Watery Diarrhea from virus/bacteria

Acute Diarrhea. Most cases of acute, watery diarrhea are caused byviruses (viral gastroenteritis). The most common ones in children are rotavirus and in adults are norovirus (this is sometimes called “cruise ship diarrhea” due to well publicized epidemics). Bacteria are a common cause of traveler’s diarrhea.

By Dr Blanca Ochoa

Acute diarrhea is one of the most commonly reported illnesses in the United States, second only to respiratory infections. Worldwide, it is a leading cause of mortality in children younger than four years old, especially in the developing world. Diarrhea that lasts less than 2 weeks is termed acute diarrhea. Persistent diarrhea lasts between 2 and 4 weeks. Chronic diarrhea lasts longer than 4 weeks.Symptoms

Diarrheal stools are those that take shape of the container, so they are often described as loose or watery. Some people consider diarrhea as an increase in the number of stools, but stool consistency is really the hallmark. Associated symptoms can include abdominal cramps fever, nausea, vomiting, fatigue and urgency. Chronic diarrhea can be accompanied by weight loss, malnutrition, abdominal pain or other symptoms of the underling illness. Clues for organic disease are weight loss, diarrhea that wakes you up at night, or blood in the stools. These are signs that your doctor will want to do a thorough evaluation to determine the cause of your symptoms. Also tell your doctor if you have a family history of celiac disease, inflammatory bowel disease (IBD), have unintentional weight loss, fever, abdominal cramping or decreased appetite. Tell your doctor if you experience bulky, greasy or very bad smelling stools.

Causes – Acute Diarrhea

Most cases of acute, watery diarrhea are caused by viruses (viral gastroenteritis). The most common ones in children are rotavirus and in adults are norovirus (this is sometimes called “cruise ship diarrhea” due to well publicized epidemics). Bacteria are a common cause of traveler’s diarrhea.

Causes – Chronic Diarrhea

Chronic diarrhea is classified as fatty or malabsorption, inflammatory or most commonly watery. Chronic bloody diarrhea may be due to inflammatory bowel disease (IBD), which is ulcerative colitis or Crohn’s disease. Other less common causes include ischemia of the gut, infections, radiation therapy and colon cancer or polyps. Infections leading to chronic diarrhea are uncommon, with the exception of parasites.

The two major causes of fatty or malabsorptive diarrhea are impaired digestion of fats due to low pancreatic enzyme levels and impaired absorption of fats due to small bowel disease. These conditions interfere with the normal processing of fats in the diet. The former is usually due to chronic pancreatitis which is a result of chronic injury to the pancreas. Alcohol damage to the pancreas is the most common cause of chronic pancreatitis in the United States. Other causes of chronic pancreatitis include cystic fibrosis, hereditary pancreatitis, trauma to the pancreas and pancreatic cancer.

The most common small bowel disease in the U.S. is celiac disease, also called celiac sprue. Crohn’s disease can also involve the small bowel. Whipple’s disease, tropical sprue, and eosinophilic gastroenteritis are some of the rare conditions that can lead to malabsorption diarrhea.

There are many causes of watery diarrhea, including carbohydrate malabsorption such as lactose, sorbitol, and fructose intolerance. Symptoms of abdominal bloating and excessive gas after consuming dairy products suggests lactose intolerance. This condition is more common in African-Americans and Asian-Americans. Certain soft drinks, juices, dried fruits and gums contain sorbitol and fructose, which can lead to watery diarrhea in people with sorbitol and fructose intolerance. Diarrhea is a frequent side effect of antibiotics. Certain other medications such as NSAIDs, antacids, antihypertensives, antibiotics and antiarrhythmics can have side effects leading to diarrhea.

Parasitic intestinal infections such as giardiasis can cause chronic diarrhea. Diabetes mellitus may be associated with diarrhea due to nerve damage and bacterial overgrowth; this occurs mainly in patients with long-standing, poorly-controlled diabetes.

Irritable bowel syndrome (IBS) is a condition often associated with diarrhea, constipation or more frequently alternating diarrhea and constipation. Other common symptoms are bloating, abdominal pain relieved with defecation and a sense of incomplete evacuation.

