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By Violetboard.com

Drotumdi O

 

5

Antioxidants, Acids, Alkali, And Cancer

drotumdioblogpostsOtumdi Omekara

In my previous articles on cancer, I did not discuss the role of acids, bases and antioxidants in detail. But with the current hype about the miraculous nature of basic water, antioxidant foods and drugs, I feel compelled to step in and set the records straight with currently available medical literature. The efficacy of organic acids, bases and antioxidants in cancer therapy is not a myth. It has biochemical basis informed by modern research. The apparent controversy surrounding this subject emanates from poor coordination of research findings.

 

I have read journal articles leaning heavily on either systemic hyperacidosis or hyperalkalosis as the dominant toxic factor in cancer development. I have also read articles claiming that cancer development is a normal adaptive response of human body. These claims are to say the least, half truths. By the end of this discussion it would have become obvious that there is no basis for undue generalizations in the management  of cancer. There still remains the need for expert judgement in formulating a cancer treatment protocol.

 

BEFORE CANCER

 

First, let me state that the human body will literally rust away like a nail left under the rain over time without inbuilt natural protective mechanisms.  To prevent rust or oxidation, most macromolecules

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By By Topearningblogs.com

Drotumdi O

Home / Insurance / Some Insight On What It Is Like To Be A Medical Writer And What Skills Are Needed

SOME INSIGHT ON WHAT IT IS LIKE TO BE A MEDICAL WRITER AND WHAT SKILLS ARE NEEDED

 BY DOUGLAS

/

ON AUGUST 30, 2017

/

AT 9:58 AM

/

IN INSURANCE

37 VIEWS

· Do you find medicine and healthcare subjects interesting?

· Do you enjoy writing in general, and have a good control of written English up to high school level?

· Then you may find medical writing a challenging but rewarding career.

· A a medical writer you may choose to work as a:

– Health columnist for a newspaper, magazine or website

– Publisher of e-books, newsletters, pamphlet, brochures, technical manuals or inserts for healthcare industries

– Healthcare research producer

– Health education material and text book writer

– Medical textbook writer and publisher

– Medical Review book writer and publisher

– A medical education website editor and content provider

The list can go on and on.

· As a medical technical writer, you may choose to go free lance or accept an employment position in healthcare organizations

· The freelance option is for those who have some savings to depend on while growing their clientele. Otherwise the start period could be very stressful financially.

· The information to be put in writing is usually in the form of medical manuscripts from individuals or research organizations in a disorganized manner.

· The information will need to be organized and formatted to meet the standards of various journal or magazine publishing companies.

· An experienced medical writer will be familiar with formats of big organizations like the American Medical Journal.

· When attending interviews a medical writer would need to present a portfolio of properly formatted writings, whether published or unpublished, in hard copy or electronic copy.

· A medical writer must double check content information with the author, and verify spellings and punctuations with quality word processing software, since there is almost zero tolerance for typos or misinformation in medical writing

· Over time a non-medical medical copy writer may take courses in basic medical sciences to qualify them to write original articles or books in hard copy or online

· How much a medical writer makes annually depends on level of education, experience, output quality, and the organization he / she works for. The pharmaceutical companies tend to pay more and, of course, are most demanding.

Medical reporters can earn from as low as $ 35, 000 per year to as high as 80, 000 per year depending of the above factors

· A freelance medical writer may need only high school education and healthcare work experience.

· But employers tend to prefer medical writers who have college degrees in medical writing, technical writing, basic medical sciences, or English language.

· There are many universities and community colleges now offering courses geared towards medical writing. For more information visit http://www.amwa.org


Otumdi Omekara
Insurance
http://ezinearticles.com/?Some-Insight-On-What-It-Is-Like-To-Be-A-Medical-Writer-And-What-Skills-Are-Needed&id=7067152

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By Rekeshsaini.com

Drotumdi O

Some Insight On What It Is Like To Be A Medical Writer And What Skills Are Needed

· Do you discover drugs and healthcare topics attention-grabbing?

· Do you take pleasure in writing typically, and have a superb management of written English as much as highschool degree?

· Then you might discover medical writing a difficult however rewarding profession.

· A a medical author you might select to work as a:

– Well being columnist for a newspaper, journal or web site

– Writer of e-books, information letters, pamphlet, brochures, technical manuals or inserts for healthcare industries

– Healthcare analysis producer

– Well being schooling materials and textual content guide author

– Medical textbook author and writer

– Medical Evaluation guide author and writer

– A medical schooling web site editor and content material supplier

The record can go on and on.

· As a medical technical author, you might select to go free lance or settle for an employment place in healthcare organizations

· The freelance possibility is for many who have some financial savings to rely upon whereas rising their clientele. In any other case the startup interval could possibly be very worrying financially.

· The data to be put in writing is normally within the type of medical manuscripts from people or analysis organizations in a disorganized method.

· The data will must be organized and formatted to fulfill the requirements of assorted journal or journal publishing firms.

· An skilled medical author might be conversant in codecs of huge organizations just like the American Medical Journal.

· When attending interviews a medical author would want to current a portfolio of correctly formatted writings, whether or not revealed or unpublished, in laborious copy or digital copy.

· A medical author should double examine content material info with the creator, and confirm spellings and punctuations with high quality phrase processing software program, since there’s virtually zero tolerance for typos or misinformation in medical writing

· Over time a non-medical medical copy author might take programs in fundamental medical sciences to qualify them to put in writing unique articles or books in laborious copy or on-line

· How a lot a medical author makes yearly will depend on degree of schooling, expertise, output high quality, and the group he/she works for. The pharmaceutical firms are inclined to pay extra and, in fact, are most demanding.

Medical writers can earn from as little as $35, 000 per 12 months to as excessive as 80, 000 per 12 months relying of the above elements

· A contract medical author might have solely highschool schooling and healthcare work expertise.

· However employers are inclined to desire medical writers who’ve faculty levels in medical writing, technical writing, fundamental medical sciences, or English language.

· There are various universities and group faculties now providing programs geared towards medical writing. For extra info go to http://www.amwa.org

Source by Otumdi Omekara

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By kipaduka.com Vet Medics

Drotumdi O

Antioxidants, Acids, Alkali and Cancer


In my previous articles on cancer, I did not discuss the role of acids, bases and antioxidants in detail. But with the current hype about the miraculous nature of basic water, antioxidant foods and drugs, I feel compelled to step in and set the records straight with currently available medical literature.

The efficacy of acids, bases and antioxidants in cancer therapy is not a myth. It has biochemical basis informed by modern research (SS Kim et al, 2004; Ian F. Robey & Lance A. Nesbit, 2013). The apparent controversy surrounding this subject emanates from poor coordination of research findings.

I have read articles (Bradley A. Web et al, 2011; Shi Q. et al, 2001; Silver M. et al, PubMed 2011) supporting systemic alkalosis or systemic hyperacidosis as the dominant toxic factor in cancer development. I have also watched video presentations claiming that cancer development is just a natural cellular adaptation to toxic environment, which is corrected by normalizing the environment.

These claims are to say the least, unbalanced truths. By the end of this discussion it would have become obvious that there is no basis for undue generalizations in the management of cancer. There still remains the need for expert judgement in formulating a cancer treatment protocol.

BEFORE CANCER

First, let me state that the human body will literally rust away like a nail left under the rain over time without inbuilt natural protective mechanisms. To prevent rust or oxidation, most macromolecules essential for human existence are shielded from molecular oxygen or oxygen equivalents with hydrogen molecules (reduction). Oxygen equivalents are those compounds that remove these protective hydrogen molecules from other compounds.

They are also called oxidizing agents. Compounds that restore these hydrogen molecules are called reducing agents. The two most important organic reducing agents in human body are glutathione and ubiquinone, while the two most important oxidizing agents are molecular oxygen and free oxygen radicals.

APOPTOSIS AND GROWTH SUPPRESSOR GENES

The human body cells are normally continuously moving from resting phase, to growth phase and then multiplication phase. This continuous state of growth and multiplication means that any organ can potentially grow to any size, depending on its natural growth rate. By inference all human beings may also grow into giants. It even suggests immortality of human beings.

Thankfully, every cell has an inbuilt apoptotic clock that ensures that it dies after a specified number of days, making room for incoming cells. Thus red blood cells, for instance, are recycled every 120 days. The size and shape of the cells of individual organs are equally limited prior to their date of apoptosis, by growth suppressor genes (notably p53, AP1, NF-kB) located in the nucleus.

Anything that hinders the functions of apoptosis and growth suppressor genes would obviously be expected to unleash uncontrolled growth and multiplication of cells in any organ of the body. This rapid growth of disorganized and poorly differentiated cells is called cancer.

All anti-growth suppression and anti-apoptosis agents are called carcinogens. They may be chemicals, radiations, biochemical molecules, acids, bases, free radicals, heat, cold, etc. But they all exert their effect by in activating apoptosis gene or growth suppressor gene. They accomplish this by corrupting the gene coding system in such a way that the codes are wrong (missense) or mean nothing (nonsense).

The code is corrupted due to the insertion of the wrong amino acid code into a gene sequence or the excision of the right amino acid code from the sequence. Consequently the t-RNA misreads or miss-senses the expression of the right apoptosis or growth suppressor protein.

TOXINS, FREE RADICALS AND CARCINOGENS

Toxins are basically those compounds whose activities will directly or indirectly lead to human rust and death by causing catabolic or destructive oxidative reactions in body tissues. The high powered toxic tissue oxidizing agents are called free radicals (ROS and RNS), which are basically free ionized oxygen or Nitrogen atoms (O2- and N2- )

When a toxin causes a gene altering damage in the nuclear region of a cell (oxidative nuclear damage) it is then known as a carcinogen. As such not all toxins are carcinogen. Aflatoxin (from mold) is not only toxic to liver cells, but ultimately causes liver cancer, making it a carcinogen.

The detoxification process mainly converts lipid soluble toxins into excretable water soluble glucuronides in three steps. In step one the toxins are aggregated and isolated in the specific organs that neutralize them.

Then glucuronic acid is attached to them in the presence of glutathione which the protective hydrogen molecules. (Note that in fighting oxidants hydrogen (non-ionized) carried by reduced NADPH is a friend, while in acid-base balance ionized hydrogen is the enemy).

Free radicals can also contribute to cancer development by inducing genetic mutation through oxidative nuclear damage, or suppress cancer growth by promoting apoptosis. Step three is the excretion of the toxins.

ANTIOXIDANTS

Compounds use to replenish hydrogen molecules in glutathione and other endogenous reductase enzymes are called antioxidants. A lot of these reducing agents occur naturally in fruits and vegetables. Others are available as drug extracts from plants and animals.

Individual antioxidants target different steps of the detox process. This is why balanced nutrition by itself goes a long way to keep our bodies toxin free. The air we breathe, the food we eat, the water we drink, and the environments we live in are all full of toxins, including heavy metals. To survive as human beings, an extensive detoxification mechanism has to exist.

Every body tissue has detox ability, but the liver, gut, and lymphoid tissues and kidneys play the dominant role. Thus most toxins are trapped, neutralized and excreted through feces, urine or bile. Stagnation or obstruction of flow in any of these three organs, generally leads to a toxic state.

Stressors and nutritional insufficiencies that weaken the immune system also contribute to toxic states allowing micro-organisms to multiply and generate additional toxic substances that must be removed.

Successful detoxification requires a lot of energy, which comes from glucose metabolism. Biochemical energy is not measured in Joules, but in ATPs (Adenosine Triphosphate). The metabolic process for converting glucose to ATP is called glycolsis.

During aerobic glycolysis one molecule of glucose combines with two molecules of ADP3- (Adenosine Diphosphate) and two ionic phosphoric acid molecules to yield two ionic ATP4- molecules and two lactate molecules. The ionic ATP4- molecule gives up one Hydrogen proton (H+) to yield one molecule of ionic ADP3-, which is reused in glycolysis.

Under anaerobic (low oxygen) conditions, ATP is generated differently. One molecule, each, of ADP3- and ionic phosphoric acid accumulated from aerobic glycolysis recombine without glucose to form one molecule of ATP4+ and one hydroxyl molecule. Two hydrogen protons combine with two bicarbonates to end up as carbonic acid inside body cells.

