Metabolic Mutation vs APS (Antiphospholipid Syndrome)

The pentose phosphate pathway appears to have a very ancient evolutionary origin. The reactions of this pathway are mostly enzyme-catalyzed in modern cells. They also occur however non-enzymatically under conditions that replicate those of the Archean ocean, and are catalyzed by metal ions, ferrous ions (Fe(II)) in particular.[2] The origins of the pathway could thus date back to the prebiotic world.

Example...PhosphorylationIn biology, D-ribose must be phosphorylated by the cell before it can be used. Ribokinase catalyzes this reaction by converting D-ribose to D-ribose 5-phosphate. Once converted, D-ribose-5-phosphate is available for the manufacturing of the amino acids tryptophan and histidine, or for use in the pentose phosphate pathway. The absorption of D-ribose is 88–100% in the small intestines (up to 200 mg/kg/h)https://en.wikipedia.org/wiki/Ribose

You can probably test yourself for this...antedotally that is by doing the same thing they do to test babies at birth...How easy could this be? Could this be wrong? I wonder how much the hospital charges for this?
The test is positive if the blood spot fails to fluoresce under ultraviolet light.

Anemia was a symptom of my pesticide poisoning
Anemia due to disorders of glutathione metabolism, including:
Glucose-6-phosphate dehydrogenase deficiency [DS:H01375];
Glutathione peroxidase deficiency;
Gamma-glutamylcysteine synthetase deficiency;
Glutathione synthetase deficiency

Description
Anemia due to disorders of glutathione metabolism is a group of red cell disorders caused by inherited abnormality of enzymes of glutathione metabolism. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymatic disorder of red blood cells in humans. It is estimated that about 400 million people are affected by this deficiency. A G6PD-deficient patient lacks the ability to protect red blood cells against oxidative stresses from certain drugs, infections, metabolic conditions, and ingestion of fava beans. GCLC catalyzes the initial and the rate-limiting step of glutathione synthesis. Deficiency of GCLC is extremely rare. GSS deficiency is a more frequent cause of glutathione deficiency.

Category
Inherited metabolic disease; Hematologic disease
Brite
Human diseases [BR:br08402]
Cardiovascular diseases
Hematologic diseases
H00668 Anemia due to disorders of glutathione metabolism
Congenital disorders of metabolism
Congenital disorders of amino acid metabolism
H00668 Anemia due to disorders of glutathione metabolism
Human diseases in ICD-10 classification [BR:br08403]
3. Diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism (D50-D89)
D55-D59 Haemolytic anaemias
D55 Anemia due to enzyme disorders
H00668 Anemia due to disorders of glutathione metabolism
BRITE hierarchy
Pathway
hsa00480
Glutathione metabolism
hsa00030
Pentose phosphate pathway
http://www.genome.jp/dbget-bin/www_bget?ds:H00668

Pentose Pathway

Fava Beans the reason people call the illness of a deficiency in G6PD to produce Glutothion, and so, calling the disease Favism. Through anecdotal evidence over the ages people knew they had the deficiency because when they ate the beans they had symptoms that could be categorized. I'm sure people caught on that their children may have it too.

Health issues
Broad beans are rich in tyramine, and thus should be avoided by those taking monoamine oxidase inhibitors.
Raw broad beans also contain the alkaloids vicine and convicine which can induce hemolytic anemia in patients with the hereditary condition glucose-6-phosphate dehydrogenase deficiency. This potentially fatal condition is called favism after the fava bean.
The seed testae contain condensed tannins of the proanthocyanidins type that could have an inhibitory activity on enzymes.

The condition is characterized by abnormally low levels of glucose-6-phosphate dehydrogenase, an enzyme involved in the pentose phosphate pathway that is especially important in the red blood cell. G6PD deficiency is the most common human enzyme defect. There is no specific treatment, other than avoiding known triggers.

