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INFLAMMATORY COMMENTS ON AGEING June 19, 2013 · by Mary Cavanagh
in Stanford Neuroblog
Excerpts:
"None of us is getting any younger. In fact, most of us can expect to live longer than ever. The world’s oldest man died just last week aged 116 and, as global life expectancy continues to increase, we’re going to have to tackle age-related frailty and functional fragility to avoid unbearable healthcare costs and provide quality of life for a growing population of centenarians. With rates of dementia as high as 60% in the over 85s1, neurodegeneration is a big issue; but treating age-related diseases in isolation may not be the most effective solution. Scientists now think of ageing as an intricate process during which tissues and cells change the way they communicate and interact, resulting in a gradual loss of function. Not exactly a simple cause-effect pairing that can be hit with a youth pill."
"One versatile and highly abundant transcription factor, and the focus of a new study in Nature2, is NFkB (nuclear factor kappa B). This molecule is a hallmark of inflammation and once activated, perpetuates inflammatory responses. However, many different cells use this molecule to transmit all sorts of messages and, as a consequence, its role in a particular signalling pathway is often difficult to pin down. In their new study, Zhang and colleagues used several tricks to see just what NFkB is up to in the brain and how its activity relates to ageing. By linking it to a fluorescent molecule, the authors were able to visualise NFkB activity in the brain. The more active the transcription factor, the brighter the signal. In this case, brains got brighter with age supporting the idea that inflammation in the brain increases as we get older. While not always bad, inflammation in the brain is a sign of altered equilibrium and contributes to several neurodegenerative diseases3-6. By injecting a non-functional version of the protein, the authors were able to interrupt NFkB activation in the brains of old mice. Interestingly, reducing NFkB activity not only reduced inflammation, but also improved cognitive function (measured by maze navigation), decreased muscle degeneration (measured by grip tests) and even extended life span."
Article at:
http://neuroblog.stanford.edu/?p=3873
Boston University, Department of Biology, Thomas Gilmore
Professor of Biology, PhD, University of California, Berkeley, 1984
Areas of interest: molecular biology, cell biology, signal transduction, cancer, molecular ecology, no date
Current Research:
"Much of our research focuses on three projects centered around transcription factor NF-kB. In one project, we seek to understand the cellular and molecular mechanisms by which altered NF-kB activity contributes to a variety of human cancers, especially lymphoid cell cancers. For example, we have found that the human REL gene, which encodes an NF-kB transcription factor, is amplified and overexpressed in many human lymphomas and can also malignantly transform avian and human lymphoid cells in tissue culture. More recently, we have also been investigating the role of NF-kB co-activator proteins called HATs (histone acectyltransferases) in human B-cell lymphoma.
In collaborative studies with Drs. John Porco and Adrian Whitty in the Chemistry Department at Boston University, we are characterizing natural and synthetic inhibitors of NF-kB signaling. Many of these inhibitors are derivatives of natural products, and may have anti-cancer or anti-inflammatory activities.
Finally, we are studying the evolutionary origins of the NF-kB pathway by characterizing NF-kB genes and proteins in simple marine organisms, such as the sea anemone Nematostella vectensis. This research may have relevance to the mechanisms by which simple marine organisms deal with the environmental stress that is currently impacting sensitive marine ecosystems. These studies are being carried out in collaboration with Drs. Les Kaufman, John Finnerty and Trevor Siggers (Biology Department, Boston University).
Article at:
http://www.bu.edu/biology/people/faculty/gilmore/
Telomerase directly regulates NF-?B-dependent transcription
Arkasubhra Ghosh, Gaye Saginc,Shi Chi Leow,Ekta Khattar, Eun Myong Shin,Ting Dong Yan,Marc Wong, Zhizhuo Zhang,Guoliang Li,
Wing-Kin Sung, Jianbiao Zhou, Wee Joo Chng, Shang Li, Edison Liu & Vinay Tergaonkar
in NATURE CELL BIOLOGY, 18 November 2012
Abstract:
"Although elongation of telomeres is thought to be the prime function of reactivated telomerase in cancers, this activity alone does not account for all of the properties that telomerase reactivation attributes to human cancer cells. Here, we uncover a link between telomerase and NF-?B, a master regulator of inflammation. We observe that while blocking NF-?B signalling can inhibit effects of telomerase overexpression on processes relevant to transformation, increasing NF-?B activity can functionally substitute for reduced telomerase activity. Telomerase directly regulates NF-?B-dependent gene expression by binding to the NF-?B p65 subunit and recruitment to a subset of NF-?B promoters such as those of IL-6 and TNF-a, cytokines that are critical for inflammation and cancer progression. As NF-?B can transcriptionally upregulate telomerase levels, our findings suggest that a feed-forward regulation between them could be the key mechanistic basis for the coexistence of chronic inflammation and sustained telomerase activity in human cancers."
Article at:
http://www.nature.com/ncb/journal/v14/n12/full/ncb2621.html
Suppression of Inflammatory Responses by Handelin, a Guaianolide Dimer from Chrysanthemum boreale, via Downregulation of NF-?B Signaling and Pro-inflammatory Cytokine Production in The Journal of Natural Products, April 1, 2014
Yuna Pyee , Hwa-Jin Chung , Tae Jun Choi , Hyen Joo Park , Ji-Young Hong , Ju Sun Kim , Sam Sik Kang , and Sang Kook Lee *
College of Pharmacy, Natural Products Research Institute, Seoul National University, Seoul 151-742, Korea
J. Nat. Prod., 2014, 77 (4), pp 917–924
DOI: 10.1021/np4009877
Copyright © 2014 The American Chemical Society and American Society of Pharmacognosy
Excerpt:
"The anti-inflammatory activity of handelin (1), a guaianolide dimer from Chrysanthemum boreale flowers, was evaluated in vivo, and the effects on mediators nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-a (TNF-a), and interleukin-1ß (IL-1ß) and the nuclear factor-?B (NF-?B) and ERK/JNK signaling pathways were investigated in vitro. Compound 1 inhibited lipopolysaccharide (LPS)-induced production of NO and PGE2 in cultured mouse macrophage RAW 264.7 cells. The suppression of NO and PGE2 production by 1 was correlated with the downregulation of mRNA and protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Compound 1 also suppressed the induction of pro-inflammatory cytokines TNF-a and IL-1ß in LPS-stimulated RAW 264.7 cells. To further clarify the transcriptional regulatory pathway in the expression of iNOS and COX-2 by 1, the role of NF-?B was determined in RAW 264.7 cells. Compound 1 inhibits the binding activity of NF-?B into the nuclear proteins. The transcriptional activity of NF-?B stimulated with LPS was also suppressed by 1, which coincided with the inhibition of I?B degradation. Compound 1 also suppressed the activation of mitogen-activated protein kinases, including ERK and JNK signaling. In addition, the LPS-stimulated upregulation of miRNA-155 expression was suppressed by 1. The oral administration of 1 inhibited acute inflammation in carrageenan-induced paw and 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced ear edema models. The serum level of IL-1ß was also inhibited by 1 in a carrageenan-induced paw edema model. These findings suggest that the suppression of NF-?B activation and pro-inflammatory cytokine production may be a plausible mechanism of action for the anti-inflammatory activity of handelin."
My interpretation:
The Koreans are also looking for an anti-inflammatory that suppresses NF-kB. They have found a compound, handelin, that comes from the Chrysanthemum flower and it appears to behave similar to anatabine citrate that appears naturally from the solance family of plants.
Article at:
http://pubs.acs.org/doi/abs/10.1021/np4009877
Vitamin D and NF-kappaB
Posted FEB 15 2014 by ADMIN in HEALTH, REEDUCATE YOURSELF
Excerpt:
"Have you heard of NF-kappaB? Most people haven’t. What does NF-kappaB mean to you? After all, the name is technical and difficult to spell. So what’s the big deal anyway?
Well for one, the discovery of NF-kappaB earned a Nobel Prize for biologist David Baltimore in 1975. It took three more decades to work out the science (and we are still working on it).
NF-kappaB is probably the hottest topic in the medical science world now. It is technically a protein complex that is a “transcription factor”. NF-kappaB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, and bacterial or viral infections.
NF-kappaB promotes the activation of inflammatory mediators – such as cytokines, prostaglandins, leukotrienes, CRP (C-reactive protein) – and promotes cellular dysfunction and tissue destruction. It promotes inflammation and cancers."
From our perspective, anything that inhibits NF-kappaB is helpful.