TOXIC ACIDOSIS

Glycolsis can be aerobic when it consumes molecular oxygen, or anaerobic when it consumes oxidizing agents. Both the detox reactions and glycolsis are driven or catalyzed by enzymes, which depend on the availability of specific micro-molecules, proteins, amino acids and vitamins as cofactors for their functions.

By the time enough ATP is generated to keep the body toxin safe, enough carbonic acid hydration of respiratory carbon dioxide (CO2) has accumulated to keep the inside of every cell perpetually acidic. In a highly toxic state, which includes rapid proliferation of cells, this intracellular acid builds up exponentially beyond survivable limits.

Cancer cells are known to rapidly outgrow their blood supplies and go into severe hypoxic states. This is why the cancer cell nucleus has to rapidly increase the expression of sodium driven proton extruding proteins and enzyme proteins through nuclear sensing of sharp rise in HIF.

Thus, by default, the Intracellular fluid (ECF) of every cell is acidic (low pH) while that of the extracellular fluid (ECF) is alkaline (high pH). It is important to note at this point that while intracellular fluids exist in compartments inside the cells, extracellular fluids coalesce to form a pool in which all body cells submerged.

This ECF pool is represented by intercellular fluid, lymph, blood, and glandular secretions, all of which feed into the circulatory system of the body. ECF acid or base build up in any part of the body is ultimately dissipated into the circulatory system, which centrally maintains a mildly basic pH of 7.20 -7.40.

In addition to mobilizing ammonium and bicarbonate ions the central buffer system has the ability to move chloride ions in and out cells (chloride shift) to maintain acid-base balance.

MEMBRANE SENSORS AND TRANSPORTERS

To keep intracellular acidity below lethal level, the inner surface of the cell membrane has acid sensors and transporters that detect abnormal rise in intracellular acidity and trigger increased extrusion of hydrogen and retention of alkaline bicarbonate ions.

This trigger is mediated by the rise in the blood level of hypoxia induced factors (HIF) and probably acidosis induced factors (AIF). On detecting this rise in HIF, the nucleus temporarily increases the expression of Na-driven proton transport proteins and histidine rich basic proteins.

The ammonium radicals on the amino acids of these basic proteins (especially histidine) serve as physiologic buffers for organic acids.

“Protonation and de-protonation has been experimentally shown to change protein structure and thus, alter protein-protein binding affinity, change protein stability, modify protein function, and alter subcellular localization (Schonichen et al., 2013b).

Evolutionarily, histidines must confer some selective advantage for cancers, as 15% of the 2000 identified somatic mutations in cancer involve histidine substitutions, with Arg-to-His being the most frequent (Kan et al., 2010)”.

The nucleus also temporarily steps up the expression of important enzyme proteins that catalyze the buffer reactions, namely mono-carboxylate, carbonic anhydrase, and aminotransferase enzymes.

In a similar manner the external surface of the cell also has alkaline sensors made up of G-protein coupled surface receptors, which also communicate with the nucleus to increase or decrease the expression of relevant proteins and enzymes. As tissue hypoxia decreases, the level of HIF decreases along with nuclear expression of proton extrusion proteins and enzymes.

Failure of this return to normalcy has been observed as one of the hallmarks of early cancer. What started out as a normal adaptive change becomes persistent because of irreversible genetic modifications that triggered it.

CELLULAR SURFACE ACID/BASE REVERSAL

The central physiological buffer system has a maximum capacity to neutralize up to 30 micromoles of acid/gram tissue/min in systemic acidosis or 5-10 micromoles of base in alkalosis.

Beyond these levels, normal body cells are unable to continue their buffer functions because the enzymes are deactivated. At this point there is a reversal of the normal acid-base distribution on either side of the cell membrane, which is lethal to normal issues. In some critical situations, chloride ions are shifted massively into all body cells (chloride shift) to urgently dilute the extracellular acidity.

But the gastric cells have the natural ability to survive in the presence of high extracellular acidity (HCl at pH of 6.6). How they manage this high extracellular acidity then becomes very important in understanding how cancer cells survive high extracellular acidity with normal intracellular acidity for their survival and proliferation. Some cancer cells are known to have accumulated genetic adaptations that enable them to survive extreme pH conditions (carbonic acid at pH of 6.6).

Gastric cells are shielded from concentrated HCl secreted into the stomach mainly by structural barriers (thick basement membrane, thick mucosal layer and thick mucous layer). There are no natural inhibitors of hydrogen potassium ATPase enzyme that catalyzes the final phase of acid excretion.

In severe cases of Peptic Ulcer Disease (PUD), Gastro-esophageal reflux (GERD), or Zollinger-Ellison Syndrome, when this natural barrier is ulcerated by concentrated HCl, some gastric lining cells undergo goblet intestinal metaplasia (transformation into ectopic intestinal epithelium in the stomach) to secrete neutralizing alkaline fluids into the stomach.

While there is no natural attempt to control the hydrogen potassium ATPase enzymes, pharmacological intervention with proton pump inhibitors (PPIs) like omeprazole has been successful in reducing gastric secretion in severe cases of chronic gastric hyperacidity.

Similarly some esophageal epithelial cells undergo gastric metaplasia to become gastric cells in the face of chronic exposure to reflux gastric acid (Barrett’s Esophagus). Acquisition of this missing ability to control hydrogen potassium ATPase and sodium driven proton extrusion by monocarboxylate enzyme appear to be critical to the survival of cancer cells

IN EARLY CANCER

It is important to note that the natural response to extracellular hyperacidity in the GIT depends on the stage and localization of the acidity. Both goblet metaplasia and gastric metaplasia have been recognized as precancerous lesions (carcinoma in situs). At the early stage of Barret esophagus, the response is only structural to prevent cell wall damage.

But when the barrier has failed in the stomach, the response is alkaline secretion. A person on preventive alkaline water will be helping to neutralize the added hypoxic acidity of early cancer in Barret’s Esophagus and chronic PUD, but not in any way preventing the occurrence of cancer itself, since proton extrusion in cancer is irreversible.

Any cancer caught at the in situ stage is usually best treated with surgical excision and radiotherapy, rather than alkaline water.The question then is: “Why did prophylactic alkaline water not prevent the metaplasia?”

The answer to that is that while oral alkali intake may cap out at micromoles of alkali per gram tissue, cancer proton extrusion acid build up ranges in nanomoles per gram tissue (a thousand times more). Also intracellular hypoxia and hyperacidity are not the only risk factors for cancer.

Radiations are known to be commonly responsible for skin cancers, even as HPV is known to be responsible for cervical cancer. Prophylactic alkalosis has not been reported to prevent any of them. Sticking to the hype that alkaline water is the best way to prevent and even cure cancer, puts people at risk of missing early opportunities to truly cure cancer.

Alkaline water intake will help the body maximize the physiological adaptive response acidosis. Unfortunately, even at maximum physiological capacity, extracellular buffers are no match for cancer intracellular proton extruders.

As the well adapted cancer cells grow and multiply freely their neighboring non-cancerous cells are rapidly destroyed by ECF hyperacidity creating more space for them to occupy. Thus cancer invasiveness has been shown to correlate with the degree of acid-base reversal across the cancer cell membrane.

At the advanced stage of cancer with ECF acidity readings in nanomols compared to orally boosted alkalinity readings in micromoles, buffer therapy has been shown to be resisted by cancer cells. One such reported example is the inefficacy of a basic drug doxorubicin used in the treatment of Leukemias and lymphomas.

Going by what has been discussed so far, it is obvious that externally sourced acids and alkali cannot be safely loaded to outweigh tumor generated levels in ECF and ICF. It is also understandable that no single pH balancing agent, can be used to treat both acid sensing and alkaline sensing cancers.

Preventive or prophylactic intake of acidic or alkaline liquids or foods remain relevant only within the physiological buffering range, when adaptive changes are still reversible. Unfortunately at that point the tumor generated acidity would have risen to resistant levels. Preventive alkaline water intake in a person with undiagnosed acid sensing cancer is not likely to retard the growth of the tumor.

Similarly preventive intake of alkaline water in a patient with undiagnosed alkaline sensing cancer will encourage it to grow and establish faster. Patients receiving treatment for emesis gravid arum (vomiting in pregnancy) for instance, cannot be on preventive alkaline regimens in the face of systemic alkalosis from heavy loss of gastric acid through vomiting.

However, it is possible that some people are unable to fully optimize the natural buffer system, due to genetic predisposition or problems related to amino acid metabolism. In such situations, preventive acid or base intake supplements the patients effort to achieve maximum physiological buffering. This can easily account for some of the spectacular results observed in some patients whose cancers were caught early.

In conclusion, the management of cancer remains complicated. When there is a strong family history or occupational predisposition for cancer, cancer screening needs to be done early to search for risk factors and genetic markers.

Where there are suggestions of cancer predisposition, full blood tests, scans, biopsies, endocrinological tests, and radiological test should be done by a primary care provider and reviewed by a team of experts in radiology, hematology, pathology, oncology surgical oncology, gastroenterology, and international medicine.

References:

Ian F. Robey and Lance A. Nesbit, Investigating Mechanisms of Alkalinization for Reducing Primary Breast Tumor Invasion

Bradley A. Webb, Michael Chimenti, Matthew P. Jacobson & Diane L. Barber, Dysregulated pH: a perfect storm for cancer progression

Silvia M. Titan1, Otávio C.E. Gebara2, Silvia H.V. Callas2, Ana O. Hoff3, Paulo M. Hoff2 and P.C.A. Galvão2, Case report: a rare cause of metabolic alkalosis, 2011

SS Kim, HW Yang, HG Kang, HH Lee, HC Lee, DS Ko… – Fertility and sterility, Quantitative assessment of ischemic tissue damage in ovarian cortical tissue with or without antioxidant (ascorbic acid) treatment, 2004 – Elsevier

M Valko, CJ Rhodes, J Moncol, MM Izakovic… – Chemico-biological… , Free radicals, metals and antioxidants in oxidative stress-induced cancer, 2006 – Elsevier

Rofstad EK, Mathiesen B, Kindem K, Galappathi K. Acidic extracellular pH promotes experimental metastasis of human melanoma cells in athymic nude mice. Cancer Res. 2006;66(13):6699-6707. doi: 10.1158/0008-5472.CAN-06-0983.

Gillies R. J. (2002). In vivo molecular imaging. J. Cell Biochem. Suppl. 39, 231-238 10.1002/jcb.10450 (monocarboxylate transporters and Na-driven proton extrusion)

Shi Q, Le X, Wang B, Abbruzzese JL, Xiong Q, He Y, Xie K. Regulation of vascular endothelial growth factor expression by acidosis in human cancer cells. Oncogene. 2001;20(28):3751-3756. doi: 10.1038/sj.onc.1204500.

Gallagher F. A., Kettunen M. I., Day S. E., Hu D. E., Ardenkjaer-Larsen J. H., Zandt R., et al. (2008). Magnetic resonance imaging of pH in vivo using hyperpolarized 13C-labelled bicarbonate. Nature 45

Gatenby R. A., Gillies R. J. (2004). Why do cancers have high aerobic glycolysis? Nat. Rev. Cancer 4, 891-899 10.1038/nrc1478 (Pasteur Effect)
Source by Otumdi Omekara

 

By SCITECHOUTPOST.COM

Drotumdi O

Home R&D Some Insight On What It Is Like To Be A Medical Writer...

Some Insight On What It Is Like To Be A Medical Writer And What Skills Are Needed

By

incync

-

June 5, 2017

17

0

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· Do you find medicine and healthcare subjects interesting?

· Do you enjoy writing in general, and have a good control of written English up to high school level?

· Then you may find medical writing a challenging but rewarding career.

· A a medical writer you may choose to work as a:

– Health columnist for a newspaper, magazine or website

– Publisher of e-books, news letters, pamphlet, brochures, technical manuals or inserts for healthcare industries

– Healthcare research producer

– Health education material and text book writer

– Medical textbook writer and publisher

– Medical Review book writer and publisher

– A medical education website editor and content provider

The list can go on and on.

· As a medical technical writer, you may choose to go free lance or accept an employment position in healthcare organizations

· The freelance option is for those who have some savings to depend on while growing their clientele. Otherwise the startup period could be very stressful financially.

· The information to be put in writing is usually in the form of medical manuscripts from individuals or research organizations in a disorganized manner.

