Archives for April 2012

First blood test to diagnose major depression in teens

Breakthrough test identifies depression and its subtypes with promise of individualized treatment

CHICAGO — A Northwestern Medicine scientist has developed the first blood test to diagnose major depression in teens, a breakthrough approach that allows an objective diagnosis by measuring a specific set of markers found in a patient’s blood.

The current method of diagnosing depression is subjective. It relies on the patient’s ability to recount his symptoms and the physician’s ability and training to interpret them.

Diagnosing teens is an urgent concern because they are highly vulnerable to depression and difficult to accurately diagnose due to normal mood changes during this age period.

The test also is the first to identify subtypes of depression. It distinguished between teens with major depression and those with major depression combined with anxiety disorder. This is the first evidence that it’s possible to diagnose subtypes of depression from blood, raising the hope for tailoring care to the different types.

“Right now depression is treated with a blunt instrument,” said Eva Redei, a professor of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine and lead investigator of the study, published in Translational Psychiatry. “It’s like treating type 1 diabetes and type 2 diabetes exactly the same way. We need to do better for these kids.”

“This is the first significant step for us to understand which treatment will be most effective for an individual patient,” added Redei, also the David Lawrence Stein Professor of Psychiatric Diseases Affecting Children and Adolescents. “Without an objective diagnosis, it’s very difficult to make that assessment. The early diagnosis and specific classification of early major depression could lead to a larger repertoire of more effective treatments and enhanced individualized care.”

The estimated rates of major depressive disorder jump from 2 to 4 percent in pre-adolescent children to 10 to 20 percent by late adolescence. Early onset of major depression in teens has a poorer prognosis than when it starts in adulthood. Untreated teens with this disease experience increases in substance abuse, social maladjustment, physical illness and suicide. Their normal development is derailed, and the disease persists into adulthood.

The depressed teens in the study were patients of Kathleen Pajer, M.D., a co-first author of the study, and her colleagues from the Research Institute of Nationwide Children’s Hospital in Columbus, Ohio. Pajer is now head of Dalhousie University’s division of child and adolescent psychiatry in Nova Scotia, Canada.

The study subjects included 14 adolescents with major depression who had not been clinically treated and 14 non-depressed adolescents, all between 15 to 19 years old. The depressed and control subjects were matched by sex and race.

Redei’s lab tested the adolescents’ blood for 26 genetic blood markers she had identified in previous research. She discovered 11 of the markers were able to differentiate between depressed and non-depressed adolescents. In addition, 18 of the 26 markers distinguished between patients that had only major depression and those who had major depression combined with anxiety disorder.

The blood analysis was done by Brian Andrus from Redei’s lab, the other co-first author of the study, who was blind to the diagnoses of the subjects.

“These 11 genes are probably the tip of the iceberg because depression is a complex illness,” Redei said. “But it’s an entree into a much bigger phenomenon that has to be explored. It clearly indicates we can diagnose from blood and create a blood diagnosis test for depression.”

Redei first isolated and identified the genetic blood markers for depression and anxiety based on decades of research with severely depressed and anxious rats. The rats mirror many behavioral and physiological abnormalities found in patients with major depression and anxiety.

Further indicating the challenge in working with depressed adolescents, none of the teens who were diagnosed with depression opted for treatment.

“Everybody, including parents, are wary of treatment, and there remains a social stigma around depression, which in the peer-pressured world of teenagers is even more devastating,” Redei said. “Once you can objectively diagnose depression as you would hypertension or diabetes, the stigma will likely disappear.”

 

Reference

Pajer K, Andrus BM, Gardner W, Lourie A, Strange B, Campo J, Bridge J, Blizinsky K, Dennis K, Vedell P, Churchill GA, Redei EE. Discovery of blood transcriptomic markers for depression in animal models and pilot validation in subjects with early-onset major depression. Transl Psychiatry (2012) 2, e101. DOI: 10.1038/tp.2012.26

 

Intravenous Vitamin C May be Beneficial in Treatment of Shingles

Intravenously administered ascorbic acid may have beneficial effects on herpes zoster-associated pain, lesions and accompanying complaintsThis according to a German study published in the April 2012 issue of the Medical Science Monitor. 

Not only the acute symptoms of herpes zoster can be diminished by high-dose vitamin C. Even long-term sequelae, like painful postherpetic neuralgia, may be mitigated or even fully avoided. 

