Orthomolecular Psychiatry: What Would Abram Hoffer Do?
L. John Hoffer, MD, PhD
Project Director, Lady Davis Institute for Medical Research; Senior Physician, Divisions of Internal Medicine and Endocrinology, Jewish General Hospital; Professor, Faculty of Medicine, McGill University; Associate Professor, School of Dietetics and Human Nutrition, McGill University
Abstract This article provides a practical explanation of orthomolecular psychiatry as practiced by my father, Abram Hoffer, a research psychiatrist and biochemist who dedicated his life to finding a cure for schizophrenia. Even after his death in 2009, Hoffer remains an icon for many people suffering from schizophrenia. The article summarizes the formal clinical trials published by Hoffer’s research group in the 1950s and 1960s, and the evolution of his clinical practice after he retired from academic psychiatry in 1967. Its content is based on Hoffer’s many publications and conversations I had with him over those many years. Given our close relationship, it’s unavoidably biased. Explicitly included are my own interpretations, updates, qualifications and disagreements, as framed by my career as an academic internist and clinical investigator. Key historical and other references are cited at the end of an article that was published in this journal in 2010 but which, unfortunately, lacks the in-text reference numbers. Interested readers may contact me for a properly annotated version. They may also consult an article published by Jonathan Prousky with similar intent to this one but a slightly different slant; it is available on the internet.
Milk Protein Allergy in Breastfeeding Infants
Kimberly Cranford, BS
Currently studying medicine at the University of Washington School of Medicine (MD candidate May 2015); student member of the American Psychiatric Association, the American College of Physicians, and the American Academy of Family Physicians; Bachelor of Science in Molecular Biology earned from the University of Wyoming; Email: email@example.com
Abstract Milk protein allergy (MPA) is a term used to describe various symptoms and clinical presentations thought to be associated with an allergy to cow’s milk protein, such as casein. The as- sociation between dairy milk consumption and certain symptoms is well known and documented. Controversy exists over whether breastfeeding infants can also have an allergic reaction to cow’s milk protein consumed from the breast milk of nursing mothers. The results of several studies show an as- sociation between allergic symptomatology in breastfeeding infants and dairy milk consumption in the mothers of those infants. The methodology for diagnosis of MPA is outlined along with treatment options. Studies have found two treatment regimens to be effective for infants with MPA. The best option is for the mother to continue breastfeeding while also doing a trial of dietary restriction of cow’s milk protein, then all bovine protein, and possibly other cross-reactive proteins like soy. The sec- ond option is for the mother to feed her infant exclusively with formula using extensively hydrolyzed or amino acid-based formulas.
Proposed Stroke and Heart Attack Mechanisms
James G. Crawford, PhD
1409 Usdasdi Drive, Brevard, NC 28712 Email: firstname.lastname@example.org Tel: 828-883-8475
Abstract This is an account of possible causes of stroke and heart attack, which include dehydration, sticky cells, high blood sugar, magnesium deficiency, and inflammation. This report does not discount the usual list of risk factors largely provided by the Framingham Studies, which includes atrial fibril- lation, high blood pressure, and cholesterol. I propose that the Framingham 50+ year effort has been severely compromised, having used cohorts mostly from wealthy countries. This effort thus appears to be more of a study of food choices than stroke and heart attack causes. A new concept for prevention of cardioembolic events is discussed where the strategy needed for prevention of cardioembolic events depends upon where you live. Subjects, who live in countries where food is rich in sugar and fat, develop cardiovascular disease of the type C, where arterial plaque leads to clot formation. Subjects, who live in the tropics, however, develop type D, characterized by dehydration and magnesium deficiency conditions. In the latter type, sickled cells and parasite-infected cells tend to clump with other deoxygenated hemoglobin, deforming red blood cells and causing blood to clot.