· The information will need to be organized and formatted to meet the standards of various journal or magazine publishing companies.

· An experienced medical writer will be familiar with formats of big organizations like the American Medical Journal.

· When attending interviews a medical writer would need to present a portfolio of properly formatted writings, whether published or unpublished, in hard copy or electronic copy.

· A medical writer must double check content information with the author, and verify spellings and punctuations with quality word processing software, since there is almost zero tolerance for typos or misinformation in medical writing

· Over time a non-medical medical copy writer may take courses in basic medical sciences to qualify them to write original articles or books in hard copy or online

· How much a medical writer makes annually depends on level of education, experience, output quality, and the organization he/she works for. The pharmaceutical companies tend to pay more and, of course, are most demanding.

Medical writers can earn from as low as $35, 000 per year to as high as 80, 000 per year depending of the above factors

· A freelance medical writer may need only high school education and healthcare work experience.

· But employers tend to prefer medical writers who have college degrees in medical writing, technical writing, basic medical sciences, or English language.

· There are many universities and community colleges now offering courses geared toward medical writing. For more information visit http://www.amwa.org



Source by Otumdi Omekara

By Glavavibase.com

Drotumdi O

Antioxidants, Acids, Alkali and Cancer

In my previous articles on cancer, I did not discuss the role of acids, bases and antioxidants in detail. But with the current hype about the miraculous nature of basic water, antioxidant foods and drugs, I feel compelled to step in and set the records straight with currently available medical literature.

The efficacy of acids, bases and antioxidants in cancer therapy is not a myth. It has biochemical basis informed by modern research (SS Kim et al, 2004; Ian F. Robey & Lance A. Nesbit, 2013). The apparent controversy surrounding this subject emanates from poor coordination of research findings.

I have read articles (Bradley A. Web et al, 2011; Shi Q. et al, 2001; Silver M. et al, PubMed 2011) supporting systemic alkalosis or systemic hyperacidosis as the dominant toxic factor in cancer development. I have also watched video presentations claiming that cancer development is just a natural cellular adaptation to toxic environment, which is corrected by normalizing the environment.

These claims are to say the least, unbalanced truths. By the end of this discussion it would have become obvious that there is no basis for undue generalizations in the management of cancer. There still remains the need for expert judgement in formulating a cancer treatment protocol.

BEFORE CANCER

First, let me state that the human body will literally rust away like a nail left under the rain over time without inbuilt natural protective mechanisms. To prevent rust or oxidation, most macromolecules essential for human existence are shielded from molecular oxygen or oxygen equivalents with hydrogen molecules (reduction). Oxygen equivalents are those compounds that remove these protective hydrogen molecules from other compounds.

They are also called oxidizing agents. Compounds that restore these hydrogen molecules are called reducing agents. The two most important organic reducing agents in human body are glutathione and ubiquinone, while the two most important oxidizing agents are molecular oxygen and free oxygen radicals.

APOPTOSIS AND GROWTH SUPPRESSOR GENES

The human body cells are normally continuously moving from resting phase, to growth phase and then multiplication phase. This continuous state of growth and multiplication means that any organ can potentially grow to any size, depending on its natural growth rate. By inference all human beings may also grow into giants. It even suggests immortality of human beings.

Thankfully, every cell has an inbuilt apoptotic clock that ensures that it dies after a specified number of days, making room for incoming cells. Thus red blood cells, for instance, are recycled every 120 days. The size and shape of the cells of individual organs are equally limited prior to their date of apoptosis, by growth suppressor genes (notably p53, AP1, NF-kB) located in the nucleus.

Anything that hinders the functions of apoptosis and growth suppressor genes would obviously be expected to unleash uncontrolled growth and multiplication of cells in any organ of the body. This rapid growth of disorganized and poorly differentiated cells is called cancer.

All anti-growth suppression and anti-apoptosis agents are called carcinogens. They may be chemicals, radiations, biochemical molecules, acids, bases, free radicals, heat, cold, etc. But they all exert their effect by in activating apoptosis gene or growth suppressor gene. They accomplish this by corrupting the gene coding system in such a way that the codes are wrong (missense) or mean nothing (nonsense).

The code is corrupted due to the insertion of the wrong amino acid code into a gene sequence or the excision of the right amino acid code from the sequence. Consequently the t-RNA misreads or miss-senses the expression of the right apoptosis or growth suppressor protein.

TOXINS, FREE RADICALS AND CARCINOGENS

Toxins are basically those compounds whose activities will directly or indirectly lead to human rust and death by causing catabolic or destructive oxidative reactions in body tissues. The high powered toxic tissue oxidizing agents are called free radicals (ROS and RNS), which are basically free ionized oxygen or Nitrogen atoms (O2- and N2- )

When a toxin causes a gene altering damage in the nuclear region of a cell (oxidative nuclear damage) it is then known as a carcinogen. As such not all toxins are carcinogen. Aflatoxin (from mold) is not only toxic to liver cells, but ultimately causes liver cancer, making it a carcinogen.

The detoxification process mainly converts lipid soluble toxins into excretable water soluble glucuronides in three steps. In step one the toxins are aggregated and isolated in the specific organs that neutralize them.

Then glucuronic acid is attached to them in the presence of glutathione which the protective hydrogen molecules. (Note that in fighting oxidants hydrogen (non-ionized) carried by reduced NADPH is a friend, while in acid-base balance ionized hydrogen is the enemy).

Free radicals can also contribute to cancer development by inducing genetic mutation through oxidative nuclear damage, or suppress cancer growth by promoting apoptosis. Step three is the excretion of the toxins.

ANTIOXIDANTS

Compounds use to replenish hydrogen molecules in glutathione and other endogenous reductase enzymes are called antioxidants. A lot of these reducing agents occur naturally in fruits and vegetables. Others are available as drug extracts from plants and animals.

Individual antioxidants target different steps of the detox process. This is why balanced nutrition by itself goes a long way to keep our bodies toxin free. The air we breathe, the food we eat, the water we drink, and the environments we live in are all full of toxins, including heavy metals. To survive as human beings, an extensive detoxification mechanism has to exist.

Every body tissue has detox ability, but the liver, gut, and lymphoid tissues and kidneys play the dominant role. Thus most toxins are trapped, neutralized and excreted through feces, urine or bile. Stagnation or obstruction of flow in any of these three organs, generally leads to a toxic state.

Stressors and nutritional insufficiencies that weaken the immune system also contribute to toxic states allowing micro-organisms to multiply and generate additional toxic substances that must be removed.

Successful detoxification requires a lot of energy, which comes from glucose metabolism. Biochemical energy is not measured in Joules, but in ATPs (Adenosine Triphosphate). The metabolic process for converting glucose to ATP is called glycolsis.

During aerobic glycolysis one molecule of glucose combines with two molecules of ADP3- (Adenosine Diphosphate) and two ionic phosphoric acid molecules to yield two ionic ATP4- molecules and two lactate molecules. The ionic ATP4- molecule gives up one Hydrogen proton (H+) to yield one molecule of ionic ADP3-, which is reused in glycolysis.

Under anaerobic (low oxygen) conditions, ATP is generated differently. One molecule, each, of ADP3- and ionic phosphoric acid accumulated from aerobic glycolysis recombine without glucose to form one molecule of ATP4+ and one hydroxyl molecule. Two hydrogen protons combine with two bicarbonates to end up as carbonic acid inside body cells.

TOXIC ACIDOSIS

Glycolsis can be aerobic when it consumes molecular oxygen, or anaerobic when it consumes oxidizing agents. Both the detox reactions and glycolsis are driven or catalyzed by enzymes, which depend on the availability of specific micro-molecules, proteins, amino acids and vitamins as cofactors for their functions.

By the time enough ATP is generated to keep the body toxin safe, enough carbonic acid hydration of respiratory carbon dioxide (CO2) has accumulated to keep the inside of every cell perpetually acidic. In a highly toxic state, which includes rapid proliferation of cells, this intracellular acid builds up exponentially beyond survivable limits.

Cancer cells are known to rapidly outgrow their blood supplies and go into severe hypoxic states. This is why the cancer cell nucleus has to rapidly increase the expression of sodium driven proton extruding proteins and enzyme proteins through nuclear sensing of sharp rise in HIF.

Thus, by default, the Intracellular fluid (ECF) of every cell is acidic (low pH) while that of the extracellular fluid (ECF) is alkaline (high pH). It is important to note at this point that while intracellular fluids exist in compartments inside the cells, extracellular fluids coalesce to form a pool in which all body cells submerged.

This ECF pool is represented by intercellular fluid, lymph, blood, and glandular secretions, all of which feed into the circulatory system of the body. ECF acid or base build up in any part of the body is ultimately dissipated into the circulatory system, which centrally maintains a mildly basic pH of 7.20 -7.40.

In addition to mobilizing ammonium and bicarbonate ions the central buffer system has the ability to move chloride ions in and out cells (chloride shift) to maintain acid-base balance.

MEMBRANE SENSORS AND TRANSPORTERS

To keep intracellular acidity below lethal level, the inner surface of the cell membrane has acid sensors and transporters that detect abnormal rise in intracellular acidity and trigger increased extrusion of hydrogen and retention of alkaline bicarbonate ions.

This trigger is mediated by the rise in the blood level of hypoxia induced factors (HIF) and probably acidosis induced factors (AIF). On detecting this rise in HIF, the nucleus temporarily increases the expression of Na-driven proton transport proteins and histidine rich basic proteins.

The ammonium radicals on the amino acids of these basic proteins (especially histidine) serve as physiologic buffers for organic acids.

“Protonation and de-protonation has been experimentally shown to change protein structure and thus, alter protein-protein binding affinity, change protein stability, modify protein function, and alter subcellular localization (Schonichen et al., 2013b).

Evolutionarily, histidines must confer some selective advantage for cancers, as 15% of the 2000 identified somatic mutations in cancer involve histidine substitutions, with Arg-to-His being the most frequent (Kan et al., 2010)”.

The nucleus also temporarily steps up the expression of important enzyme proteins that catalyze the buffer reactions, namely mono-carboxylate, carbonic anhydrase, and aminotransferase enzymes.

In a similar manner the external surface of the cell also has alkaline sensors made up of G-protein coupled surface receptors, which also communicate with the nucleus to increase or decrease the expression of relevant proteins and enzymes. As tissue hypoxia decreases, the level of HIF decreases along with nuclear expression of proton extrusion proteins and enzymes.

Failure of this return to normalcy has been observed as one of the hallmarks of early cancer. What started out as a normal adaptive change becomes persistent because of irreversible genetic modifications that triggered it.

CELLULAR SURFACE ACID/BASE REVERSAL

The central physiological buffer system has a maximum capacity to neutralize up to 30 micromoles of acid/gram tissue/min in systemic acidosis or 5-10 micromoles of base in alkalosis.

Beyond these levels, normal body cells are unable to continue their buffer functions because the enzymes are deactivated. At this point there is a reversal of the normal acid-base distribution on either side of the cell membrane, which is lethal to normal issues. In some critical situations, chloride ions are shifted massively into all body cells (chloride shift) to urgently dilute the extracellular acidity.

But the gastric cells have the natural ability to survive in the presence of high extracellular acidity (HCl at pH of 6.6). How they manage this high extracellular acidity then becomes very important in understanding how cancer cells survive high extracellular acidity with normal intracellular acidity for their survival and proliferation. Some cancer cells are known to have accumulated genetic adaptations that enable them to survive extreme pH conditions (carbonic acid at pH of 6.6).

Gastric cells are shielded from concentrated HCl secreted into the stomach mainly by structural barriers (thick basement membrane, thick mucosal layer and thick mucous layer). There are no natural inhibitors of hydrogen potassium ATPase enzyme that catalyzes the final phase of acid excretion.

In severe cases of Peptic Ulcer Disease (PUD), Gastro-esophageal reflux (GERD), or Zollinger-Ellison Syndrome, when this natural barrier is ulcerated by concentrated HCl, some gastric lining cells undergo goblet intestinal metaplasia (transformation into ectopic intestinal epithelium in the stomach) to secrete neutralizing alkaline fluids into the stomach.

While there is no natural attempt to control the hydrogen potassium ATPase enzymes, pharmacological intervention with proton pump inhibitors (PPIs) like omeprazole has been successful in reducing gastric secretion in severe cases of chronic gastric hyperacidity.

