Depriving Deadly Brain Tumors Of Cholesterol , parasites need cholesterol

Depriving Deadly Brain Tumors Of Cholesterol May Be Their Achilles’ Heel

Summary: Depriving glioblastoma brain cancer cells of cholesterol caused tumor regression and prolonged survival in mouse models of the disease, a new study reports.

Source: UCSD.

In mouse models, alternative approach proves promising against hard-to-treat cancer.

Researchers at University of California San Diego School of Medicine, Ludwig Institute for Cancer Research and The Scripps Research Institute, with colleagues in Los Angeles and Japan, report that depriving deadly brain cancer cells of cholesterol, which they import from neighboring healthy cells, specifically kills tumor cells and caused tumor regression and prolonged survival in mouse models.

The findings, published in the online October 13 issue of Cancer Cell, also present a potential alternative method for treating glioblastomas (GBM), the most common and most aggressive form of brain cancer. GBMs are extremely difficult to treat. The median survival rate is just over 14 months, with few treated patients living five years or more past diagnosis.

Adult brain cancers are almost universally fatal, in part because of the biochemical composition of the central nervous system (CNS) and the blood-brain barrier, which selectively and protectively limits the passage of molecules from the body into the brain, but which also blocks most existing chemotherapies, contributing to treatment failure.

This includes blocking small molecule inhibitors that target growth factor receptors, which have not proven to be effective with brain cancers, possibly due to their inability to get past the blood-brain barrier and achieve sufficiently high levels in the central nervous system.

“Researchers have been thinking about ways to deal with this problem,” said senior author Paul S. Mischel, MD, a member of the Ludwig Cancer Research branch at UC San Diego and professor in the UC San Diego School of Medicine Department of Pathology. “We have been challenged by the fact that GBMs are among the most genomically-well characterized forms of cancer, with clear evidence of targetable driver oncogene mutations but this information has yet to benefit patients, at least in part, because the drugs designed to target these oncogenes have difficulty accessing their targets in the brain. We have been trying to find an alternative way to use this information to develop more effective treatments.

“One such approach stems from the observation that oncogenes (mutated genes) can rewire the biochemical pathways of cells in ways that make them dependent on proteins that are not themselves encoded by oncogenes. Targeting these ‘oncogene-induced co-dependencies’ opens up a much broader pharmacopeia, including the use of drugs that aren’t traditionally part of cancer drug pipelines but have better pharmacological properties.”

In previous research, Mischel and others had noted GBM cells cannot synthesize cholesterol, which is vital to cell structure and function, particularly in the brain. Instead, GBM cells derive what they need from brain cells called astrocytes, which produce cholesterol in abundance. Roughly 20 percent of total body cholesterol is found in the brain.

When normal cells have sufficient cholesterol, they convert some of it into molecules called oxysterols, which activate a receptor in the cell’s nucleus — the liver X receptor (LXR) — to shut down the uptake of cholesterol.

“So when normal cells get enough cholesterol, they stop making it, stop taking it up and start pumping it out,” said Mischel. “We found that in GBM cells, this mechanism is completely disrupted. They’re like parasites of the brain’s normal cholesterol system. They steal cholesterol and don’t have an off switch. They just keep gobbling the stuff up.”

Image shows an MRI brain scan of a glioblastoma patient.

GBM cells ensure their cholesterol supply by suppressing the production of oxysterols, the researchers said, ensuring cells’ LXRs remain inactive.

The research team, including Andrew Shaiu and Tim Gahman of Ludwig’s Small Molecule Development team at UC San Diego, identified an experimental metabolic disease drug candidate named LXR-623 that activates LXRs.

In mouse models, LXR-623 easily crossed the blood-brain barrier to bind with LXRs in normal cells, stimulating the production of oxysterols and the reduction of cholesterol. There was no effect upon healthy neurons and other brain cells, the scientists found, but GBM cells were deprived of vital cholesterol, resulting in cell death and tumor regression.

“Disrupting cholesterol import by GBM cells caused dramatic cancer cell death and shrank tumors significantly, prolonging the survival of the mice,” said Mischel. “The strategy worked with every single GBM tumor we looked at and even on other types of tumors that had metastasized to the brain. LXR-623 also had minimal effect on astrocytes or other tissues of the body.”

