Archive for the ‘Archived’ Category

Are “Frankenfoods” Really All that Scary?

Wednesday, December 14th, 2011

Here’s an article regarding GMO foods.  The best policy for optimal health and thus a healthy scalp is to avoid all GMO foods.

Please note: The below is a quoted article, not in my words, posted here for posterity. It’s talking about cancer, but it has relevant educational points on GMO foods, genetically mutilated foods if you want my opinion.

 

Article:

 

Are “Frankenfoods” Really All that Scary?

Those who make and eat GM (genetically modified) foods say they’re the answer to mass starvation and disease. Those who shun GM technology say it’ll be the cause of mass starvation and disease. They call these foods “Frankenfoods,” with a nod to Frankenstein, the monster humanoid created by runaway, out-of-control science.

GM food is a hot-button issue right now. The subject arouses intense emotions, often based on a minimum of information. Most important of all is the question of how GM foods might affect our long-term health. Let’s first look at the facts.


When food meets technology

GM foods come from genetically modified organisms (GMOs). They consist of food organisms that were modified via molecular biology techniques that promote selective breeding.

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Selenium and the control of thyroid hormone metabolism.

Friday, July 1st, 2011

-:: This Abstract is posted here for posterity and archival purposes only ::-

Thyroid. 2005 Aug;15(8):841-53.
Selenium and the control of thyroid hormone metabolism.
Köhrle J.

Institut für Experimentelle Endokrinologie und Endokrinologisches Forschungs-Centrum der Charité EnForCé, Charité Universitätsmedizin Berlin, Berlin, Germany. josef.koehrle@charite.de

Abstract

Thyroid hormone synthesis, metabolism and action require adequate availability of the essential trace elements iodine and selenium, which affect homeostasis of thyroid hormone-dependent metabolic pathways.

The three selenocysteine-containing iodothyronine deiodinases constitute a novel gene family. Selenium is retained and deiodinase expression is maintained at almost normal levels in the thyroid gland, the brain and several other endocrine tissues during selenium deficiency, thus guaranteeing adequate local and systemic levels of the active thyroid hormone T(3).

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Due to their low tissue concentrations and their mRNA SECIS elements deiodinases rank high in the cellular and tissue-specific hierarchy of selenium distribution among various selenoproteins.

While systemic selenium status and expression of abundant selenoproteins (glutathione peroxidase or selenoprotein P) is already impaired in patients with cancer, disturbed gastrointestinal resorption, unbalanced nutrition or patients requiring intensive care treatment, selenium-dependent deiodinase function might still be adequate.

However, disease-associated alterations in proinflammatory cytokines, growth factors, hormones and pharmaceuticals modulate deiodinase isoenzyme expression independent from altered selenium status and might thus pretend causal relationships between systemic selenium status and altered thyroid hormone metabolism.

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Study: Effects of combined iodine and selenium deficiency on thyroid hormone metabolism in rats

Friday, July 1st, 2011

-:: This Abstract is posted here for posterity and archival purposes only ::-

Am J Clin Nutr. 1993 Feb;57(2 Suppl):240S-243S.

Effects of combined iodine and selenium deficiency on thyroid hormone metabolism in rats.

Beckett GJ, Nicol F, Rae PW, Beech S, Guo Y, Arthur JR.

University Department of Clinical Chemistry, Royal Infirmary, Edinburgh, UK.

Abstract

This paper compares the effects of combined iodine and selenium deficiency, of single deficiencies of these trace elements, and of no deficiency on thyroid hormone metabolism in rats.

In rats deficient in both trace elements, thyroidal triiodothyronine (T3), thyroidal thyroxin (T4), thyroidal total iodine, hepatic T4, and plasma T4 were significantly lower, and plasma thyroid-stimulating hormone (TSH) and thyroid weight were significantly higher than in rats deficient in iodine alone.

Plasma and hepatic T3 concentrations were similar in the dietary groups. Hepatic type I iodothyronine deiodinase (ID-I) activity was inhibited by selenium deficiency irrespective of the iodine status. Type II deiodinase (ID-II) activity in the brain was significantly higher and in pituitary, significantly lower in combined deficiency than in iodine deficiency alone.

These data show that selenium can play an important role in determining the severity of the hypothyroidism associated with iodine deficiency.

PMID:
8427196
[PubMed - indexed for MEDLINE]
Source: http://www.ncbi.nlm.nih.gov/pubmed/8427196

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Study: The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health.

Friday, July 1st, 2011

-:: This Abstract is posted here for posterity and archival purposes only ::-

Thyroid. 2002 Oct;12(10):867-78.

The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health.

Zimmermann MB, Köhrle J.

Laboratory for Human Nutrition, Swiss Federal Institute of Technology, Zürich, Switzerland. Michael.zimmermann@ilw.agrt.ethz.ch
Abstract

Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function.

Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation.

Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes.

Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure.

In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism.

