Archives for August 2012

Zinc and Inflammation

Zinc deficiency affects nearly 2 billion people in the developing world resulting in growth retardation, hypogonadism, immune dysfunction and cognitive impairment. Additionally, the roles of this divalent cation in the human body have not been clearly elucidated, since the essentiality of zinc has only been known within the last 50 years. However, it has been clearly documented that the supplementation of zinc improves many conditions such as; acute diarrhea in children, the common cold, infections in the elderly, oxidative stress and generation of inflammatory cytokines. Janet Ludwig, Ph.D. has worked in this area of study specifically modifying cellular injury by zinc supplementation.

This presentation from a webinar in May 2012 explore the following areas in order to begin to understand the therapeutic role of zinc in many inflammatory conditions:

•             Zinc roles in the body-metalloenzymes

•             Zinc as an antioxidant and anti-inflammatory agent

•             Membrane stabilization by zinc

•             Inflammatory diseases ameliorated by zinc supplementation.

 

 

Janet Ludwig, PhD

Janet Ludwig, PhD has worked in the area of zinc and inflammation for more than 25 years. She was at the Division of Surgical Biology at the Arizona Health Sciences Center studying zinc and cell injury induced by alcohol and carbon tetrachloride, an effective hepatotoxin. Additionally, she studied the mechanisms and structural identification of the potent class of inflammatory mediators, Platelet-Activating Factors (PAFs), at the Department of Pathology, University of Texas Health Sciences Center in San Antonio. She has taught courses in inflammation, biochemistry and nutrition at various Universities. She also travels to Bangkok, Thailand to give nutritional advice in a non-governmental organization that aids in improving the conditions for impoverished women and their children. Currently she is on the Hawthorn University faculty.

 

Cancer is Curable Now

The documentary “Cancer is Curable Now” (2010) brings together more than 30 international, holistic professionals who have been working passionately in the field of cancer alternatives — doctors, scientists, researchers and writers from around the world.

Marcus Freudenmann and his wife Sabrina, a naturopathic doctor, traveled the world with their four children for almost 3 years to meet the experts. Their mission was to create a film about natural cancer treatments that would “wake up the world.” This video  is the result of their work.

What Really Causes Schizophrenia

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. Dr. Foster was professor of geography at the University of Victoria.

Using evidence from disciplines as diverse as history, geography, biochemistry and genetics, Dr. Foster demonstrates in the book “What Really Causes Schizophrenia” (2003) that schizophrenia is caused by the hallucinogen adrenochrome and its derivatives. Effective treatment involves orthomolecular substances that reduce adrenochrome production or mitigate its impact.

Dr. Abram Hoffer (1917 – 2009) wrote in 2004 a book review of “What Really Causes Schizophrenia” in the Journal of Orthomolecular Medicine. For more information on the science and research based on Dr.Foster’s work, visit The Harold Foster Foundation and Foster Health.

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Good Diets Fight Bad Alzheimer Genes

Diets high in fish oil have a beneficial effect in patients at risk

Scientists today agree that there are five molecules that are known to affect or cause Alzheimer’s disease, which plagues an estimated five million Americans. The potency of these molecules is linked to environmental factors such as diet and lifestyle.

Professor Daniel Michaelson of Tel Aviv University’s Department of Neurobiologyat the George S. Wise Faculty of Life Sciences has illuminating news about one of these five molecules — APOE, created by the apolipoprotein E gene found in all of our bodies.

Professor Michaelson says APOE comes in two forms, a “good” APOE gene and a “bad” APOE gene, called APOE4. He has developed animal models to investigate the effects of diet and environment on carriers of APOE4, the presence of which is a known risk factor for Alzheimer’s. It appears in 50% of all Alzheimer’s patients, and in 15% of the general population which due to APOE4 is the population which is at risk of getting the disease.

The good news? A diet high in Omega 3 oils and low in cholesterol appears to significantly reduce the negative effects of the APOE4 gene in mouse models.

