Welcome To Tony Pantalleresco Radio Show notes – November 8th 2014
As usual Tony has been very busy putting together some amazing information on health and welness
Topics in this show:
Niacin and Schizophrenia– History and Opportunity
Healing the Kidneys with Sodium Bicarbonate (Baking Soda)
Effects of poor eating habits persist even after diet is improved
Alzheimer’s Disease and Parkinson’s Disease. A Dietary Connection
Biological fat with a sugar attached essential to maintaining brain’s supply of stem cells
Niacin and Schizophrenia– History and Opportunity
by Nick Fortino, PhD Candidate
(OMNS Oct 27, 2014) Schizophrenia is usually treated with prescription antipsychotic drugs, many of which produce severe adverse effects (1-6); are linked to an incentive for monetary profit benefiting pharmaceutical corporations (7-13); lack sufficient evidence for safety and efficacy (9, 14); and have been grossly misused (15-20). Orthomolecular (nutritional) medicine provides another approach to treating schizophrenia, which involves the optimal doses of vitamin B3-also known as niacin, niacinamide, nicotinamide, or nicotinic acid-in conjunction with an individualized protocol of multiple vitamins. The orthomolecular approach involves treating “mental disease by the provision of the optimum molecular environment for the mind, especially the optimum concentrations of substances normally present in the human body” (21).
Evidence for the Niacin Treatment of Schizophrenia
Vitamin B3 as a treatment for schizophrenia is typically overlooked, which is disconcerting considering that historical evidence suggests it effectively reduces symptoms of schizophrenia, and has the added advantage, in contrast to pharmaceuticals, of mild to no adverse effects (22-35). After successful preliminary trials treating schizophrenia patients with niacin, pilot trials of larger samples commenced in 1952-reported in 1957 by Hoffer, Osmond, Callbeck, and Kahan. Dr. Abram Hoffer began an experiment involving 30 patients who had been diagnosed with acute schizophrenia. Participants were given a series of physiological and psychological tests to measure baseline status and were subsequently assigned randomly to treatment groups. Nine subjects received a placebo, 10 received nicotinic acid, and 11 received nicotinamide (the latter two are forms of vitamin B3). All participants received treatment for 42 days, were in the same hospital, and received psychotherapy from the same group of clinicians. The two experimental groups were administered three grams of vitamin B3 per day. Each of the three treatment groups improved, but the two vitamin B3 groups improved more than the placebo group as compared to baseline measures. At one year follow up, 33% of patients in the placebo group remained well, and 88% of patients in the B3 groups remained well. These results inspired many subsequent trials, and those that replicated the original method produced similarly positive results.
That schizophrenia may be caused or aggravated by a deficiency of essential nutrients appears to have eluded the majority of the health care providers serving the schizophrenic population, as evidenced by the fact that “antipsychotic medications represent the cornerstone of pharmacological treatment for patients with schizophrenia” (36). Waves of different antipsychotic drugs have been developed throughout the last 60 years, which have not decreased the prevalence of schizophrenia; in fact it has increased (15, 37).–Although dangerous when taken in high doses and for a long period of time, the value of antipsychotics appears to be that in the short term they can help to bring some control to schizophrenic symptoms, not by curing the condition but by inducing a neurological effect that is qualitatively different from the schizophrenic state. Dr. Hoffer acknowledged their value and in his private practice he would introduce antipsychotics and vitamins simultaneously because antipsychotics work rapidly and vitamins work more slowly, so a person could benefit from the short term relief from symptoms that antipsychotics provide while the vitamins slowly, but surely, healed the deficiency causing the schizophrenic symptoms. This also allowed for a much easier process of tapering from the drugs.
“For schizophrenia, the recovery rate with drug therapy is under 15%. With nutritional therapy, the recovery rate is 80%.” – Abram Hoffer, MD, PhD
More Research Needed
Further research into the orthomolecular treatment of schizophrenia is imperative. Saha, Chant, and McGrath (38) found that mortality rates in schizophrenia have increased in recent decades and warned, “in light of the potential for second-generation antipsychotic medications to further adversely influence mortality rates in the decades to come, optimizing the general health of people with schizophrenia warrants urgent attention.” The orthomolecular approach may be, at least, an integral part of a treatment program that optimizes general health and leads to a life free from schizophrenic symptoms.–Questions abound regarding individuals’ experiences while on these different treatments. Particularly the psychological and relational, or, intrapersonal and interpersonal experience while on antipsychotics versus an orthomolecular treatment must be more thoroughly documented because it is in this domain that a person ascertains his/her quality of life. And only the person who has these experiences can provide such an account; no psychiatrist peering in from outside a one-way mirror on a person hearing voices, nor any brain image, nor any valid and reliable measure can ever reflect the person’s living qualitative experience as accurately as the person can[F1] . This is why I have designed a multiple case study to explore in depth the experiences of individuals successfully treating their schizophrenia using orthomolecular medicine. The central research question is: What is the experience of individuals with schizophrenia who switched from using antipsychotics to orthomolecular medicine to treat their condition?