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Study: Fat maintenance is a predictor of the murine lifespan response to dietary restriction

Thursday, June 16th, 2011

This article archives the study titled: Fat maintenance is a predictor of the murine lifespan response to dietary restriction:

1) Article

Article: Mouse study turns fat-loss/longevity link on its head – Science Daily, 5/3/11

“studied the effect of food restriction on fat and weight loss in 41 genetically different strains of mice. The scientists then correlated the amount of fat reduction to life span … The answer: Mice that maintained their fat actually lived longer. Those that lost fat died earlier … People are best advised to adopt a moderate approach, not losing all fat but definitely not keeping unhealthy amounts of fat, either … None of the mice in this study were what we would consider to be obese”

Archived article: Mouse-Study-Turns-Fat-Loss-longevity-Link-on-Its-Head.pdf

2) Journal reference:

Chen-Yu Liao, Brad A. Rikke, Thomas E. Johnson, Jonathan A.L. Gelfond, Vivian Diaz, James F. Nelson. Fat Maintenance Is a Predictor of the Murine Lifespan Response to Dietary Restriction. Aging Cell, 2011; DOI: 10.1111/j.1474-9726.2011.00702.x

Journal Summary:

Fat maintenance is a predictor of the murine lifespan response to dietary restriction     1. Chen-Yu Liao1,2,    2. Brad A. Rikke3,    3. Thomas E. Johnson3,4,    4. Jonathan A. L. Gelfond2,5,    5. Vivian Diaz2,    6. James F. Nelson1,2  Article first published online: 25 APR 2011  DOI: 10.1111/j.1474-9726.2011.00702.x
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Too Much Fluoride/Bromide/Chlorine & Not Enough Iodine

Monday, June 13th, 2011

Nature. 2006 Apr 13 “Reactive oxygen species have a causal role in multiple forms of insulin resistance”

Thursday, May 26th, 2011

Nature. 2006 Apr 13;440(7086):944-8.
Reactive oxygen species have a causal role in multiple forms of insulin resistance.
Houstis N, Rosen ED, Lander ES.
Source

Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02141, USA.
Abstract

Insulin resistance is a cardinal feature of type 2 diabetes and is characteristic of a wide range of other clinical and experimental settings. Little is known about why insulin resistance occurs in so many contexts. Do the various insults that trigger insulin resistance act through a common mechanism? Or, as has been suggested, do they use distinct cellular pathways? Here we report a genomic analysis of two cellular models of insulin resistance, one induced by treatment with the cytokine tumour-necrosis factor-alpha and the other with the glucocorticoid dexamethasone. Gene expression analysis suggests that reactive oxygen species (ROS) levels are increased in both models, and we confirmed this through measures of cellular redox state. ROS have previously been proposed to be involved in insulin resistance, although evidence for a causal role has been scant. We tested this hypothesis in cell culture using six treatments designed to alter ROS levels, including two small molecules and four transgenes; all ameliorated insulin resistance to varying degrees. One of these treatments was tested in obese, insulin-resistant mice and was shown to improve insulin sensitivity and glucose homeostasis. Together, our findings suggest that increased ROS levels are an important trigger for insulin resistance in numerous settings.

PMID:
16612386
[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez/16612386?dopt=Abstract&holding=f1000,f1000m,isrctn

Food Irradiation Research

Tuesday, May 24th, 2011

There is no direct scientific link between food irradiation and hair loss (yet). I avoid all food that has been cold pasteurized (irradiated). We simply do not know enough about the safety. My logic? Unless proven safe, irradiation is not. Food irradiation is being shoved down our throats (similarly to Fluoridation and Pasteurization). For years, food irradiation has been promoted as a simple process that can be used to effectively and significantly reduce food-borne illnesses around the world.

A thorough review of the literature reveals a paucity of adequate research conducted to specifically address health concerns that may directly result from the consumption of irradiated food. Here’s some info so you can learn what the FDA, corporations and their scientists deem good for you (and their wallets).

 

-:: Note: This article serves to archive research and articles written on food irradiation for archival, preservation, dissemination and educational purposes ::-


PDF Document Archive:

Below you see attached PDF documents relating to food irradiation

Top 10 Problems with Irradiated Food (Top10.pdf) – Public Citizen

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British Journal of Dermatology – April 2006 – “Inhibitory autocrine factors produced by the mesenchyme-derived hair follicle dermal papilla may be a key to male pattern baldness”

Tuesday, May 24th, 2011

Archived study

British Journal of Dermatology – Volume 154, Issue 4, pages 609–618, April 2006

Inhibitory autocrine factors produced by the mesenchyme-derived hair follicle dermal papilla may be a key to male pattern baldness

1. K. Hamada1,2,3,
2. V.A. Randall1

Article first published online: 20 FEB 2006

DOI: 10.1111/j.1365-2133.2006.07144.x

Summary

Background Androgenetic alopecia, or male pattern baldness, is a common, progressive disorder where large, terminal scalp hairs are gradually replaced by smaller hairs in precise patterns until only tiny vellus hairs remain. This balding can cause a marked reduction in the quality of life. Although these changes are driven by androgens, most molecular mechanisms are unknown, limiting available treatments. The mesenchyme-derived dermal papilla at the base of the mainly epithelial hair follicle controls the type of hair produced and is probably the site through which androgens act on follicle cells by altering the regulatory paracrine factors produced by dermal papilla cells. During changes in hair size the relationship between the hair and dermal papilla size remains constant, with alterations in both dermal papilla volume and cell number. This suggests that alterations within the dermal papilla itself play a key role in altering hair size in response to androgens. Cultured dermal papilla cells offer a useful model system to investigate this as they promote new hair growth in vivo, retain characteristics in vitro which reflect their parent follicle’s response to androgens in vivo and secrete mitogenic factors for dermal papilla cells and keratinocytes.

