However, Davis said a movement has begun with people turning away from wheat – and dropping substantial weight. –“If three people lost eight pounds, big deal,” he said. “But we’re seeing hundreds of thousands of people losing 30, 80, 150 pounds. Diabetics become no longer diabetic; people with arthritis having dramatic relief. People losing leg swelling, acid reflux, irritable bowel syndrome, depression, and on and on every day.”–To avoid these wheat-oriented products, Davis suggests eating “real food,” such as avocados, olives, olive oil, meats, and vegetables. “(It’s) the stuff that is least likely to have been changed by agribusiness,” he said. “Certainly not grains. When I say grains, of course, over 90 percent of all grains we eat will be wheat, it’s not barley… or flax. It’s going to be wheat. –“It’s really a wheat issue.”–Some health resources, such as the Mayo Clinic, advocate a more balanced diet that does include wheat. But Davis said on “CTM” they’re just offering a poor alternative. –“All that literature says is to replace something bad, white enriched products with something less bad, whole grains, and there’s an apparent health benefit – ‘Let’s eat a whole bunch of less bad things.’ So I take…unfiltered cigarettes and replace with Salem filtered cigarettes, you should smoke the Salems. That’s the logic of nutrition, it’s a deeply flawed logic. What if I take it to the next level, and we say, ‘Let’s eliminate all grains,’ what happens then?—“That’s when you see, not improvements in health, that’s when you see transformations in health.” http://www.cbsnews.com/8301-505269_162-57505149/modern-wheat-a-perfect-chronic-poison-doctor-says/?tag=cbsnewsSectionContent.8 *********************************************************************** Nutritional Supplement Offers Promise in Treatment of Unique Form of Autism ScienceDaily (Sep. 6, 2012) — An international team of researchers, led by scientists at the University of California, San Diego and Yale University schools of medicine, have identified a form of autism with epilepsy that may potentially be treatable with a common nutritional supplement.–The findings are published in the Sept. 6, 2012 online issue of Science.–Roughly one-quarter of patients with autism also suffer from epilepsy, a brain disorder characterized by repeated seizures or convulsions over time. The causes of the epilepsy are multiple and largely unknown. Using a technique called exome sequencing, the UC San Diego and Yale scientists found that a gene mutation present in some patients with autism speeds up metabolism of certain amino acids. These patients also suffer from epileptic seizures. The discovery may help physicians diagnose this particular form of autism earlier and treat sooner.–The researchers focused on a specific type of amino acid known as branched chain amino acids or BCAAs. BCAAs are not produced naturally in the human body and must be acquired through diet. During periods of starvation, humans have evolved a means to turn off the metabolism of these amino acids. It is this ability to shut down that metabolic activity that researchers have found to be defective in some autism patients.—“It was very surprising to find mutations in a potentially treatable metabolic pathway specific for autism,” said senior author Joseph G. Gleeson, MD, professor in the UCSD Department of Neurosciences and Howard Hughes Medical Institute investigator. “What was most exciting was that the potential treatment is obvious and simple: Just give affected patients the naturally occurring amino acids their bodies lack.”—Gleeson and colleagues used the emerging technology of exome sequencing to study two closely related families that have children with autism spectrum disorder. These children also had a history of seizures or abnormal electrical brain wave activity, as well as a mutation in the gene that regulates BCAAs. In exome sequencing, researchers analyze all of the elements in the genome involved in making proteins.—In addition, the scientists examined cultured neural stem cells from these patients and found they behaved normally in the presence of BCAAs, suggesting the condition might be treatable with nutritional supplementation. They also studied a line of mice engineered with a mutation in the same gene, which showed the condition was both inducible by lowering the dietary intake of the BCAAs and reversible by raising the dietary intake. Mice treated with BCAA supplementation displayed improved neurobehavioral symptoms, reinforcing the idea that the approach could work in humans as well.–“Studying the animals was key to our discovery,” said first author Gaia Novarino, PhD, a staff scientist in Gleeson’s lab. “We found that the mice displayed a condition very similar to our patients, and also had spontaneous epileptic seizures, just like our patients. Once we found that we could treat the condition in mice, the pressing question was whether we could effectively treat our patients.”