Risk Factors

Exposure to infectious agents is the major risk factor for acute diarrhea. Bacteria and viruses are often transmitted by the fecal-oral route, so hand washing and hygiene are important to prevent infection. Soap and water are better because alcohol-based hand sanitizers may not kill viruses. Medications such as antibiotics and drugs that contain magnesium products are also common offenders. Recent dietary changes can also lead to acute diarrhea. These including intake of coffee, tea, colas, dietetic foods, gums or mints that contain poorly absorbable sugars. Acute bloody diarrhea suggests a bacterial cause like Campylobacter, Salmonella or Shigella or Shiga-toxin E. coli. Traveler’s diarrhea is common in those who travel to developing countries and results from exposure to bacterial pathogens most commonly enterotoxigenic E. coli. The best method of prevention is to avoid eating and drinking contaminated or raw foods and beverages.


Most episodes of acute diarrhea resolve quickly without antibiotic therapy and with simple dietary modifications. See a doctor if you feel ill, have bloody diarrhea, severe abdominal pain or diarrhea lasting more than 48 hours. In patients with mild acute diarrhea, no laboratory evaluation is needed because the illness generally resolves quickly. Your doctor may perform stool tests for bacteria and parasites if your diarrhea is severe or bloody or if you traveled to an area where infections are common. If you have severe diarrhea, blood tests will be helpful to guide replacement of fluid and electrolytes and minerals such as magnesium, potassium and zinc that can become depleted.

If you have chronic diarrhea, your doctor will want to further assess etiologic factors or complications of diarrhea by obtaining several tests. These can include a blood count to look for anemia and infections, an electrolyte and kidney function panel to assess for electrolyte abnormalities and renal insufficiency, and albumin to assess your nutritional status.

A stool sample may help define the type of diarrhea. The presence of fat, microscopic amounts of blood, and white blood cells will help determine if a fatty, inflammatory, or watery diarrhea is present. A bacterial culture and ova/parasite studies of a stool specimen will also help determine if an infectious etiology is present.

Endoscopic examination of the colon with flexible sigmoidoscopy or colonoscopy and upper endoscopy are helpful in detecting the etiology of chronic diarrhea, as this allows direct examination of the bowel mucosa and the ability to obtain biopsies for microscopic evaluation. Double-balloon enteroscopy and capsule endoscopy are sometimes used to examine the mucosa of the small intestine that lies beyond the reach of conventional endoscopes.

Radiographic studies such as an upper GI series or barium enema are not routinely performed in the evaluation of chronic diarrhea, and have largely been replaced by cross-sectional imaging. Ultrasound and CT scan of the abdomen can be helpful to evaluate the bowel, pancreas and other intra-abdominal organs.

Treating Acute Diarrhea

It is important to take plenty of fluid with sugar and salt to avoid dehydration. Salt and sugar together in a beverage help your intestine absorb fluids. Milk and dairy products should be avoided for 24 to 48 hours as they can make diarrhea worse. Initial dietary choices when refeeding should begin with soups and broth.

Anti-diarrheal drug therapy can be helpful to control severe symptoms, and includes bismuth subsalicylate and antimotility agents such as loperamide. These, however, should be avoided in people with high fever or bloody diarrhea as they can worsen severe colon infections and in children because the use of anti-diarrheals can lead to complications of hemolytic uremic syndrome in cases of Shiga-toxin E. coli (E. coli 0157:H7).

Your doctor may prescribe antibiotics if you have high fever, dysentery, or moderate to severe traveler’s diarrhea. Some infections such as Shigella always require antibiotic therapy.

Treatment of chronic diarrhea depends on the etiology of the chronic diarrhea. Often, empiric treatment can be provided for symptomatic relief, when a specific diagnosis is not reached, or when a diagnosis that is not specifically treatable is reached.

Antimotility agents such as loperamide are the most effective agents for the treatment of chronic diarrhea. They reduce symptoms as well as stool weight. Attention should be paid to replacing any mineral and vitamin deficiencies, especially calcium, potassium, magnesium and zinc.