Article at:
http://www.expatglobalventures.com/health/vitamin-d-and-nf-kappab/
Cancer Rx: The $100,000 Myth by Donald W Light and Hagop Kantarjian, May 2014 in AARP Bulletin
Excerpts:
"Every patient with cancer wants the most effective treatment, but drug prices have become staggering. Eleven of the 12 new cancer drugs approved in 2012 were priced above $100,000 annually, and a 20 to 30 percent copayment can make them unaffordable even for well-insured patients."
Article at:
http://pubs.aarp.org/aarpbulletin/201405?pg=23#pg23
Forget Cholesterol, Inflammation's the Real Enemy - CBN.com
The Christian Broadcasting Network The Christian Broadcasting Network·--short 14 minute video on chronic inflammation Published on Feb 4, 2013
Excerpt;
"A growing number of medical experts say weight gain, heart disease, and other illnesses are not caused by high cholesterol, but by something different: inflammation.."
Video at:
A Test for Alzheimer's Disease Raises Thorny Ethical Issues
Experts weigh in on value of knowing without availability of effective treatments by Peter Jaret, AARP Bulletin, May 2014
Excerpt:
"When researchers recently announced a promising new blood test for Alzheimer's disease — one that could be as simple to perform as a standard cholesterol test — reactions were mixed. While some experts heralded the news, others worried that, until effective treatments are available, learning that you're likely to develop Alzheimer's could cause more harm than good.
To know or not to know
Experts say that developing a test for Alzheimer's allows for the possibility of more effective treatment. "The main problem with treating Alzheimer's disease today is that the medicines are probably given too late to do much good," says Howard Federoff, M.D., professor of neurology at Georgetown University Medical Center, who was part of the team that developed the test. "Our research reports a biomarker that will allow us to select patients who have very early disease, and we can determine if medicines are more effective when given earlier."
Article at:
http://www.aarp.org/health/brain-health/info-2014/alzheimers-disease-blood-test.html?cmp=NLC-RSS-DAILY-BULLETIN-DSO-050814-H1-338869
Big surprise: Payers don't trust pharma. The fix? Risky trials and transparency May 8, 2014 | By Tracy Staton in Fierce Pharma
Excerpts:
"Just in case you need more evidence that U.S. payers and pharma companies are at loggerheads, check out Ernst & Young's latest report on the pharma industry. It shows that drugmakers have certain opinions about their products and prices--and the people who write the checks have an entirely different set.
For one thing, drugmakers don't generate the kind of trial data payers want. Pharmacy benefit managers and other gatekeepers--not to mention healthcare providers--are most interested in comparative data. They want to see strong evidence that new meds are better.
But pharma companies try to avoid studies pitting their new products against older (and often cheaper) alternatives. That's too risky. Consider Eli Lilly's ($LLY) trial pitting its blood thinner Effient against the standard of care, Plavix; no dice. Or Merck ($MRK) testing its combination cholesterol pill Vytorin against Zocor, one of the combo's components; also a dud. So placebo remains the comparator of choice, at least until a drugmaker sees a competitive advantage in a head-to-head trial."
"Which leads us to pharma's reputation problem. According to Ernst & Young's research, less than half of payers consider industry data to be credible. That's the perceived "truth deficit"--a term coined by former Merck CEO Dick Clark--that has afflicted pharma companies for years now."
R]estoring trust with payers and the public is perhaps the most urgent and important issue facing the pharmaceutical industry today," Glen Giovannetti, EY's global life sciences leader, said in a statement. "This is no longer just about doing the right thing--it's about doing the right thing for business. Companies urgently need to become more consistent, proactive and transparent in trust-building initiatives."
Read more: Big surprise: Payers don't trust pharma. The fix? Risky trials and transparency - FiercePharma http://www.fiercepharma.com/story/big-surprise-payers-dont-trust-pharma-fix-risky-trials-and-transparency/2014-05-08#ixzz318yIUKtE
Harvard researchers find protein that could reverse the aging process By Anthony Wood May 7, 2014 in Gizmag.com
Excerpts:
"Researchers from the Harvard Stem Cell Institute (HSCI) have shown that injections of a protein dubbed GDF11, when administered to older mice, appear to cause a reversal of many signs of aging. Analysis showed that every major organ system tested displayed signs of improvement, with the protein even appearing to reverse some of the DNA damage which is synonymous with the aging process itself.
The protein GDF11 is found in humans as well as mice, and is now being considered for possible human testing due to its surprising and apparently regenerative properties."
"In terms of human applications, it is hoped that a drug derived from GDF11 will lead to a cure for conditions such as diastolic heart failure. This condition is a defect which eventually causes one or more of the ventricles of the heart to deteriorate while attempting to fill the heart with blood, in order to pump it around the body. There is also a possibility that a GDF11-inspired drug could be used to combat Alzheimer's, a condition synonymous with the aging process.
Looking to the future, the team will continue studies of the GDF11 protein, with a view to begin human medical trials within three to five years."
Article at:
http://www.gizmag.com/gdf11-protein-aging-mice-harvard/31929/?utm_source=Gizmag+Subscribers&utm_campaign=85884528c3-UA-2235360-4&utm_medium=email&utm_term=0_65b67362bd-85884528c3-76708937
Breastfeeding lowers risk of chronic inflammation: study in Xinhua English News dated April 23, 2014
"LONDON, April 23 (Xinhua) -- Breastfeeding duration is linked to chronic inflammation risk in early adulthood, which indicates the chances of cardiovascular and metabolic diseases, a new study said Wednesday.
When immune system goes wrong, it would "overreact" and attack healthy organs, which causes chronic inflammation. Previous research showed that chronic inflammation increases the risk of heart disease, strokes and type 2 diabetes.
The new study, published in British scientific journal Proceedings of the Royal Society B, found a "significant" association between duration of breastfeeding and levels of C-reactive protein (CRP), a key biomarker of inflammation, in blood samples of young adults.
Researchers from Northwestern University in the United States and other American universities analyzed blood samples of nearly 7,000 participants aged 24 to 32, 44.8 percent of whom were breastfed as infants.
Compared with individuals not breastfed, CRP concentrations were 20.1 percent, 26.7 percent, 29.6 percent and 29.8 percent lower among individuals breastfed for less than three months, three to six months, six to twelve months and greater than twelve months, respectively.
The authors of the paper concluded that, shorter durations of breastfeeding predict elevated concentrations of CRP in young adulthood, indicating increased risk for cardiovascular and metabolic diseases.
Scientific research has found numerous benefits of breastfeeding for infants. In Britain, the Department of Health recommends six months of exclusive breastfeeding."
Article at:
http://news.xinhuanet.com/english/health/2014-04/23/c_133284497.htm
PERIODONTAL DISEASE AND SYSTEMIC HEALTH in American Academy of Periodontology, perio.org, no date
Excerpt:
"Research has shown that periodontal disease is associated with several other diseases. For a long time it was thought that bacteria was the factor that linked periodontal disease to other disease in the body; however, more recent research demonstrates that inflammation may be responsible for the association. Therefore, treating inflammation may not only help manage periodontal diseases but may also help with the management of other chronic inflammatory conditions"
Article at:
http://www.perio.org/consumer/other-diseases
The Nutrition Debate #187: Chronic Systemic Inflammation and C-reactive protein (hsCRP) in the Nutrition Debate dated: THURSDAY, FEBRUARY 27, 2014
Excerpts:
"Chronic systemic inflammation is a whole other thing and is mostly unrecognized. So, why should we care? Dr. Art Ayers, a PhD biomedical researcher with a special interest in inflammation and disease, puts it this way: “Inflammation is the foundation for cancer and degenerative/autoimmune diseases. Small changes in diet and exercise, e.g. omega-3 oils, vitamin D, low starch, and maintaining muscle mass, can dramatically alter predisposition to disease and aging, and minimize the negative impact of genetic risks. His blog, “Cooling Inflammation,” is on my personal Blogger “reading list.”
"A common cause of Chronic Systemic Inflammation is periodontitis, an inflammatory disease affecting the tissues that surround and support the teeth. Periodontitis is caused by microorganisms on the tooth's surfaces, along with an overly aggressive immune response by pro-inflammatory cytokines, lymphocytes & macrophages against these microorganisms."
"The Google heading “Inflammation” includes the following: “Chronic inflammation is widely observed in obesity.”[31] The obese commonly have many elevated markers of inflammation, including: CRP (C-reactive protein)[34][35]”; “Waist circumference correlates significantly with systemic inflammatory response,[37]” and “C-reactive protein (CRP) is generated at a higher level in obese people. Mild elevation in CRP increases risk of heart attacks, strokes…and high blood pressure.”