Men get this through inheritance, and it is unusual for women... No doctor has ever checked me for this mutation...
Signs and symptoms
Most individuals with G6PD deficiency are asymptomatic.
Symptomatic patients are almost exclusively male, due to the X-linked pattern of inheritance, but female carriers can be clinically affected due to unfavorable lyonization, where random inactivation of an X-chromosome in certain cells creates a population of G6PD-deficient red blood cells coexisting with normal red cells. A typical female with one affected X chromosome will show the deficiency in approximately half of her red blood cells. However, in rare cases, including double X deficiency, the ratio can be much more than half, making the individual almost as sensitive as a male.
Abnormal red blood cell breakdown (hemolysis) in G6PD deficiency can manifest in a number of ways, including the following:
Prolonged neonatal jaundice, possibly leading to kernicterus (arguably the most serious complication of G6PD deficiency)
Hemolytic crises in response to:
Illness (especially infections)
Drugs
Certain foods, most notably broad beans
Certain chemicals

Diabetic ketoacidosis
Very severe crises can cause acute kidney failure
Favism may be formally defined as a hemolytic response to the consumption of broad beans. All individuals with favism show G6PD deficiency. However, not all individuals with G6PD deficiency show favism. Favism is known to be more prevalent in infants and children, and G6PD genetic variant can influence chemical sensitivity. Other than this, the specifics of the chemical relationship between favism and G6PD are not well understood.
6-phosphogluconate dehydrogenase (6PGD) deficiency has similar symptoms and is often mistaken for G6PD deficiency, as the affected enzyme is within the same pathway, however these diseases are not linked and can be found within the same patient.

Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme in the pentose phosphate pathway. G6PD converts glucose-6-phosphate into 6-phosphoglucono-δ-lactone and is the rate-limiting enzyme of this metabolic pathway that supplies reducing energy to cells by maintaining the level of the reduced form of the co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH). The NADPH in turn maintains the supply of reduced glutathione in the cells that is used to mop up free radicals that cause oxidative damage.
The G6PD / NADPH pathway is the only source of reduced glutathione in red blood cells (erythrocytes). The role of red cells as oxygen carriers puts them at substantial risk of damage from oxidizing free radicals except for the protective effect of G6PD/NADPH/glutathione.
People with G6PD deficiency are therefore at risk of hemolytic anemia in states of oxidative stress. Oxidative stress can result from infection and from chemical exposure to medication and certain foods.

G6PD deficiency is the most common human enzyme defect (Frank, 2005). 6-Phosphogluconate dehydrogenase (6PGD) is the third enzyme of the pentose phosphate metabolic pathway, catalyzing the conversion of 6-PGA (6 phosphogluconate) to Driboluse-5-phosphate in the presence of NADP+. The reaction, catalyzed by 6PGD, yields NADPH, which protects the cell against oxidant agents by producing reduced glutathione (GSH) (Bianchi et al., 2001; Lehninger et al., 2000). Glutathione reductase (GR; NADPH: oxidized glutathione oxidoreductase, EC 1.6.4.2), a flavoprotein, is an important enzyme which catalizes convertion of oxidized glutathione into reduced glutathione. The enzyme uses NADPH as electron donor for the reduction of GSSG. GR enables several vital functions of the cell such as the detoxification of free radicals and reactive oxygen species as well as protein and DNA biosynthesis by maintaining a high ratio of GSH/GSSG (Schirmer et al., 1989; Rendón et al., 2004). 

We observed that the activities of the enzymes decreased with increasing deltamethrin concentrations and exposure time. The pesticide had greater inhibitory effect on gill enzymes than on muscle, liver and kidney enzymes. Many environmental pollutants including fungicides and pesticides are capable of inducing oxidative stress in aquatic animals. Oxidative stress occurs as a result of the effect of xenobiotics causing disturbances in antioxidant enzyme systems and, as a result, the oxidative stress resulting from the production of reactive oxygen species (ROS) has gained considerable interest in the field of ecotoxicology (Kappus, 1987; Lemaire et al., 1996). The induction of antioxidant expression by the fungicides and pesticides reflects the activation of defense mechanisms in organisms to counteract ROS toxicity.