Calcium in our foods and bodies


The effects of calcium on human cells are specific, meaning that different types of cells respond in different ways. However, in certain circumstances, its action may be more general. Ca2+ ions are one of the most widespread second messengers used in signal transduction. They make their entrance into the cytoplasm either from outside the cell through the cell membrane via calcium channels (such as Calcium-binding proteins or voltage-gated calcium channels), or from some internal calcium storages such as the endoplasmic reticulum[3] and mitochondria. Levels of intracellular calcium are regulated by transport proteins that remove it from the cell. For example, the sodium-calcium exchanger uses energy from the electrochemical gradient of sodium by coupling the influx of sodium into cell (and down its concentration gradient) with the transport of calcium out of the cell. In addition, the plasma membrane Ca2+ ATPase (PMCA) obtains energy to pump calcium out of the cell by hydrolysing adenosine triphosphate (ATP). In neurons, voltage-dependent, calcium-selective ion channels are important for synaptic transmission through the release of neurotransmitters into the synaptic cleft by vesicle fusion of synaptic vesicles.

Calcium’s function in muscle contraction was found as early as 1882 by Ringer. Subsequent investigations were to reveal its role as a messenger about a century later. Because its action is interconnected with cAMP, they are called synarchic messengers. Calcium can bind to several different calcium-modulated proteins such as troponin-C (the first one to be identified) and calmodulin, proteins that are necessary for promoting contraction in muscle.

In the endothelial cells which line the inside of blood vessels, Ca2+ ions can regulate several signaling pathways which cause the smooth muscle surrounding blood vessels to relax.[citation needed] Some of these Ca2+-activated pathways include the stimulation of eNOS to produce nitric oxide, as well as the stimulation of Kca channels to efflux K+ and cause hyperpolarization of the cell membrane. Both nitric oxide and hyperpolarization cause the smooth muscle to relax in order to regulate the amount of tone in blood vessels.[7] However, dysfunction within these Ca2+-activated pathways can lead to an increase in tone caused by unregulated smooth muscle contraction. This type of dysfunction can be seen in cardiovascular diseases, hypertension, and diabetes.

Calcium: magnesium ratio is 60:40 and always taken with Vit C, Vit D3 and zinc and in afternoon while iron rich foods is eaten in the morning since calcium and iron cancels each other out.

Hypocalcemia and Sepsis

hypoHypocalcemia varies from an asymptomatic biochemical abnormality to a life-threatening disorder, depending on the duration, severity, and rapidity of development. Hypocalcemia is caused by loss of calcium from or insufficient entry of calcium into the circulation.

Hypoparathyroidism is the most common cause of hypocalcemia and often develops because of surgery in the central neck requiring radical resection of head and neck cancers. It develops in 1% to 2% of patients after total thyroidectomy.

The hypocalcemia may be transient, permanent, or intermittent, as with vitamin D deficiency during the winter. Autoimmune hypoparathyroidism is seen as an isolated defect or as part of polyglandular autoimmune syndrome type I in association with adrenal insufficiency and mucocutaneous candidiasis. Most of these patients have autoantibodies directed against the calcium-sensing receptor. Congenital causes of hypocalcemia include activating mutations of calcium-sensing receptor, which has reset the calcium–parathyroid hormone (PTH) relation to a lower serum calcium level. Mutations affecting intracellular processing of the pre-pro-PTH molecule are also described and lead to hypoparathyroidism, hypocalcemia, or both. Finally, some cases are associated with hypoplasia or aplasia of the parathyroid glands; the best known is DiGeorge syndrome.

Pseudohypoparathyroidism is a group of disorders with postreceptor resistance to PTH. One classic variant is Albright’s hereditary osteodystrophy, associated with low stature, round facies, short digits, and mental retardation. Hypomagnesemia induces PTH resistance and also affects PTH production. Severe hypermagnesemia (>6 mg/dL) can lead to hypocalcemia by inhibiting PTH secretion. Vitamin D deficiency leads to hypocalcemia when associated with decreased dietary calcium intake. The low calcium level stimulates PTH secretion (secondary hyperparathyroidism), leading to hypophosphatemia.

Rhabdomyolysis and tumor lysis syndrome cause loss of calcium from the circulation when large amounts of intracellular phos-phate are released and precipitate calcium in bone and extraskeletal tissues. A similar mechanism causes hypocalcemia with phosphate administration.

Acute pancreatitis precipitates calcium as a soap in the abdomen, causing hypocalcemia. Hungry bone syndrome is hypocalcemia after surgery for hyperparathyroidism (HPT) in patients with severe prolonged disease (secondary or tertiary HPT in renal failure). Serum calcium is rapidly deposited into the bone. Hungry bone syndrome is rarely seen after correction of longstanding metabolic acidosis or after thyroidectomy for hyperthyroidism.