Mischel suggested the GBM strategy could be implemented in clinical trials using drug-candidates under development or in early trials.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Co-authors of this paper include: first author Genaro R. Villa, Yuchao Gu, Xin Rong, Cynthia Hong, Timothy F. Cloughesy, UCLA; Jonathan J. Hulce, Kenneth M. Lum, Michael Martini and Benjamin F. Cravatt, TSRI; Ciro Zanca, Junfeng Bi, Shiro Ikegami, Gabrielle L. Cahill, Huijun Yang, Kristen M. Turn, Feng Liu, Gary C. Hon, David Jenkins, Aaron M. Armando, Oswald Quehenberger, Frank B. Furnari, and Webster K. Cavenee, UC San Diego; and Kenta Masui and Peter Tontonoz, Tokyo Women’s Medical University.

Funding: Funding for this research came, in part, from the National Cancer Institute (F31CA186668), the National Institute for Neurological Diseases and Stroke (NS73831, NS080939), the Defeat GBM Program of the National Brain Tumor Society, the Ben and Catherine Ivy Foundation, the Ziering Family Foundation and the National Institutes of Health (CA132630).

Source: Scott LaFee – UCSD
Image Source: NeuroscienceNews.com image is credited A. Christaras.
Original Research: The study will appear in Cancer Cell.


All parasites may be metabolising cholesterol

The requirement of cholesterol for internalization of eukaryotic pathogens like protozoa (Leishmaniasis, Malaria and Toxoplasmosis) and the exchange of cholesterol along with other metabolites during reproduction in Schistosomes (helminths) under variable circumstances are poorly understood. In patients infected with some other helminthes, alterations in the lipid profile have been observed. Also, the mechanisms involved in lipid changes especially in membrane proteins related to parasite infections remain uncertain. Present review of literature shows that parasites induce significant changes in lipid parameters, as has been shown in the in vitro study where substitution of serum by lipid/cholesterol in medium and in experimental models (in vivo). Thus changes in lipid profile occur in patients having active infections with most of the parasites. Membrane proteins are probably involved in such reactions. All parasites may be metabolising cholesterol, but the exact relationship with pathogenic mechanism is not clear. So far, studies suggest that there may be some factors or enzymes, which allow the parasite to breakup and consume lipid/cholesterol.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142336/

Step 1 to cancer free: Limit stress that leads to high blood glucose and lipids

Adrenals and liver come to the rescue as blood sugar levels drop.  The endocrine pancreas, liver and adrenal glands work to normalize blood sugar and triglycerides.

Take care of your stress so it will be easier for you to prevent obesity, depression, sugar cravings and nerve pain which may start to happen at around 55 years of age. When we take care of our stress level, we take care of our metabolism , brain , whole body and we then prevent chronic diseases that lead to cancer.

Activities to make you happy

Beach stroll, dancing, watching comedians , laughing , sleeping at nigh, massage , happy and loving friends and relationships , spending time with family and friends , playing with your pets, gardening , singing , praying , deep breathing exercise, meditation

Side effects of chronically elevated cortisol can include:

Anxiety , Autoimmune diseases , Cancer,  Chronic fatigue syndrome , Common Colds , Hormone imbalance , Irritable bowel disease , Thyroid conditions , Weight loss resistance

Needed nutrients

Digestive enzymes, vitamin C (citrus, kiwi, berries, tamarind), vitamin B, L-carnitine, chromium, anti-oxidants, fiber-rich foods (squash, yams, sulfur family of garlic and onions, greens, okra, radish), spearmint, ginger, beets, carrots, all root crops, sprouts, pineapple, papaya , taurine rich foods (breastmilk, sea algae, fish)

Adaptogenic herbs

  1. Eleuthero ginseng
  2. Holy basil
  3. Rodiola rosea
  4. ashwagandha
  5. Astralagus
  6. Sour date
  7. Mimosa pudica
    Extracts of Mimosa pudica are successful in wiping out harmful bacteria and can be useful in antibacterial products
  8. Medicinal mushrooms
    Mushrooms are rich in B vitamins such as riboflavin (B2), folate (B9), thiamine (B1), pantothenic acid (B5), and niacin (B3).
  9. Licorice root
  10. Valerian

 

Zinc, copper and magnesium to fight diabetes and neurodegeneration

Dear GF with diabetes,

If you are not 12,000 miles away from me, I will bring sesame seeds, pumpkin seeds and cashew (raw and unsalted). I will massage you with special oils. Take care, I hope to see you soon.