A Call for Participants
Inclusion criteria for this study are: over age 18, diagnosed as having schizophrenia, treated for a period of time primarily with antipsychotics, and are currently treated by or were cured by an orthomolecular protocol. Participation will consist of three interviews with the researcher (in person or online video conference), each of which will focus on a distinct period: symptomatic but unmedicated, primarily using antipsychotic drugs, and primarily using orthomolecular medicine. The researcher will also request one interview with the orthomolecular practitioner if possible, the diagnosing psychiatrist if possible, and at least two close friends and/or family members about their experiences of relating with the primary participant during these different periods. Anonymity is guaranteed if requested.–I am a Psychology Ph.D. student and this is my dissertation study. I never had the privilege of meeting Dr. Hoffer, but his spirit, conviction, and massive production of great work have inspired my writing this dissertation. Toward that latter part of his career, he commented on the nature of schizophrenia treatment research:
Case histories have disappeared from journal articles, as if living patients no longer existed or counted for very much. Instead, authors describe their methods, describe what criteria they used in selecting their groups of patients which were used in their prospective double blind controlled studies, and provide ample charts and statistics. I have read many papers where it is impossible to get any feeling for a single patient. (29)[F2]
This dissertation attempts to address this deficit of qualitative data. The narrative accounts that multiple case studies yield are invaluable, and can be accessible and relatable for people in a position of gathering information about schizophrenia treatments for themselves or a loved one. This dissertation is not an attempt to prove the legitimacy of the orthomolecular treatment; Dr. Hoffer and others have dedicated their professional lives to that endeavor. This is meant to explore the experience of the treatment, especially as it compares to the experience of the antipsychotic treatment. I am recruiting from a very small population of people, so I ask you to consider participating if you fit the criteria, or pass this invitation along to someone you know who fits the criteria. I can be reached by phone (408) 840-1253 or email (email@example.com) to answer questions and/or to begin the research process.
1. Arana, G. W. (2000). An overview of side effects caused by typical antipsychotics. Journal of Clinical Psychiatry, 61(8), 5-11. http://www.ncbi.nlm.nih.gov/pubmed/10811237.
2. Ciranni, M. A., Kearney, T. E., & Olson, K. R. (2009). Comparing acute toxicity of first- and second-generation antipsychotic drugs: A 10-year, retrospective cohort study. The Journal of Clinical Psychiatry, 70(1), 122-129. http://www.ncbi.nlm.nih.gov/pubmed/19192473
3. Ho, B. C., Andreasen, N. C., Ziebell, S., Pierson, R., & Magnotta, V. (2011). Long-term antipsychotic treatment and brain volumes: A longitudinal study of first-episode schizophrenia. Archives of General Psychiatry, 68(2), 128. http://www.ncbi.nlm.nih.gov/pubmed/21300943
4. Pope, H. G., Keck, P. E., & McElroy, S. L. (1986). Frequency and presentation of neuroleptic malignant syndrome in a large psychiatric hospital. The American Journal of Psychiatry, 143(10), 1227-1233. http://www.ncbi.nlm.nih.gov/pubmed/2876647
5. Saddichha, S., Manjunatha, N., Ameen, S., & Akhtar, S. (2008). Diabetes and schizophrenia-effect of disease or drug? Results from a randomized, double blind, controlled prospective study in first-episode schizophrenia. Acta Psychiatrica Scandinavica, 117, 342-347. http://www.ncbi.nlm.nih.gov/pubmed/18307585
6. Woods, S. W., Morgenstern, H., Saksa, J. R., Walsh, B. C., Sullivan, M. C., Money, R., Hawkins, K. A., Gueorguieva, R. V., & Glazer, W. M. (2010). Incidence of tardive dyskinesia with atypical and conventional antipsychotic medications: Prospective cohort study. The Journal of Clinical Psychiatry, 71(4), 463-475. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109728/
7. Angell, M. (2004). The truth about the drug companies: How they deceive us and what to do about it. New York, N.Y.: Random House LLC.