Exercise is not enough — and may be worse

Prof. Daniel Michaelson

In differentiating between the good and bad variants of the APOE gene, Professor Michaelson and his team studied many variables. They determined that while a rich and stimulating environment is good for carriers of “good” APOE, the same environment has a negative effect on those at risk for Alzheimer’s because they carry the APOE4 gene. While this environment stimulated the formation of new neuronal connections in the “good APOE” mice, it caused the death of brain neurons in the “bad APOE” mice. The stimulating environment included running wheels and tubes for hiding and sliding, as well as ropes and other toys for the mice to play on, replaced and updated with new toys weekly. Those in a non-stimulating environment had access to no toys at all.

“Conditions that are generally considered good can be harmful if the mouse is a carrier of the APOE4 gene. Extrapolating this to the human population, individuals with the bad APOE4 gene are more susceptible to stress caused by an environment that stimulates their brain,” says Professor Michaelson.

The following is an abstract of a study by the research group of Professor Michaelson. The study is published in Journal of Alzheimer’s Disease (2012; 28 (3): 667-83):

“Apolipoprotein E4 (apoE4) is the most prevalent genetic risk factor for Alzheimer’s disease (AD). Epidemiological studies revealed that consumption of docosahexaenoic acid (DHA: 22 : 6 (ω3)), a major brain polyunsaturated fatty acid, is protective for AD and that elevated cholesterol levels are an AD risk factor. We presently investigated the extent to which the pathological effects of apoE4 in vivo can be prevented by consuming fish oil (DHA) or can be modified by cholesterol. Accordingly, apoE3- and apoE4-targeted replacement mice were subjected, following weaning, to a fish oil dietenriched in DHA and to a cholesterol-containing diet under regular and enriched environments. Cholesterol metabolism in the hippocampus and the corresponding phospholipid and fatty acid levels were affected by fish oil (DHA) and cholesterol diets and by environmental stimulation. Importantly, cholesterol metabolism and the fatty acid levels were not affected by apoE4. The phospholipid levels were, however, affected by apoE4. This effect was most pronounced in the cholesterol-fed mice and was abolished by the fish oil (DHA) diet. ApoE4 elevated hippocampal intraneuronal amyloid-β levels under regular conditions and lowered them following environmental stimulation, relative to those of the apoE3 mice. ApoE4 also elevated the levels of the presynaptic transporters Vglut and Vgat, and decreased behavioral performance in an object recognition test. Importantly, all of these apoE4 phenotypes were abolished by the fish oil (DHA) diet, whereas the cholesterol diet modified them. These findings suggest that a fish oil (DHA)diet could be used to attenuate the effects of apoE4 in AD.”

When it’s good, it’s good

“The main take-away message here is that good diets can alleviate the effects of bad genes. Of course nutritionists have had this general idea for a while, but it’s nice to be able to show that this approach can be applied to specifically counteract the negative effects of Alzheimer’s disease-related genes,” says Professor Michaelson.

 

 Reference

Kariv-Inbal Z, Yacobson S, Berkecz R, Peter M, Janaky T, Lütjohann D, Broersen LM, Hartmann T, Michaelson DM. The isoform-specific pathological effects of apoE4 in vivo are prevented by a fish oil (DHA) diet and are modified by cholesterol. J Alzheimers Dis 2012; 28 (3): 667-83.

 

Strawberry Extract Protects Against UVA Rays

The experiment shows that strawberry extract added to skin cell cultures acts as a protector against UVA rays.

An experiment has shown that strawberry extract added to skin cell cultures acts as a protector against ultraviolet radiation as well as increasing its viability and reducing damage to DNA. Developed by a team of Italian and Spanish researchers, the study opens the door to the creation of photoprotective cream made from strawberries.

“We have verified the protecting effect of strawberry extract against damage to skins cells caused by UVA rays,” as explained to SINC by Maurizio Battino, researcher at the Università Politecnica delle Marche in Italy and lead author of the jointly Spanish and Italian study. The results are published in the ‘Journal of Agricultural Food Chemistry‘.