Several medications (e.g., ethylenediaminetetraacetic acid [EDTA], citrate present in transfused blood, lactate, foscarnet) chelate calcium in the circulation, sometimes producing hypocalcemia in which ionized calcium is decreased, cohereas total calcium may be normal. Extensive osteoblastic skeletal metastases (prostate and breast cancers) may also cause hypocalcemia. Chemotherapy, including cisplatin, 5-fluorouracil, and leucovorin, causes hypocalcemia mediated through hypomagnesemia. Hypocalcemia after surgery can be mediated by the citrate content of transfused blood or by a large volume of fluid administration and hypoalbuminemia. Patients with sepsis demonstrate hypocalcemia usually associated with hypoalbuminemia.

Ionized means charged. Sepsis is the other cause of hypocalcemia (absence of PTH secretion or hypoparathyroidism). Low calcium, high magnesium and low Vitamin D3. Can also be congenital (mutations of CaSR, PTH, and parathyroid aplasia)

Supplementation of calcium 60%, magnesium 40% with zinc, Vitamin D and C and should be taken before eating food rich in iron since iron cancels calcium absorption.

Metabolic pathway provides cues for cancer, aging and health care

metabolic path.JPGIn biochemistry, a metabolic pathway is a linked series of chemical reactions occurring within a cell. The reactants, products, and intermediates of an enzymatic reaction are known as metabolites, which are modified by a sequence of chemical reactions catalyzed by enzymes.[1] In a metabolic pathway, the product of one enzyme acts as the substrate for the next. These enzymes often require dietary minerals, vitamins, and other cofactors to function.

Different metabolic pathways function based on the position within a eukaryotic cell and the significance of the pathway in the given compartment of the cell.[2] For instance, the citric acid cycle, electron transport chain, and oxidative phosphorylation all take place in the mitochondrial membrane. In contrast, glycolysis, pentose phosphate pathway, and fatty acid biosynthesis all occur in the cytosolof a cell.[3]

There are two types of metabolic pathways that are characterized by their ability to either synthesize molecules with the utilization of energy (anabolic pathway) or break down of complex molecules by releasing energy in the process (catabolic pathway).[4] The two pathways complement each other in that the energy released from one is used up by the other. The degradative process of a catabolic pathway provides the energy required to conduct a biosynthesis of an anabolic pathway.[4] In addition to the two distinct metabolic pathways is the amphibolic pathway, which can be either catabolic or anabolic based on the need for or the availability of energy.[5]

Pathways are required for the maintenance of homeostasis within an organism and the flux of metabolites through a pathway is regulated depending on the needs of the cell and the availability of the substrate. The end product of a pathway may be used immediately, initiate another metabolic pathway or be stored for later use. The metabolism of a cell consists of an elaborate network of interconnected pathways that enable the synthesis and breakdown of molecules (anabolism and catabolism)

Glycolysis, Oxidative Decarboxylation of Pyruvate, and Tricarboxylic Acid (TCA) Cycle

Net reactions of common metabolic pathways

Each metabolic pathway consists of a series of biochemical reactions that are connected by their intermediates: the products of one reaction are the substrates for subsequent reactions, and so on. Metabolic pathways are often considered to flow in one direction. Although all chemical reactions are technically reversible, conditions in the cell are often such that it is thermodynamically more favorable for flux to flow in one direction of a reaction. For example, one pathway may be responsible for the synthesis of a particular amino acid, but the breakdown of that amino acid may occur via a separate and distinct pathway. One example of an exception to this “rule” is the metabolism of glucose. Glycolysis results in the breakdown of glucose, but several reactions in the glycolysis pathway are reversible and participate in the re-synthesis of glucose (gluconeogenesis).

  • Glycolysis was the first metabolic pathway discovered:
  1. As glucose enters a cell, it is immediately phosphorylated by ATP to glucose 6-phosphate in the irreversible first step.

  2. In times of excess lipid or protein energy sources, certain reactions in the glycolysis pathway may run in reverse in order to produce glucose 6-phosphate which is then used for storage as glycogen or starch.