8. Berenson, A. (2007, January 05). Lilly settles with 18,000 over zyprexa. The New York Times, pp. 1-2. Retrieved from http://www.nytimes.com/2007/01/05/business/05drug.html?_r=0
9. Kendall, T. (2011). The rise and fall of atypical antipsychotics. The British Journal of Psychiatry, 199(4), 266-268. doi:10.1192/bjp.bp.110.083766 http://www.ncbi.nlm.nih.gov/pubmed/22187726
10. Moynihan, R., & Alan, C. (2005). Selling sickness: How the world’s biggest pharmaceutical companies are turning us all into patients. New York, N.Y.: Nation Books.
11. Moynihan, R., Heath, I., & Henry, D. (2002). Selling sickness: the pharmaceutical industry and disease mongering. British Medical Journal, 324(7342), 886. http://www.ncbi.nlm.nih.gov/pubmed/11950740
12. Scherer, F. M. (1993). Pricing, profits, and technological progress in the pharmaceutical industry. The Journal of Economic Perspectives, 7(3), 97-115. https://www.aeaweb.org/articles.php?doi=10.1257/jep.7.3.97
13. Spielmans, G. I., & Parry, P. I. (2009). From evidence-based medicine to marketing-based medicine: Evidence from internal industry documents. Journal of Bioethical Inquiry, 7(1), 13-29. doi:10.1007/s11673-010-9208-8 http://link.springer.com/article/10.1007%2Fs11673-010-9208-8#page-1
14. Lieberman, J. A., Stroup, T. S., McEvoy, J. P., Swartz, M. S., Rosenback, R. A., Perkins, D. O., Keefe, R. S. E., Davis, S. M., Davis, C. E., Lebowitz, B. D., Severe, J., Hsiao, J. K. (2005). Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. The New England Journal of Medicine, 353(12), 1209-1223. http://www.ncbi.nlm.nih.gov/pubmed/17335312
15. Whitaker, R. (2010). Anatomy of an epidemic: Magic bullets, psychiatric drugs, and the astonishing rise of mental illness in America. New York, N.Y.: Crown Publishers.
16. Kuehn, B. M. (2010). Questionable antipsychotic prescribing remains common, despite serious risks. Journal of the American Medical Association, 303(16), 1582-1584. http://www.ncbi.nlm.nih.gov/pubmed/20424239
17. Moran, M. (2011). Misuse of antipsychotics widespread in nursing homes. Psychiatric News, 46(11), 2. http://psychnews.psychiatryonline.org/newsarticle.aspx?articleid=108671
18. Ray, W. A., Federspiel, C. F., & Schaffner, W. (1980). A study of antipsychotic drug use in nursing homes: Epidemiologic evidence suggesting misuse. American Journal of Public Health, 70(5), 485-491. http://www.ncbi.nlm.nih.gov/pubmed/6103676
19. Stevenson, D. G., Decker, S. L., Dwyer, L. L., Huskamp, H. A., Grabowski, D. C., Metzger, E. D., & Mitchell, S. L. (2010). Antipsychotic and benzodiazepine use among nursing home residents: Findings from the 2004 National Nursing Home Survey. The American journal of Geriatric Psychiatry: Official Journal of the American Association for Geriatric Psychiatry, 18(12), 1078-1092. http://www.ncbi.nlm.nih.gov/pubmed/20808119
20. Szaz, T. (1974). The myth of mental illness: Foundations of a theory of personal conduct. New York, N.Y.: Harper Perennial.
21. Pauling, L. (1968). Orthomolecular psychiatry. Varying the concentrations of substances normally present in the human body may control mental disease. Orthomolecular psychiatry. Science, 160, 265-271. http://www.ncbi.nlm.nih.gov/pubmed/5641253
22. Cleckley, H. M., Sydenstricker, V. P., & Geeslin, L. E. (1939). Nicotinic acid in the treatment of atypical psychotic states. The Journal of the American Medical Association, 112(21), 2107-2110. http://jama.jamanetwork.com/article.aspx?articleid=288714