Objectives To investigate whether cultured dermal papilla cells from balding follicles secrete altered amounts/types of mitogenic factors for dermal papilla cells than those from larger, normal follicles. We also aimed to determine whether rodent cells would recognize mitogenic signals from human cells in vitro and whether factors produced by balding dermal papilla cells could alter the start of a new mouse hair cycle in vivo.

Methods Dermal papilla cells were cultured from normal, balding and almost clinically normal areas of balding scalps and their ability to produce mitogenic factors compared using both human and rat whisker dermal papilla cells as in vitro targets and mouse hair growth in vivo.

Results Normal scalp cells produced soluble factors which stimulated the growth of both human scalp and rat whisker dermal papilla cells in vitro, demonstrating dose-responsive mitogenic capability across species. Although balding cells stimulated some growth, this was much reduced and they also secreted inhibitory factor(s). Balding cell media also delayed new hair growth when injected into mice.

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Autoimmune Disease, Pathogens and Hair Loss

Thursday, May 12th, 2011

Pathogens are possibly one of the reasons men and women experience autoimmune diseases and patterned hair loss.

Very few realize how many pathogens we have as humans. Do not confuse pathogens with beneficial bacteria and probiotics. The sicker you are the more complex your hair loss (and health issues) is.

hypomethylation is a major contributor to autoimmune diseases. Read: Methylation and Hair Loss

Watch this interesting video on pathogens:

 

In this video, Amy Proal speaks at the Ljubljana 7th International Congress on Autoimmunity, on May 6, 2010. Her topic is “Metagenomic Symbiosis between Bacterial and Viral Pathogens in Autoimmune Disease.”

Summary of video:
Metagenomic research involves the collective genomes of microbes
Different microbial genomes can combine to cause a pathogenic state
Many new novel microbes have been discovered in the human body (thousands)
A part of the human microbiome project
It is possible that in auto immune disease, the anti bodies are not creating a response to self but to these pathogens Even tissue considered sterile like the amniotic fluid turned out to have 1000s of microbes not known before..
Pathogens exist in blood and inside the cells of the immune system themselves
H pyloric also in blood.
How does chronic disease develop? alter body metabolism and attack the vitamin d receptor.
Viruses and bacteria evolved to survive by slowing activity of vit D receptor!
They slow the body’s defense mechanism, HIV takes over VDR activity, many other pathogens slow VDR activity and other receptors that control immune response.
The Immune system slows after acquiring one pathogen, then it is easier to acquire more and more pathogens
Viral, fungal, bacterial, this is termed “successive infection”
An inflammatory disease state is due to the sum of microbes human accumulates and thus shifts further away from homeostasis.
People develop inflammatory disorders such as ones diagnosed as autoimmune, or the typical aches as in normal aging
The Epstein-barr virus (EBV) linked to celiac, MS, rheumatoid arthritis, lupus, crohn’s, schizophrenia, and many other autoimmune disease
A 1 microbe 1 disease approach not viable
Where do we pick up these pathogens? everywhere: father’s sperm, mother, medicine, donated blood, air, even cigarettes
With current autoimmune treatment, the Pathogens remain alive and cause person to become sicker
Amy works at the Autoimmunity research foundation .. They are treating auto immune disease by stimulating the immune system not suppressing it, with success.
This is a paradigm shift

Amy closes by suggesting, in cases of autoimmune disease: “don’t palliate, stimulate”

Quote:

it is entirely possible that in autoimmune disease the antibodies are not being produced as antibodies to self but are instead being produced in reaction to these pathogens.

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Disclaimer: I must say this: The information presented herein is for informational purposes only. Consult your doctor, practitioner, and/or pharmacist for any health problem and before using any supplements, making dietary changes, or before making any changes in prescribed medications.
All posts are strictly opinions meant to foster debate, education, comment, teaching, scholarship and research under the "fair use doctrine" in Section 107 of U.S. Code Title 17. No statement of fact is made and/or should be implied. Please verify all the articles on this site for yourself. The Information found here should in no way to be construed as medical advice. If You have a health issue please consult your professional medical provider. Everything here is the authors own personal opinion as reported by authors based on their personal perception and interpretation as a part of authors freedom of speech. Nothing reported here should be taken as medical advice, diagnosis or prescription; medical advice should only be taken from your health care provider. Consume the information found on this web site under your own responsibility. Please, do your own research; reach your own conclusions, and take personal responsibility and personal control of your health.