  • Metabolic pathways are often regulated by feedback inhibition.
  • Some metabolic pathways flow in a ‘cycle’ wherein each component of the cycle is a substrate for the subsequent reaction in the cycle, such as in the Krebs Cycle (see below).
  • Anabolic and catabolic pathways in eukaryotes often occur independently of each other, separated either physically by compartmentalization within organelles or separated biochemically by the requirement of different enzymes and co-factors.

Catabolic pathway (catabolism)

A catabolic pathway is a series of reactions that bring about a net release of energy in the form of a high energy phosphate bond formed with the energy carriers Adenosine Diphosphate (ADP) and Guanosine Diphosphate (GDP) to produce Adenosine Triphosphate (ATP) and Guanosine Triphosphate (GTP), respectively. The net reaction is, therefore, thermodynamically favorable, for it results in a lower free energy for the final products.[6] A catabolic pathway is an exergonic system that produces chemical energy in the form of ATP, GTP, NADH, NADPH, FADH2, etc. from energy containing sources such as carbohydrates, fats, and proteins. The end products are often carbon dioxide, water, and ammonia. Coupled with an endergonic reaction of anabolism, the cell can synthesize new macromolecules using the original precursors of the anabolic pathway.[7] An example of a coupled reaction is the phosphorylation of fructose-6-phosphate to form the intermediate fructose-1,6-bisphosphate by the enzyme phsophofructokinase accompanied by the hydrolysis of ATP in the pathway of glycolysis. The resulting chemical reaction within the metabolic pathway is highly thermodynamically favorable and, as a result, irreversible in the cell.[8]

{\displaystyle Fructose-6-Phosphate+ATP\longrightarrow Fructose-1,6-Bisphosphate+ADP}{\displaystyle Fructose-6-Phosphate+ATP\longrightarrow Fructose-1,6-Bisphosphate+ADP}

Cellular respiration

Main article: Cellular respiration

A core set of energy-producing catabolic pathways occur within all living organisms in some form. These pathways transfer the energy released by breakdown of nutrients into ATP and other small molecules used for energy (e.g. GTP, NADPH, FADH). All cells can perform anaerobic respirationby glycolysis. Additionally, most organisms can perform more efficient aerobic respiration through the citric acid cycle and oxidative phosphorylation. Additionally plants, algae and cyanobacteria are able to use sunlight to anabolically synthesize compounds from non-living matter by photosynthesis.

Gluconeogenesis Mechanism

Anabolic pathway (anabolism)

In contrast to catabolic pathways, are the anabolic pathways that require an input of energy in order to conduct the construction of macromolecules such as polypeptides, nucleic acids, proteins, polysaccharides, and lipids. The isolated reaction of anabolism is unfavorable in a cell due to a positive Gibbs Free Energy (+ΔG); thus, an input of chemical energy through a coupling with an exergonic reaction is necessary.[9] The coupled reaction of the catabolic pathway affects the thermodynamics of the reaction by lowering the overall activation energy of an anabolic pathway and allowing the reaction to take place.[10] Otherwise, an endergonic reaction is non-spontaneous.

An anabolic pathway is a biosynthetic pathway, meaning that it combines smaller molecules to form larger and more complex ones.[11] An example is the reversed pathway of glycolysis, otherwise known as gluconeogenesis, which occurs in the liver and sometimes in the kidney in order to maintain proper glucose concentration in the blood and to be able to supply the brain and muscle tissues with adequate amount of glucose. Although gluconeogenesis is similar to the reverse pathway of glycolysis, it contains three distinct enzymes from glycolysis that allow the pathway to occur spontaneously.[12] An example of the pathway for gluconeogenesis is illustrated in the image titled “Gluconeogenesis Mechanism“.


Changes in mineral metabolism in chronic kidney disease, an ebook


With progression of chronic kidney disease (CKD), disorders of mineral metabolism appear. The classic sequence of events begins with a deficit of calcitriol synthesis and retention of phosphorus. As a result of this, serum calcium decreases and parathyroid hormone (PTH) is stimulated, producing in the bone the high turnover (HT) bone disease known as osteitis fibrosa while on the other extreme we find the forms of low turnover (LT) bone disease.

Initially associated with aluminum intoxication, these diseases are now seen primarily in older and/or diabetic patients, who in a uremic setting have relatively low levels of PTH to maintain normal bone turnover.