23. Hoffer, A. (1962). Niacin Therapy in Psychiatry. Springfield, Il: C. C. Thomas.
24. Hoffer, A. (1963). Nicotinic acid: An adjunct in the treatment of schizophrenia. American Journal of Psychiatry, 120, 171-173. http://www.ncbi.nlm.nih.gov/pubmed/13963912
25. Hoffer, A. (1966). The effect of nicotinic acid on the frequency and duration of re-hospitalization of schizophrenic patients: A controlled comparison study. International Journal of Neuropsychiatry, 2(3), 234-240. http://www.ncbi.nlm.nih.gov/pubmed/4225426
26. Hoffer, A. (1970a). Childhood schizophrenia: A case treated with nicotinic acid and nicotinamide. Schizophrenia, 2, 43-53. http://orthomolecular.org/library/jom/1970/pdf/1970-v02n01-p043.pdf
27. Hoffer, A. (1973). A neurological form of schizophrenia. Canadian Medical Association Journal, 108, 186-194. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1941147/
28. Hoffer, A. (1994). Chronic schizophrenic patients treated ten years or more. Journal of Orthomolecular Medicine, 9(1), 7-37. http://orthomolecular.org/library/jom/1994/pdf/1994-v09n01-p007.pdf
29. Hoffer, A. (1996). Inside schizophrenia: Before and after treatment. Journal of Orthomolecular Medicine, 11(1), 45-48. http://orthomolecular.org/library/jom/1996/pdf/1996-v11n01-p045.pdf
30. Hoffer, A. & Fuller, F. (2009). Orthomolecular treatment of schizophrenia. Journal of Orthomolecular Medicine, 24(3,4), 151-159. http://orthomolecular.org/library/jom/2009/pdf/2009-v24n01-p009.pdf
31. Hoffer, A., & Osmond, H. (1964). Treatment of schizophrenia with nicotinic acid: A ten year follow up. Acta Psychiatrica Scandinavica, 40, 171-189. doi:10.1111/j.1600-0447.1964.tb05744.x http://www.ncbi.nlm.nih.gov/pubmed/14235254.
32. Hoffer, A., & Osmond, H. (1980). Schizophrenia: Another long term follow-up in Canada. Orthomolecular Psychiatry, 9(2), 107-113. http://psycnet.apa.org/psycinfo/1981-13316-001
33. Hoffer, A., Osmond, H., Callbeck, M. J., & Kahan, I. (1957). Treatment of schizophrenia with nicotinic acid and nicotinamide. Journal of Clinical and Experimental Psychopathology, 18(2), 131-157. http://www.ncbi.nlm.nih.gov/pubmed/13439009
34. Tung-Yep, T. (1981). The use of orthomolecular therapy in the control of schizophrenia-a study preview. The Australian Journal of Clinical Hypnotherapy, 2(2), 111-116. http://schizophreniabulletin.oxfordjournals.org/content/12/1/141.full.pdf
35. Verzosa, P. L. (1976). A report on a twelve-month period of treating metabolic diseases using mainly vitamins and minerals on the schizophrenias. Orthomolecular Psychiatry, 5(4), 253-260. http://www.orthomolecular.org/library/jom/1976/pdf/1976-v05n04-p253.pdf
36. Gilmer, T. P., Dolder, C. R., Lacro, J. P., Folsom, D. P., Lindamer, L., Garcia, P., & Jeste, D. V. (2004). Adherence to treatment with antipsychotic medication and health care costs among Medicaid beneficiaries with schizophrenia. American Journal of Psychiatry, 161(4), 692-699. http://www.ncbi.nlm.nih.gov/pubmed/15056516
37. McGrath, J., Saha, S., Chant, D., & Welham, J. (2008). Schizophrenia: A concise overview of incidence, prevalence, and mortality. Epidemiologic Reviews, 30, 67-76. http://www.ncbi.nlm.nih.gov/pubmed/18480098.
38. Saha, S., Chant, D., & McGrath, J. (2007). A systematic review of mortality in schizophrenia. Archives of General Psychiatry, 64(10), 1123-1131. http://www.ncbi.nlm.nih.gov/pubmed/17909124
Healing the Kidneys with Sodium Bicarbonate (Baking Soda)
Posted by Dr Sircus on November 11, 2009 | Filed under Medicine, Sodium Bicarbonate (Baking Soda)
Sodium bicarbonate is not only an excellent agent for natural chemotherapy, bringing as it does higher O2 levels through increased alkalinity to the cells, it is also one of the most basic medicines we have for kidney disease. New research by British scientists at the Royal London Hospital shows that sodium bicarbonate can dramatically slow the progress of chronic kidney disease. We don’t need a thousand years of tests to understand something as simple as water and it is quite the same with bicarbonate, which is always present in the best drinking waters. Bicarbonate acts to stimulate the ATPase by acting directly on it. -The simple household product used for baking, cleaning, bee stings, treating asthma, cancer and acid indigestion is so effective in treating kidney disease that it prevents patients from having to be put on kidney machines. The findings have been published in the Journal of the American Society of Nephrology. Bicarbonate is a truly strong universal concentrated nutritional medicine that works effectively in many clinical situations that we would not normally think of. It is a prime emergency room and intensive care medicine that can save a person’s life in a heartbeat and it is also a supermarket item that you can take right off the shelf and use for more things than one can imagine – including diaper rash. -Dr. SK Hariachar, a nephrologist who oversees the Renal Hypertension Unit in Tampa Florida stated, upon seeing the research on bicarbonate and kidney disease, ”I am glad to see confirmation of what we have known for so long. I have been treating my patients with bicarbonate for many years in attempts to delay the need for dialysis, and now we finally have a legitimate study to back us up. Not only that, we have the added information that some people already on dialysis can reverse their condition with the use of sodium bicarbonate”. -John, a dialysis technician at the same center as Dr. Hariachar, who used to be on dialysis himself for 2 years as a result of kidney failure, had his kidneys miraculously start functioning to the point where dialysis was no longer needed. He states that he was prescribed oral doses of sodium bicarbonate throughout his treatment, and still takes it daily to prevent recurrences of kidney failure. Dr. Hariachar maintains though, that not everyone will be helped by taking bicarbonate. He says that those patients who have difficulty excreting acids, even with dialysis using a bicarbonate dialysate bath, that, “oral bicarbonate makes all the difference.”