"
Dan Brown--"I was diagnosed a Type 2 diabetic in 1986. I started a Very Low Carb diet (Atkins Induction) in 2002 to lose weight. I didn’t realize at the time that it would put my diabetes in clinical remission, or that I would be able to give up almost all of my oral diabetes meds. I also didn’t understand that, as I lost weight and continued to eat Very Low Carb, my blood lipids would dramatically improve (doubling my HDL and cutting my triglycerides by 2/3rds) and that my blood pressure would drop from 130/90 to 110/70 on the same meds. Over the years I changed from Atkins to the Bernstein Diet (designed for diabetics) and, altogether lost 170 pounds. I later regained some and then lost most of it again. As long as I eat Very Low Carb, I am not hungry and I have lots of energy. And I no longer have any of the indications of Metabolic Syndrome. My object, as long as I have excess body fat, is to remain continuously in a ketogenic state, both for blood glucose regulation and continued weight loss. I expect that this regimen will continue to provide the ancillary benefits of improved blood lipids and blood pressures as well."
Blog at:
http://www.thenutritiondebate.com/2014/02/the-nutrition-debate-187-chronic.html
Modulation of obesity-induced inflammation by dietary fats: mechanisms and clinical evidence in Nutrition Journal 2014, Published: 29 January 2014
Kim-Tiu Teng1*, Chee-Yan Chang2, Lin Faun Chang3 and Kalanithi Nesaretnam1
* Corresponding author: Kim-Tiu Teng kt.teng@gmail.com
Author Affiliations
1 Product Development and Advisory Services, Malaysian Palm Oil Board (MPOB), 6 Persiaran Institusi, Bandar Baru Bangi, 43000 Kajang, Selangor, Malaysia
2 epartment of Molecular Medicine, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia
3 Department of Medicine, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia
Abstract
"Obesity plays a pivotal role in the development of low-grade inflammation. Dietary fatty acids are important modulators of inflammatory responses. Saturated fatty acids (SFA) and n-6 polyunsaturated fatty acids (PUFA) have been reported to exert pro-inflammatory effects. n-3 PUFA in particular, possess anti-inflammatory properties. Numerous clinical studies have been conducted over decades to investigate the impact of dietary fatty acids on inflammatory response in obese individuals, however the findings remained uncertain. High fat meals have been reported to increase pro-inflammatory responses, however there is limited evidence to support the role of individual dietary fatty acids in a postprandial state. Evidence in chronic studies is contradictory, the effects of individual dietary fatty acids deserves further attention. Weight loss rather than n-3 PUFA supplementation may play a more prominent role in alleviating low grade inflammation. In this context, the present review provides an update on the mechanistic insight and the influence of dietary fats on low grade inflammation, based on clinical evidence from acute and chronic clinical studies in obese and overweight individuals."
Article at:
http://www.nutritionj.com/content/13/1/12
The Relationship between Sugar and Inflammation in Low Carb Magazine by Dr Nancy Appleton PhD
Excerpts:
"Scientists have long linked oedema, arthritis and inflammatory bowel disease with inflammation. Only recently the medical community has implicated the process to diabetes, certain cancers and other unsolvable degenerative conditions. The latest research links heart disease more to various inflammatory conditions than to high cholesterol. Researchers are doing their best to come up with anti-inflammatory drugs and other cures for this inflammation."
"One of the biggest offenders of inflammation is ingestion of sugar. By sugar I mean table sugar, brown sugar, raw sugar, turbinado sugar, honey (even raw), maple sugar, corn sweetener, dextrose, glucose, fructose and any other word that ends in an "ose", barley malt, rice syrup, liquid cane sugar, concentrated fruit juice and others. Don't be fooled by the name organic when it applies to sugar. Sugar is sugar, organic or not, and the following will explain exactly what can happen in the body when you eat as little as two teaspoons."
"Dr William Philpott, in his book BRAIN ALLERGIES says, "One of the most important systemic functions of the pancreas is to supply proteolytic enzymes (enzymes from the pancreas that aid in the digestion of proteins into polypeptides and then amino acids) which act as regulatory mechanisms over inflammatory reactions in the body. Poor digestion of proteins to amino acids occurs as a consequence of insufficient pancreatic proteolytic enzymes. As a result, unusable inflammation evoking protein molecules are absorbed through the intestinal mucosa and circulate in the blood, reaching tissues in partially digested form."
"From my clinical experience, acne and water retention also are caused by food allergy. Ulcerative colitis and Crohn's disease are also caused by undigested protein.(16) The nonusable protein can go anywhere in the blood and cause problems. At this time our immune system looks at this undigested food as a foreign invader, and our immune system comes to our defence and removes this foreign protein from our blood.(l7),(l8)
When we consume sugar over and over, we weaken our body tissues, our white blood cells
and our immune system.(l9),(20) Our white cells and other tissues need protein to function optimally. The cells can not get the correct protein when it is not digested and assimilated properly.
When our body tissues and immune system are weak, we can not fend off foreign invaders. Not only are we now susceptible to degenerative diseases but also infectious diseases. Whatever infectious disease we will get depends on what bacteria or virus is in the environment, and the weakness in our genetic blueprint determines what tissue will be affected and to which degenerative disease we are susceptible.
Sugar in the amount that we eat today (over 150 lbs, or over 1/2 cup a day,) continually upsets our body chemistry, causes the inflammatory process and leads to disease. The less sugar you eat, the less inflammation, and the stronger the immune system to defend us against infectious and degenerative diseases."
Article at:
http://www.lowcarbmonthly.com/general-health/the-relationship-between-sugar-and-inflammation.html
UCSF, Stanford and Johns Hopkins join FDA partnership to speed drug development May 6, 2014 | By Emily Mullin in Fierce Biotech Research
Excerpts:
"At a time when Big Pharma is increasingly tapping academic institutions for expertise in informatics and data-driven computer models for drug discovery, the FDA has selected Johns Hopkins University, Stanford University and the University of California, San Francisco (UCSF) for a new initiative aimed at streamlining the drug development and approval process.
Under the FDA's Centers of Excellence in Regulatory Science and Innovation (CERSI) program, UCSF will be the site of a new regulatory science center on the West Coast. The center will bring together researchers in the UCSF School of Pharmacy and Stanford University in an effort to help spur new approaches in drug development."
"The pharmaceutical and biotech industries are facing huge challenges, with the majority of drugs failing in clinical trials because they are not effective," said Kathy Giacomini, a professor in the UCSF School of Pharmacy and co-chair of the UCSF Center for Quantitative Pharmacology, in a statement. "These new computer-based models are enabling us to predict how the human body metabolizes a drug, the drug's toxicity and its effectiveness in preventing and treating various human diseases, as well as how that varies across a population of diverse people. This partnership will enable us to develop new models and methods, and also move these technologies out of academia and into practice."
Read more: UCSF, Stanford and Johns Hopkins join FDA partnership to speed drug development - FierceBiotech Research http://www.fiercebiotechresearch.com/story/ucsf-stanford-and-johns-hopkins-join-fda-partnership-speed-drug-development/2014-05-06#ixzz3153Eu3pv
Anatabine for MS treatment?; New target found for Alzheimer's;
February 5, 2013 in Fierce Biotech Research (just a reminder what Dr Mullan is doing.)
Article:
Star Scientific Reports Publication of First Peer-Reviewed Article on the Effects of Anatabine in an Animal Model of Multiple Sclerosis
February 5, 2013
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GLEN ALLEN, Va., Jan. 31, 2013 /PRNewswire/ -- Star Scientific, Inc. (STSI) today announces publication of the first peer-reviewed article examining the effects of anatabine in a mouse model of the debilitating autoimmune and neurodegenerative disease multiple sclerosis (MS). The study, conducted by the Company's research partner, The Roskamp Institute, was designed to determine whether anatabine had beneficial effects on the development of experimental autoimmune encephalomyelitis (EAE) in mice, which is a standard mouse model of MS. Some of the findings were previously presented at Neuroscience 2012, an international scientific convention; however, the article in PLOS ONE contains complete results of the study, and the article was subjected to the peer review evaluation process prior to publication.
The Roskamp researchers found that orally administered anatabine significantly reduced neurological disability and improved motor coordination of EAE mice. In particular, paralysis of the hind limbs was markedly suppressed in the anatabine treated group, and neurological symptoms were delayed in the anatabine treated group compared to the placebo group.