 

Martin Schencking, Claudia Vollbracht, Gabriele Weiss, Jennifer Lebert, Andreas Biller, Birgitt Goyvaerts, and Karin Kraft

Intravenous Vitamin C in the treatment of shingles: Results of a multicenter prospective cohort study
Med Sci Monit 2012; 18 (4): CR 215-224 

 

ABSTRACT

Background: Vitamin C is an immune-relevant micronutrient, which is depleted in viral infections and this deficiency seems to play a critical role in the pathogenesis of herpes infections and in the development of postherpetic neuralgia. The objective of this observational multicenter study was to evaluate the utilization, safety and efficacy of intravenously administrated vitamin C in patients with shingles.

Material/Methods: Between April 2009 and December 2010 16 general practitioners recorded data of 67 participants with symptomatic herpes zoster who received vitamin C intravenously (Pascorbin® 7.5 g/50 ml) for approximately 2 weeks in addition to standard treatment. The assessment of pain (VAS) and the dermatologic symptoms of shingles such as hemorrhagic lesions and the number of efflorescences were investigated in a follow-up observation phase of up to 12 weeks.

Results: Mean declines of pain scores (VAS), number of affected dermatomes and efflorescences, and the presence of hemorrhagic vesicles between the baseline and follow-up assessments at 2 and 12 weeks were statistically significant. Overall, 6.4% of the participants experienced post-herpetic neuralgia. Common complaints such as general fatigue and impaired concentration also improved during the study. The effects and the tolerability of the treatment were evaluated positively by the physicians. The risk of developing PHN was reduced.

Conclusions: The data presented here provide evidence that concomitant use of intravenously administered ascorbic acid may have beneficial effects on herpes zoster-associated pain, dermatologic findings and accompanying common complaints. To confirm our findings, randomized, placebo-controlled clinical studies are necessary.

 

Nutrition and Physical Degeneration

A Comparison of Primitive and Modern Diets and Their Effects 

Dr. Weston A. Price (1870 – 1948) was a Cleveland dentist, who has been called the Charles Darwin of Nutrition. Searching for the causes of dental decay and physical degeneration he observed daily in his dental practice, he turned from test tubes and microscopes to study people with fine teeth the isolated primitives.

In 1939, he published Nutrition and Physical Degeneration. The book startled the worlds of science and nutrition with its documented evidence of primitive populations encountering civilisation, adopting modern diets, and finding that their health worsened. It remains the basic book in this area and is essential reading for those concerned with food and health.

Nutrition and Physical DegenerationTitle: Nutrition and Physical Degeneration Author: Weston A. Price * A Project Gutenberg of Australia eBook * eBook No.: 0200251h.html Language: English Date first posted: 2002 Date most recently updated: April 2012 Project Gutenberg of Australia eBooks are created from printed editions which are in the public domain in Australia, unless a copyright notice is included.

Embedly Powered

 

Read More

The Price-Pottenger Nutrition Foundation (PPNF)

Weston A. Price Foundation

Weston Price, Wikipedia article

 

Why all migraine patients should be treated with magnesium

Magnesium, the second most abundant intracellular cation, is essential in many intracellular processes and appears to play an important role in migraine pathogenesis. Routine blood tests do not reflect true body magnesium stores since <2 % is in the measurable, extracellular space, 67 % is in the bone and 31 % is located intracellularly. Lack of magnesium may promote cortical spreading depression, hyperaggregation of platelets, affect serotonin receptor function, and influence synthesis and release of a variety of neurotransmitters. Migraine sufferers may develop magnesium deficiency due to genetic inability to absorb magnesium, inherited renal magnesium wasting, excretion of excessive amounts of magnesium due to stress, low nutritional intake, and several other reasons. There is strong evidence that magnesium deficiency is much more prevalent in migraine sufferers than in healthy controls. Double-blind, placebo-controlled trials have produced mixed results, most likely because both magnesium deficient and non-deficient patients were included in these trials. This is akin to giving cyanocobalamine in a blinded fashion to a group of people with peripheral neuropathy without regard to their cyanocobalamine levels. Both oral and intravenous magnesium are widely available, extremely safe, very inexpensive and for patients who are magnesium deficient can be highly effective. Considering these features of magnesium, the fact that magnesium deficiency may be present in up to half of migraine patients, and that routine blood tests are not indicative of magnesium status, empiric treatment with at least oral magnesium is warranted in all migraine sufferers.