Similarly some esophageal epithelial cells undergo gastric metaplasia to become gastric cells in the face of chronic exposure to reflux gastric acid (Barrett’s Esophagus). Acquisition of this missing ability to control hydrogen potassium ATPase and sodium driven proton extrusion by monocarboxylate enzyme appear to be critical to the survival of cancer cells

IN EARLY CANCER

It is important to note that the natural response to extracellular hyperacidity in the GIT depends on the stage and localization of the acidity. Both goblet metaplasia and gastric metaplasia have been recognized as precancerous lesions (carcinoma in situs). At the early stage of Barret esophagus, the response is only structural to prevent cell wall damage.

But when the barrier has failed in the stomach, the response is alkaline secretion. A person on preventive alkaline water will be helping to neutralize the added hypoxic acidity of early cancer in Barret’s Esophagus and chronic PUD, but not in any way preventing the occurrence of cancer itself, since proton extrusion in cancer is irreversible.

Any cancer caught at the in situ stage is usually best treated with surgical excision and radiotherapy, rather than alkaline water.The question then is: “Why did prophylactic alkaline water not prevent the metaplasia?”

The answer to that is that while oral alkali intake may cap out at micromoles of alkali per gram tissue, cancer proton extrusion acid build up ranges in nanomoles per gram tissue (a thousand times more). Also intracellular hypoxia and hyperacidity are not the only risk factors for cancer.

Radiations are known to be commonly responsible for skin cancers, even as HPV is known to be responsible for cervical cancer. Prophylactic alkalosis has not been reported to prevent any of them. Sticking to the hype that alkaline water is the best way to prevent and even cure cancer, puts people at risk of missing early opportunities to truly cure cancer.

Alkaline water intake will help the body maximize the physiological adaptive response acidosis. Unfortunately, even at maximum physiological capacity, extracellular buffers are no match for cancer intracellular proton extruders.

As the well adapted cancer cells grow and multiply freely their neighboring non-cancerous cells are rapidly destroyed by ECF hyperacidity creating more space for them to occupy. Thus cancer invasiveness has been shown to correlate with the degree of acid-base reversal across the cancer cell membrane.

At the advanced stage of cancer with ECF acidity readings in nanomols compared to orally boosted alkalinity readings in micromoles, buffer therapy has been shown to be resisted by cancer cells. One such reported example is the inefficacy of a basic drug doxorubicin used in the treatment of Leukemias and lymphomas.

Going by what has been discussed so far, it is obvious that externally sourced acids and alkali cannot be safely loaded to outweigh tumor generated levels in ECF and ICF. It is also understandable that no single pH balancing agent, can be used to treat both acid sensing and alkaline sensing cancers.

Preventive or prophylactic intake of acidic or alkaline liquids or foods remain relevant only within the physiological buffering range, when adaptive changes are still reversible. Unfortunately at that point the tumor generated acidity would have risen to resistant levels. Preventive alkaline water intake in a person with undiagnosed acid sensing cancer is not likely to retard the growth of the tumor.

Similarly preventive intake of alkaline water in a patient with undiagnosed alkaline sensing cancer will encourage it to grow and establish faster. Patients receiving treatment for emesis gravid arum (vomiting in pregnancy) for instance, cannot be on preventive alkaline regimens in the face of systemic alkalosis from heavy loss of gastric acid through vomiting.

However, it is possible that some people are unable to fully optimize the natural buffer system, due to genetic predisposition or problems related to amino acid metabolism. In such situations, preventive acid or base intake supplements the patients effort to achieve maximum physiological buffering. This can easily account for some of the spectacular results observed in some patients whose cancers were caught early.

In conclusion, the management of cancer remains complicated. When there is a strong family history or occupational predisposition for cancer, cancer screening needs to be done early to search for risk factors and genetic markers.

Where there are suggestions of cancer predisposition, full blood tests, scans, biopsies, endocrinological tests, and radiological test should be done by a primary care provider and reviewed by a team of experts in radiology, hematology, pathology, oncology surgical oncology, gastroenterology, and international medicine.

References:

Ian F. Robey and Lance A. Nesbit, Investigating Mechanisms of Alkalinization for Reducing Primary Breast Tumor Invasion

Bradley A. Webb, Michael Chimenti, Matthew P. Jacobson & Diane L. Barber, Dysregulated pH: a perfect storm for cancer progression

Silvia M. Titan1, Otávio C.E. Gebara2, Silvia H.V. Callas2, Ana O. Hoff3, Paulo M. Hoff2 and P.C.A. Galvão2, Case report: a rare cause of metabolic alkalosis, 2011

SS Kim, HW Yang, HG Kang, HH Lee, HC Lee, DS Ko… – Fertility and sterility, Quantitative assessment of ischemic tissue damage in ovarian cortical tissue with or without antioxidant (ascorbic acid) treatment, 2004 – Elsevier

M Valko, CJ Rhodes, J Moncol, MM Izakovic… – Chemico-biological… , Free radicals, metals and antioxidants in oxidative stress-induced cancer, 2006 – Elsevier

Rofstad EK, Mathiesen B, Kindem K, Galappathi K. Acidic extracellular pH promotes experimental metastasis of human melanoma cells in athymic nude mice. Cancer Res. 2006;66(13):6699-6707. doi: 10.1158/0008-5472.CAN-06-0983.

Gillies R. J. (2002). In vivo molecular imaging. J. Cell Biochem. Suppl. 39, 231-238 10.1002/jcb.10450 (monocarboxylate transporters and Na-driven proton extrusion)

Shi Q, Le X, Wang B, Abbruzzese JL, Xiong Q, He Y, Xie K. Regulation of vascular endothelial growth factor expression by acidosis in human cancer cells. Oncogene. 2001;20(28):3751-3756. doi: 10.1038/sj.onc.1204500.

Gallagher F. A., Kettunen M. I., Day S. E., Hu D. E., Ardenkjaer-Larsen J. H., Zandt R., et al. (2008). Magnetic resonance imaging of pH in vivo using hyperpolarized 13C-labelled bicarbonate. Nature 45

Gatenby R. A., Gillies R. J. (2004). Why do cancers have high aerobic glycolysis? Nat. Rev. Cancer 4, 891-899 10.1038/nrc1478 (Pasteur Effect)



Source by Otumdi Omekara

By herzkrankheit.blogspot.com (German Translation)

Drotumdi O


How Physicians Treat A Patient Who Complains of Chest Pain (German Translation)

 


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Herzkrankheit


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Wie behandeln Someone Who Compains of Chest Pains Klagt


Wie ein Patient, der Schmerzen in der Brust klagt behandelt wird, hängt von der Diagnose ab. Um eine Diagnose von Schmerzen in der Brust zu machen, wird ein Arzt zunächst eine detaillierte Geschichte der exakten Lage der Schmerz, wo es strahlt, wie lange es schon auf, wie es angefangen hat, alle damit verbundenen Symptome gewesen, alle bisherigen Folgen und wie es gelöst wurde. Der Arzt wird auch über die Geschichte von


Bluthochdruck, periphere arterielle Verschlusskrankheit, Schlaganfall, hoher Cholesterinspiegel, hoher Triglycerid, Lungenentzündung, Lungenembolie, Pneumothorax, Diabetes, Nierenerkrankungen, Magengeschwür, Refluxkrankheit, Gallenblase, Lebererkrankungen, Pankreatitis fragen , Brust Verletzungen, Familiengeschichte oder Herzinfarkt, Medikamente Geschichte vor allem Aspirin und Nitroglycerin Verwendung usw.


Basierend auf den Ergebnissen dieser Geschichte, wird der Arzt durchführen allgemeine körperliche Untersuchung, durch einen fokussierten Brust Prüfung gefolgt. Er / sie wird prüfen, abtasten, abhorchen (mit einem Stethoskop), Ausschreibung Flecken, Schwellungen, wuchtet, Frakturen, abnorme Herztöne, abnormale Atemgeräusche, abdominale Zärtlichkeit, Zärtlichkeit Gallenblase, Niere und Pankreas Zärtlichkeit usw. 


Die Arme und Beine wird auf Anzeichen für einen Schlaganfall untersucht werden, während die Augen auf Anzeichen von inneren Blutungen im Kopf untersucht werden. Weiter wird der Patient zu dem EKG-Gerät für eine EKG-Aufzeichnung, um auszuschließen, ischämischer Herzkrankheit oder Herzinfarkt, die die größte Bedrohung ist eingehängt werden. 


Blut wird auch für Herz-Enzym und Koagulationstests gesammelt weiter für Herzinfarkt doppelt überprüfen. Wenn es einen Vorschlag für einen Herzinfarkt, wird der Patient schnell in der Intensivstation aufgenommen. Tragbare Brust x-ray ist auf der Intensivstation durchgeführt, um auszuschließen, Lungenembolie, Pneumonie und Pneumothorax. Ein CT-Scan des Kopfes und der Brust wird auch getan werden, um auszuschließen, Schlaganfall und


Lungenembolie. Sofortige Antikoagulation Behandlungen einschließlich Aspirin gestartet werden, wenn es irgendein Vorschlag Gefäßverschluss im Herzen oder im Gehirn durch ein Blutgerinnsel. Nitroglycerin und selektive Betablocker werden initiiert, um die Blutversorgung der Muskeln zu erhöhen hören, wenn es einen hohen Verdacht auf Herzinfarkt. Inzwischen wird der Patient auf Sauerstoffmaske und elektronische Herz und Lunge Monitor setzen. 


Die Sauerstoffsättigung, Blutdruck, Puls und Atemfrequenz sind für jegliche negativen Veränderungen überwacht. Notfall-Reanimation griffbereit für möglich Herzstillstand oder Arrhythmien (unregelmäßiger hören Beats). Der AED Maschine griffbereit im Falle der Herz aufhört zu schlagen oder beginnt zu schlagen unregelmäßig oder zu schnell.


Zu diesem Zeitpunkt ist würde sich ziemlich klar gewesen, wo die Schmerzen in der Brust kommen wird. Wenn so die spezifische Behandlung wird nach den üblichen Zeitpläne fortgesetzt. Ansonsten Erkundungen der abdominalen Diagnosemöglichkeiten werden begonnen, um auszuschließen, Magengeschwür, PUD, Reflux, Alle Blase Krankheit und Pankreatitis. 


Detaillierte Untersuchungen sind in der Regel durchgeführt, wenn der Patient auf der Intensivstation stabilisiert wird und auf der Station. Die weitere Behandlung wird dann auf nachfolgende Ergebnisse und abschließende Diagnose abhängig.  




 

By webmagnates.org

Drotumdi O


Why Older Women Break Their Hip Bones So Easily
 

 




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Why Older Women Break Their Hip Bones So Easily

http://www.webmagnates.org


Fifty five percent of all Americans aged over 50 years have osteoporosis or thin spongy bone, that is highly susceptible to compression and breakage. One out of every two white women in US will fracture a bone in her lifetime. Although all long bones and vertebral bones are vulnerable, the most common fractures affect the hip bones. About 20% of post-menopausal women who fracture their hip bone die within a year of the fracture, while 20% of these women often have a second fracture one year down the road. 


The cost of treatment and nursing home rehabilitation of hip bone fracture patients runs into about one billion dollars a year. Currently about 10 million Americans have mild bone thinning or osteopenia. Another 34 million people have severe bone thinning or osteoporosis. This number is expected to increase in the years ahead with many more US citizens growing older.


Osteoporosis is mostly attributable to bone thinning usually after the age of 35 years, for various reasons. The normal rate of bone thinning due to age is 0-3% to 0,5% per year. Bone density usually peaks at the age 25 and remains there for another 10 years. Genes (family history), environment, sex, ethnicity, hormones, and medications influence bone density. 


Men tend to have heavier bones than women, even as African Americans tend to have heavier bones than Caucasians and Asian Americans. The short supply of sunshine in North America reduces the availability of Vitamin D, which normally helps the absorption of dietary calcium.


Women are particularly vulnerable to osteoporosis because of the progressive decrease in the level of estrogen needed to support bone density after the menopausal age of 45 years. Bone thinning is accelerated to 2% - 4% with up 25 % to 30% loss of bone density by age 55. The spongy nature of the bone is produced by normal formation of protein structure (collagen) of the bone without adequate calcification. 