Connie

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Zinc and Diabetes – Diabetes Self-Management

https://www.diabetesselfmanagement.com › Blog › Amy Campbell

Mar 26, 2007 – Zinc is also necessary for the formation of insulin in the pancreas’s beta cells. For these reasons, researchers have looked at the role of zinc supplementation in the prevention and treatment of Type 2 diabetes—unfortunately, without success. However, new light has been shed on the role of zinc indiabetes.

Effects of zinc supplementation on diabetes mellitus: a systematic …

by R Jayawardena – ‎2012 – ‎Cited by 133 – ‎Related articles

Apr 19, 2012 – Zinc is important in insulin action and carbohydrate metabolism [11]. Oxidative stress plays an important role in the pathogenesis of diabetes and its complications. … Animal studies have shown that Zinc supplementation improves fasting insulin level and fasting glucose in mice [16].

Introduction · ‎Methods · ‎Results · ‎Discussion

Zinc Benefits for Diabetes: Natural Blood Sugar Control and More …

Dec 8, 2017 – Are you looking for natural blood sugar control techniques? … Zinc benefits include promoting healthy insulin function, providing natural blood sugar control, and might even help to preventdiabetes in the first place. … Take command of your diabetes, simplify blood sugar management …

Low zinc levels could be associated with prediabetes risk

Nov 9, 2017 – Scientists have observed an association between zinc metabolism and the development of prediabetes. The findings suggest that lower concentrations of trace elements in the blood (particularly zinc) play an important role in prediabetes development, although they do not yet understand why.

Zinc supplements for diabetics | Diabetes Forum • The Global …

https://www.diabetes.co.uk › Forums › Diabetes Discussion › Ask A Question

Dec 20, 2012 – 14 posts – ‎5 authors

I have heard that people who suffer from auto-immune conditions are often severely deficient in zinc. Does anyone know anything about this? It’s not something that has ever been mentioned by consultants etc. I am interested in doing the zinc taste test to check for deficiency, but am not sure how accurate it …

Zinc Supplementation in Patients with Type 2 Diabetes – EndocrineWeb

Apr 26, 2016 – Zinc Supplementation in Patients with Type 2 Diabetes. … To gauge the effects of zincsupplementation on patients’ fasting blood glucose levels, HbA1c, serum zinc concentration, and serum insulin levels, the researchers conducted a meta-analysis of randomized trials.

Take Zinc If Your Diabetes Is High – Diabetes Developments

Feb 27, 2016 – If you are healthy, you may not need to take a zinc supplement. But if your health isn’t good enough, a new meta-analysis indicates that you probably need to take one. The study categorizes people with type 2 diabetes as “non-healthy.” zinc (1). The mineral zinc plays an important role in how our bodies …

Prediabetes Patients Improve Fasting Glucose with Zinc

http://www.diabetesincontrol.com › Conditions › Prediabetes

Apr 16, 2016 – Six-month regimen of 30 mg zinc sulfate once daily found effective compared with those on placebo, according to study. In Diabetes Research and Clinical Practice, Australian researchers used a cohort of 55 adults, mean age of 44, to assess whether participants would improve fasting glucose with zinc …

Zinc supplements and blood sugars – Diabetes Daily

https://www.diabetesdaily.com › Forum › General › Type 2 Diabetes

Sep 27, 2017 – Before I was diagnosed prediabetic, for at least a year I felt tired & sleepy after lunch. Like 6 months before my diagnosis, I was taking 50 mg zinc a day for a month to see if it helps me build muscle. It did help. Looking back, during that month of taking zinc, I had a lot more energy & I definitely didn’t feel …

Image shows the work Shank3.

ZINC MAY HELP REVERSE BRAIN CHANGES IN AUTISM

According to researchers, cellular changes in the brain caused by genetic mutations associated with Autism can be reversed with the help of zinc. READ MORE…

Study reveals role of specific lipids in accelerating or curbing bacterial infection

Study reveals role of specific lipids in accelerating or curbing bacterial infection

Lipids appear to play an important role in infections. According to researchers from the University of Maastricht in Maastricht, The Netherlands, and the University of Maryland, Baltimore (UMB) in Baltimore, Md., USA, specific lipids can greatly accelerate bacterial infection.

With the help of mass spectrometry imaging (MSI), researchers showed that specific mammalian lipids could also provide protection against the same infection. Their discovery offers hope for future treatment of vulnerable patients in hospitals or development of preventative treatments for travellers to risk areas in certain parts of the world.