The team prepared human skin cell cultures (fibroblasts) and added strawberry extract in different concentrations (0.05, 0.25 and 0.5 mg/ml), the only exception being the control extract. Using ultraviolet light, the samples were then exposed to a dose “equivalent to 90 minutes of midday summer sun in the French Riviera.”

Data confirm that the strawberry extract, especially at a concentration of 0.5 mg/ml, displays photoprotective properties in those fibroblasts exposed to UVA radiation, it increases cell survival and viability and decreases damage in the DNA when compared with control cells.

“These aspects are of great importance as they provide protection for cell lines subject to conditions that can provoke cancer and other skin-related inflammatory and degenerative illnesses,” outlines Battino.

The researcher recognises that this is the “first step in determining the beneficial effects of strawberries in our diet or as a possible compound source for ‘food integrators’ or cosmetics for instance.”

The redness of anthocyanins

But what molecules give strawberries their photoprotective properties? Scientists suspect that it could be the anthocyanins, which are pigments that give leaves, flowers and fruits their red colour. Analyses have confirmed that extracts are rich in such substances.

“These compounds have important anti-inflammatory, antioxidant and anti-tumour properties and are capable of modulating enzymatic processes,” explains another of the authors, Sara Tulipani from the University of Barcelona. She adds that “we have not yet found a direct relationship between their presence and photoprotective properties.”

“At the moment the results act as the basis for future studies evaluating the ‘bioavailability’ and ‘bioactivity’ of anthocyanins in the dermis and epidermis layers of the human skin, whether by adding them to formulations for external use or by ingesting the fruit itself,” states Tulipani.

Also made up of researchers from the Universities of Salamanca and Granada, in its previous works the team had already demonstrated that strawberries (Fragaria x ananassa) strengthen the red bloods cells and protect the stomach from the effects of alcohol.

 

Reference

Giampieri F, Alvarez-Suarez JM, Tulipani S, Gonzàles-Paramàs AM, Santos-Buelga C, Bompadre S, Quiles JL, Mezzetti B, Battino M. Photoprotective Potential of Strawberry (Fragaria × ananassa) Extract against UV-A Irradiation Damage on Human Fibroblasts. Journal of Agricultural Food Chemistry 2012; 60 (9): 2322-7.

 

Fat, Sick & Nearly Dead

100 pounds overweight, loaded up on steroids and suffering from a debilitating autoimmune disease, Joe Cross is at the end of his rope and the end of his hope. In the mirror he saw a 310 lb man whose gut was bigger than a beach ball and a path laid out before him that wouldn’t end well— with one foot already in the grave, the other wasn’t far behind. FAT, SICK & NEARLY DEAD (2010) is an inspiring film that chronicles Joe’s personal mission to regain his health.

With doctors and conventional medicines unable to help long- term, Joe turns to the only option left, the body’s ability to heal itself. He trades in the junk food and hits the road with juicer and generator in tow, vowing only to drink fresh fruit and vegetable juice for the next 60 days. Across 3,000 miles Joe has one goal in mind: To get off his pills and achieve a balanced lifestyle.

While talking to more than 500 Americans about food, health and longevity, it’s at a truck stop in Arizona where Joe meets a truck driver who suffers from the same rare condition. Phil Staples is morbidly obese weighing in at 429 lbs; a cheeseburger away from a heart-attack. As Joe is recovering his health, Phil begins his own epic journey to get well.

What emerges is nothing short of amazing – an inspiring tale of healing and human connection.
Part road trip, part self-help manifesto, FAT, SICK & NEARLY DEAD defies the traditional documentary format to present an unconventional and uplifting story of two men from different worlds who each realize that the only person who can save them is themselves.