The study results also showed that anatabine supplementation resulted in suppression of several pro-inflammatory molecules (cytokines) in the blood and in the spleen of the EAE mice. The observed reduction in the levels of several inflammatory molecules provides evidence that the experimental autoimmune process has been reduced. Anatabine also significantly suppressed STAT3 and NF-kB activation in the spleen and the brain of the EAE mice. These two intracellular transcription factors (proteins) regulate a large array of inflammatory genes including cytokines, suggesting a mechanism by which anatabine antagonizes pro-inflammatory cytokine production.
In addition, the researchers found that anatabine reduced the infiltration of inflammatory cells in the brain and significantly prevented demyelination in the spinal cord of EAE mice. In humans, demyelination in the spinal cord is associated with muscle weakness and paralysis in MS. Therefore, the researchers concluded that the "data suggest that anatabine may be effective in the treatment of MS."
Dr. Michael Mullan, President and CEO of the Roskamp Institute, commented, "The most remarkable results were the clear inhibition of brain inflammation and the degeneration of the spinal cord by anatabine and the accompanying inhibition of the severe paralysis that usually accompanied the model."
Dr. Daniel Paris, the primary author of the article and Head of Research and Development at the Roskamp Institute, added, "The oral administration of anatabine potently reduced the neurological deficits and abrogated the pathological lesions in the spinal cord that are responsible for the development of paralysis in this mouse model of multiple sclerosis (MS). In addition our work also explains the beneficial activity of anatabine in this MS model by showing that this compound prevents the activation of key molecules that orchestrate the propagation of inflammation in the central nervous system and the periphery."
The full title of the study is, "Amelioration of Experimental Autoimmune Encephalomyelitis by Anatabine," and can be viewed here: http://dx.plos.org/10.1371/journal.pone.0055392. This study builds upon earlier research conducted by the Roskamp Institute, which showed that the natural alkaloid anatabine displays anti-inflammatory properties and readily crosses the blood brain barrier, suggesting it could represent an important compound for mitigating many types of neuro-inflammatory conditions.
PLOS ONE is an international, peer-reviewed, open-access, scientific journal.
Read more: Anatabine for MS treatment?; New target found for Alzheimer's; - FierceBiotech Research http://www.fiercebiotechresearch.com/story/anatabine-ms-treatment-new-target-found-alzheimers/2013-02-05#ixzz31502ytAz
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GlaxoSmithKline and Galapagos succeed in psoriasis after two setbacks April 17, 2014 | By Damian Garde in Fierce Biotech
Excerpts:
"Galapagos and partner GlaxoSmithKline ($GSK) say their anti-inflammation candidate hit its mark in a mid-stage trial on psoriasis, a stroke of good news for a drug beset by developmental slipups.
The treatment, GSK2586184, met its primary endpoint of improving psoriasis severity at 12 weeks in a 66-patient Phase IIa study, the partners said, and the two reported no serious adverse events. GSK is running the placebo-controlled study on its own, and, under a 2012 deal between the duo, Galapagos is in line for up to $47 million in milestones and a cut of sales if the drug makes its way to market.
That seemed like a shaky proposition after Galapagos revealed in February that its Big Pharma partner had halted a Phase II study of GSK2586184 in lupus due to lack of effect and put on hold a Phase I/II trial testing the drug in ulcerative colitis. GSK's moves pinned any hopes for the JAK1 inhibitor on the then-pending psoriasis study, and now, in light of the drug's latest success, the U.K. giant said it plans to review the data before deciding whether to press on into Phase III.
Galapagos' next big readout is due in June, when it expects to report Phase II data on GLPG0974, an unpartnered FFA inhibitor with potential in ulcerative colitis. And the collaboration-inclined biotech is working with AbbVie ($ABBV) on the mid-stage rheumatoid arthritis treatment GLPG0634 and the preclinical cystic fibrosis drug GLPG1837. Alongside partners Johnson & Johnson ($JNJ) and Servier, Galapagos is developing treatments in oncology and a slew of inflammatory diseases.
Last month, the Belgian company sold off its contract research arm to Charles River Laboratories ($CRL) for $179 million, moving away from its once-diversified model to better focus on its pipeline.
Read more: GlaxoSmithKline and Galapagos succeed in psoriasis after two setbacks - FierceBiotech http://www.fiercebiotech.com/story/glaxosmithkline-and-galapagos-succeed-psoriasis-after-two-setbacks/2014-04-17#ixzz314wr3oSG
AstraZeneca continues to chop back, spotlights immuno-oncology PhIII
April 24, 2014 | By John Carroll in Fierce Biotech
Excerpts:
"AstraZeneca ($AZN) is continuing its campaign to refashion its image as it tries to shake off past setbacks and unsuccessful units and turn analysts' attention to its brightest pipeline prospects, particularly in cancer."
"AstraZeneca is concentrating R&D on a few key areas: oncology, cardiovascular and metabolic diseases, and respiratory and inflammation, reports Reuters"
Read more: AstraZeneca continues to chop back, spotlights immuno-oncology PhIII - FierceBiotech http://www.fiercebiotech.com/story/astrazeneca-continues-chop-back-spotlights-immuno-oncology-phiii/2014-04-24#ixzz314vNGfp7
Celgene shells out $710M for a PhIII Crohn's drug with billions on the line, April 24, 2014 | By Damian Garde in Fierce Pharma
Excerpt:
"As Big Pharma trades billions for whole business units, the deal-inclined Celgene ($CELG) has quietly paid $710 million to get its hands on a late-stage Crohn's disease contender in a deal that could spiral out to 10 figures.
Celgene is handing over $710 million upfront to Ireland's Nogra Pharma to get its hands on GED-0301, an oral antisense drug that targets the messenger RNA Smad7 to treat moderate to severe Crohn's symptoms. Antisense therapies are synthetic copies of nucleic acids designed to treat diseases by shutting down the genes that cause them, usually by binding to mRNA.
Under the agreement, Nogra is in line for up to $815 million more in development milestones and $1.1 billion in sales payouts if the drug ever hits $4 billion in a year, bringing the maximum deal value to about $2.6 billion."
"The drug joins Celgene's small but promising anti-inflammatory pipeline, led by apremilast, a blockbuster hopeful that picked up its first FDA nod to treat psoriatic arthritis last month with a make-or-break verdict on psoriasis expected by September. The company is also running a Phase II trial on the cancer drug Pomalyst in systemic sclerosis and conducting early-stage work on CC-220 for a variety of inflammatory diseases.
Read more: Celgene shells out $710M for a PhIII Crohn's drug with billions on the line - FierceBiotech http://www.fiercebiotech.com/story/celgene-forks-over-710m-phiii-crohns-drug/2014-04-24#ixzz314t2PFNU
First Million-Dollar Drug Near After Prices Double on Dozens of Treatments By Robert Langreth Apr 30, 2014 in Bloomberg
Excerpt:
"Earl Harford, a retired professor, recently bought a month’s worth of the pills he needs to keep his leukemia at bay. The cost: $7,676, or three times more than when he first began taking the pills in 2001. Over the years, he has paid more than $140,000 from his retirement savings to cover his share of the drug’s price."
"Starting prices for new drugs are escalating as well. Today, a cholesterol-lowering treatment for certain rare cases costs $311,000 a year and a cystic fibrosis medicine -- developed partly with funding from a charity -- costs $300,000 annually. Fifteen cancer drugs introduced in the last five years cost more than $10,000 a month, according to data from Memorial Sloan Kettering Cancer Center.
Analysts, meanwhile, predict the first $1 million drug treatment may be just around the corner."
"While generic drugs pushed by insurers and the government now make up 86 percent of all medicines used in the U.S., that hasn’t reduced total spending on prescription medicines. In 2012, Americans spent $263 billion, or 11 percent more than the $236 billion spent in 2007, according to U.S. government data.
“We have been consistently noticing that as manufacturers near the end of their product’s life cycle, they are seeking larger price hikes than they previously did,” said Sharon Frazee, vice president for research at Express Scripts Holding Co., one of the country’s largest pharmacy benefit managers.
Last year, increases in prices for existing branded prescription drugs accounted for $20 billion of the industry’s 2013 sales growth, offsetting $19.3 billion in revenue declines due to patent expirations, according to the IMS Institute for Healthcare Informatics. Discounts and rebates counteracted some of the price increases, according to the report."
"The downside is financial strain on patients. “Every day in my clinic there are patients who start discussing they can’t afford this drug or that drug” because it costs too much, said Hagop Kantarjian, a leukemia doctor at M.D. Anderson Cancer Center in Houston, who wrote an article in the medical journal Blood in which a group of 100 hematology doctors protested the “unsustainable” costs of leukemia drugs."