The findings of the research team, led by American researchers Robert Ernst and Alison Scott at UMB and Maastricht University Distinguished Professor Ron Heeren, were published Nov. 6 in the journal, Proceedings of the National Academy of Sciences (PNAS).

Mass Spectrometry Imaging
Mass spectrometry imaging is an imaging technique in which molecular maps of a pathological tissue section can be compiled from a single experiment. Researchers use the technique to determine exactly where certain molecules are located and how their distribution is affected by pathogenic bacteria, for instance. “This technique enables us to analyse thousands of molecules with a single measurement,” Heeren explains. “What is special about our research is that we were able to use this method in order to capture for the first time the molecular changes which occur during a bacterial infection, mainly revealing the role of lipids in the further evolution of such an inflammation. This result means that we’ll be able in future to determine the severity of an infection accurately within half an hour. Based on the type of lipid, we’ll also know how the inflammation will behave in a patient.”

Protect or accelerate
To test their ability to use MSI to track disease progression, the scientists injected a healthy mouse with the highly pathogenic bacteria Francisella novicida (Fn). Through MSI, the researchers were then able to create an accurate molecular map of the infection’s evolution, predominantly based on lipids. In doing so, it became clear that certain lipids significantly accelerated the infection, although these lipids should never be seen as separate from their spatial context in the tissue. “The distribution of lipids in the host – the patient – appears to have a tremendous effect on the immune system. For this reason, lipids are a strong determining factor in the aggressiveness of a bacterial infection,” Heeren concludes. “It is now important to establish a kind of library, in which we can precisely identify which lipids play a role in accelerating infection and which lipids have a positive effect on the immune response.”

Alison Scott PhD, research associate professor at the University of Maryland School of Dentistry (UMSOD) and guest researcher at Maastricht University, hopes that this knowledge will help develop drugs that could be used to treat vulnerable patients and help them form the right lipids in the right places to dampen infection.

Applicability of this study
Although the researchers specifically used MSI to track Fn infection in this study, the techniques could be applied to a wide range of diseases. “The methodology underlying the study is relevant to any infection and positions us to expand work in the field of the role of lipids in both the bacteria and the host. It allows researchers to identify host-based pathways for therapeutic treatment to control bacterial infection and inflammation. I hope to start looking at airway infections such as pseudomonas,” says Scott.

This kind of research is only made possible by collaborations across disciplines. “This study shows the value of highly collaborative projects bringing together microbiologists and mass spectrometry experts to define the finite interactions between a bacteria and a host,” says Robert “Bob” Ernst, PhD, the senior investigator involved in the study and professor and vice chair of the Department of Microbial Pathogenesis at UMSOD and an adjunct professor at the University of Maryland School of Medicine (UMSOM).

The research presented here opens up many research avenues, both into the applicability of MSI for disease studies and the development of therapeutics that target lipids to treat infection, according to Ernst and colleagues, who include Kari Ann Shirey, PhD, assistant professor in UMSOM’s Department of Microbiology and Immunology.

New Link Found Between Diabetes and Alzheimer’s

Summary: Researchers report a drug used to treat diabetes may be successful at treating Alzheimer’s disease also.

Source: University of Aberdeen.

Drugs used to treat diabetes could also be used to treat Alzheimer’s disease, and vice versa, according to new research from the University.

This is also the first study of its kind to show that Alzheimer’s disease can lead to diabetes, as opposed to diabetes occurring first as was previously thought.

The study reports that Alzheimer’s Disease and type 2 diabetes are so closely related that drugs currently used to control glucose levels in diabetes may also alleviate the symptoms and progression of Alzheimer’s disease.

The paper, published in the journal Diabetologia, found for the first time that dementia-related complications within the brain can also lead to changes in glucose handling and ultimately diabetes. This is contrary to what was previously thought – that diabetes begins with a malfunction in the pancreas or a high fat, high sugar diet.

The research was led by Professor Bettina Platt who formed a unique collaboration between her Alzheimer’s research team and the diabetes research team led by Professor Mirela Delibegovic. The teams were keen to investigate why the two diseases are so commonly found together in elderly patients.

The researchers developed a model of Alzheimer’s disease and were surprised to find that increased levels of a gene involved in the production of toxic proteins in the brain not only led to Alzheimer’s -like symptoms, but also to the development of diabetic complications.