—Using a nutritional supplement purchased at a health food store at a specific dose, the scientists reported that they could correct BCAA levels in the study patients with no ill effect. The next step, said Gleeson, is to determine if the supplement helps reduce the symptoms of epilepsy and/or autism in humans.—“We think this work will establish a basis for future screening of all patients with autism and/or epilepsy for this or related genetic mutations, which could be an early predictor of the disease,” he said. “What we don’t know is how many patients with autism and/or epilepsy have mutations in this gene and could benefit from treatment, but we think it is an extremely rare condition.” Co-authors are Paul El-Fishawy, Child Study Center, Yale University School of Medicine; Hulya Kayserili, Medical Genetics Department, Istanbul University, Turkey; Nagwa A. Meguid, Rehab O. Khalil, Adel F. Hashish and Hebatalla S. Hashem, Department of Research on Children with Special Needs, National Research Centre, Cairo, Egypt; Eric M. Scott, Jana Schroth, Jennifer L. Silhavy, Neurogenetics Laboratory, Howard Hughes Medical Institute, Department of Neurosciences, UC San Diego; Majdi Kara, Pediatric Department, Tripoli Children’s Hospital, Libya; Tawfeq Ben-Omran, Clinical and Metabolic Genetics Division, Department of Pediatrics, Hamad Medical Corporation, Doha, Qatar; A. Gulhan Ercan-Sencicek, Stephan J. Sanders and Matthew W. State, Program on Neurogenetics, Child Study Center, Department of Psychiatry and Department of Genetics, Yale University School of Medicine; Abha R. Gupta, Child Study Center, Department of Pediatrics, Yale University School of Medicine; Dietrich Matern, Biochemical Genetics Laboratory, Department of Laboratory Medicine and Pathology, Mayo Clinic; Stacy Gabriel, Broad Institute of Harvard and Massachusetts Institute of Technology; Larry Sweetman, Institute of Metabolic Disease, Baylor Research Institute; Yasmeen Rahimi and Robert A. Harris, Roudebush VA Medical Center and Department of Biochemistry and Molecular Biology, Indiana University School of Medicine.–Funding for this research came, in part, from the National Institutes of Health (grants P1HD070494, R01NS048453, P30NS047101, RC2MH089956, K08MH087639, T32MH018268, U54HG003067), the Center for Inherited Disease Research, the Simons Foundation Research Initiative, Veterans Administration Merit Award, the German Research Foundation, the American Academy of Child and Adolescent Psychiatry Pilot Research Award/Elaine Schlosser Lewis Fund and the American Psychiatric Association/Lilly Research Fellowship.—Story Source-The above story is reprinted from materials provided by University of California, San Diego, via Newswise. –Journal Reference-Gaia Novarino, Paul El-Fishawy, Hulya Kayserili, Nagwa A. Meguid, Eric M. Scott, Jana Schroth, Jennifer L. Silhavy, Majdi Kara, Rehab O. Khalil, Tawfeg Ben-Omran, A. Gulhan Ercan-Sencicek, Adel F. Hashish, Stephan J. Sanders, Abha R. Gupta, Hebatalla S. Hashem, Dietrich Matern, Stacey Gabriel, Larry Sweetman, Yasmeen Rahimi, Robert A. Harris, Matthew W. State, and Joseph G. Gleeson. Mutations in BCKD-kinase Lead to a Potentially Treatable Form of Autism with Epilepsy. Science, 2012; DOI: 10.1126/science.1224631 ************************************************************************ Myocardial infarction in relation to mercury and fatty acids from fish: a risk-benefit analysis based on pooled Finnish and Swedish data in men1,2,3,4
- Maria Wennberg,
- Ulf Strömberg,
- Ingvar A Bergdahl,
- Jan-Håkan Jansson,
- Jussi Kauhanen,
- Margareta Norberg,
- Jukka T Salonen,
- Staffan Skerfving,
- Tomi-Pekka Tuomainen,
- Bengt Vessby, and
- Jyrki K Virtanen
- 1From the Departments of Public Health and Clinical Medicine, Occupational and Environmental Medicine (MW and IAB), Medicine (J-HJ), and Epidemiology and Global Health (MN), Umeå University, Umeå, Sweden; the Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden (US and SS); the Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland (JK, T-PT, and JKV); Metabolic Analytical Services Oy, Helsinki, Finland (JTS); and the Department of Public Health and Caring Science, Uppsala University, Uppsala, Sweden (BV).
- ↵2 This article reflects the views of the authors only; the European Union is not liable for any use that may be made of the information. Funding sources had no role in the study design; the collection, analysis, or interpretation of data; the writing of the report; or the decision to submit the manuscript for publication.
- ↵3 Supported by the European Union [Sixth Framework Programme: PHIME (Public Health Impact of long-term, low-level Mixed Element Exposure in susceptible population strata); grant FOOD-CT-2006-016253] and the Swedish Research Council Formas. Additional support was provided by the Academy of Finland (grant 121206; to JKV), the Foundation of Medical Research in Skellefteå, and the Research Unit, Department of Medicine, Skellefteå Hospital.
- ↵4 Address reprint requests and correspondence to M Wennberg, Occupational and Environmental Medicine, Umeå University, 901 87 Umeå, Sweden. E-mail: [email protected].
