Feeds:
Posts
Comments

Glyphosate Causes Irreversible Abnormal Growth & Delayed Development of Embryonic Rat Neuronal Cells. Primary rat neuronal cultures exposed to glyphosate showed abnormal morphology, delayed differentiation and decreased activity of a Wnt signalling pathway involved in embryonic development Dr Eva Sirinathsinghji

A new study finds that cultured embryonic rat neurones exposed to sub-lethal doses of glyphosate show a delay in development characterised by reduced neuronal polarisation, complexity and morphology. Underlying the abnormalities was reduced activity of a Wnt protein Wnt5a, a signalling transduction molecule, as well as its downstream signalling effector CaMKII (Ca2+/calmodulin-dependent protein kinase II). Effects of glyphosate were rescued through the restoration of normal Wnt signalling activity, validating its involvement in glyphosate’s neurotoxic effects.

The toxicity of glyphosate herbicides and their formulation products are widely recognised in the scientific literature, with evidence accumulating on its neurotoxic effects.

http://www.i-sis.org.uk/Glyphosate_Causes_Abnormal_Neuronal_Development.php Continue Reading »

Inherited determinants of Crohn’s disease and ulcerative colitis phenotypes: a genetic association study

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(15)00465-1/abstract

Crohn’s disease and ulcerative colitis are the two major forms of inflammatory bowel disease; treatment strategies have historically been determined by this binary categorisation. Genetic studies have identified 163 susceptibility loci for inflammatory bowel disease, mostly shared between Crohn’s disease and ulcerative colitis. We undertook the largest genotype association study, to date, in widely used clinical subphenotypes of inflammatory bowel disease with the goal of further understanding the biological relations between diseases.

Methods
This study included patients from 49 centres in 16 countries in Europe, North America, and Australasia. We applied the Montreal classification system of inflammatory bowel disease subphenotypes to 34 819 patients (19 713 with Crohn’s disease, 14 683 with ulcerative colitis) genotyped on the Immunochip array. We tested for genotype–phenotype associations across 156 154 genetic variants. We generated genetic risk scores by combining information from all known inflammatory bowel disease associations to summarise the total load of genetic risk for a particular phenotype. We used these risk scores to test the hypothesis that colonic Crohn’s disease, ileal Crohn’s disease, and ulcerative colitis are all genetically distinct from each other, and to attempt to identify patients with a mismatch between clinical diagnosis and genetic risk profile.

Findings
After quality control, the primary analysis included 29 838 patients (16 902 with Crohn’s disease, 12 597 with ulcerative colitis). Three loci (NOD2, MHC, and MST1 3p21) were associated with subphenotypes of inflammatory bowel disease, mainly disease location (essentially fixed over time; median follow-up of 10·5 years). Little or no genetic association with disease behaviour (which changed dramatically over time) remained after conditioning on disease location and age at onset. The genetic risk score representing all known risk alleles for inflammatory bowel disease showed strong association with disease subphenotype (p=1·65 × 10−78), even after exclusion of NOD2, MHC, and 3p21 (p=9·23 × 10−18). Predictive models based on the genetic risk score strongly distinguished colonic from ileal Crohn’s disease. Our genetic risk score could also identify a small number of patients with discrepant genetic risk profiles who were significantly more likely to have a revised diagnosis after follow-up (p=6·8 × 10−4).

Interpretation
Our data support a continuum of disorders within inflammatory bowel disease, much better explained by three groups (ileal Crohn’s disease, colonic Crohn’s disease, and ulcerative colitis) than by Crohn’s disease and ulcerative colitis as currently defined. Disease location is an intrinsic aspect of a patient’s disease, in part genetically determined, and the major driver to changes in disease behaviour over time.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(15)00465-1/abstract

The #1 Nutrition Rule I Live By: A Cardiologist Explains by Dr. Robert Ostfeld

My brother Daniel died from an incurable disease when he was three. I was seven, and I remember wanting to throw stamps into his grave so he could write us. I was too shy and did not. Ever since then, I’ve wanted to help people. One thing led to another and I went to medical school and ultimately became a cardiologist. Over the years, I had the opportunity to train with many wonderful and brilliant physicians and scientists.

But despite my many years at Yale and Harvard, I never learned much about nutrition. And this odd gap, I have come to learn, is quite common. It was only after my formal education was complete that I started to learn more.