Professor Platt said of her research: “Many people are unaware of the relationship between diabetes and Alzheimer’s disease, but the fact is that around 80% of people with Alzheimer’s disease also have some form of diabetes or disturbed glucose metabolism. This is hugely relevant as Alzheimer’s is in the vast majority of cases not inherited, and lifestyle factors and comorbidities must therefore be to blame.

“Our research teams are particularly interested in the impact of lifestyle related factors in dementia and by collaborating with experts in diabetes and metabolism, we have been able to investigate the nature of the link in great detail.

“Until now, we always assumed that obese people get type 2 diabetes and then are more likely to get dementia – we now show that actually it also works the other way around.

blue brain

“Additionally, it was previously believed that diabetes starts in the periphery, i.e. the pancreas and liver, often due to consumption of an unhealthy diet, but here we show that dysregulation in the brain can equally lead to development of very severe diabetes – so again showing that diabetes doesn’t necessarily have to start with your body getting fat – it can start with changes in the brain.

“This study provides a new therapeutic angle into Alzheimer’s disease and we now think that some of the compounds that are used for obesity and diabetic deregulation might potentially be beneficial for Alzheimer’s patients as well. The good news is that there are a number of new drugs available right now which we are testing to see if they would reverse both Alzheimer’s and diabetes symptoms. We will also be able to study whether new treatments developed for Alzheimer’s can improve both, the diabetic and cognitive symptoms.”

ABOUT THIS ALZHEIMER’S DISEASE ARTICLE

Finding: The research was funded by R, Simcox, Romex Oilfield Chemicals, the Scottish Alzheimer’s Research UK network, British Heart Foundation, Diabetes UK and European Foundation for the Study of Diabetes/Lilly programme grant.

Source: Wendy Skene – University of Aberdeen
Image Source: This NeuroscienceNews.com image is adapted from the University of Aberdeen press release.
Original Research: Full open access research for “Neuronal human BACE1 knockin induces systemic diabetes in mice” by Kaja Plucińska, Ruta Dekeryte, David Koss, Kirsty Shearer, Nimesh Mody, Phillip D. Whitfield, Mary K. Doherty, Marco Mingarelli, Andy Welch, Gernot Riedel, Mirela Delibegovic, and Bettina Platt in Diabetologia. Published online May 2 2016 doi:10.1007/s00125-016-3960-1

University of Aberdeen. “New Link Found Between Diabetes and Alzheimer’s.” NeuroscienceNews. NeuroscienceNews, 21 June 2016.
<http://neurosciencenews.com/diabetes-alzheimers-neurology-4531/&gt;.

Abstract

Neuronal human BACE1 knockin induces systemic diabetes in mice

Aims

β-Secretase 1 (BACE1) is a key enzyme in Alzheimer’s disease pathogenesis that catalyses the amyloidogenic cleavage of amyloid precursor protein (APP). Recently, global Bace1 deletion was shown to protect against diet-induced obesity and diabetes, suggesting that BACE1 is a potential regulator of glucose homeostasis. Here, we investigated whether increased neuronal BACE1 is sufficient to alter systemic glucose metabolism, using a neuron-specific human BACE1 knockin mouse model (PLB4).

Methods

Glucose homeostasis and adiposity were determined by glucose tolerance tests and EchoMRI, lipid species were measured by quantitative lipidomics, and biochemical and molecular alterations were assessed by western blotting, quantitative PCR and ELISAs. Glucose uptake in the brain and upper body was measured via 18FDG-PET imaging.

Results

Physiological and molecular analyses demonstrated that centrally expressed human BACE1 induced systemic glucose intolerance in mice from 4 months of age onward, alongside a fatty liver phenotype and impaired hepatic glycogen storage. This diabetic phenotype was associated with hypothalamic pathology, i.e. deregulation of the melanocortin system, and advanced endoplasmic reticulum (ER) stress indicated by elevated central C/EBP homologous protein (CHOP) signalling and hyperphosphorylation of its regulator eukaryotic translation initiation factor 2α (eIF2α). In vivo 18FDG-PET imaging further confirmed brain glucose hypometabolism in these mice; this corresponded with altered neuronal insulin-related signalling, enhanced protein tyrosine phosphatase 1B (PTP1B) and retinol-binding protein 4 (RBP4) levels, along with upregulation of the ribosomal protein and lipid translation machinery. Increased forebrain and plasma lipid accumulation (i.e. ceramides, triacylglycerols, phospholipids) was identified via lipidomics analysis.

Conclusions/interpretation

Our data reveal that neuronal BACE1 is a key regulator of metabolic homeostasis and provide a potential mechanism for the high prevalence of metabolic disturbance in Alzheimer’s disease.