Kidneys Produce Bicarbonate
The exocrine section of the pancreas has been greatly ignored in the treatment of diabetes even though its impairment is a well documented condition. The pancreas is primarily responsible for the production of enzymes and bicarbonate necessary for normal digestion of food. Bicarbonate is so important for protecting the kidneys that even the kidneys get into the act of producing bicarbonate and now we know the common denominator between diabetes and kidney disease. When the body is hit with reductions in bicarbonate output by these two organs,’ acid conditions build and then entire body physiology begins to go south. Likewise when acid buildup outstrips these organs normal bicarbonate capacity cellular deterioration begins.-The kidneys alone produce about two hundred and fifty grams (about half a pound) of bicarbonate per day in an attempt to neutralize acid in the body. -The kidneys monitor and control the acidity or “acid-base” (pH) balance of the blood. If the blood is too acidic, the kidney makes bicarbonate to restore the bloods pH balance. If the blood is too alkaline, then the kidney excretes bicarbonate into the urine to restore the balance. Acid-base balance is the net result of two processes, first, the removal of bicarbonate subsequent to hydrogen ion production from the metabolism of dietary constituents; second, the synthesis of “new” bicarbonate by the kidney. -It is considered that normal adults eating ordinary Western diets have chronic, low-grade acidosis which increases with age. This excess acid, or acidosis, is considered to contribute to many diseases and to contribute to the aging process. Acidosis occurs often when the body cannot produce enough bicarbonate ions (or other alkaline compounds) to neutralize the acids in the body formed from metabolism and drinking highly acid drinks like Coke, Pepsi and we are even seeing reports on bottled mineral water being way too acidic.-Acid-buffering by means of base supplementation is one of the major roles of dialysis. Bicarbonate concentration in the dialysate (solution containing water and chemicals (electrolytes) that passes through the artificial kidney to remove excess fluids and wastes from the blood, also called “bath.”) should be personalized in order to reach a midweek pre-dialysis serum bicarbonate concentration of 22 mmol/l. Use of sodium bicarbonate in dialysate has been shown in studies to better control some metabolic aspects and to improve both treatment tolerance and patients’ life quality. Bicarbonate dialysis, unlike acetate-free biofiltration, triggers mediators of inflammation and apoptosis.-One of the main reasons we become acid is from over-consumption of protein. Eating meat and dairy products may increase the risk of prostate cancer, research suggests. We would find the same for breast and other cancers as well. Conversely mineral deficiencies are another reason and when you combine high protein intake with decreasing intake of minerals you have a disease in the making through lowering of pH into highly acidic conditions. When protein breaks down in our bodies they break into strong acids.-Unless a treatment actually removes acid toxins from the body and increases oxygen, water, and nutrients most medical interventions come to naught.-These acids must be excreted by the kidneys because they contain sulfur, phosphorus or nitrogen which cannot break down into water and carbon dioxide to be eliminated as the weak acids are. In their passage through the kidneys these strong acids must take a basic mineral with them because in this way they are converted into their neutral salts and don’t burn the kidneys on their way out. This would happen if these acids were excreted in their free acid form.-Substituting a sodium bicarbonate solution for saline infusion prior to administration of radiocontrast material seems to reduce the incidence of nephropathy. – Dr. Thomas P. Kennedy
American Medical Association
Bicarbonate ions neutralize the acid conditions required for chronic inflammatory reactions. Hence, sodium bicarbonate is of benefit in the treatment of a range of chronic inflammatory and autoimmune diseases. Sodium bicarbonate is a well studied and used medicine with known effects. Sodium bicarbonate is effective in treating poisonings or overdoses from many chemicals and pharmaceutical drugs by negating their cardiotoxic and neurotoxic effects. It is the main reason it is used by orthodox oncology – to mitigate the highly toxic effects of chemotherapy.-Sodium bicarbonate possesses the property of absorbing heavy metals, dioxins and furans. Comparison of cancer tissue with healthy tissue from the same person shows that the cancer tissue has a much higher concentration of toxic chemicals, pesticides, etc.-Sodium bicarbonate injection is indicated in the treatment of metabolic acidosis, which may occur in severe renal disease, uncontrolled diabetes, and circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. The acid/alkaline balance is one of the most overlooked aspects of medicine. In general, the American public is heavily acid, excepting vegetarians, and even their bodies have to face increasing levels of toxic exposure, which help turn the body to acidic pH conditions.-For more detailed information feel free to consult my book Sodium Bicarbonate E-Book that’s with a reasonable price, or for a more personal approach check my Consultations page.