I’ve never seen anything come close to the depth of benefits that a plant-based diet provides. I’ve now been at Montefiore Medical Center in the Bronx, where I am the Director of Preventive Cardiology, for many years. When I first started, I did all of the things I was trained to do. I prescribed guideline-based medications and recommended a variety of medical procedures — all of which can be very helpful.

http://www.mindbodygreen.com/0-22610/the-1-nutrition-rule-i-live-by-a-cardiologist-explains.html Continue Reading »

Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity Contributed by Bruce S. McEwen, October 20, 2015 (sent for review August 12, 2015; reviewed by Bita Moghaddam and Johannes M. H. M. Reul)   http://www.pnas.org/content/112/48/14960

Chronic stress alters the hippocampal responses to familiar and novel stressors, behaviorally, physiologically, and epigenetically. In the aftermath of chronic stress in WT mice and in mice with a BDNF loss-of-function allele without any applied stress, there is a window of plasticity that allows familiar and novel experiences to alter anxiety- and depressive-like behaviors, reflected also in electrophysiological changes in the dentate gyrus (DG) in vitro. A consistent biomarker of mood-related behaviors in DG is reduced type 2 metabotropic glutamate (mGlu2), which regulates the release of glutamate. Within this window, familiar stress rapidly and epigenetically up-regulates mGlu2 by a P300-driven histone H3 lysine 27 acetylation and improves mood behaviors. This transient epigenetic plasticity may be useful for treatment of stress-related disorders where dysregulaton of glutamate is involved.

http://www.pnas.org/content/112/48/14960

Continue Reading »

Glyphosate is Carcinogenic

The WHO expert panel reclassified glyphosate as ‘probably carcinogenic’ more than 40 years after it was brought to market, but the range of available evidence is sufficient to classify it definitely carcinogenic.

The WHO IARC reclassified glyphosate as ‘probable carcinogen’ based on ‘limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals’, supported by strong evidence that glyphosate and glyphosate formulations are genotoxic, and strong evidence that glyphosate and its metabolite AMPA, and glyphosate formulations cause oxidative stress; both oxidative stress and genotoxicity being key characteristics of carcinogens.

Regarding carcinogenicity in humans, we have reviewed the main evidence presented in the glyphosate part of the IARC Monograph 112 [10], which showed that glyphosate exposure is associated with increased risk of non-Hodgkin’s lymphoma from several large epidemiological studies as well as smaller studies, and single studies have found non-significant RRs or ORs for glyphosate exposure and several cancer sites. In addition, we have presented further relevant evidence from the formal scientific literature as well as reports from non-government organizations.

First, glyphosate use has gone up rapidly and enormously worldwide especially since glyphosate-tolerant genetically modified crops were introduced. The global glyphosate market demand in 2012 was 718 600 tonnes [35], with GM crops accounting for 45.2 % of the total demand, and glyphosate for ~25 % of the global pesticide market [36]. Glyphosate and its residues have heavily contaminated air, soil, and water worldwide, constituting a major increase in pesticide burden on public health. It is to be found not only generally in human and livestock urine through exposure in food and feed (as well as in drinking water, and through inhalation from the air and absorption through the skin), but also in all livestock tissues tested and in mother’s milk, contradicting all the claims of the manufacturer that glyphosate does not accumulate in soil or leach into water, and that it does not bio-accumulate in tissues.

Second, although no post-market health monitoring has been done for either GM crops or glyphosate, it is significant that US government data show a marked deterioration of public health, with increase in incidence of 22 diseases including 6 cancers – liver, thyroid, bladder, pancreas, kidney and myeloid leukaemia – closely tracking the increase in GM crops planted and glyphosate used in the country [8]. For 22 diseases, the Pearson correlation coefficients were calculated between incidence and % GM crops and between incidence and glyphosate usage. Most of the 44 coefficients are greater than 0.91, with none of them falling below 0.81, and those for incidence of cancers and glyphosate use among the highest.

Glyphosate’s carcinogenic potential has been known to Monsanto and the US EPA from long term animal experiments since the early 1980s but repeatedly dismissed. This has resulted in two decades of people and planet being poisoned by glyphosate herbicides on a misclassification of ‘noncarcinogenic’ that has allowed the manufacturer to claim it is ‘safe’ and perpetrating many other falsehoods to promote its ubiquitous and liberal use Dr Mae-Wan Ho and Prof Peter T. Saunders

http://www.i-sis.org.uk/Glyphosate_is_Carcinogenic.php Continue Reading »

Pesticide Exposure found to cause Parkinsons Disease as Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease

http://www.neurology.org/content/82/5/419.short

The objective of this study was to determine whether environmental and genetic alterations of neuronal aldehyde dehydrogenase (ALDH) enzymes were associated with increased Parkinson disease (PD) risk in an epidemiologic study.