Osteomalacia is also included in this group, which after the disappearance of aluminum intoxication is rarely observed. LT forms of hyperparathyroidism facilitate the exit of calcium (Ca) and phosphorus (P) from bone, whereas the adynamic bone limits the incorporation of Ca and P into bone tissue.

Therefore, both forms facilitate the availability of Ca and P, which ends up being deposited in soft tissues such as arteries. The link between bone disease and vascular calcifications in CKD is now a well-established phenomenon.

Diagnostic strategies Calcium, Phosphorus

They have little capacity to predict underlying bone disease, but their regular measurement is decisive for therapeutic management of the patient, especially in the dose titration stages of intestinal phosphorus binders, vitamin D analogs or calcimimetics. Ideally, Ca++ should be used, but total Ca is routinely used. It is recommended to adjust albumin levels in the event of hypoalbuminemia (for each g/dL of decrease in albumin, total serum Ca decreases 0.9 mg/dL). The following formula facilitates rapid calculation of corrected total calcium: Corrected total Ca (mg/dL) = total Ca (mg/dL) + 0.8 [4-albumina (g/dL)]. Parathyroid hormone “Intact” PTH is the biochemical parameter that best correlates with bone histology (levels measured with the Allegro assay from Nichols Institute Diagnostics, no longer available).

Various assays are currently available that use antibodies against different fragments of the molecule, but they have significant intermethod variability and have not been validated. A whole PT assay (1-84) is currently unavailable. A consensus to establish uniform criteria for PTH measurement remains to be established. During the dose titration stages of intestinal phosphorus binders, vitamin D analogs or calcimimetics, more frequent measurement may be required based on clinical judgment.

Calcifediol (25(OH) D3 )

It is important to maintain adequate levels of 25(OH)D3 (> 30 ng/mL), since they will be the substrate for production of 1- 25(OH)2 D3, and their deficiency aggravates hyperthyroidism. Determining 25(OH)D3 levels every 6-12 months is a recommended guideline.

Other markers of bone turnover (osteocalcin, total and bone alkaline phosphate, free pyridolines in serum, and C-terminal telopeptide of collagen) do not improve the predictive power of PTH and therefore their systematic use is not justified.

Radiologic studies Radiologic studies are of little diagnostic utility, because biochemical changes precede radiologic changes. Systematic radiologic evaluation of the skeleton in asymptomatic patients is not justified at present. They are useful as the first step in the study to detect vascular calcifications and amyloidosis due to b2-microglobulin and in symptomatic and at risk patients to detect vertebral fractures.

Bone densitometry

Dual energy x-ray absorptiometry (DEXA) is the standard method to determine bone mineral density (usually in the femoral neck and vertebrae). It provides information on changes in bone mineral content, but not on the type of underlying bone disease. It is useful for follow-up of bone mass or for the study of bone mass changes in the same patient. Its value as a predictor of the risk of fracture has not been demonstrated in patients on kidney replacement therapy or with advanced chronic kidney disease. It is indicated in patients with fractures or risk factors for osteoporosis. Bone biopsy: The “gold standard” for diagnosis of bone disease. With improved knowledge of the value of noninvasive parameters, its use is infrequent.


The recommended diet for the patient with CKD is traditionally based on protein restriction and phosphorus restriction for control of mineral metabolism. A favorable circumstance is that there is a close relationship between protein and phosphorus intake. In CKD stages 3, 4 and 5, it is recommended to restrict phosphorus intake to between 0.8-1 g/day when serum levels of phosphorus and PTH are above the recommended range. This is approximately equivalent to a diet of 50-60 g of protein. This reasonable antiproteinuric strategy that also restricts phosphorus intake is nutritionally safe. What should we tell them to eat? In a practical and oversimplified way, we recommend the following daily intake: Animal proteins: 1 serving (100-120 g), dairy products: 1 serving (equivalent to 200-240 mL of milk or 2 yoghourts), bread, cereals, pastas (1 cup of pasta, rice or legumes + some bread or cookies), vegetables and fruits relatively freely, but with moderation. 4.2. Medication Vitamin D supplements should be provided if serum levels are less than 30 ng/mL. In Spain, vitamin D3 (cholecalciferol) is marketed as Vitamin D3 Berenguer 2,000 IU/mL of solution. Combinations of calcium with cholecalciferol are also available. Most of the dosage forms contain approximately 500 mg of Ca+ and 400 IU of cholecalciferol.