 Origin of the Bicarbonate Stimulation of Torpedo Electric Organ Synaptic Vesicle ATPase. Joan E. Rothlein 1 Stanley M. Parsons. Department of Chemistry and the Marine Science Institute, University of California, Santa Barbara, Santa Barbara, California, U.S.A.
 Levine DZ, Jacobson HR: The regulation of renal acid secretion: New observations from studies of distal nephron segments. Kidney Int 29:1099–1109, 1986
 JAMA 2004;291:2328-2334,2376-2377.
 These include, Benzotropines (valium) cyclic antidepressants (amytriptayine), organophosphates, methanol (Methyl alcohol is a cheap and potent adulterant of illicit liquors) Diphenhydramine (Benedryl), Beta blockers (propanalol) Barbiturates, and Salicylates (Aspirin). Poisoning by drugs that block voltage-gated sodium channels produces intraventricular conduction defects, myocardial depression, bradycardia, and ventricular arrhythmias. Human and animal reports suggest that hypertonic sodium bicarbonate may be effective therapy for numerous agents possessing sodium channel blocking properties, including cocaine, quinidine, procainamide, flecainide, mexiletine, bupivacaine, and others.
Effects of poor eating habits persist even after diet is improved
Date-November 3, 2014
Source-Federation of American Societies for Experimental Biology
Almost everyone knows that improving your eating habits will most likely improve your health. What most people may not know, however, is that the effects of poor eating habits persist long after dietary habits are improved. In a new report appearing in the November 2014 issue of the Journal of Leukocyte Biology, scientists use mice to show that even after successful treatment of atherosclerosis (including lowering of blood cholesterol and a change in dietary habits) the effects of an unhealthy lifestyle still affect the way the immune system functions. This change in function occurs largely because poor eating habits alter the way genes express themselves, including genes related to immunity. This change in gene expression (epigenetics) ultimately keeps the risk of cardiovascular disorders higher than it would be had there been no exposure to unhealthy foods in the first place.–“I hope that this study demonstrates the importance of diet-induced changes in the epigenome and encourages further research into the interaction between dietary patterns, DNA methylation and disease,” said Erik van Kampen, a researcher involved in the work from the Division of Biopharmaceutics at the Leiden Academic Centre for Drug Research at Leiden University in Leiden, The Netherlands.–To make their discovery, scientists used two groups of mice that had an altered gene making them more susceptible to developing high blood cholesterol and atherosclerosis. These mice were either fed a high-fat, high-cholesterol diet (Western-type diet, WTD) or a normal diet (chow). After a long period of feeding, bone marrow was isolated from the mice and transplanted into mice with a similar genetic background that had their own bone marrow destroyed. The recipient mice were left on chow diet for several months, after which the development of atherosclerosis in the heart was measured. The number and status of immune cells throughout the body and epigenetic markings on the DNA in the bone marrow also were examined. They found that DNA methylation, an epigenetic signature, in the bone marrow was different in mice that received bone marrow from the WTD-fed donors compared to the mice receiving bone marrow from chow-fed donors. Furthermore, these mice had large differences in their immune system and increased atherosclerosis.–“We’ve long known that lifestyle and nutrition could affect immune system function,” said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. “The ability of nutritional history to have durable affects on immune cells demonstrated in this new report could have profound implications for treatment of diseases with immune underpinnings. The length of such effects will be critical to determine and it will be interesting to examine the effects of drugs that can modify epigenetics.”–Story Source-The above story is based on materials provided by Federation of American Societies for Experimental Biology. Note: Materials may be edited for content and length.—Journal Reference-E. van Kampen, A. Jaminon, T. J. C. van Berkel, M. Van Eck. Diet-induced (epigenetic) changes in bone marrow augment atherosclerosis. Journal of Leukocyte Biology, 2014; 96 (5): 833 DOI: 10.1189/jlb.1A0114-017R
Alzheimer’s Disease and Parkinson’s Disease. A Dietary Connection
By Fred Kummerow, Ph.D.