Cigarette smoking, alcohol consumption, low protein and low calcium diets, as well as malabsorption from celiac sprue or biliary cirrhosis can all contribute to low bone density and easy bone fracture in older women.


Diseases like hyperthyroidism, anorexia nervosa or vigorous exercises (common among teenagers) can eventually cause amenorrhea (cessation of menses) with secondary bone thinning. Stroke and chronic arthritis, which cause immobility, also lead to loss of bone density. 


Abnormally high level of parathyrioid hormone, which normally maintains the normal level of blood calcium ends up stripping the bones of calcium, with marked reduction in density. High level of parathyroid hormone is often found in some forms of lung cancer as a paraneoplastic syndrome. Long-term use of heparin (blood thinner), phenythoin (anticonvulsant) and prednisolone (steroid) may also lead to loss of bone density.


Based on the what has been discussed so far it becomes necessary for every woman above 45 years to be aware of the high risk of bone fracture from osteoporosis and seek to be on a physician-prescribed preventive program. This includes X-ray and DEXA scan monitoring (T score of - 2.5 of or higher), adequate moderate outdoor exercises, and preventive medications like Alendronate (Fosamax) and estrogen replacement therapy (ERT).

By cancer323.blogspot.com

Drotumdi O


cancer

 


http://cancer323.blogspot.com

 


Saturday, 9 February 2013

 

 


cancer


Cancer Overview: Types, Causes, Diagnosis And Treatment
By Otumdi Omekara


Cancer is the name given to a cell that has lost its normal physiological or natural growth control and multiplies very rapidly to produce a large new growth called a tumor or neoplasm (swelling). This new growth or neoplasm could be confined to the local region or directly invade the surrounding tissues. It may also break out with tumor particles carried by blood to distant parts of the body. This is what determines the stage of the tumor.


Such cancers that invade neighboring tissues or spread to distant organs as said to be malignant. Those confined to the original tissue type are said to be benign. The level of disorganization of the tissue architecture also gives a sense of whether the tumor is benign or malignant. Benign cancers are not as dangerous as malignant cancers, although large ones depending on their locations could produce dangerous pressure effects as happens with fibroids causing abortions.


Cancers can arise from virtually any tissue of the body, in the presence of the right stimulus and genetic predisposition. The stimuli that initiate cancer could be radiations (x-ray, solar, etc), chemicals like carbon tetrachloride or asbestos or cigarette smoke, drugs used in early pregnancy, biochemicals like VEGF, etc. The stimuli generally alter the genetic code of the individual cells to disable the tumor suppressor genes that prevent uncontrolled cell growth or ensure programmed cell death (apoptosis)


Different tissues are sensitive to different stimuli, but those cells that naturally grow rapidly are most sensitive to cancer stimuli. Such tissues include the skin, testis, ovaries, breast, uterus, liver, spleen, gastro-intestinal tract, growing bones, blood cell, lungs, lymph nodes etc. The commonest cancers therefore involve the lungs (carcinoma), blood (leukemia), lymphoid tissues (lymphoma), bones (osteoma or steosarcoma), skin (carcinoma), liver (hepatoma), ovaries (cystadenoma or cystadenocarcinoma).

 


The destructive potential of a particular cancer depends on the type and location. Lung and breast cancers are known to be the two leading causes of death among women in the US. Colon cancer kills a lot of men and women. Leukemia kills a lot children in America by destroying their bone marrows and making them very anemic. Prostate cancer kills a lot men each year in the US. Sun exposure causes a lot of skin cancer in States like Florida. Tumors affecting blood vessels cause them to be fragile and bleed easily. This can be a huge problem in the eyes and brain.


The general approach to treatment of cancers is to detect them early when they are still very local and ablate them surgically, thermally (diathermy) or cryoscopically (freezing). Surgical biopsy is used to obtain some of the cancer tissue for laboratory examination and classification. Early stage cancers are generally cured by surgical excision.


Mid stage cancers, involve both wide surgical dissection, as in breast cancer, and radiation therapy to kill off residual cancer cells. Late stage cancer is mostly treated with chemotherapy and radiation. Leukemias, often involve the wiping out of patients' bone marrow cells and replacing them with donor cells.


Author: Dr. O. Omekara


URL: http://www.droomekara.com


Email: tumex@droomekara.com


Phone: 19712085909


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By MAOADMIN

Drotumdi O


EBOLA FAST FACTS



moaadmin | November 6, 2014 | News | No Comments


The current Ebola hemorrhagic fever outbreak has been described as the largest in history and the first of its kind in West Africa. The disease is related to but distinct from Lasa fever which had an outbreak in Nigeria in th 1980s. Four types affecting human beings include: Ebola Zaire, Ebola Sudan, Ebola Ivory Cost and Ebola Bundibugyo


Ebola hemorrhagic fever affects both animals (primates like monkeys) and human beings and can be transmitted between the two species. Transmission is mainly through body fluids entering broken skins or mucosa membranes. Ebola virus causes severe damages to the major organs of the body and often causes blood clotting failure with massive internal bleeding; hence the name hemorrhagic fever. It is a deadly disease without intensive supportive treatment.


The current FDA approved antiviral drugs are ineffective against Ebola virus, hence the death rate from Ebola infection is up to 95%. Researchers have noticed a continuous change in the genetic make up of Ebola virus between 2014 and 2024, as it switches human hosts. The current outbreak has been traced to an initial animal to human transmission in Central Africa, with human to human spread to West Africa


As of October 14, 2014, over 2470 people have been infected and over 1300 people have been killed by Ebola virus in West Africa. These numbers are said to be increasing exponentially. Only one death has been reported in Dallas Texas in the US, of a Liberian male who contracted the disease before leaving for US. One of the nurses who attended to the dead patient has just been diagnosed with Ebola infection, is not in critical condition.


Failure of personal protective equipment (PPE) protocol has been suggested, and US healthcare workers are getting actively prepared to handle potential outbreaks in their institutions. All healthcare workers presented with patients with high fever must ask about their travel history and instantly commence universal precautionary measures


The US Congress has approved mandatory screening of all passengers from West Africa for high fever and other symptoms at the international airports. All travellers entering the US with symptoms of Ebola infection must be observed in isolation for a specified period before they can enter the country. The National Institute of Health (NIH) has warned the US Congress about possible Ebola epidemic and even pandemic without aggressive national and international Ebola infection preventive measures. Some legislators are calling for restriction of inbound flights from Liberia, Sierra Leone, or Guinea. However, the US Congress is yet to have a debate on that call


If Ebola symptoms presented after visitors have made contact with US residents, their contacts must also be traced and observed in isolation, The homes and surroundings of their hosts are also actively disinfected by specially equipped CDC crew. The same precaution was taken for the first US patient recently diagnosed with Ebola hemorrhagic fever in Texas. Contact with potential Ebola patients must be avoided without adequate personal protective wears.


A $50 Billion dollar public health aid package for the affected countries has also been approved by US congress, along with over 1000 military personnel to help with Ebola epidemic containment efforts. An Ebola Response Team has also been established in the US by the Center for Disease Prevention (CDC) to step in immediately the diagnosis of the Ebola is confirmed in any part the country. The team is to help with patient management expertise, provision and supervision of proper use of personal protective equipment (PPE), transportation, environmental disinfection, and more.


New vaccine testing on US Ebola patients brought back from West Africa is providing modest hope of arresting the speed of Ebola infection. Ebola virus is not airborne, so there is no need for panic among unexposed individuals, who have made no direct contacts with infected patients. Ebola virus produces symptoms after up to 21 days, when and only when it becomes infectious


The symptoms of Ebola hemorrhagic fever include: fever of up to 103°F, flu-like symptoms, stomach upset, general body ache, muscle weakness, loss of appetite, diarrhea, nausea, vomiting, malaise, and mild headache, skin rashes, sore throat, and gastrointestinal bleeding. In severe cases coma and death may follow hypotensive shock.


These symptoms are produced by viral invasion of the blood, liver, kidneys, and other vital organs, including the central nervous system. Toxic pyrogens disrupt the hypothalamic thermoregulatory system, allowing the body temperature to rise up to 103°F. Severe damage to the liver cuts off production of clotting factors leading to generalized bleeding disorder.


In general, epithelial cells lining the skin and mucous membranes normally release interferon – alpha (IFN-alpha) from CD4 T lymphocytes and immunoglobulin-M (IgM) from CD8 B- lymphocytes immediately invading viruses are detected. IFN-alpha activates natural killer (NK) cells which destroy the viruses. About 24 hours later activated CD4 T-Helper lymphocytes switch immunoglobulin production from IgM to IgA which protects secretory surfaces from bacterial invasion. When the viral load overwhelms this natural defense mechanism, symptoms of the disease begin to manifest. Vaccine development is aimed at stimulating increased production of natural killer cells specifically targeted at Ebola virus genome.


From what is happening in West Africa, the World Health Organization (WHO) has warned that without aggressive preventive measures and logistic supports, there might soon be up to 10,000 new Ebola hemorrhagic fever patients daily. The US president has also called on those nations who have some resources to offer to step up to the plate and send aid packages to Sierra Leone, Liberia and Guinea.


Source by Otumdi Omekara

By veterinaryvet.com

Drotumdi O


  http://www.veterinaryvet.com


Autism Spectrum Diseases - The Importance of Early Diagnosis - I

by Otumdi Omekara


posted in Health and Fitness


Autism Spectrum Diseases - The Importance of Early Diagnosis - I


Health and Fitness: Autism • Published: November 12, 2014


The ability of parents to suspect that their baby may have autism is very critical to early diagnosis and intervention. This article is aimed at getting parents to the point where they are able to ask: Is this autism or what? How early this question is answered in a child's life, goes a long way to determine whether he/she will live a dependent or independent life. A high index of suspicion is so important because having had previous normal children does not exclude the possibility of having an autistic baby.


The risk of having autism is highest (90%) for a concordant twin of a known autistic kid. Other siblings have only 35% risk of being diagnosed with autism. Autism usually presents enough symptoms and signs for accurate diagnosis by the age of two. As such many federal and state government programs for supporting autistic children require that it is diagnosed before his/her second birth day for them to qualify.


In response to the growth of autism as a source of disability in the US, Congress passed the Children's Health Act in 2000, mandating several activities that included the establishment of a new autism research network. This legislation led to the birth of five NIH institutes charged with the responsibility of researching into the causes, diagnosis, early detection, prevention and treatment of autism.


Yet a CDC autism survey in 2009 showed that 1 in 110 US kids was at risk of developing autism, with boys being four to five times more likely to be affected than girls. A significant number of high-functioning autistic kids diagnosed in 2000 are now in their early twenties and need vocational employments as people with liability. There are many federal, state and county programs currently available to assist higher functioning autistic adults with independent living, job procurement, community inclusion, speech therapy and mental health care.


Since 2000 a lot has been learned about autism neurobiology, diagnosis, intervention genetics, and services. The number of autism support resources have also grown dramatically. One key knowledge that has emerged from the various research efforts is that autism is a broad spectrum disorder including several members of a group of disorder known as pervasive developmental disorders (PDDs).


Autism is therefore presently classified in the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. (DSMV--IV-TR) as Autism Spectrum Disorder (ASD). The DSMV-IV describes ASD as a group of five pervasive brain. disorders (AD, AS, PDD-NOS, RD, and PCDD) which variably impair a child's ability to communicate, socialize, behave normally. and reason at age-appropriate levels. AD is the classic autism disorder. AS is Asperger's Syndrome. PDD-NOS is Pervasive Developmental disorders Not Otherwise Specified. RS IS Rett Syndrome while CDD is Childhood Disintegrative Disorder.


The classic ASD is a neuro-psychiatric developmental disorder affecting the brain in such a way that an individual's communication, socialization, behavioral, cognitive (reasoning) abilities are compromised to various extents. It is the extent to which these adaptive skills are compromised that differentiates one PDD from the other. It also accounts for the spectral nature of autism. In severe ASD the IQ is substantially reduced adding the fourth component, cognitive (reasoning) impairment to the picture.


This same compromise accounts for the highly variable levels of disability observed among individuals diagnosed with ASD. Some autism patients are so minimally affected as in Rett disorder that they live independently without supervision. Others are so severely affected, as in classic ASD, that they need 24/7 residential care, as well as assistance with activities of daily living (ADL).