Antioxidant enzymes, such as GR, G6PD and 6PGD, have major direct or indirect effects on antioxidant systems and they are useful biomarkers because they are involved in regenerating reduced glutathione (GSH) from glutathione disulfide (GSSG). Glucose-6-phosphate dehydrogenase and 6- phosphogluconate dehydrogenase are indirect antioxidant enzymes in the pentose phosphate pathway and responsible for NADPH production. Because fish tend to adapt to oxidative conditions when exposed to pesticides, fungicides or other pollutants, relatively high levels of GR, G6PD and 6PGD enzymes are expressed in the muscle, liver, kidney, and gills of fish (Stephensen et al., 2000). Nevertheless, because of complex interactions and interrelationships among individual components, the physiological role of these enzymes in the cells is poorly understood. On the other hand, inhibited activity of enzymes caused by exposure to fungicide or pesticide may be due to several reasons; first is production of O2

−
(Bagnasco et al., 2000), second is direct action of fungicides and pesticides on the synthesis of the enzyme (Bainy et al., 1993; Oruç & Uner, 2000), and finally through direct inhibition of enzyme activity both in vivo and in vitro.

No link...most are from Wiki

The conversion of nicotinamide adenine dinucleotide phosphate to its reduced form in erythrocytes is the basis of diagnostic testing for the deficiency. This usually is done by fluorescent spot test. Different gene mutations cause different levels of enzyme deficiency, with classes assigned to various degrees of deficiency and disease manifestation. Because acute hemolysis is caused by exposure to an oxidative stressor in the form of an infection, oxidative drug, or fava beans, treatment is geared toward avoidance of these and other stressors. Acute hemolysis is self-limited, but in rare instances it can be severe enough to warrant a blood transfusion. Neonatal hyperbilirubinemia may require treatment with phototherapy or exchange transfusion to prevent kernicterus. The variant that causes chronic hemolysis is uncommon because it is related to sporadic gene mutation rather than the more common inherited gene mutation.

Cases of sporadic gene mutation occur in all populations.

A total deficiency of G6PD is incompatible with life.

The test is positive if the blood spot fails to fluoresce under ultraviolet light.
In field research, where quick screening of a large number of patients is needed, other tests have been used; however, they require definitive testing to confirm an abnormal result.9,10 Tests based on polymerase chain reaction detect specific mutations and are used for population screening, family studies, or prenatal diagnosis.6

In patients with acute hemolysis, testing for G6PD deficiency may be falsely negative because older erythrocytes with a higher enzyme deficiency have been hemolyzed. Young erythrocytes and reticulocytes have normal or near-normal enzyme activity. Female heterozygotes may be hard to diagnose because of X-chromosome mosaicism leading to a partial deficiency that will not be detected reliably with screening tests.

G6PD deficiency is one of a group of congenital hemolytic anemias, and its diagnosis should be considered in children with a family history of jaundice, anemia, splenomegaly, or cholelithiasis, especially in those of Mediterranean or African ancestry.

Testing should be considered in children and adults (especially males of African, Mediterranean, or Asian descent) with an acute hemolytic reaction caused by infection, exposure to a known oxidative drug, or ingestion of fava beans.

Although rare, G6PD deficiency should be considered as a cause of any chronic nonspherocytic hemolytic anemia across all population groups.

Newborn screening for G6PD deficiency is not performed routinely in the United States, although it is done in countries with high disease prevalence. The World Health Organization recommends screening all newborns in populations with a prevalence of 3 to 5 percent or more in males.
http://www.aafp.org/afp/2005/1001/p1277.html

G6PDdeficiency.org They have a food and drug to avoid list  People with G6PD deficiency have compromised reduced glutathione and when they take fluoroquinolones they oxidate most of their glutathione left in their body. They can also end up with hemolytic anemia.
Unfortunately most doctors do not take this seriously.
People who become ill from the drug fluoroquinolones are calling themselves Floxies..They are having all the symptoms as me with antiphospholipid anticardiolipin syndrome I was diagnosed with. And what I find really interesting is some doctors also said I had rheumatoid arthritis and wanted me to take that drug...!!! 