"How drug companies price medicines “is one of the industry’s dirty secrets,” said Bernard Munos, a former Eli Lilly executive who founded InnoThink Center for Research in Biomedical Innovation, an Indianapolis consulting firm. “Everyone is engaging in extreme prices because they can get away with it.”
The revenue from higher prices has helped companies hit by steep declines as patents ended on blockbusters, like Lipitor. Patients have also gained from important new treatments for diseases such as multiple sclerosis, cystic fibrosis and rare forms of cancer -- including diseases that at one time were neglected because the patient populations were viewed as too small to be profitable."
"Additionally, as products lose revenue because of competition, drugmakers will sometimes raise prices to make up the difference. For example, prescriptions for Biogen Idec Inc.’s multiple sclerosis drug Avonex have slowly declined in the U.S. in recent years because of competition. At the same time Avonex’s wholesale price has risen, growing by 147 percent to $1,363.50 per injection this year from $552.19 in late 2007, according to data from DRX. After discounts, the DRX analysis found a typical health plan pays around $1,177 per injection."
Article at;
http://www.bloomberg.com/news/2014-04-30/drug-prices-defy-gravity-doubling-for-dozens-of-products.html
Report: Drug prices skyrocketing, with no end in sight May 1, 2014 | By Arlene Weintraub in Fierce Pharma
Excerpt:
"
Despite a wave of M&A deals aimed at increasing efficiency and lowering expenses in the pharmaceutical industry, drug prices continue to rise, with several drug companies nearly doubling the costs of key products over the last 7 years. That's the conclusion of an analysis prepared for Bloomberg by DRX, a California-based provider of health software.
According to the DRX analysis, Merck ($MRK), Novartis ($NVS), Eli Lilly ($LLY), and Pfizer ($PFE) are among the companies that have hiked prices by at least 75% since 2007. The cost of Lilly's diabetes drug Humulin was up an incredible 354% during the period, while Sanofi's ($SNY) popular Lantus rose 160%. Even Pfizer's former cholesterol blockbuster Lipitor, which went off-patent in 2011, was on the list--its price has risen 102% since 2007."
"It's not just diabetes that's driving up drug prices. The DRX analysis found huge price increases for some cancer medications, including Novartis' Gleevec to treat chronic myeloid leukemia, which costs $306.43 for a single pill this year--up from $118.78 in 2007. The price of Roche's ($RHHBY) lung cancer drug Tarceva rose 90% during the studied time period, while that of Bristol-Myers Squibb's ($BMY) leukemia drug Sprycel doubled.
While this all might seem a small price to pay for medicines that can save lives, the healthcare system is likely to suffer if drug spending continues to be out-of-whack with spending on other commonly purchased goods. As Bloomberg points out, while the prices of some drugs have been doubling, the consumer price index has risen just 12% since 2007."
Article at:
http://www.fiercepharma.com/story/report-drug-prices-skyrocketing-no-end-sight/2014-05-01#ixzz314l5ybVt
Subscribe at FiercePharma
Chronic Acidity Leads To Chronic Inflammation and Chronic Inflammation Leads To Cancer by Robert O. Young D.Sc., Ph.D. in Articles of Health dated Sunday, April 20, 2014
Excerpt:
""Chronic Acidity from an Acidic Lifestyle Leads to Inflammation that Leads to Cancer that Leads to Death! Now you know the pathology of cancer and death". Dr. Robert O. Young
. . .
Our body’s immune system forms a defensive shield that any fighting force would be proud of. One of its most powerful weapons is inflammation, a carefully orchestrated maneuver designed to eliminate enemies such as bacteria, injured cells and chemical irritants. Without it, we probably wouldn’t survive beyond infancy.
But inflammation has a split personality – one that can wreak havoc for those unfortunate enough to experience it. And we now know that inflammation’s dark side is a powerful force in cancer development, where it aids and abets tumor growth and spread around the body. The longer the inflammation persists, the higher the risk of associated carcinogenesis. http://www.cancernetwork.com/review-article/chronic-inflammation-and-cancer#sthash.gedvxqlo.dpuf
A new study shows how inflammation can help cause cancer. Chronic inflammation due to infection or to conditions such as chronic inflammatory bowel disease is associated with up to 25 percent of all cancers.
http://www.sciencedaily.com/releases/2011/04/110419091159.htm
Chronic Acidity Leads To Chronic Inflammation and Chronic Inflammation Leads To Cancer. Therefore the cause of cancer is excess tissue and organ acidity which has not been properly neutralized or eliminated through the four channels of elimination - urination, defecation, perspiration or respiration. So what causes chronic acidity? An acidic lifestyle and diet. the ingestion of meat, dairy, sugar, lack of exercise and stress are the primary contributors to chronic acidity that leads to inflammation, cancer and then death.
Article at:
http://articlesofhealth.blogspot.com/2014/04/chronic-acidity-leads-to-chronic.html
Chronic Inflammation PERIODONTAL DENTISTRY | 22. APR, 2014 BY ANTHONY FERRERA in Burlingame Dentistry
Excerpt:
"But sometimes an immune system doesn’t know when to stop. It smolders beneath the surface, destroying the very tissue it’s supposed to heal. This potential volcano at the core of your body is called Chronic Inflammation. CI is thought to trigger such diseases as heart disease, cancer, stroke, diabetes, Alzheimer’s and gum disease.
A simple blood test for chronic inflammation focuses on C-reactive protein (CRP), which the liver produces when inflammation is present. Individuals with the highest levels of CRP are three times as likely as those with the lowest levels to suffer a heart attack within six years.
Your mouth can present evidence of CI — sore or bleeding gums. That is periodontal disease (gum disease), and it needs to be treated as soon as it is detected to reduce the risk.
Here’s how you may be able to reduce CI:
Brush and floss twice daily
Lose weight
Stop smoking, or don’t start
Control your blood pressure
Exercise regularly
Schedule time for meditation or prayer
Eliminate sugars, refined starches, and processed foods from your diet, replacing them with fresh fruits and vegetables rich in antioxidants, whole foods high in fiber, and healthy fats such as nuts and small fish.
Treat periodontal disease in its early stage"
(So, even the dentists are concerned about chronic inflammation.)
Article at:
http://www.burlingamedentistry.com/blog/chronic-inflammation/
Aging Process Speeded By Chronic Inflammation by Beth Balen on March 31, 2014 in Guardian's Liberty Voice
Excerpts:
"Healthspan: the years of life spent relatively free of disability and serious illness. A study from the Yale School of Medicine released in the October, 2013, issue of Cell Metabolism shows that chronic inflammation can speed the aging process and significantly reduce healthspan.
Chronic inflammation is different from the swelling that occurs with a specific injury, such as a sprained ankle. Acute inflammation can typically be resolved with ice and time. Chronic inflammation is a slowly advancing disturbance that cannot be felt or tested for.
It starts with the immune system, the body’s first line of defense against damage or harm. During the aging process the body’s cells change, causing the immune system to produce low-level, chronic inflammation throughout the body. The Yale research is the first to show that inflammation is directly linked to functional deterioration during aging.
The Yale study has identified an immune sensor, Nlrp3, as the specific trigger of inflammation. Nlrp3 is activated with age and is the common start of inflammation-driven functional decline. This inflammation is associated with many chronic age-related diseases, including gout, arthritis, diabetes, impaired memory, and Alzheimer’s disease."
"Vishwa Deep Dixit, Yale School of Medicine and lead author of the study said the question is whether the trigger for aging that causes low-level inflammation can be switched off to slow the onset of the chronic diseases that occur with age.
If the Nlrp3 immune sensor could be manipulated to reduce or delay the chronic inflammation that speeds the aging process, it could possibly lead to prolonged healthspan, and old age reasonably free of disability or disease."
"As the population over 50 increases, doctors are seeing an associated increase in age-related diseases. Researchers now say treating those individual diseases may be wrong, and that they may be more effectively handled by treating the chronic inflammation shown to speed the aging process."
Article at:
http://guardianlv.com/2014/03/aging-process-speeded-by-chronic-inflammation/
Get A Grip On Arthritis and other inflammatory disorders by Lorna Vanderhaeghe
Excerpts:
"Stress, bacteria, viruses, parasites, environmental poisons, certain foods (including sugar), smoking, high blood-insulin levels and obesity are just a few of the factors that promote inflammation. The fact that we are living a lot longer than our ancestors did may also be contributing to inflammation; as we age, our ability to shut off the inflammatory process often weakens. "
"The foods you choose can either promote or prevent inflammation. Foods containing arachidonic acid, such as eggs, organ meats (including liver, heart and giblets), beef and dairy products promote inflammation. "
"We know that overeating promotes the inflammatory response and suppresses the immune system. Tests performed by the National Institute on Aging revealed that when animals were fed 50 percent fewer calories per day, their immune response improved, the amount of inflammatory cytokines in circulation was reduced, thymus size was maintained and inflammation-fighting T-cell function improved."