Journal of Neural Transmission, Online First™ – SpringerLinkMagnesium, the second most abundant intracellular cation, is essential in many intracellular processes and appears to play an important role in migraine pathogenesis. Routine blood tests do not reflect true body magnesium stores since <2 % is in the measurable, extracellular space, 67 % is in the bone and 31 % is located intracellularly.

Embedly Powered

Reference

Mauskop A, Varughese J. Why all migraine patients should be treated with magnesium. J Neural Transm. 2012 Mar 18. [Epub ahead of print]

 

Antioxidant may disrupt Alzheimer’s disease process

According to new study published in the Journal of Alzheimer’s Disease

Alzheimer’s disease (AD) is now the sixth leading cause of death among Americans, affecting nearly 1 in 8 people over the age of 65. There is currently no treatment that alters the course of this disease. However, an increasing amount of evidence suggests that changes in the way the body handles iron and other metals like copper and zinc may start years before the onset of AD symptoms. A new study shows that reducing iron levels in blood plasma may protect the brain from changes related to AD.

In the current study a group of investigators from led by Dr. Othman Ghribi, PhD, Associate Professor, Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota School of Medicine and Health Sciences, rabbits were fed a high-cholesterol diet which caused them to accumulate plaques of a small protein called beta-amyloid (Aβ). These plaques are toxic to neurons and central to the development of Alzheimer’s disease. The rabbits also developed changes in tau protein, which is part of the skeleton of neurons. When this protein becomes heavily phosphorylated, the ability of neurons to conduct electrical signals is disrupted. Following treatment with a drug called deferiprone (an iron chelator), the iron level in the rabbits’ blood plasma was reduced and the levels of both beta-amyloid and phosphorylated tau in the brain were returned to normal levels.

Another degenerative process in AD involves the production of reactive oxygen species (ROS) that can damage neurons in the brain. Deferiprone is also thought to suppress this reactive oxygen damage caused by free iron in the bloodstream, however in this study there was no difference in reactive oxygen species in the treated group. It appears that iron in the AD brain is located in the wrong places – in particular it accumulates to very high levels in the cores of beta-amyloid plaques and is very reactive in this setting.

According to Dr. Ghribi, “Our data show that treatment with the iron chelator deferiprone opposes several pathological events induced by a cholesterol-enriched diet…Deferiprone reduced the generation of Aβ and lowered levels of tau phosphorylation.” While there was no effect on ROS levels, he comments that “It is possible that a higher dose of deferiprone, or combination therapy of deferiprone together with an antioxidant to prevent ROS generation would more-fully protect against the deleterious effects of cholesterol-enriched diet that are relevant to AD pathology.”

Noted expert on metals metabolism research on AD Ashley Bush, MD, PhD, Mental Health Research Institute, Melbourne, Australia, adds that “this research highlights the role of metal ions as key modulators for the toxic interactions of risk factors for Alzheimer’s disease, in this case cholesterol. Drugs targeting these metal interactions hold promise as disease-modifying agents.”

 

Reference

Prasanthi JR, Schrag M, Dasari B, Marwarha G, Kirsch WM, Ghribi O. Deferiprone Reduces Amyloid-β and Tau Phosphorylation Levels but not Reactive Oxygen Species Generation in Hippocampus of Rabbits Fed a Cholesterol-Enriched Diet. J Alzheimers Dis. 2012 Mar 9. [Epub ahead of print]

 

Red Wine Compound May Fight Obesity

Kee-Hong Kim found that piceatannol, a compound found in red wine and several fruits, blocks immature fat cells from growing. (Purdue Agricultural Communication photo/Tom Campbell)

A compound found in red wine, grapes and other fruits, and similar in structure to resveratrol, is able to block cellular processes that allow fat cells to develop, opening a door to a potential method to control obesity, according to a Purdue University study.

Kee-Hong Kim, an assistant professor of food science, and Jung Yeon Kwon, a graduate student in Kim’s laboratory, reported in this week’s issue of the Journal of Biological Chemistry that the compound piceatannol blocks an immature fat cell’s ability to develop and grow.

While similar in structure to resveratrol – the compound found in red wine, grapes and peanuts that is thought to combat cancer, heart disease and neurodegenerative diseases – piceatannol might be an important weapon against obesity. Resveratrol is converted to piceatannol in humans after consumption.

“Piceatannol actually alters the timing of gene expressions, gene functions and insulin action during adipogenesis, the process in which early stage fat cells become mature fat cells,” Kim said. “In the presence of piceatannol, you can see delay or complete inhibition of adipogenesis.”