Neck pain and MTHFR gene , folate , methionine

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My co-worker complained of chronic neck pain and her doctor prescribed a med and an iron pill. My mom uses Zyflamend in evening (with calcium and magnesium supplement in 60:40 ratio with Vit D, zinc and C) and iron rich food for lunch and avoided inflammatory foods such as red meat and eggplant.  I suggested a massage stroke (using the thumb in one downward motion from neck to back) and oil mixed with eucalyptus, tea tea oil and apricot oil.  A Fluradix liquid iron supplement with whole foods in the morning will also help, including raisins,liver,dark chocolate and blackstrap mollases.  A chronic pain is indicative of a deep rooted health issue that must be addressed at the core. There genes that affect how we absorb iron. Vit C rich foods and vinegar help in the absorption of iron (eaten in the morning and noon) and calcium (eaten in the evening because iron and calcium cancels each other).  I will always add probiotics and prebiotics in this health issue.

  1. Avoid taking folic acid blocking or depleting drugs, such as birth control pills or Methyltrexate
  2. Avoid taking proton pump inhibitors, like Prilosec or Prevacid or antacids, like Tums, which may block essential Vitamin B12 absorption
  3. Have your homocysteine measured, which if elevated may indicate a problem with methylation or a deficiency of B12 or folate.  If your homocysteine is elevated, limit your intake ofmethionine-rich foods
  4. Avoid eating processed foods, many of which have added synthetic folic acid.  Instead eat whole foods with no added chemicals or preservatives.
  5. Get your daily intake of leafy greens, like spinach, kale, swiss chard or arugula, which are loaded with natural levels of folate that your body can more easily process.
  6. Eat hormone-free, grass-fed beef, organic pastured butter or ghee, and eggs from free-range, non-GMO fed chickens.
  7. Remove any mercury amalgams with a trained biologic dentist.  Avoid aluminum exposure in antiperspirants or cookware.  Avoiding heavy metal or other toxic exposure is important.
  8. Make sure you supplementing with essential nutrients, like methyl-B12, methyl-folate, TMG, N-acetylcysteine, riboflavin, curcumin, fish oil, Vitamins C, D, E, and probiotics.  If you are double homozygous for MTHFR mutations, you should proceed very cautiously with methyl-B12 and methyl-folate supplementation as some people do not tolerate high doses.  Introduce nutrients one by one and watching for any adverse reactions.  Use extreme caution when supplementing with niacin, which can dampen methylation.
  9. Make time for gentle detox regimens several times per week.  These could include infrared sauna, epsom salt baths, dry skin brushing, and regular exercise or sweating.

See MTHFR gene mutation, iron and neck pain

methio 4.JPG

Cancer fighting diet


parsleycilantrosulfur-richyellowgreens.JPGWith regards to a cancer treatment, every food that we eat or drink can be categorized into several different categories:

  • Foods that feed and strengthen the cancer cells and/or the microbes in the cancer cells and body. Examples would be: refined sugar (e.g. see: Challenge Cancer Website), refined flour, soda pop, dairy products, etc.
  • Foods that cause cancer (e.g. trans fatty acids [margarine, french fries and virtually every other processed food you buy], aspartame [Diet Coke, NutraSweet, Equal, etc.], MSG, polyunsaturated oils [e.g. corn oil], etc.)
  • Foods that directly interfere with alternative treatments for cancer (e.g. chlorine, fluoride, alcohol, coffee, etc.)
  • Foods that occupy and distract the immune system from focusing on killing the cancer cells (e.g. beef, turkey, etc.)
  • Foods that contain nutrients that kill the cancer cells, stop the spread of cancer, or in some other way help treat the cancer (e.g. purple grapes with seeds and skin, red raspberries with seeds, strawberries with seeds, broccoli, cauliflower, several herbs, carrots, pineapples, almonds, etc.)

Cooking destroys the enzymes in the vegetables and make them far less digestible and far less effective in treating cancer. Pasteurizing any food or drink also does this.

Read More http://www.cancertutor.com/alt_diet/

Oxalic acid in whole foods is deadly to cancer cells

50% of the foods a cancer patients eats should have high oxalic acid content.