"It is known that even an extra 20 pounds can create an abundance of inflammation in the human body and lower overall immunity. Weight management is an important aspect of maintaining a balanced immune system and controlling inflammation. With over 50 percent of North Americans overweight, and an additional 15 percent or more classed as obese, public health care planners expect to see a tremendous increase in inflammatory diseases. Fat cells act like immune cells and secrete inflammatory factors (histamines and cytokines), especially during weight gain. The more fat cells you have, the more potential there is for inflammation.
"Inflammatory cytokines are secreted at a higher rate by those who have insomnia, compared to those who do not. During sleep, the body regenerates and the immune system calms down. Lack of restorative sleep is a major promoter of inflammation. People with rheumatoid arthritis or other autoimmune disorders know this, because lack of sleep due to pain associated with their condition promotes further flare-ups and more pain.
Up to 33 percent of North Americans are in chronic pain, which disables more people than cancer and heart disease combined. Lost workdays, workers' compensation claims and medical expenses associated with chronic pain are estimated to cost the both Canada and the U.S. over US$100 billion annually."
Article at:
http://www.healthyimmunity.com/books/get-a-grip-on-arthritis/Causes-of-Chronic-Inflammation.asp
How inflammation makes you fat and diabetic (and vice versa)
by CHRIS KRESSER in Health for the Twenty First Century
Excerpts:
"The idea that inflammation precedes diabesity is supported by the observation that humans with other chronic inflammatory conditions are at higher risk of developing T2DM. For example, about one-third of chronic Hepatitis C patients develop T2DM, and those with rheumatoid arthritis are also at higher risk.
Second, inflammation begins in the fat cells themselves. Fat cells are the first to be affected by the development of obesity. As fat mass expands, inflammation increases. One mechanism for this may be dysfunction of the mitochondria (the “power plant” of our cells) caused by the additional stress obesity places on cellular function. Another mechanism may be oxidative stress. As more glucose is delivered to the fat cells, they produce an excess of reactive oxygen species (ROS) which in turn starts an inflammatory cascade within the cell.
Third, inflammation of the fat tissue causes insulin resistance, which is the primary feature of T2DM. TNF-a, a cytokine (small protein) released during the inflammatory response, has been repeatedly shown to cause insulin resistance. Several other proteins involved with inflammation, such as MCP-1 and C-Reactive protein, have also been shown to cause insulin resistance.
Fourth, inflammation of the brain (specifically the hypothalamus) causes leptin resistance, which often precedes and accompanies insulin resistance and T2DM. Leptin is a hormone that regulates appetite and metabolism. It does this through its effect on the hypothalamus. When the hypothalamus becomes resistant to leptin, glucose and fat metabolism are impaired and weight gain and insulin resistance result.
Finally, inflammation of the gut causes leptin and insulin resistance. This may occur via an increase in lipopolysaccharide (LPS), an endotoxin produced by Gram-negative bacteria in the gut. LPS has been shown to cause inflammation, insulin resistance in the liver and weight gain."
"Collectively, these findings are consistent with the theory I presented in the last article that obesity is an autoimmune, inflammatory disorder.
As we’ve seen, inflammation is both the cause and the result of diabesity. Once obesity and/or insulin resistance have been established, each can further stimulate the production of inflammatory cytokines, forming a vicious cycle of inflammation and diabesity.
It follows, then, that the key to preventing and treating diabesity is reducing inflammation. Unfortunately, few clinicians treating diabesity today understand this. Focusing exclusively on regulating blood sugar and fat hormones without addressing other potential causes of inflammation is bound to produce inferior results.
What are these “other causes” of inflammation? In a phrase: the modern lifestyle. Specifically, dietary triggers (fructose, wheat and industrial seed oils), stress, poor sleep, gut dysbiosis and environmental toxins all cause inflammation on their own. When combined together, they are an explosive mix."
Article at:
http://chriskresser.com/how-inflammation-makes-you-fat-and-diabetic-and-vice-versa
Only within the last 3 months or so has there been an explosion in information about chronic inflammation. Seems like many researchers and doctors have zeroed in their information and opinion about what chronic inflammation is all about. Why all the interest now? Maybe they have connected the dots where in the past there were not enough dots? Whatever it is, my data mining and meta searches are exploding with info now about chronic inflammation. Even with all this interest, the only thing I see about remedies have to do with proper diets and avoidance of pathogens and carcinogens. There have been some discussion about statins being used because of their anti-inflammatory characteristics, but there have been arguments against it because some say cholesterol should not be lowered. You can go on and on, but you as an investor should explore all the current science and decide how to invest. I, myself, think anatabine citrate will poke it's head up one day and become better known when and if STSI can demonstrate clinical efficacy as it becomes a drug. It amazes me how much big pharma has influence in the business of drugs and the publication of research. I put these postings up so you can see the science building up around chronic inflammation. So far, no one has a magic bullet and big pharma has no solution on Alzheimers. For example, an article today in Reuters:
"A deal to share Phase III costs and share eventual profits was probably the easiest approach, he told reporters on Wednesday, but AstraZeneca could also out-license the product and take a royalty on any eventual sales.
AstraZeneca believes its BACE inhibitor could potentially sell as much as $5 billion a year, but it gives it only a 9 percent chance of success on a risk adjusted basis given the high failure rate in the disease sector."
As you can see the stakes are high but traditional research into
Alzheimers show a poor yield. (maybe AstraZeneca doesn't see it's BACE solution working too well?) Most big pharmas are getting desperate because their pipelines are diminishing and their current clinical trials and research are showing very poor results. They know that chronic inflammation and Alzheimers are the next big thing in prescription drugs, their life depends on coming up with solutions. With what you know about Anatabloc, what do you think the potentials are?
Arthritis Research Looks to Unlock Secrets of Heart Disease and Depression in Scientific American dated Apr 29, 2014 |By Iain McInnes and The Conversation UK
Excerpts:
"“Arthritis is for old people, right?”
This is an outdated view of a spectrum of diseases that affect people of all ages in the population. In the past decade, there has been a revolution in the understanding and treatment of many forms of arthritis, particularly one devastating variety, namely rheumatoid.
So what is rheumatoid arthritis? Those afflicted suffer pain, swelling and progressive deformity of joints if untreated.
The core problem seems to be uncontrolled inflammation – the immune system that normally faithfully defends us against infection turns its offensive molecular and cellular power upon the joints, which leads to substantial damage."
"Recent landmark studies clearly associate the risk of getting rheumatoid arthritis with smoking both directly and passively. Those with the disease who smoke are considerably less likely to respond to therapy. Some estimate that smoking cessation could reduce the future disease burden by up to 30%.
A second major advance has been new understanding of the vital importance of the bacteria we all carry in our gastrointestinal tract – the “human microbiome”. Variations in these bacterial populations are now associated with development of several diseases related to immune dysfunction.
New data suggests a link between rheumatoid arthritis and these variations. But the value of this for diagnosis or treatment is unknown and many more studies will be required."
"Inflammation and other diseases
A vital recent discovery has been that rheumatoid arthritis brings medical challenges beyond the joint. It also increases the risks of heart attacks, strokes, depression, poor concentration and bone fractures via accelerated osteoporosis (bone thinning). The mechanisms underlying these phenomena are not entirely clear but seem to emanate from the same inflammatory pathways that drive the primary attack on the joint.
Unravelling these pathways will be important not only to reduce risks in sufferers, but also because these pathways illuminate the potential mechanisms that could operate in the wider primary diseases of these tissues. There are already many studies that implicate inflammation in atherosclerosis (narrowing of the arteries) and coronary heart disease (leading to angina and heart attacks).
These discoveries are likely to lead to new and exciting preventative and therapeutic strategies that could impact millions of the population. Similarly inflammatory pathways are implicated in a variety of mood disorders, especially depression, raising hopes of new treatment options for these most difficult of human conditions."
"While all this has been happening, two fundamental developments have led to a revolution in treatment over the past decade. The first is a change in the strategic approach to how the disease is managed. Rheumatologists now choose clear targets for treatment and adhere to widely endorsed treatment guidelines and algorithms.
The second development has been the advent of a variety of new medicines that capitalise on the explosion of knowledge about the pathology of the disease, in a sign that modern molecular medicine is truly delivering.