A Diet High in Choline During Pregnancy May Mean Less Stress for Baby

New research from Cornell University indicates that pregnant women who increase choline intake in the third trimester of pregnancy may reduce the risk of the baby developing metabolic and chronic stress-related diseases like high blood pressure and diabetes later in life (1). The results, published in the latest edition of the Journal of the Federation of American Societies for Experimental Biology (The FASEB Journal), suggest that choline, a nutrient found in high quantities in eggs, may help protect against the effects of a mother’s stress during pregnancy (1).

Previous research indicates high exposure to the stress hormone cortisol during pregnancy, often due to maternal anxiety or depression, may make offspring vulnerable to stress-induced illness and chronic conditions (2, 3). This finding adds to the growing body of evidence demonstrating the importance of choline in fetal development.

A Closer Look at the Study

Twenty-four women in the third trimester of pregnancy were randomly assigned to consume either 480 milligrams (mg) choline per day or 930 mg per day for 12 weeks prior to delivery. Researchers collected maternal and placental blood samples as well as samples of placental tissue. They then compared cortisol levels and genetic differences among all the samples. The researchers observed lower levels of cortisol in the placental cord and changes in cortisol-regulating genes in both the placental and fetal tissue among women in the higher choline intake group. “The study findings raise the exciting possibility that a higher maternal choline intake may counter some of the adverse effects of prenatal stress on behavioral, neuroendocrine, and metabolic development in the offspring,” says Marie Caudill, PhD, Cornell University, who is an author of the study and a leading choline researcher.

Choline: A Vital Nutrient

Choline is especially important for pregnant women – it has been shown to play an important role in fetal and infant brain development, affecting the areas of the brain responsible for memory and life-long learning ability. In addition, research shows women with diets low in choline have four times greater risk of having babies with neural tube defects, such as spina bifida (4).

Emerging research also shows choline may have additional benefits in other areas, including:

  • Breast cancer prevention: A study funded by the National Institutes of Health concluded that dietary choline is associated with a 24 percent reduced risk of breast cancer (5).
  • Anti-inflammatory: Foods rich in choline may help reduce the risk of inflammation associated with chronic diseases such as cardiovascular disease, bone loss, dementia and Alzheimer’s disease (6).
  • Brain function: Choline also promotes adult brain function by preserving the structure of brain cell membranes and is an essential component of acetylcholine, the neurotransmitter involved in memory function and muscle control (7).

The Incredible Excellent Source of Choline

Despite its important role in the body, only one in 10 Americans is meeting the Adequate Intake (AI) guidelines for choline (8). Eggs are an excellent source of choline, containing 125 mg per egg. Neva Cochran, registered dietitian and nutrition communications consultant, explains that the nutritional benefits of eggs are not merely limited to choline. “Not only are eggs an excellent source of choline, they contain many other nutrients pregnant women need most, such as high-quality protein, iron and folate—all for just about 15 cents apiece,” says Cochran.

In order to get adequate amounts of choline, Cochran suggests the following tips:

  • Find it in Food: A great way to get your daily dose of choline is to include choline-rich foods in the diet, such as eggs, lean beef, cauliflower and peanuts. Also keep in mind most multivitamins, even prenatal vitamins, provide far less than the Adequate Intake for choline.
  • Don’t Skip the Yolk: Choline is found exclusively in the egg yolk, not the white. Nearly half of the protein and most of the vitamins and minerals are also contained in the yolk.

 

References

1. Jiang, X., J. Yan, A. A. West, C. A. Perry, O. V. Malysheva, S. Devapatla, E. Pressman, F. Vermeylen, and M. A. Caudill. Maternal choline intake alters the epigenetic state of fetal cortisol-regulating genes in humans. FASEB J 2012; 26: 3563-3574.

2. Levitt, N. S., Lindsay, R. S., Holmes, M. C., and Seckl, J. R. Dexamethasone in the last week of pregnancy attenuates hippocampal glucocorticoid receptor gene expression and elevates blood pressure in the adult offspring in the rat. Neuroendocrinology 1996; 64: 412.