And some are even being diagnosed with Antiphospholipid too!
High doses of "Synkavite"< (insert name of any Xenobiotic) caused haemolysis (destruction of red blood cells) and high serum bilirubin levels...I had high Bilirubin levels too! You should have seen my blood the 1st time I was poisoned in 1995...It was brown, and and looked like clumpy balls a little smaller then a marble in the syringe when they took my blood...But, of course there was no explanation, or concern over this...

That was the beginning of my research and education...I bought a book called "How We Die", and took a 1 month vacation to Maui, where my daughter lived, to see her for the last time, and her me...I could hardly lift my arms and walk with so much pain in my muscles and joints...My eyes were as fuzzy, and muddled as my brain...Then I went home, and laid in bed 8 months...

This time, 2008, I also had "peripheral vascular collapse. " All the veins in my arms and legs just stopped working...they dissappeared...and I had absolutly nopulse in any part they tried to find one... I had to work hard to stay alive at that point.Stopping the morphine (that slowed my heart) and drinking coffee and cokes to force actions to push blood to these areas...I switched to Percocets for pain (all my tissues, limbs, and joints were in pain and swelling), but only for a short time, 8 months, did I take the pills...then stopped in order to let my liver have as much health as possible to help me.
New Ethicals Compendium also warns that the use of Konakion can cause jaundice and kernicterus in infants. Other listed side effects include flushing, sweating, cyanosis, a sense of chest constriction, and peripheral vascular collapse.

All of these pharma drugs causing all these problems too...esp. those that are affecting "sensitive" people, example: G6PD...


Mitochondrial “Collateral Damage” Thanks to Big Pharma
Iatrogenic Drug and Vaccine-induced Mitochondrial Disorders

"I include excerpts from just three examples from a multitude of peer-reviewed medical journal articles that have been trying to tell us clinicians (and our most aware patients) that there are many common, preventable disorders that the powers-that-be want us to believe are either the fault of the patient-victim (“shame-on-you”) or are simply inherited from our guilty parents (and thus neither preventable nor curable).

Many of these disorders (see list below) are actually caused by prescription drugs, vaccines and/or other toxic chemicals that are poisoning the mitochondria in our brains, nerves, muscles and other organs. Thus we are being afflicted by preventable, iatrogenic- or industry-caused diseases. Both realities are taboo subjects in the current era of mind-control by America’s powerful, profit-motivated, multinational corporations in BigPharma, BigChemical, BigMedicine, BigMedia, BigFood and BigAgribusiness industries. That pervasive group prefers our ignorance, and each of them spends unlimited amounts of money to ensure it.
The avarice of these industries for larger market-share, higher share price, bigger profits, lower wages and more aggressive wealth extraction knows no bounds, and their brain-disabling products makes their goals ever easier to attain.

http://www.globalresearch.ca/mitochondrial-collateral-damage-thanks-to-big-pharma/5447650

Every single chemical corporation has a spin off Pharma Corporation!

This is how GMOs hurt us...They are poison...
Pusztai found, to his own surprise, that consumption by rats of G-E potatoes had a "profound physiological effect" on their growth and development. Dr Pusztai, a research scientist with a world reputation, has published over 200 papers on lectin, a protein which is a natural insecticide found in the snowdrop flower.

In his 1998 experiments, he fed lectin to rats. The rats who ate potatoes mixed together with lectin suffered no ill effects. But the rats who ate potatoes into which lectin had been genetically engineered became ill.

Pusztai sums up the situation as follows: two harmless substances, potato and lectin, were found to become toxic after genetic modification.

GM (genetically modified foods) are modified by splicing 'lectins' from one plant family to another. This is extremely problematic. If you know you react to a particular plant family but that lectin has been put in a plant not of that family you may consume the 'toxic to you' lectin, have the reaction/response and not know the cause.
http://www.krispin.com/lectin.html

Our newborns in the USA are in danger at the hospital when they are 1st born...because of all of the above...