These new medicines include small chemical drugs and larger biologic drugs – the latter are proteins that mimic those that operate in the immune system itself. These have brought substantial improvements in outcomes."
Article at:
http://www.scientificamerican.com/article/arthritis-research-looks-to-unlock-secrets-of-heart-disease-and-depression/?&WT.mc_id=SA_HLTH_20140506
Chronic Diseases Data at The Marshall Protocal Knowledge Base, Autoimmunity Research Foundation.
Excerpts:
"The last half century has seen a steady increase in the incidence and prevalence of chronic inflammatory diseases with further increases expected. According to the Marshall Pathogenesis, a number of factors are to blame:
misuse of antibiotics especially Beta-lactam antibiotics
vitamin supplementation including folic acid but especially vitamin D
novel vectors for sharing pathogens including blood donation
widespread adoption of compulsory mass vaccinations"
"Manifestations of both arteriosclerosis1 2 and cardiac disease3 can be observed in mummies of ancient Egypt. Ötzi the Neolithic Iceman who lived around 3300 BC was found to have arthritis.4 Yet, it is only recently that rates of certain chronic diseases have appeared to escalate.
At the beginning of the twentieth century, infectious diseases were the leading cause of death worldwide. In the United States, three diseases — tuberculosis, pneumonia, and diarrhoeal disease — caused 30% of deaths.5 By the end of the twentieth century, in most of the developed world, mortality from infectious diseases had been replaced by mortality from chronic illnesses such as heart disease, cancer and stroke.6
According to a recent Nature paper there were 36 million deaths from “noncommunicable diseases” in 2008, or 63% of all deaths worldwide."
"In 2000, approximately 125 million Americans (45% of the population) had chronic conditions and 61 million (21% of the population) had multiple chronic conditions.10
According to a 2004 report:
In 2004, almost half of all Americans, or 133 million people, live with a chronic condition. … People with chronic conditions account for 83 percent of health care spending and those with five or more chronic conditions have an average of almost fifteen physician visits and fill over 50 prescriptions in a year."
"The rate of chronic health conditions among children in the United States increased from 12.8% in 1994 to 26.6% in 2006, particularly for asthma, obesity, and behavior and learning problems, according to results of a new prospective study published in the 2010 paper in Journal of the American Medical Association.11"
"In the United States, the number of people with chronic conditions is projected to increase steadily for the next 30 years.19 Partnership for Solutions National Program Office estimates that it will reach 157 million by 2010 while another estimate says that figure will be 140 million."(graph shows 118 million in 1995 with chronic diseases in U.S. climbing to 171 million in 2030.)
"Obesity rates worldwide have doubled in the last three decades, even as blood pressure and cholesterol levels have dropped, according to several studies published in a 2011 issue of Lancet.22 In 1980, about 5 percent of men and 8 percent of women worldwide were obese. By 2008, the rates were nearly 10 percent for men and 14 percent for women. That means 205 million men and 297 million women were obese. An additional 1.5 billion adults were overweight.
Another team concluded in a recent meta-analysis that if Americans keep gaining weight at the current rate, 75 percent of U.S. adults will be overweight and 41 percent obese by the year 2015. A 2002 paper concluded that “the prevalence of obesity is increasing globally, with nearly half a billion of the world’s population now considered to be overweight or obese.”23"
"Diabetes
In a 2010 paper, Boyle predicted that one-third of the U.S. population will have diabetes by 2050. In a 2002 paper, Edwin Gale concluded that the incidence of childhood diabetes (type I diabetes) began to steadily increase at almost the same time – from the 1950s onwards.25 This increase had been identified in a range of developed countries including the United States, Sardinia, and Northern Europe.26
According to a 2009 paper in Diabetes care, the number of people with diabetes in the United States is expected to double over the next 25 years. That would bring the total by 2034 to about 44.1 million people with the disease, up from 23.7 million today"
"It has been predicted that atherosclerosis will be the primary cause of death in the world by 2020"
There is a TON of data here for chronic diseases, worth looking at and studying for a while.
website at:
http://mpkb.org/home/pathogenesis/epidemiology
"Inflammation and the Host Response to Injury is a large-scale collaborative research program supported by the National Institute of General Medical Sciences, a division of the National Institutes of Health. Our NIH investigators agreed that the most important biological problem to tackle in the area of injury research centered on the innate inflammatory response, and specifically, to improve our systems level understanding of the key regulatory elements, and their relative roles and importance that drive the host's response to serious injury and its accompanying severe systemic inflammation
The problem could only be addressed by first acquiring large amounts of new data ("discovery-driven approach"). It was evident to our participating investigators that our limited success in developing appropriate therapeutic interventions for the treatment of the severe trauma or burn injured patient has been the result of an incomplete understanding of the integrated host response to injury. The excitement of the group focused on our potential to pay attention to experimental detail and data gathering capacity along with the potential to derive greater accuracy and informational content in ever smaller and more enriched samples, and to ultimately introduce genome-wide microarray technologies and high throughput proteomics to clinical medicine. Such an improved understanding would lead to genomic and proteomic markers that predict ultimate outcomes both good and bad, and would suggest new targets for further basic and clinical research, as well as fruitful targets for pharmacological and immunomodulatory interventions.
We continue our work towards reaching our Program deliverables and contributions, which should include: (1) a well-annotated clinical database of rich genomic and proteomic information; (2) new technology for application in clinical studies (microfluidic cell separations, novel custom gene chip); (3) novel bioinformational, statistical and pathway analysis tools for the exploration of the genomic and proteomic data; and (4) gene sets with high predictability of multiple organ failure and other clinical trajectories.
Very detailed, technical website focused on both acute and chronic inflammation causes, immune functions, injury and inflammation, inflammatory diseases, and commonly asked questions/answers.
Website at:
http://www.gluegrant.org/index.htm
Autoimmune diseases fact sheet at womenshealth.gov
Excerpts:
"Our bodies have an immune system, which is a complex network of special cells and organs that defends the body from germs and other foreign invaders. At the core of the immune system is the ability to tell the difference between self and nonself: what's you and what's foreign. A flaw can make the body unable to tell the difference between self and nonself. When this happens, the body makes autoantibodies (AW-toh-AN-teye-bah-deez) that attack normal cells by mistake. At the same time special cells called regulatory T cells fail to do their job of keeping the immune system in line. The result is a misguided attack on your own body. This causes the damage we know as autoimmune disease. The body parts that are affected depend on the type of autoimmune disease. There are more than 80 known types."
Lengthy website explaining details of autoimmune disorders, their cause, symptoms, and management.
Link is:
https://www.womenshealth.gov/publications/our-publications/fact-sheet/autoimmune-diseases.html
The cells that make us fat discovered: these are triggered by inflammation in Doc Salus article.
Excerpts:
"A study conducted by a group of Viennese endocrinologists, published on the International Journal of Obesity (Zeyda M et al, Int J Obes (Lond) 2007 Jun 26; [Epub ahead of print]), shed new light on the triggers of weight-gain and its correlation with low-grade inflammation. Thanks to these results, it is today even clearer why people showing food-related inflammation may develop insulin resistance more easily.
Zeyda et al. Work is not the sole one: since 2004, Mitchell Lazar has published on Science data showing why macrophages may produce resistin as a simple response to low-grade inflammation and cause insulin-resistance and fat accumulation in adipose cells as a defensive response.
By demonstrating how BAFF, a cytokine deeply linked to food-related inflammation, leads directly to situations of insulin resistance, various other articles have finally identified the bridge from inflammation to weight-gain, as well as to the stimulation of adipokines that lead to obesity.
Clearly, a diet able to control food-related inflammatory events (intolerances) may help recover one’s own ideal weight, reducing the fat body mass and increasing the lean body mass.
It is clear that an intoxicated and inflamed organism has the tendency to gain weight, and why people with food allergies often put on weight without understanding the reasons behind it.
The key to understand these phenomena stands in the production of inflammatory cytokines (like BAFF, for example) and in the activation of those macrophages residing into the adipose tissue, usually known for their anti-inflammatory role but in reality also able to drive pro-inflammatory cytokines production and lead to insulin resistance, if negatively affected by diet and low-grade inflammation.
In other words, these cells can lay the foundations to conditions similar to those present in diabetes, facilitating the fat body mass increase.
Today we can measure the level of inflammatory cytokines within the organism and starting from this we can understand the level of on-going inflammation. We can follow the inflammatory trend along the course of a diet and of a supportive therapy, aimed at reducing the insulin resistance."