Methods: A novel ex vivo assay was developed to identify pesticides that can inhibit neuronal ALDH activity. These were investigated for PD associations in a population-based case-control study, the Parkinson’s Environment & Genes (PEG) Study. Common variants in the mitochondrial ALDH2 gene were genotyped to assess effect measure modification (statistical interaction) of the pesticide effects by genetic variation.

Results: All of the metal-coordinating dithiocarbamates tested (e.g., maneb, ziram), 2 imidazoles (benomyl, triflumizole), 2 dicarboxymides (captan, folpet), and 1 organochlorine (dieldrin) inhibited ALDH activity, potentially via metabolic byproducts (e.g., carbon disulfide, thiophosgene). Fifteen screened pesticides did not inhibit ALDH. Exposures to ALDH-inhibiting pesticides were associated with 2- to 6-fold increases in PD risk; genetic variation in ALDH2 exacerbated PD risk in subjects exposed to ALDH-inhibiting pesticides.

Conclusion: ALDH inhibition appears to be an important mechanism through which environmental toxicants contribute to PD pathogenesis, especially in genetically vulnerable individuals, suggesting several potential interventions to reduce PD occurrence or slow or reverse its progression.

http://www.neurology.org/content/82/5/419.short/reply#neurology_el_61067

How to Support Sustainable Agriculture by Janis Levy
Several things we can do to help sustainable agriculture and sustain the Earth
1. Eat organic, for your health and to support farmers who aren’t doing harm, who are growing with very few chemicals, which are used sparingly. Eat organic 100% of the time. You can do this! If hard for you to do, please do your best! smile emoticon

2. Support small, organic farmers as much as possible. At your grocery store, look for organic B companies. And buy from local organic farmers (especially those who are using regenetative ag/permaculture methods) at farmers markets or visit their farms.

3. Even if organic, cut down significantly on meat purchases. That will free up your food budget for more organic veggie/fruit purchases.

4. Buy less processed/packaged foods. Processed food have more of a “carbon footprint”, (more transportation costs are involved, for example).

5. Grow your own organic food crops, using regenetative ag/permaculture methods. Learn about what that means – making your own compost, designing your landscape so everything works with nature and has a beneficial relationship, conserving water, etc.

If you don’t have land, containers are a good option. No sunlight? Grow lamps. No time, rather buy organic at grocery? That works. (You might consider donating food scraps to someone who composts. I do. I store in the freezer.)

At the very least, learn about it. Then, if your own conditions aren’t condusive, you can still teach others. Take a permaculture class, some given on weekends, some online. Learn about it so you can teach other people. You can share informative posts, too. Help this grow until everyone with front and back yards is growing organic food crops, rather than lawns. How cool would that be!! smile emoticon Help GROW this and Outgrow Monsanto!!

6. Cut down on paper use. Buy recycled paper at the very least. Also plastic – use glass, as much as possible. Recycle. Be as resourceful as possible, in your own home.

7. Speaking of homes, you can also support Earth, with other products you use for home care and personal care. The less toxic chemicals the better. Protect our water systems and your family.

8. Cut down on gasoline use. Some ideas – Carpool, ride a bicycle, use public transportation. Plan your trips so you can do errands together in one location. This reduces the use of fossil fuels and you’re not giving as much money to companies like Exxon, BP, etc.

And there’s another reason. Do you know what ethanol is made from? It’s made from Monsanto’s genetically engineered Roundup Ready Corn (also RR Soy, but mostly corn). About 40% of RR Corn is used for ethanol. Besides all the harm Roundup Ready genetically engineered crops/agriculture/foods are doing to our health, the cultivation of these crops, this agriculture (monoculture) is destroying the soil, habitats, the bees (neonicotinoids are applied to seeds), biodiversity, small farms, and much more!! It’s the very opposite of Agroecology. Chemical agriculture destroys Earth’s delicate ecological balance and is a large factor in climate change. Please consider this and cut down on buying gasoline.
Every bit helps.

Follow

Get every new post delivered to your Inbox.

Join 1,599 other followers