Over a period of 10 days or more, immature fat cells, called preadipocytes, go through several stages to become mature fat cells, or adipocytes.

“These precursor cells, even though they have not accumulated lipids, have the potential to become fat cells,” Kim said. “We consider that adipogenesis is an important molecular target to delay or prevent fat cell accumulation and, hopefully, body fat mass gain.”

Kim found that piceatannol binds to insulin receptors of immature fat cells in the first stage of adipogenesis, blocking insulin’s ability to control cell cycles and activate genes that carry out further stages of fat cell formation. Piceatannol essentially blocks the pathways necessary for immature fat cells to mature and grow.

Piceatannol is one of several compounds being studied in Kim’s laboratory for its health benefits, and it is also present in different amounts in red grape seeds and skin, blueberries, passion fruit, and other fruits.

Kim would like to confirm his current finding, which is based on a cell culture system, using an animal model of obesity. His future work would also include determining methods for protecting piceatannol from degrading so that concentrations large enough would be available in the bloodstream to stop adipogenesis or body fat gain.

“We need to work on improving the stability and solubility of piceatannol to create a biological effect,” Kim said.

 

Reference

Jung Yeon Kwon, Sang Gwon Seo, Yong-Seok Heo, Shuhua Yue, Ji-Xin Cheng, Ki Won Lee, and Kee-Hong Kim. Piceatannol, Natural Polyphenolic Stilbene, Inhibits Adipogenesis via Modulation of Mitotic Clonal Expansion and Insulin Receptor-dependent Insulin Signaling in Early Phase of Differentiation. J Biol Chem 2012; 287: 11566-11578.

 

 

An Orthomolecular Approach to Diabetes

Julian Whitaker, MD (born August 7, 1944), graduated from Dartmouth College in 1966, and received his medical training at Emory University Medical School  in Atlanta in 1970. He is a member of the American Medical Association and is board certified in anti-aging medicine.

In 1979 Dr. Whitaker opened the Whitaker Wellness Institute in Newport Beach, California, and today it is the nation’s largest and most comprehensive alternative medicine clinic. At this clinic they have unparalleled success treating diabetes. Their personalized nutritional protocols at and weight-loss strategies have helped thousands of patients reduce their reliance on insulin and oral diabetes drugs — often eliminating them altogether.

 

Eating flavonoids protects men against Parkinson’s disease

Men who eat flavonoid-rich foods such as berries, tea, apples and red wine significantly reduce their risk of developing Parkinson’s disease, according to new research by Harvard University and the University of East Anglia (UEA).

Published April 4 in the journal Neurology®, the findings add to the growing body of evidence that regular consumption of some flavonoids can have a marked effect on human health. Recent studies have shown that these compounds can offer protection against a wide range of diseases including heart disease, hypertension, some cancers and dementia.

This latest study is the first study in humans to show that flavonoids can protect neurons against diseases of the brain such as Parkinson’s.

Around 130,000 men and women took part in the research. More than 800 had developed Parkinson’s disease within 20 years of follow-up. After a detailed analysis of their diets and adjusting for age and lifestyle, male participants who ate the most flavonoids were shown to be 40 per cent less likely to develop the disease than those who ate the least. No similar link was found for total flavonoid intake in women.

The research was led by Dr Xiang Gao of Harvard School of Public Health in collaboration with Prof Aedin Cassidy of the Department of Nutrition, Norwich Medical School at UEA.

“These exciting findings provide further confirmation that regular consumption of flavonoids can have potential health benefits,” said Prof Cassidy.

“This is the first study in humans to look at the associations between the range of flavonoids in the diet and the risk of developing Parkinson’s disease and our findings suggest that a sub-class of flavonoids called anthocyanins may have neuroprotective effects.”

Prof Gao said: “Interestingly, anthocyanins and berry fruits, which are rich in anthocyanins, seem to be associated with a lower risk of Parkinson’s disease in pooled analyses. Participants who consumed one or more portions of berry fruits each week were around 25 per cent less likely to develop Parkinson’s disease, relative to those who did not eat berry fruits. Given the other potential health effects of berry fruits, such as lowering risk of hypertension as reported in our previous studies, it is good to regularly add these fruits to your diet.”

Flavonoids are a group of naturally occurring, bioactive compunds found in many plant-based foods and drinks. In this study the main protective effect was from higher intake of anthocyanins, which are present in berries and other fruits and vegetables including aubergines, blackcurrants and blackberries. Those who consumed the most anthocyanins had a 24 per cent reduction in risk of developing Parkinson’s disease and strawberries and blueberries were the top two sources in the US diet.