“Neuronal human BACE1 knockin induces systemic diabetes in mice” by Kaja Plucińska, Ruta Dekeryte, David Koss, Kirsty Shearer, Nimesh Mody, Phillip D. Whitfield, Mary K. Doherty, Marco Mingarelli, Andy Welch, Gernot Riedel, Mirela Delibegovic, and Bettina Platt in Diabetologia. Published online May 2 2016 doi:10.1007/s00125-016-3960-1

Reduced level of calcium, lipids, proteins, nucleic acids and glycogen levels in mice liver due to aluminium exposure

Determination of aluminium induced metabolic changes in mice liver: A Fourier transform infrared spectroscopy study.
In this study, we made a new approach to evaluate aluminium induced metabolic changes in liver tissue of mice using Fourier transform infrared spectroscopy analysis taking one step further in correlation with strong biochemical evidence.
This finding reveals the alterations on the major biochemical constituents, such as lipids, proteins, nucleic acids and glycogen of the liver tissues of mice. The peak area value of amide A significantly decrease from 288.278±3.121 to 189.872±2.012 between control and aluminium treated liver tissue respectively.
Amide I and amide II peak area value also decrease from 40.749±2.052 to 21.170±1.311 and 13.167±1.441 to 8.953±0.548 in aluminium treated liver tissue respectively. This result suggests an alteration in the protein profile.

The absence of olefinicCH stretching band and CO stretching of triglycerides in aluminium treated liver suggests an altered lipid levels due to aluminium exposure. Significant shift in the peak position of glycogen may be the interruption of aluminium in the calcium metabolism and the reduced level of calcium.
The overall findings exhibit that the liver metabolic program is altered through increasing the structural modification in proteins, triglycerides and quantitative alteration in proteins, lipids, and glycogen. All the above mentioned modifications were protected in desferrioxamine treated mice.
Histopathological results also revealed impairment of aluminium induced alterations in liver tissue. The results of the FTIR study were found to be in agreement with biochemical studies and which demonstrate FTIR can be used successfully to indicate the molecular level changes.

Sivakumar S, Sivasubramanian J, Khatiwada CP, Manivannan J, Raja B. Spectrochim Acta A Mol Biomol Spectrosc. 2013 Mar 21;110C:241-248. doi: 10.1016/j.saa.2013.03.056
Department of Physics, Annamalai University, Annamalai Nagar 608 002, Tamil Nadu, India. Electronic address: girihari777@yahoo.com.

About desferrioxamine, a chelating agent to get rid of excess iron or other metals in the bodyDesferal injections contain the active ingredient desferrixoamine mesilate, which is a type of medicine called a chelating agent.
Desferrioxamine is a medicine that binds to excess iron in the body. It is then excreted in the urine and faeces, thereby reducing iron levels in the body.
Iron is an essential part of haemoglobin, the oxygen-carrying pigment found in red blood cells. In normal situations, iron balance is tightly controlled. Most average diets supply adequate amounts of iron and any amounts excess to requirements are excreted. In certain circumstances, the normal control mechanisms are overwhelmed, leading to an accumulation of iron in the body (iron overload). Iron builds up in the cells of the kidneys, heart, liver, brain and other organs, and can cause congestive heart failure, cirrhosis of the liver and diabetes if left untreated.
Iron overload occurs most commonly as a result of repeated blood transfusions. These might be necessary to treat bone marrow failure (eg caused by radiation, chemotherapy, viruses or hereditary reasons) or blood disorders like thalassaemia or anaemias. Or it may be as a result of iron storage disease, eg haemochromatosis. In this condition, excessive amounts of iron are absorbed from the gut and deposited in the tissues.
Iron overload can also occur as the result of iron overdosage (iron poisoning).
Desferrioxamine is given to bind to and remove excess iron in all these situations.

Read more: http://www.netdoctor.co.uk/heart-and-blood/medicines/desferal.html#ixzz2QZimUf5i

Connie’s comments: Alzheimer’s and Parkinson’s diseases are believed to be be caused by metal toxins such as aluminum. Use stainless steel cooking pots and pans.

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Collected by
Connie Dello Buono

Connie Dello Buono ; motherhealth@gmail.com

Call for part time or full time business or job 408-854-1883 in financial planning, college planning, retirement planning and helping others with their idle money to work for them at 13%, tax free, safe and secured with free health benefits