Abstract Background: Exposure to methylmercury from fish has been associated with increased risk of myocardial infarction (MI) in some studies. At the same time, marine n−3 (omega-3) PUFAs[U1] are an inherent constituent of fish and are regarded as beneficial. To our knowledge, no risk-benefit model on the basis of data on methylmercury, PUFA, and MI risk has yet been presented. Objective: The objective of this study was to describe how exposure to both marine n−3 PUFAs and methylmercury relates to MI risk by using data from Finland and Sweden. Design: We used matched case-control sets from Sweden and Finland that were nested in population-based, prospective cohort studies. We included 361 men with MI from Sweden and 211 men with MI from Finland. MI risk was estimated in a logistic regression model with the amount of mercury in hair (hair-Hg) and concentrations of n−3 PUFAs (EPA and DHA) in serum (S-PUFA) as independent variables. Results: The median hair-Hg was 0.57 μg/g in Swedish and 1.32 μg/g in Finnish control subjects, whereas the percentage of S-PUFA was 4.21% and 3.83%, respectively. In combined analysis, hair-Hg was associated with higher (P = 0.005) and S-PUFA with lower (P = 0.011) MI risk. Our model indicated that even a small change in fish consumption (ie, by increasing S-PUFA by 1%) would prevent 7% of MIs, despite a small increase in mercury exposure. However, at a high hair-Hg, the modeled beneficial effect of PUFA on MI risk was counteracted by methylmercury. [U2] Conclusions: Exposure to methylmercury was associated with increased risk of MI, and higher [U3] S-PUFA concentrations were associated with decreased risk of MI. Thus, MI risk may be reduced by the consumption of fish high in PUFAs and low in methylmercury. [U4] ********************************************************************** Supplement Your Stem Cells—how to look at this study ScienceDaily (Apr. 7, 2010) — A nutritional supplement could stimulate the production of stem cells integral for repairing the body. Research published in BioMed Central’s open access Journal of Translational Medicine suggests that a commercially-available supplement can increase the blood circulation of hematopoietic stem cells, which can give rise to all blood cells, and endothelial progenitor cells, which repair damage to blood vessels.—Thomas E. Ichim from Medistem Incorporated, USA worked with a team of 13 researchers from industry and academia to further investigate whether this supplement, containing a cocktail of green tea, astralagus, goji berry extracts, ‘good’ bacteria Lactobacillus fermentum, antioxidant ellagic acid, immune enhancer beta 1,3 glucan and vitamin D3, was able to increase the number of stem cells circulating in the blood. They recruited 18 healthy adults aged between 20 and 72 who stopped any other dietary supplements 4-5 days [U5] before starting a two-week course of this supplement, taking it twice daily. The researchers took blood from the participants before they started the course and on days 1, 2, 7 and 14 to test for signs of stem cell activity by looking for cells expressing the genetic stem cell markers CD133, CD34 and KDR. They then confirmed whether taking the supplement changed the overall levels of hematopoietic stem cells and endothelial progenitor cells in the blood by using HALO (Hematopoietic Assay via Luminescent Output) and colony forming assays respectively.—Hematopoietic stem cells and endothelial progenitor cells increased after taking the nutritional supplement, suggesting that the supplement may be a useful stimulator for both types of stem cells. In this study, the levels of these stem cells peaked at 2-7 days and started to drop at 14 days, suggesting that this supplement could be used for continuous treatment for conditions associated with decreases in these stem cells such as Alzheimer’s Disease. Other therapeutic treatments used to recruit hematopoietic stem cells are not viable as long-term solutions due to costs and increased health risks caused by the extremely high levels of stem cells that these treatments maintain in the blood.—“To our knowledge, this is the first study demonstrating profound mobilization effect with possible clinical significance by a food supplement-based approach,” say the authors, adding, “Indeed it may be possible that our supplement could be beneficial in conditions associated with reduced progenitor cells such as diabetes or in smokers which possess lower baseline values as compared to controls.” Although they are quick to add, “However, given commercial pressures associated with this largely unregulated field, we propose detailed scientific investigations must be made before disease-associated claims are made by the scientific community.”–Story Source-The above story is reprinted from materials provided by BioMed Central, via EurekAlert!, a service of AAAS. –Journal Reference-Nina A Mikirova, James A Jackson, Ron Hunninghake, Julian Kenyon, Kyle WH Chan, Cathy A Swindlehurst, Boris Minev, Amit N Patel, Michael P Murphy, Leonard Smith, Famela Ramos, Doru T Alexandrescu, Thomas E Ichim and Neil H Riordan. Nutraceutical augmentation of circulating endothelial progenitor cells and hematopoietic stem cells in human subjects. Journal of Translational Medicine, (in press) [link]