The findings must now be confirmed by other large epidemiological studies and clinical trials.

Parkinson’s disease is a progresssive neurological condition affecting one in 500 people, which equates to 127,000 people in the UK. There are few effective drug therapies available.

Dr Kieran Breen, director of research at Parkinson’s UK said: “This study raises lots of interesting questions about how diet may influence our risk of Parkinson’s and we welcome any new research that could potentially lead to prevention.

“While these new results look interesting there are still a lot of questions to answer and much more research to do before we really know how important diet might be for people with Parkinson’s.”

 

Reference

Gao X, Cassidy A, Schwarzschild MA, Rimm EB, Ascherio A. Habitual intake of dietary flavonoids and risk of Parkinson disease. Neurology, 2012 DOI: 10.1212/WNL.0b013e31824f7fc4

 

A Nutritional Approach to AIDS

According to Bradfield & Foster ( 2006) is it possible to reverse all the  symptoms of AIDS in dying patients using  nutrition alone. This requires selenium and the amino acids, cysteine, tryptophan and glutamine.

Dr. Harold D. Foster, Ph.D. (1933-2009) was one of the giants in orthomolecular medicine with boundless enthusiasm and a prolific gift of writing. He was a researcher with a soaring scientific mind who made unique contributions to the understanding of health and disease.

Starting in 2004, a series of medical trials were conducted based on Dr. Foster’s research into the geographical correlations seen with HIV/AIDS, focusing on the nutritional deficiencies caused by the virus and the disease.

“HIV encodes for one of the human glutathione peroxidases. As a result, as it is replicated it deprives HIV-seropositive individuals of the selenoenzyme glutathione peroxidase and its four key components, namely selenium, cysteine, glutamine and tryptophan. Slowly but surely, this depletion process causes severe deficiencies of all these nutrients. Their lack, in turn, is behind the major symptoms of AIDS, including the collapse of the immune system, increased susceptibility to cancer, myocardial infarction, depression, muscle wasting, diarrhea, psychosis and dementia” (excerpted from hdfoster.com).

Marnie Bradfield & Harold D. Foster concluded in 2006 the following in an article in  Journal of Orthomolecular Medicine:

Several conclusions appear obvious from the African nutritional trials being used to test the efficacy of selenium and amino acids as a treatment for HIV/AIDS. Firstly, it is possible to reverse all the symptoms of AIDS in dying patients using nutrition alone. Secondly, this requires selenium and the amino acids, cysteine,tryptophan and glutamine. Thirdly, while selenium alone can slow HIV replication, eventually HIV/AIDS patients also need amino acid supplements. These can be given temporarily until deficiencies are corrected. The patients can then return to selenium supplementation alone for several months, until the more complex nutritional mixture is again required for another month. There appear to be no adverse side affects from these nutritional treatments and patients are delighted with their greatly improved health status.

For more information on the science and research based on Dr.Foster’s work, visit The Harold Foster Foundation and Foster Health

 

References

Bradfield M, Foster HD. The Successful Orthomolecular Treatment of AIDS: Accummulating Evidence from Africa. Journal of Orthomolecular Medicine 2006; 21 (4): 193-196.

Foster HD. What Really Causes AIDS. TraffordPublishing, Victoria BC. 2002.

 

 

A Safe Protocol for Amalgam Removal

Dr. Dana Colson graduated from Dentistry in 1977 from the University of Toronto, Canada. She has practiced holistic, mercury free and mercury safe dentistry since 1983. Dr. Colson is aware that mercury vapor and dental infections can have a negative impact on overall health. Because of this concern, she focus on patient education and strive to remove mercury amalgam (silver) fillings in a safe way. She has now published a review article about this topic in the Journal of Environmental and Public Health.

 

 

Dana G. Colson

A safe protocol for amalgam removal

J Environ Public Health 2012; 2012: 517391 

 

ABSTRACT

Today’s environment has different impacts on our body than previous generations. Heavy metals are a growing concern in medicine. Doctors and individuals request the removal of their amalgam (silver mercury) restorations due to the high mercury content. A safe protocol to replace the silver mercury filling will ensure that there is minimal if any absorption of materials while being removed. Strong alternative white composite and lab-processed materials are available today to create a healthy and functioning mouth. Preparation of the patient prior to the procedure and after treatment is vital to establish the excretion of the mercury from the body.