The rest of the PDDs then fit in at various levels between these two extremes. How ASD selectively targets and alters the areas of the brain responsible for emotions, speech, behavior and reasoning is still being actively researched. These target areas include the limbic system (amygdala and nucleus accombens), and the ventromedial prefrontal cortex and the frontal lobe.


The understanding of how these areas have been genetically altered by other disorders affecting them, coupled with observations in traumatic or surgical lobotomy, have both provided some insight into the possible risk factors for autism. What is known so far is that ASD is triggered by multiple and random gene alterations (frame shift mutation or gene duplication, or deletion), on chromosomes 15 and 16. Gene deletion or duplication leads to a frame shift mutation, which in turn leads to the production of a neutral protein, a destructive protein, or an enhancing protein in the target areas of the brain.
(See Part II on Article List)
Article Source: http://EzineArticles.com/8806407


Autism Spectrum Diseases - The Importance of Early Diagnosis - II
10:35  Health  No comments


When neutral proteins are produced, mild ASD will occur due to inadequate production of synaptic adhesion proteins (neuroligin, neurexin, MDGA1 and MDGA2) needed for normal mood, speech and behavior. When a toxic protein results it would destroy the target sites, and impair their functions.On rare occasions, a mutant synaptic adhesion protein may have an enhancing protein which may lead to a super-functioning ASD patient. Synaptic protein abnormalities have been associate with autism and schizophrenia. In order to easily recognize an abnormal pattern of child development, one needs to have a sense of what is normal.


After having two normal kids a mom might get a sense of what is normal in child development. But a new mom will need help knowing what to expect. She needs to know that at birth, a newborn baby will have a grabbing and reaching behavior or the startle reflex. The newborn is also able to initiate facial grimace, as well as cry and cling for attachment. As early as 1 week a newborn can distinguish mom's smell from dad's smell. A normal newborn, in the first couple of months is attracted to bright, colorful, moving objects, and can distinguish voice sound from ordinary noise.


Prior to the 8th week, the baby exhibits reflex (endogenous) smile. But by week 8, the baby responds to faces with a smile (exogenous or social smile). By week 12, the smile becomes selective for familiar faces only (preferential social smile). The newborn quickly learns to draw attention to personal needs by crying aloud. The loud cry usually builds up from unhappy face to grunting to sobbing to cry outburst with tear stream. As the child grows older he/she learns to kick off bed covers in protest and roll into ready to crawl position with head lifted up and eyes scanning for parents. In general the manifestations of autism are related to the child's tendency to be disinterested in the environment, to be inflexible with habits and mannerisms, and to be emotionally numb. Two early sign of inflexibility often overlooked in a newborn are the selective feeding on only one breast and selective sleeping in only one position.


The autistic newborn may also only fall asleep when the room is pitch dark or clutching a specific part of his/her body. Some may insist on having their thumb in their mouth before they can fall asleep. One of the earliest obvious suggestions that something may be wrong is the absence social smile between three to four months after birth.There may also be absence of eye contacts or tracking eye movements. It becomes more obvious that something is wrong between ages 6 and 12, when a child fails to develop normal emotional, speech and play patterns, and makes only repetitive sounds and hand movements.Synaptic failures between primary cortical sensory areas (visual, auditory, and somatosennsory) and association cortex, prevents learning and memory formation that occurs through the association of particular emotions with specific stimuli, place and objects.


Normally, the smiley face of a mom breastfeeding her baby stimulates increased dopamine release in the pleasure center (nucleus accumbens), and causes the baby to return a smile whenever a physiologic need is met. The pleasure of social interaction by itself may directly create a positive memory in a normal child through the hippocampus without nuerotransmitter surge in nucleus accombens. The script recorded in the hypocampus is played over and over by the autistic kid for every emotional situation, until there occurs a strong intrusive override by way of teaching. This accounts for the repetitive and non-interactive, domineering style of communication exhibited by autistic individuals. A negative emotion creates a diminished desire for the stimulus, by reducing the level of dopamine, which normally causes a craving for the stimulus.


This association of negative emotion with withdrawal occurs in the amygdala, the limbic nucleus for harm avoidance. Dopamine reduction is produced by a surge of serotonin into the synapses, which creates the feeling of satisfaction and switches off the stimulus. Two other neurotransmitters, mGluR2 and mGluR3, inhibit the opening of dopamine receptors, thereby further reducing its craving effect and increasing the harm avoidance response. The craving response and harm avoidance response are modulated by the ventromedial prefrontal cortical association area, which is the center for problem solving reward with a strong kink to the limbic system.

Author: Dr. O. Omekara

http://www.Droomekara.com

PO Box 91221, Portland OR, 97291

tumex@droomekara.com

9712085909

Article Source: http://EzineArticles.com/?expert=Otumdi_Omekara

By FASTSSDHOSTING.NET

Drotumdi O


FASTSSDHOSTNG.NET

 


ANTIOXIDANTS, ACIDS, ALKALI AND CANCER

In my previous articles on cancer, I did not discuss the role of acids, bases and antioxidants in detail. But with the current hype about the miraculous nature of basic water, antioxidant foods and drugs, I feel compelled to step in and set the records straight with currently available medical literature.

The efficacy of acids, bases and antioxidants in cancer therapy is not a myth. It has biochemical basis informed by modern research (SS Kim et al, 2004; Ian F. Robey & Lance A. Nesbit, 2013). The apparent controversy surrounding this subject emanates from poor coordination of research findings.


I have read articles (Bradley A. Web et al, 2011; Shi Q. et al, 2001; Silver M. et al, PubMed 2011) supporting systemic alkalosis or systemic hyperacidosis as the dominant toxic factor in cancer development. I have also watched video presentations claiming that cancer development is just a natural cellular adaptation to toxic environment, which is corrected by normalizing the environment.


These claims are to say the least, unbalanced truths. By the end of this discussion it would have become obvious that there is no basis for undue generalizations in the management of cancer. There still remains the need for expert judgement in formulating a cancer treatment protocol.

BEFORE CANCER................

Source by Otumdi Omekara

 

By CheerCoach.com

Drotumdi O

 


Antioxidants, Acids, and Cancer


In my previous articles on cancer, I did not discuss the role of acids, bases and antioxidants in detail. But with the current hype about the miraculous nature of basic water, antioxidant foods and drugs, I feel compelled to step in and set the records straight with currently available medical literature.

The efficacy of acids, bases and antioxidants in cancer therapy is not a myth. It has biochemical basis informed by modern research (SS Kim et al, 2004; Ian F. Robey & Lance A. Nesbit, 2013). The apparent controversy surrounding this subject emanates from poor coordination of research findings.


Source by Otumdi Omekara

By STAFF PICK.com

Drotumdi O


POSTED ON FEBRUARY 3, 2016 POSTED IN STAFF PICK BY STAFF PICK

Cancer Overview: Types, Causes, Diagnosis And Treatment

Cancer is the name given to a cell that has lost its normal physiological or natural growth control and multiplies very rapidly to produce a large new growth called a tumor or neoplasm (swelling). This new growth or neoplasm could be confined to the local region or directly invade the surrounding tissues. It may also break out with tumor particles carried by blood to distant parts of the body. This is what determines the stage of the tumor.


Such cancers that invade neighboring tissues or spread to distant organs as said to be malignant. Those confined to the original tissue type are said to be benign. The level of disorganization of the tissue architecture also gives a sense of whether the tumor is benign or malignant. Benign cancers are not as dangerous as malignant cancers, although large ones depending on their locations could produce dangerous pressure effects as happens with fibroids causing abortions.


Cancers can arise from virtually any tissue of the body, in the presence of the right stimulus and genetic predisposition. The stimuli that initiate cancer could be radiations (x-ray, solar, etc), chemicals like carbon tetrachloride or asbestos or cigarette smoke, drugs used in early pregnancy, biochemicals like VEGF, etc. The stimuli generally alter the genetic code of the individual cells to disable the tumor suppressor genes that prevent uncontrolled cell growth or ensure programmed cell death (apoptosis)


Different tissues are sensitive to different stimuli, but those cells that naturally grow rapidly are most sensitive to cancer stimuli. Such tissues include the skin, testis, ovaries, breast, uterus, liver, spleen, gastro-intestinal tract, growing bones, blood cell, lungs, lymph nodes etc. The commonest cancers therefore involve the lungs (carcinoma), blood (leukemia), lymphoid tissues (lymphoma), bones (osteoma or steosarcoma), skin (carcinoma), liver (hepatoma), ovaries (cystadenoma or cystadenocarcinoma).

 


The destructive potential of a particular cancer depends on the type and location. Lung and breast cancers are known to be the two leading causes of death among women in the US. Colon cancer kills a lot of men and women. Leukemia kills a lot children in America by destroying their bone marrows and making them very anemic. Prostate cancer kills a lot men each year in the US. Sun exposure causes a lot of skin cancer in States like Florida. Tumors affecting blood vessels cause them to be fragile and bleed easily. This can be a huge problem in the eyes and the brain.


The general approach to treatment of cancers is to detect them early when they are still very local and ablate them surgically, thermally (diathermy) or cryoscopically (freezing). Surgical biopsy is used to obtain some of the cancer tissue for laboratory examination and classification. Early stage cancers are generally cured by surgical excision.


Mid stage cancers, involve both wide surgical dissection, as in breast cancer, and radiation therapy to kill off residual cancer cells. Late stage cancer is mostly treated with chemotherapy and radiation. Leukemias, often involve the wiping out of patients’ bone marrow cells and replacing them with donor cells.


About The Author
Dr. Otumdi Omekara is a preventive medicine specialist and medical publisher with over two decades of clinical practice experience and over a decade of provider management experience. His passion for patient education drives his medical content article writing and publishing. He was a health educator at Oregon DHS Center for Disease Control from 2001 to 2002. Prior to that he volunteered at NE Portland Neighborhood Clinic as a health educator from 1997 to 2002. Since 2002 he has been the Chief Consultant at Dromekara.com Health & Fitness Publishing. He can be reached online or by mail: PO Box 91221 Portland Oregon 97291.


Syndicated By EzineArticles
 

By Learnaboutcancer.com

Drotumdi O


LEARN ABOUTCANCER.COM


Posted by admin

Antioxidants, Acids, Alkali and Cancer
 In my previous articles on cancer, I did not discuss the role of acids, bases and antioxidants in detail. But with the current hype about the miraculous nature of basic water, antioxidant foods and drugs, I feel compelled to step in and set the records straight with currently available medical literature.


The efficacy of acids, bases and antioxidants in cancer therapy is not a myth. It has biochemical basis informed by modern research (SS Kim et al, 2004; Ian F. Robey & Lance A. Nesbit, 2013). The apparent controversy surrounding this subject emanates from poor coordination of research findings.


I have read articles (Bradley A. Web et al, 2011; Shi Q. et al, 2001; Silver M. et al, PubMed 2011) supporting systemic alkalosis or systemic hyperacidosis as the dominant toxic factor in cancer development. I have also watched video presentations claiming that cancer development is just a natural cellular adaptation to toxic environment, which is corrected by normalizing the environment.


These claims are to say the least, unbalanced truths. By the end of this discussion it would have become obvious that there is no basis for undue generalizations in the management of cancer. There still remains the need for expert judgments in formulating a cancer treatment protocol.


BEFORE CANCER


First, let me state that the human body will literally rust away like a nail left under the rain over time without inbuilt natural protective mechanisms. To prevent rust or oxidation, most macromolecules essential for human existence are shielded from molecular oxygen or oxygen equivalents with hydrogen molecules (reduction). Oxygen equivalents are those compounds that remove these protective hydrogen molecules from other compounds.


They are also called oxidizing agents. Compounds that restore these hydrogen molecules are called reducing agents. The two most important organic reducing agents in human body are glutathione and ubiquinone, while the two most important oxidizing agents are molecular oxygen and free oxygen radicals.


APOPTOSIS AND GROWTH SUPPRESSOR GENES

The human body cells are normally continuously moving from resting phase, to growth phase and then multiplication phase. This continuous state of growth and multiplication means that any organ can potentially grow to any size, depending on its natural growth rate. By inference all human beings may also grow into giants. It even suggests immortality of human beings.