Oxalic Acid Foods List: Carrot juice, with a little beet juice, is a common cancer treatment. Both foods are high in oxalic acid.  Note: Cooked your greens (steamed, do not over cook) and eat calcium-rich whole foods.

Foods High in Oxalic Acid

High levels of oxalic acid can have harmful effects on the body. When the concentration of oxalic acid in the body increases, it precipitates out as crystals, that irritate the body tissues, and can get lodged in the kidneys and bladder as ‘stones’. When the acid combines with minerals like calcium, it forms an interlocking compound that destroys the nutritional value of both, resulting in deficiency of the minerals.


There are several vegetables containing high amount of oxalic acid and should be cooked well (not eaten raw) for people with recurrent kidney stones or other such conditions. The United States Department of Agriculture has ranked parsley, highest in oxalic acid content, as it contains about 1.70g of oxalic acid per 100g.

  • Beets
  • Sweet potatoes
  • Celery
  • Dandelion greens
  • Eggplant
  • Kale
  • Chives
  • Broccoli
  • Carrots
  • Green Pepper
  • Parsnips
  • Potatoes
  • Pumpkin
  • Spinach
  • Squash
  • Turnip greens
  • Watercress
  • Okra
  • Collards
  • Escarole
  • Leeks
  • Purslane
  • Radish
  • Cassava


Certain fruits have a high oxalic acid content. They are as follows:

  • Concord grapes
  • Kiwi
  • Lemon peel
  • Figs
  • Blueberries
  • Raspberries
  • Plums
  • Tangerines
  • Starfruit
  •  Nuts and Seeds

  • Peanuts
  • Almonds
  • Hazel nuts
  • Brazil nuts
  • Pecans
  • Sesame seeds
  • Poppy Seeds
  • Sunflower seeds
  • Cashews
  • Legumes and Grains

Majority of legumes are rich in oxalic acid. Some of them are as follows:

  • Black beans
  • Kidney beans
  • Garbanzo beans
  • Lima beans
  • Brussels sprouts
  • Whole wheat
  • Oatmeal
  • Buckwheat
  • Amaranth
  •  Other Foods

Oxalic acid is mainly present in plant products. A lot of spices and condiments also contain a considerable amount of oxalic acid. Tea leaves are known to contain among the highest measured concentration of the acid. However, as only a small amount of leaves are used for brewing, the content of the acid in many tea beverages is quite low. Here are some other foods containing it:

  • Cinnamon
  • Ginger
  • Lettuce
  • Soy products
  • Chocolate
  • Cocoa
  • Tea
  • Beer

Increase the amount of calcium/magnesium (60:40 ratio) in your diet, avoiding processed and pasteurized food.

Low amounts of calcium in your diet will increase your chances of forming calcium oxalate kidney stones. Many people are afraid to eat calcium because of the name “calcium oxalate stones.” However, calcium binds oxalate in the intestines. A diet rich in calcium helps reduce the amount of oxalate being absorbed by your body, so stones are less likely to form. Eat calcium rich foods and beverages every day (2 to 3 servings) from dairy foods or other calcium-rich foods.

Also, eating high calcium foods at the same time as high oxalate food is helpful; for example have low fat cheese with a spinach salad or yogurt with berries. If you take a calcium supplement, calcium citrate is the preferred form.

Limit Vitamin C content of your diet.

Oxalate is produced as an end product of Vitamin C (ascorbic acid) metabolism. Large doses of Vitamin C may increase the amount of oxalate in your urine, increasing the risk of kidney stone formation. If you are taking a supplement, do not take more than 500 mg of Vitamin C daily.

Drink the right amount of fluids every day.

It is very important to drink plenty of liquids. Your goal should be 10-12 glasses a day. At least 5-6 glasses should be water. You may also want to consider drinking lemonade. Research suggests that lemonade may be helpful in reducing the risk of calcium oxalate stone formation.

Eating the right amount of protein daily.

Eating large amounts of protein may increase the risk of kidney stone formation. Your daily protein needs can usually be met with 2-3 servings a day, or 4 to 6 ounces. Eating more than this if you are at risk at kidney stones is unnecessary.

Reduce the amount of sodium in your diet. Eat seaweeds.