Article at:
http://www.docsalus.com/blog/2013/12/12/the-cells-that-make-us-fat-discovered-these-are-triggered-by-inflammation/
Gut-Wrenching: New Studies Reveal the Insidious Effects of Glyphosate article in Cornucopia News By Pamela Coleman, PhD
Farm and Food Policy Analyst
The Cornucopia Institute
Excerpts:
"The acute toxicity of glyphosate is relatively low, meaning that accidentally ingesting it will likely not cause immediate harm. Chronic toxicity—the effects of continually ingesting glyphosate residues in food—is cause for concern. Glyphosate interferes with fundamental biochemical reactions and may predispose humans to obesity, Alzheimer’s, Parkinson’s, and other health problems.
It’s easy to overlook these effects. Toxicity studies on laboratory animals are typically short term, often only a few months. The harm from low-level, chronic exposure can only be seen after a long period of time, often years, or even decades. The real guinea pigs in this case are humans.
From a scientific perspective, it is impossible to prove that a chemical ingested on food can harm a person’s health decades later. However, it is possible to study the specific biochemical action of the pesticide, and then examine the diseases that have been related to malfunction of that biochemical pathway."
Article at:
http://www.cornucopia.org/2014/03/gut-wrenching-new-studies-reveal-insidious-effects-glyphosate/
Glyphosate Is The Elephant in the Room. See:
Glyphosate news, articles and information at:
http://www.naturalnews.com/glyphosate.html
Really bad stuff!
The Statin Myth — It's Inflammation, Not Cholesterol
Wednesday, 02 Oct 2013 by Russell Blaylock M.D.
Excerpt:
"The latest studies show that inflammation is an independent risk factor for heart disease that is much stronger than any measure of cholesterol. A study of two statin drugs, atorvastatin and pravastatin, found that patients with low hsCRP levels had fewer heart attacks no matter their LDLcholesterol level, and they had more heart attacks if their hsCRP was elevated regardless of their LDLcholesterol level. The same thing has been found for stroke risk.
Few physicians who prescribe statin drugs know that the link between elevated cholesterol levels and strokes has never been established, but the link to inflammation is strong and is supported by many laboratory and clinical studies.
Why won’t the drug manufacturers and physicians who promote statin drugs just change their policy and give statin drugs only to people with increased inflammation?
It all comes down to dollars. If I make lowering cholesterol my goal — especially a drastic decrease — I can convince doctors that everyone, even children, should take
them for a lifetime. Yet, if I use hsCRP or other measures of inflammation as the criteria for prescribing statins, the drug would not be given to 75 percent to 80 percent of people presently prescribed to them. That is a massive loss of revenue.
Now that the statin promoters have admitted that inflammation, not elevated cholesterol, is the cause of atherosclerosis, we can examine ways to reduce inflammation in our bodies (and our blood vessels in particular) rather than using statin drugs.
Most chronic diseases and conditions, such as metabolic syndrome and abdominal fat, are associated with chronic inflammation."
Article at:
http://www.newsmaxhealth.com/Dr-Blaylock/cholesterol-statin-drugs-inflammation-DrRussell-Blaylock/2013/10/02/id/528866/
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It seems to me that with our over consumption of Fructose metabolizing into fat, high levels of Vitamin D deficiency in the world, and Glyphosate toxicity pervading our food chain---CHRONIC INFLAMMATION IS THE END CONCLUSION. The Monsanto Roundup information is especially disturbing. If you haven't read the previous postings, I suggest you do so and reach your own conclusion. So what is STSI worth?
Monsanto’s Roundup Herbicide May Be Most Important Factor in Development of Autism and Other Chronic Disease Article and video by Dr Mercola.
Excerpts:
"In 2009, a French court found Monsanto guilty of lying; falsely advertising its Roundup herbicide as "biodegradable," "environmentally friendly" and claiming it "left the soil clean."
"While Monsanto insists that Roundup is as safe to humans as aspirin, Seneff and Samsel’s research tells a different story altogether. Their report, published in the journal Entropy1, argues that glyphosate residues, found in most commonly consumed foods in the Western diet courtesy of GE sugar, corn, soy and wheat, “enhance the damaging effects of other food-borne chemical residues and toxins in the environment to disrupt normal body functions and induce disease.”
"Interestingly, your gut bacteria are a key component of glyphosate’s mechanism of harm.
Monsanto has steadfastly claimed that Roundup is harmless to animals and humans because the mechanism of action it uses (which allows it to kill weeds), called the shikimate pathway, is absent in all animals. However, the shikimate pathway IS present in bacteria, and that’s the key to understanding how it causes such widespread systemic harm in both humans and animals.
The bacteria in your body outnumber your cells by 10 to 1. For every cell in your body, you have 10 microbes of various kinds, and all of them have the shikimate pathway, so they will all respond to the presence of glyphosate!
Glyphosate causes extreme disruption of the microbe’s function and lifecycle. What’s worse, glyphosate preferentially affects beneficial bacteria, allowing pathogens to overgrow and take over. At that point, your body also has to contend with the toxins produced by the pathogens. Once the chronic inflammation sets in, you’re well on your way toward chronic and potentially debilitating disease. In the interview above, Dr. Seneff reviews a variety of chronic diseases, explaining how glyphosate contributes to each condition. So to learn more, I urge you to listen to it in its entirety. It’s quite eye-opening."
"It's important to understand that the glyphosate sprayed on conventional and genetically engineered crops actually becomes systemic throughout the plant, so it cannot be washed off. It's inside the plant. For example, genetically engineered corn has been found to contain 13 ppm of glyphosate, compared to zero in non-GMO corn. At 13 ppm, GMO corn contains more than 18 times the “safe” level of glyphosate set by the EPA. Organ damage in animals has occurred at levels as low as 0.1 ppm. If that’s not reason enough to become a label reader to avoid anything with corn in it, such as corn oil or high fructose corn syrup, I don’t know what is.
You’d also be wise to stop using Roundup around your home, where children and pets can come into contact with it simply by walking across the area.
Until the US requires genetically engineered (GE) foods to be labeled, the only way you can avoid GE ingredients is to make whole, fresh organic foods the bulk of your diet, and to only buy 100% USDA certified organic processed foods. Meats need to be grass-fed or pastured to make sure the animals were not fed GE corn or soy feed.
Last but not least, do not confuse the “natural” label with organic standards.
The natural label is not based on any standards and is frequently misused by sellers of GE products. Growers and manufacturers of organic products bearing the USDA seal, on the other hand, have to meet the strictest standards of any of the currently available organic labels. In order to qualify as organic, a product must be grown and processed using organic farming methods that recycle resources and promote biodiversity. Crops must be grown without synthetic pesticides, bioengineered genes, petroleum-based fertilizers, or sewage sludge-based fertilizers."
Article/video at:
http://articles.mercola.com/sites/articles/archive/2013/06/09/monsanto-roundup-herbicide.aspx
What is Inflammation? article at Gene Smart Wellness
Excerpts:
"Current figures from the Centers for Disease Control and Prevention (CDC) put the prevalence of obesity among adults at about 66 percent. A recent study from Johns Hopkins University School of Medicine concluded that if we were to continue at the present rate, “by 2048, all American adults would become overweight or obese.”
"Nearly 24 million Americans—8 percent of the population—have diabetes, according to statistics released by the CDC in 2008. Even more shocking have been the data from individual states. In 1991, only nine states had diabetes rates of 7 to 8 percent, with none higher. By 2001, 43 states had diabetes rates of at least 7 to 8 percent, with Mississippi, Alabama, and Florida exceeding 10 percent. Estimates are that by 2025, the number of Americans with the disease will be close to 50 million.
Arthritis and joint disease affect 43 million people in the United States, almost 20 percent of the population. This number is expected to surpass 60 million by 2020.
More than 5 million Americans have Alzheimer’s disease, with the direct and indirect costs of Alzheimer’s and other dementias topping $148 billion annually, according to the Alzheimer’s Association.
Article at:
http://www.genesmart.com/pages/what-is-inflammation-/69.php
You need to read the fine print. If you listened to the question/answer section at the end of the video(newest version), he says Vitamin D supplementation adequate to bring your D level up to normal PREVENTS the numerous conditions he cites. IT DOES NOT TREAT OR CURE the problem. So, D helps reduce the chances of chronic inflammation (my words) but may not have an effect on existing chronic inflammation caused problems. My take is that if you are still young, Vitamin D is very useful to prevent problems caused by D deficiencies. As you get older, if you have chronic inflammation, you need to look at alternatives. (again, my interpretation of what he is saying)