3. Levitt, N. S., Lambert, E. V., Woods, D., Hales, C. N., Andrew, R., and Seckl, J. R. Impaired glucose tolerance and elevated blood pressure in low birth weight, nonobese, young South African adults: early programming of cortisol axis. J Clin Endocrinol Metab 2000; 85: 4611.

4. Shaw GM, et al. Periconceptional dietary intake of choline and betaine and neural tube defects in offspring. Am J Epidemiol 2004; 160: 102-9.

5. Xu X, et al. Choline metabolism and risk of breast cancer in population-based study. FASEB J 2008; 22: 1-8.

6. Cho E, et al. Dietary choline and betaine assessed by food-frequency questionnaire in relation to plasma total homocysteine concentration in the Framingham Offspring Study. AJCN 2006; 83: 905-11.

6. Cho E, et al. Dietary choline and betaine assessed by food-frequency questionnaire in relation to plasma total homocysteine concentration in the Framingham Offspring Study. AJCN 2006; 83: 905-11.

7. Moeller SM, et al. The Potential Role of Dietary Xanthophylls in Cataract and Age-Related Macular Degeneration. J Am Coll Nutr 2000; 19 (5): 522S-527S.

8. Jensen HH, et al. Choline in the diets of the US population: NHANES, 2003-2004. Abstract presented at Experimental Biology 2007.

 

Evidence of Parallels Between Mercury Intoxication and the Brain Pathology in Autism

Although there may be genetic or developmental components to autism, the evidence in this current review of the brain findings in autism clearly indicates the reality of brain injury in Autism Spectrum Disorders (ASD); moreover, the brain injury symptoms which characterize autism closely correspond to those seen in sub-acute mercury (Hg) intoxication. The evidence presented in this paper is consistent with Hg being identified as either causal or contributory, working synergistically with other compounds or pathogens in producing the brain pathology observed in those diagnosed with ASD.

Their review article is published in Acta Neurobiologiae Experimentalis (2012; 72 (2): 113-153). This peer-reviewed journal is published by Nencki Institute of Experimental Biology in Warsaw, Poland. 

 

Janet K. Kern, David A. Geier, Tapan Audhya, Paul G. King, Lisa K. Sykes, and Mark R. Geier

Evidence of parallels between mercury intoxication and the brain pathology in autism

Acta Neurobiol Exp (Wars) 2012; 72 (2): 113-153 

 

ABSTRACT

The purpose of this review is to examine the parallels between the effects mercury intoxication on the brain and the brain pathology found in autism spectrum disorder (ASD). This review finds evidence of many parallels between the two, including: (1) microtubule degeneration, specifically large, long-range axon degeneration with subsequent abortive axonal sprouting (short, thin axons); (2) dentritic overgrowth; (3) neuroinflammation; (4) microglial/astrocytic activation; (5) brain immune response activation; (6) elevated glial fibrillary acidic protein; (7) oxidative stress and lipid peroxidation; (8) decreased reduced glutathione levels and elevated oxidized glutathione; (9) mitochondrial dysfunction; (10) disruption in calcium homeostasis and signaling; (11) inhibition of glutamic acid decarboxylase (GAD) activity; (12) disruption of GABAergic and glutamatergic homeostasis; (13) inhibition of IGF-1 and methionine synthase activity; (14) impairment in methylation; (15) vascular endothelial cell dysfunction and pathological changes of the blood vessels; (16) decreased cerebral/cerebellar blood flow; (17) increased amyloid precursor protein; (18) loss of granule and Purkinje neurons in the cerebellum; (19) increased pro-inflammatory cytokine levels in the brain (TNF-alppha, IFN-gamma, IL-1beta, IL-8); and (20) aberrant nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB). This review also discusses the ability of mercury to potentiate and work synergistically with other toxins and pathogens in a way that may contribute to the brain pathology in ASD. The evidence suggests that mercury may be either causal or contributory in the brain pathology in ASD, possibly working synergistically with other toxic compounds or pathogens to produce the brain pathology observed in those diagnosed with an ASD.