Thankfully, every cell has an inbuilt apoptotic clock that ensures that it dies after a specified number of days, making room for incoming cells. Thus red blood cells, for instance, are recycled every 120 days. The size and shape of the cells of individual organs are equally limited prior to their date of apoptosis, by growth suppressor genes (notably p53, AP1, NF-kB) located in the nucleus.


Anything that hinders the functions of apoptosis and growth suppressor genes would obviously be expected to unleash uncontrolled growth and multiplication of cells in any organ of the body. This rapid growth of disorganized and poorly differentiated cells is called cancer.


All anti-growth suppression and anti-apoptosis agents are called carcinogens. They may be chemicals, radiations, biochemical molecules, acids, bases, free radicals, heat, cold, etc. But they all exert their effect by in activating apoptosis gene or growth suppressor gene. They accomplish this by corrupting the gene coding system in such a way that the codes are wrong (missense) or mean nothing (nonsense).


The code is corrupted due to the insertion of the wrong amino acid code into a gene sequence or the excision of the right amino acid code from the sequence. Consequently the t-RNA misreads or miss-senses the expression of the right apoptosis or growth suppressor protein.


Source by Otumdi Omekara 

By Antioxidant Foods.com

Drotumdi O


Foods Rich in Antioxidant All about Foods Rich in Antioxidants


 






 

 










 



Antioxidant Foods April 3, 2016

2016-03-03T05:20:54

Antioxidants, Acids, Alkali and Cancer


In my previous articles on cancer, I did not discuss the role of acids, bases and antioxidants in detail. But with the current hype about the miraculous nature of basic water, antioxidant foods and drugs, I feel compelled to step in and set the records straight with currently available medical literature.


The efficacy of acids, bases and antioxidants in cancer therapy is not a myth. It has biochemical basis informed by modern research (SS Kim et al, 2004; Ian F. Robey & Lance A. Nesbit, 2013). The apparent controversy surrounding this subject emanates from poor coordination of research findings.


I have read articles (Bradley A. Web et al, 2011; Shi Q. et al, 2001; Silver M. et al, PubMed 2011) supporting systemic alkalosis or systemic hyperacidosis as the dominant toxic factor in cancer development. I have also watched video presentations claiming that cancer development is just a natural cellular adaptation to toxic environment, which is corrected by normalizing the environment.


source: Otumdi Omekara, MD.

 

By Brain-and-balance.com

Drotumdi O

http://body-and-balance.com


Antioxidants, Acids, Alkali and Cancer

 


Posted on May 20, 2016 by Partner-Denmark

 


In my previous articles on cancer, I did not discuss the role of acids, bases and antioxidants in detail. But with the current hype about the miraculous nature of basic water, antioxidant foods and drugs, I feel compelled to step in and set the records straight with currently available medical literature.

 


The efficacy of acids, bases and antioxidants in cancer therapy is not a myth. It has biochemical basis informed by modern research (SS Kim et al, 2004; Ian F. Robey & Lance A. Nesbit, 2013). The apparent controversy surrounding this subject emanates from poor coordination of research findings.

 


I have read articles (Bradley A. Web et al, 2011; Shi Q. et al, 2001; Silver M. et al, PubMed 2011) supporting systemic alkalosis or systemic hyperacidosis as the dominant toxic factor in cancer development. I have also watched video presentations claiming that cancer development is just a natural cellular adaptation to toxic environment, which is corrected by normalizing the environment.

 


These claims are to say the least, unbalanced truths. By the end of this discussion it would have become obvious that there is no basis for undue generalizations in the management of cancer. There still remains the need for expert judgement in formulating a cancer treatment protocol.

 


BEFORE CANCER

 


First, let me state that the human body will literally rust away like a nail left under the rain over time without inbuilt natural protective mechanisms. To prevent rust or oxidation, most macromolecules essential for human existence are shielded from molecular oxygen or oxygen equivalents with hydrogen molecules (reduction). Oxygen equivalents are those compounds that remove these protective hydrogen molecules from other compounds.

 


They are also called oxidizing agents. Compounds that restore these hydrogen molecules are called reducing agents. The two most important organic reducing agents in human body are glutathione and ubiquinone, while the two most important oxidizing agents are molecular oxygen and free oxygen radicals.

 


APOPTOSIS AND GROWTH SUPPRESSOR GENES

 


The human body cells are normally continuously moving from resting phase, to growth phase and then multiplication phase. This continuous state of growth and multiplication means that any organ can potentially grow to any size, depending on its natural growth rate. By inference all human beings may also grow into giants. It even suggests immortality of human beings.

 


Thankfully, every cell has an inbuilt apoptotic clock that ensures that it dies after a specified number of days, making room for incoming cells. Thus red blood cells, for instance, are recycled every 120 days. The size and shape of the cells of individual organs are equally limited prior to their date of apoptosis, by growth suppressor genes (notably p53, AP1, NF-kB) located in the nucleus.

 


Anything that hinders the functions of apoptosis and growth suppressor genes would obviously be expected to unleash uncontrolled growth and multiplication of cells in any organ of the body. This rapid growth of disorganized and poorly differentiated cells is called cancer.

 


All anti-growth suppression and anti-apoptosis agents are called carcinogens. They may be chemicals, radiations, biochemical molecules, acids, bases, free radicals, heat, cold, etc. But they all exert their effect by in activating apoptosis gene or growth suppressor gene. They accomplish this by corrupting the gene coding system in such a way that the codes are wrong (missense) or mean nothing (nonsense).

 


The code is corrupted due to the insertion of the wrong amino acid code into a gene sequence or the excision of the right amino acid code from the sequence. Consequently the t-RNA misreads or miss-senses the expression of the right apoptosis or growth suppressor protein.

 


TOXINS, FREE RADICALS AND CARCINOGENS

 


Toxins are basically those compounds whose activities will directly or indirectly lead to human rust and death by causing catabolic or destructive oxidative reactions in body tissues. The high powered toxic tissue oxidizing agents are called free radicals (ROS and RNS), which are basically free ionized oxygen or Nitrogen atoms (O2- and N2- )

 


When a toxin causes a gene altering damage in the nuclear region of a cell (oxidative nuclear damage) it is then known as a carcinogen. As such not all toxins are carcinogen. Aflatoxin (from mold) is not only toxic to liver cells, but ultimately causes liver cancer, making it a carcinogen.

 


The detoxification process mainly converts lipid soluble toxins into excretable water soluble glucuronides in three steps. In step one the toxins are aggregated and isolated in the specific organs that neutralize them.

 


Then glucuronic acid is attached to them in the presence of glutathione which the protective hydrogen molecules. (Note that in fighting oxidants hydrogen (non-ionized) carried by reduced NADPH is a friend, while in acid-base balance ionized hydrogen is the enemy).

 


Free radicals can also contribute to cancer development by inducing genetic mutation through oxidative nuclear damage, or suppress cancer growth by promoting apoptosis. Step three is the excretion of the toxins.

 


ANTIOXIDANTS

 


Compounds use to replenish hydrogen molecules in glutathione and other endogenous reductase enzymes are called antioxidants. A lot of these reducing agents occur naturally in fruits and vegetables. Others are available as drug extracts from plants and animals.

 


Individual antioxidants target different steps of the detox process. This is why balanced nutrition by itself goes a long way to keep our bodies toxin free. The air we breathe, the food we eat, the water we drink, and the environments we live in are all full of toxins, including heavy metals. To survive as human beings, an extensive detoxification mechanism has to exist.

 


Every body tissue has detox ability, but the liver, gut, and lymphoid tissues and kidneys play the dominant role. Thus most toxins are trapped, neutralized and excreted through feces, urine or bile. Stagnation or obstruction of flow in any of these three organs, generally leads to a toxic state.

 


Stressors and nutritional insufficiencies that weaken the immune system also contribute to toxic states allowing micro-organisms to multiply and generate additional toxic substances that must be removed.

 


Successful detoxification requires a lot of energy, which comes from glucose metabolism. Biochemical energy is not measured in Joules, but in ATPs (Adenosine Triphosphate). The metabolic process for converting glucose to ATP is called glycolsis.

 


During aerobic glycolysis one molecule of glucose combines with two molecules of ADP3- (Adenosine Diphosphate) and two ionic phosphoric acid molecules to yield two ionic ATP4- molecules and two lactate molecules. The ionic ATP4- molecule gives up one Hydrogen proton (H+) to yield one molecule of ionic ADP3-, which is reused in glycolysis.

 


Under anaerobic (low oxygen) conditions, ATP is generated differently. One molecule, each, of ADP3- and ionic phosphoric acid accumulated from aerobic glycolysis recombine without glucose to form one molecule of ATP4+ and one hydroxyl molecule. Two hydrogen protons combine with two bicarbonates to end up as carbonic acid inside body cells.

 


TOXIC ACIDOSIS

 


Glycolsis can be aerobic when it consumes molecular oxygen, or anaerobic when it consumes oxidizing agents. Both the detox reactions and glycolsis are driven or catalyzed by enzymes, which depend on the availability of specific micro-molecules, proteins, amino acids and vitamins as cofactors for their functions.

 


By the time enough ATP is generated to keep the body toxin safe, enough carbonic acid hydration of respiratory carbon dioxide (CO2) has accumulated to keep the inside of every cell perpetually acidic. In a highly toxic state, which includes rapid proliferation of cells, this intracellular acid builds up exponentially beyond survivable limits.

 


Cancer cells are known to rapidly outgrow their blood supplies and go into severe hypoxic states. This is why the cancer cell nucleus has to rapidly increase the expression of sodium driven proton extruding proteins and enzyme proteins through nuclear sensing of sharp rise in HIF.

 


Thus, by default, the Intracellular fluid (ECF) of every cell is acidic (low pH) while that of the extracellular fluid (ECF) is alkaline (high pH). It is important to note at this point that while intracellular fluids exist in compartments inside the cells, extracellular fluids coalesce to form a pool in which all body cells submerged.

 


This ECF pool is represented by intercellular fluid, lymph, blood, and glandular secretions, all of which feed into the circulatory system of the body. ECF acid or base build up in any part of the body is ultimately dissipated into the circulatory system, which centrally maintains a mildly basic pH of 7.20 -7.40.

 


In addition to mobilizing ammonium and bicarbonate ions the central buffer system has the ability to move chloride ions in and out cells (chloride shift) to maintain acid-base balance.

 


MEMBRANE SENSORS AND TRANSPORTERS

 


To keep intracellular acidity below lethal level, the inner surface of the cell membrane has acid sensors and transporters that detect abnormal rise in intracellular acidity and trigger increased extrusion of hydrogen and retention of alkaline bicarbonate ions.

 


This trigger is mediated by the rise in the blood level of hypoxia induced factors (HIF) and probably acidosis induced factors (AIF). On detecting this rise in HIF, the nucleus temporarily increases the expression of Na-driven proton transport proteins and histidine rich basic proteins.

 


The ammonium radicals on the amino acids of these basic proteins (especially histidine) serve as physiologic buffers for organic acids.

 


“Protonation and de-protonation has been experimentally shown to change protein structure and thus, alter protein-protein binding affinity, change protein stability, modify protein function, and alter subcellular localization (Schonichen et al., 2013b).

 


Evolutionarily, histidines must confer some selective advantage for cancers, as 15% of the 2000 identified somatic mutations in cancer involve histidine substitutions, with Arg-to-His being the most frequent (Kan et al., 2010)”.

 


The nucleus also temporarily steps up the expression of important enzyme proteins that catalyze the buffer reactions, namely mono-carboxylate, carbonic anhydrase, and aminotransferase enzymes.

 


In a similar manner the external surface of the cell also has alkaline sensors made up of G-protein coupled surface receptors, which also communicate with the nucleus to increase or decrease the expression of relevant proteins and enzymes. As tissue hypoxia decreases, the level of HIF decreases along with nuclear expression of proton extrusion proteins and enzymes.

 


Failure of this return to normalcy has been observed as one of the hallmarks of early cancer. What started out as a normal adaptive change becomes persistent because of irreversible genetic modifications that triggered it.

 


CELLULAR SURFACE ACID/BASE REVERSAL

 


The central physiological buffer system has a maximum capacity to neutralize up to 30 micromoles of acid/gram tissue/min in systemic acidosis or 5-10 micromoles of base in alkalosis.