For the past 70 years I have been researching lipids (fats) and their relationship to heart disease. I found that patients who ate an overabundance of deep fat fried foods and too much polyunsaturated fatty acids (PUFAs) produced a chemical change in the composition of their arteries. –When I analyzed the blood of these patients I found that their arteries had an increase of calcification. If these patients continue to eat these oxidized fats, the calcification will completely block their arteries. Heart disease can be prevented if these foods are not consumed. —-The oils generally used in deep fat frying, like soybean oil (and other vegetable oils) are readily oxidized because they contain linoleic and linolenic acids. These acids are easily oxidized. Prolonged exposure to air causes them to pick up oxygen and become oxidized. Repeated use just creates more oxidation.—In my laboratory we have fed weanling rats oils that had been heated at various temperatures. The rats that were fed the high temperature fats (365°F / 180°C) had lower growth rates than the rats that were fed lower temperature fats. Any foods that have been deep fried should be avoided, including potato chips and fried food from fast-food restaurants. Oils that are high in linoleic acid and linolenic acid should be avoided. —-The current research is on Alzheimer’s disease (AD) and Parkinson’s disease (PD.—AD is the most common cause of dementia. During the course of the disease, the chemistry and structure of the brain changes, leading to the death of brain cells. The challenges in AD research today include discovering methods to diagnose patients in an earlier stage and to find new treatments to prevent or cure the disease.–The brain is 81% lipids and over half of these lipids are phospholipids (fatlike, phosphorus-containing substances). PUFAs, which are easily oxidized (combined with oxygen), attach to the phospholipid molecule creating oxidative stress. The damaging consequences of oxidative stress have been implicated in a variety of very different human disorders including arteriosclerosis and diseases of the nervous system. Oxidative stress is an important pathogenic factor in AD. –I believe, just like heart disease patients, people with AD are eating too many polyunsaturated fatty acids (PUFAs) and deep fried foods. The American Heart Association and the National Institute of Health have recommended increasing PUFA consumption and decreasing saturated fat intake. Doing this increases free radicals when it is not offset with enough antioxidant rich fruits and vegetables. —Free radical damage accumulates with age. They may cause cells to function poorly or even die. When free radicals overwhelm the body’s ability to regulate them, oxidative stress occurs. An excess of oxidative stress can lead to the oxidation of lipids and proteins.
The research on preventing heart disease can also be used to prevent brain diseases. Tissue from the brain of someone who had AD is receptive to dyes that do not stain normal tissue suggesting that a chemical change occurred. –I suspect this chemical change occurs during oxidation of PUFAs. Discoverying that PUFAs are easily oxidized in the arterial cells and this could also be a factor in brain cells. The fact that AD is steadily increasing is alerting to the fact that –there is something wrong in the diet of these patients. –The Idea that AD and PD can be alleviated by monitoring the diets of patients with these diseases. A recent study at UCLA has shown that cognitive decline can be reversed by controlling the diet.–Patients eliminated simple carbohydrates and processed food from their diets. They increased their consumption of vegetables and fruits and limited their consumption of fish to non-farmed. The patients increased their sleep to almost 8 hours nightly, exercised 4-5 times per week and reduced their stress with meditation and relaxation.[F3] These patients also fasted three hours between meals and 12 hours between dinner and breakfast[F4] . The personalized therapeutic program was used based on the underlying pathogenesis of AD. Nine out of ten showed improvement and improvements have been sustained after two and one half years. This shows that more extensive therapeutic trials are needed. –The aim of my research is to find a way to prevent AD by analyzing the lipid plasma for two oxysterols. These two oxysterols were present in the plasma of the patients who needed bypass operations and are present in the food supply as frying fats and powdered egg yolk. My hypothesis is based on my studies of preventing calcification of the coronary arteries. I want to show that these two components are in the blood of patients with AD. — Controlling the amount of oxidation and consuming a healthy balanced diet the body can rid itself of the oxidized polyunsaturated fat. If this is the cause of Alzheimer’s disease, proper nutrition will end this terrible disease.[F5] –The diet plan that I would suggest would be to eat three balanced meals a day. Including 3 serving of protein, 5 -8 servings of fruits and vegetables, 3 servings of whole dairy products, at least one egg daily and eliminating simple carbohydrates and processed foods. Adequate amounts of sleep and exercise would also be encouraged. I then hope to continue this research with Parkinson’s disease patients. –.