 


Beyond these levels, normal body cells are unable to continue their buffer functions because the enzymes are deactivated. At this point there is a reversal of the normal acid-base distribution on either side of the cell membrane, which is lethal to normal issues. In some critical situations, chloride ions are shifted massively into all body cells (chloride shift) to urgently dilute the extracellular acidity.

 


But the gastric cells have the natural ability to survive in the presence of high extracellular acidity (HCl at pH of 6.6). How they manage this high extracellular acidity then becomes very important in understanding how cancer cells survive high extracellular acidity with normal intracellular acidity for their survival and proliferation. Some cancer cells are known to have accumulated genetic adaptations that enable them to survive extreme pH conditions (carbonic acid at pH of 6.6).

 


Gastric cells are shielded from concentrated HCl secreted into the stomach mainly by structural barriers (thick basement membrane, thick mucosal layer and thick mucous layer). There are no natural inhibitors of hydrogen potassium ATPase enzyme that catalyzes the final phase of acid excretion.

 


In severe cases of Peptic Ulcer Disease (PUD), Gastro-esophageal reflux (GERD), or Zollinger-Ellison Syndrome, when this natural barrier is ulcerated by concentrated HCl, some gastric lining cells undergo goblet intestinal metaplasia (transformation into ectopic intestinal epithelium in the stomach) to secrete neutralizing alkaline fluids into the stomach.

 


While there is no natural attempt to control the hydrogen potassium ATPase enzymes, pharmacological intervention with proton pump inhibitors (PPIs) like omeprazole has been successful in reducing gastric secretion in severe cases of chronic gastric hyperacidity.

 


Similarly some esophageal epithelial cells undergo gastric metaplasia to become gastric cells in the face of chronic exposure to reflux gastric acid (Barrett’s Esophagus). Acquisition of this missing ability to control hydrogen potassium ATPase and sodium driven proton extrusion by monocarboxylate enzyme appear to be critical to the survival of cancer cells

 


IN EARLY CANCER

 


It is important to note that the natural response to extracellular hyperacidity in the GIT depends on the stage and localization of the acidity. Both goblet metaplasia and gastric metaplasia have been recognized as precancerous lesions (carcinoma in situs). At the early stage of Barret esophagus, the response is only structural to prevent cell wall damage.

 


But when the barrier has failed in the stomach, the response is alkaline secretion. A person on preventive alkaline water will be helping to neutralize the added hypoxic acidity of early cancer in Barret’s Esophagus and chronic PUD, but not in any way preventing the occurrence of cancer itself, since proton extrusion in cancer is irreversible.

 


Any cancer caught at the in situ stage is usually best treated with surgical excision and radiotherapy, rather than alkaline water.The question then is: “Why did prophylactic alkaline water not prevent the metaplasia?”

 


The answer to that is that while oral alkali intake may cap out at micromoles of alkali per gram tissue, cancer proton extrusion acid build up ranges in nanomoles per gram tissue (a thousand times more). Also intracellular hypoxia and hyperacidity are not the only risk factors for cancer.

 


Radiations are known to be commonly responsible for skin cancers, even as HPV is known to be responsible for cervical cancer. Prophylactic alkalosis has not been reported to prevent any of them. Sticking to the hype that alkaline water is the best way to prevent and even cure cancer, puts people at risk of missing early opportunities to truly cure cancer.

 


Alkaline water intake will help the body maximize the physiological adaptive response acidosis. Unfortunately, even at maximum physiological capacity, extracellular buffers are no match for cancer intracellular proton extruders.

 


As the well adapted cancer cells grow and multiply freely their neighboring non-cancerous cells are rapidly destroyed by ECF hyperacidity creating more space for them to occupy. Thus cancer invasiveness has been shown to correlate with the degree of acid-base reversal across the cancer cell membrane.

 


At the advanced stage of cancer with ECF acidity readings in nanomols compared to orally boosted alkalinity readings in micromoles, buffer therapy has been shown to be resisted by cancer cells. One such reported example is the inefficacy of a basic drug doxorubicin used in the treatment of Leukemias and lymphomas.

 


Going by what has been discussed so far, it is obvious that externally sourced acids and alkali cannot be safely loaded to outweigh tumor generated levels in ECF and ICF. It is also understandable that no single pH balancing agent, can be used to treat both acid sensing and alkaline sensing cancers.

 


Preventive or prophylactic intake of acidic or alkaline liquids or foods remain relevant only within the physiological buffering range, when adaptive changes are still reversible. Unfortunately at that point the tumor generated acidity would have risen to resistant levels. Preventive alkaline water intake in a person with undiagnosed acid sensing cancer is not likely to retard the growth of the tumor.

 


Similarly preventive intake of alkaline water in a patient with undiagnosed alkaline sensing cancer will encourage it to grow and establish faster. Patients receiving treatment for emesis gravid arum (vomiting in pregnancy) for instance, cannot be on preventive alkaline regimens in the face of systemic alkalosis from heavy loss of gastric acid through vomiting.

 


However, it is possible that some people are unable to fully optimize the natural buffer system, due to genetic predisposition or problems related to amino acid metabolism. In such situations, preventive acid or base intake supplements the patients effort to achieve maximum physiological buffering. This can easily account for some of the spectacular results observed in some patients whose cancers were caught early.

 


In conclusion, the management of cancer remains complicated. When there is a strong family history or occupational predisposition for cancer, cancer screening needs to be done early to search for risk factors and genetic markers.

 


Where there are suggestions of cancer predisposition, full blood tests, scans, biopsies, endocrinological tests, and radiological test should be done by a primary care provider and reviewed by a team of experts in radiology, hematology, pathology, oncology surgical oncology, gastroenterology, and international medicine.

 


References:
Ian F. Robey and Lance A. Nesbit, Investigating Mechanisms of Alkalinization for Reducing Primary Breast Tumor Invasion
Bradley A. Webb, Michael Chimenti, Matthew P. Jacobson & Diane L. Barber, Dysregulated pH: a perfect storm for cancer progression
Silvia M. Titan1, Otávio C.E. Gebara2, Silvia H.V. Callas2, Ana O. Hoff3, Paulo M. Hoff2 and P.C.A. Galvão2, Case report: a rare cause of metabolic alkalosis, 2011
SS Kim, HW Yang, HG Kang, HH Lee, HC Lee, DS Ko… – Fertility and sterility, Quantitative assessment of ischemic tissue damage in ovarian cortical tissue with or without antioxidant (ascorbic acid) treatment, 2004 – Elsevier
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By Sambath Vita Medicine HEALTH PUBLICATION

Drotumdi O

Preventive Medicine Failure: The Flint Michigan Example - Medicine
 Sambath Vita    Medicine    10:42 AM


The crucial role of preventive medicine is usually not quite apparent until there is a costly blatant failure as presently exemplified at Flint Michigan. The dangerous effect of lead poisoning on modern society is so well recognized that homes and public water supply systems built in the US in the last two decades have been totally free of lead pipes.


Older homes and public water supply systems have either been repiped or demolished for obvious safety reasons. Cities that are unable to identify all their old lead pipe connections use corrosion control to protect inner lining of city water pipes. When these basic preventive measures (Kemper, Alex et al, 2007) were overlooked in Flint Michigan, a huge water crisis quickly developed.


Flint City had been buying healthy Huron Lake water treated at Detroit water plants for over fifty years prior to 2013. But in 2013 the city voted to switch over to a cheaper water pipeline being built to Lake Huron. This caused Detroit City to abruptly cancel their water supply contract leaving Flint without water supply.


On April 25, 2014, in a desperate move to maintain water supply to 100, 000 Flint citizens Darnell Earley, an emergency city manager, appointed by Governor Rick Snyder, decided (Reissman, D.B. et al, 2001) to switch their water supply to the corrosive Flint river water, without corrosion control and against expert warning. Experts had recommended a short term contract renewal with Detroit City to by Flint City the time it needed for lead pipe replacement and corrosion control, at an estimated cost of 1.5 million dollars. But that recommendation was overtaken by even


Soon after the switch Flint households started reporting fowl odor from their their tap water, along with brown discoloration. The local DEQ tested and confirmed E. Coli in Flint watersystem. Chlorine was introduced into the water system to clear the bacteria, and citizens were reassured that the city water safe. By January 2015, a toxic level of chlorine byproducts, Total Trihalomethanes (TTHM) was reported in the Flint water system.


Between April and June 4014, Flint residents started reporting deeper browning of their tap water, hair loss, and neurological symptoms in their kids. The DEQ tested samples of Flint City water and said it met federal standards of < 5 parts per million of lead (Handler, Phoebe, etal, 2016). It even went as far as reporting to EPA that Flint City was compliant in their use of erosion control, which was not true.


Flint citizens became suspicious of their DEQ, and started conducting their own water testing and blood testing for lead (Carty Denise C. et al, 2016). The found toxic levels of lead in their tap water. Dr. Mona Hanna-Attisha a pediatrician at Hurley Medical Center, also discovered a rise in the number of school kids with high blood lead from 2.9% - 4.9% since the switch in April 2014. So they invited an expert, Dr. Edwards, a city water lead control advocate, from Virginia Tech to come and test their tap water samples. He confirmed toxic levels of lead in the water samples and notified the city council


In less than three months the toxic Flint river water had badly eroded the inner lining of the all the underground lead pipes delivering water to Flint City. Lead began leaching into the water city water system and turning the water progressively brown.


Media pressure from Dr Edward's EPA report and The Rachel Maddow Show reports on MSNBC lead to the declaration of public health emergency in Flint City by Governor Rick Snyder on Ocober16, 2015. Even with the declaration of a disaster, Governor Rick Snyder allegedly would not reach out to the federal government for disaster relief fund, until presidential candidate Hillary Clinton called him out on MSNBC.


Flint citizens, who are predominantly blacks, took to the streets in protest against Governor Snyder, accusing him of racism. In an affect to contain the situation, the state government has now put the pediatrician who blew the whistle in charge of the Flint water crisis disaster control committee. But the citizens are still calling for the resignation of Governor Schnider.


Of all the complications of lead poisoning (Hou Shunngxing et al., 2016; Korfmacher.Katerina S., et al, 2016), the one that will cost Michigan State the most is the brain damage in school kids (Finkelstein, Myra et al, 2016). Those kids with low IQ and learning disorder will not only be a loss, but also a financial burden to the state economy for decades to come. Compare that to a couple of million dollars that would have contained the Michigan river leaching in the first place. This is a good example of what preventive medicine should not be in the 21st century.


References:
Kemper, Alex R., Rebecca L. Uren, and Sharon R. Hudson. "Childhood Lead Poisoning Prevention Activities Within Michigan Local Public Health Departments." Public Health Reports 122.1 (2007): 88-92. Print.
Hou, Shuangxing et al. "A Clinical Study of the Effects of Lead Poisoning on the Intelligence and Neurobehavioral Abilities of Children." Theoretical Biology & Medical Modelling 10 (2013): 13. PMC. Web. 1 Feb. 2016.
Korfmacher, Katrina S., and Michael L. Hanley. "Are Local Laws the Key to Ending Childhood Lead Poisoning?" Journal of health politics, policy and law 38.4 (2013): 757-813. PMC. Web. 1 Feb. 2016.
Carty, Denise C. et al. "Racism, Health Status, and Birth Outcomes: Results of a Participatory Community-Based Intervention and Health Survey." Journal of Urban Health�: Bulletin of the New York Academy of Medicine 88.1 (2011): 84-97. PMC. Web. 1 Feb. 2016.
Finkelstein, Myra E. et al. "Lead Poisoning and the Deceptive Recovery of the Critically Endangered California Condor." Proceedings of the National Academy of Sciences of the United States of America 109.28 (2012): 11449-11454.PMC. Web. 1 Feb. 2016
Reissman, D B et al. "Use of Geographic Information System Technology to Aid Health Department Decision Making about Childhood Lead Poisoning Prevention Activities." Environmental Health Perspectives 109.1 (2001): 89-94. Print.
Handler, Phoebe, and Daniel Brabander. "Increased Incidence and Altered Risk Demographics of Childhood Lead Poisoning: Predicting the Impacts of the CDC's 5 µg/dL Reference Value in Massachusetts (USA)." International Journal of Environmental Research and Public Health 9.11 (2012): 3934-3942. PMC. Web. 1 Feb. 2016.