Fred A. Kummerow, Ph.D.
Adjunct professor in biochemistry at the University of Illinois
Biological fat with a sugar attached essential to maintaining brain’s supply of stem cells
Date-November 3, 2014
Source-Medical College of Georgia at Georgia Regents University
Dr. Robert Yu, MCG neuroscientist and corresponding author of the study in The Journal of Neuroscience and Dr. Jing Wang, MCG postdoctoral fellow and the study’s first author.
Fat and sugar aren’t usually considered healthy staples, but scientists have found that a biological fat with a sugar attached is essential for maintaining the brain’s store of stem cells.–Neural stem cells help the brain develop initially, then repopulate brain cells lost to usual cell turnover as well as to a trauma or malady, such as a head injury or stroke.–While the cell population and activity decrease as a natural part of aging, scientists at the Medical College of Georgia at Georgia Regents University are studying how neural stem cells are normally maintained with the long-term goal of helping the supply stay robust despite aging as well as infirmity.–They have discovered that in mice missing the sugar containing lipid ganglioside GD3, neural stem cells have a dramatically impaired ability to self-renew, said Dr. Robert K. Yu, MCG neuroscientist and corresponding author of the study in The Journal of Neuroscience.–The scientists focused on brain areas with typically the largest supply of neural stem cells: an area just below several midbrain cavities filled with cerebrospinal fluid, called the subventricular zone, as well as the hippocampus, a major center for learning and memory.–Mice missing ganglioside GD3 on the membranes of neural stem cells had much smaller supplies of the cells in these key areas throughout life and expressed signs of lost hope with behaviors such as not actively seeking dry land when placed in water, Yu said. Additionally, the mice had impaired maintenance of the area of the brain involved in the sense of smell as well as the portion of the hippocampus that enables formation of new memories.–The changes, which correlate with aging or illness, were corrected when GD3 was restored.–“If GD3 is missing, we found these neural stem cells cannot be maintained throughout life; they are reduced by a big percentage even in a one-month-old mouse,” said Dr. Jing Wang, MCG postdoctoral fellow and the study’s first author. In fact, by one month of life, there was about a 60 percent reduction in the supply and by six months, which is considered aged in a mouse, there were only a handful of neural stem cells remaining, Wang said.–The scientists note that in healthy young mice, GD3 is abundant but seems to naturally decrease with age.–A Yu and Wang paper published in the journal PNAS in 2013 showed that GD3 is the predominant ganglioside in mouse neural stem cells where it interacts with epidermal growth factor receptors, also found on the cell surface. GD3 plays an important role in growth factor signaling, which, in turn, tells neural stem cells to proliferate or die.–“In a normal situation, that growth factor enables the neural stem cells to reproduce more stem cells,” Wang said. “This gives us a better idea about how our neural stem cell population is maintained over our life. Our long-term goal is to use endogenous neural stem cells for repair of brain or spinal cord damage, so we need to learn how they proliferate, how to keep them inside the brain.”–The two are optimistic that one day manipulating levels of growth factors and sugar-containing lipids will enable a more steadfast supply of neural stem cells throughout life, although getting the substances into the brain is a challenge. It’s already known that, at least in rats, exercise can also help.–Neural stem cells are able to self-renew, in theory at least, forever. Their ability to maintain a steady supply of themselves and to differentiate into different types of brain cells are their most important properties, Yu said.–Next steps include examining the role of other growth factors and gangliosides.–Yu is the Georgia Research Alliance Eminent Scholar Chair in Molecular and Cellular Neurobiology. The studies were funded by the National Institutes of Health and the Veterans Administration.-Story Source-The above story is based on materials provided by Medical College of Georgia at Georgia Regents University. Note: Materials may be edited for content and length.–Journal Reference-J. Wang, A. Cheng, C. Wakade, R. K. Yu. Ganglioside GD3 Is Required for Neurogenesis and Long-Term Maintenance of Neural Stem Cells in the Postnatal Mouse Brain. Journal of Neuroscience, 2014; 34 (41): 13790 DOI: 10.1523/JNEUROSCI.2275-14.2014
Suggestions to consider—MCT Oils- Glycerol—Octacosanol—ATP—Ribose—Saturated Fats—these are components that activate the body on several fronts and support immune functions—regeneration—immune protecting—