Systemic Lupus Erythematosus - A possible treatment

    Summary: Lupus is caused by a defect in the body's auto-immune system. It is characterized by muscle weakness, arthritis caused by a the deterioration of the body's connective tissues, as well as attacks on other organs. Because of the non-specific nature of these connective tissue breakdowns it can be difficult to diagnose. When treated with Chloroquin, tunnel vision can result. Because of its inflammatory nature, it conventionally invites treatment using corticosteroid such as Cortisone or Prednisone. In some cases, may bring on epiliform attacks, induced a combination of excess insulin and hypoglycemia. As a patient may be overly sensitive/or is already producing too much corticosteroids, which has led to the slow degradation of connective tissue and cartilage, more corticosteroids can attack the shoulder or hip joints.

    Another treatment involves the use of Aralin (Chloroquin) which can cause damage to the eyes. Because the unbalance in the immune system Lupus often appears before pregnancy with little or no effect on the unborn child. It is thought that some factor is released during pregnancy that is designed to protect the fetus. After birth, that factor is no longer present, and lupus returns..

     A characteristic of lupus is sensitivity to ultra-violet radiation in sunlight that can further weaken the immune system.

    A possibility may exist that the normal linkage between tryptophan and serotonin may be defective as the normal effects of SSRI's seem, at times, to be reversed. A clue to this is based on Lupus going into remission during pregnancy when the body produces an enzyme named IDO, which seems to block tryptophan. When it is not present, T-cells cannot reproduce. This might be a clue to auto-immune diseases such as Lupus. A supportive link is the deep depression found in Lupus patients and the sudden gain in strength during pregnancy.

    Another possible link may be misfolding of certain genes in women and truncated genes in men. A clue might be found in dendritic errors. One item caught my attention. Perhaps Lupus might be the result of a misfolding in chains of protein. This might suggest that by supplying the missing vitamins that are normally in a body, a degree of remission may be possible. This required a intesive study; looking for possible anomalies!

    Presenting symptoms: Any group comprising rheumathroid arthritis, ataxia, poor circulation, nervous manner or nervous exhaustion, muscle weakness, coughing accompanied by chest pain, sunlight sensitivity that produces rashes and/or fever, hypoglycemia, anemia, possible stuttering, a history of recurrent eyestrain, headaches on wakening, depression and/or panic attacks. It is identifiable by raw appearing red areas on the cheeks and forehead, together with inexplicable fatigue, persistent bruising, T-cell and blood protein abnormalities, that can be diagnosed by an antinuclear antibody test.

    A Creatine test may also be useful as Lupus can affect kidney function. Possible lower levels of Coenzyme Q10. Possible above normal levels of Monoamine oxidase (MAO) and/or a low level of L-tyrosine and/or an unstable serotonin chemistry.

    Elevated homocystene levels are possible. Possible link from dyslexia and Meares-Iren syndrome or taste acuity may be diminished. A higher or corticosteroid or insulin level than normal may be present.

    Supporting familial symptoms: Tuberculosis - Pneumonia, Diabetes - heart problems - anxiety - excessive anger – a tendency for bipolarism and/or attacks of panic - short stature - retinitus pigmentosa - susceptibility to yeast or fungus infections - possible yeast or carbohydrate intolerance - Celiac - Autism - possible lactose intolerance - possible Protein intolerance - possible intolerance to soy proteins scleradermia - smoking.

    A possible link may be a lack of normal levels of viamin D, as exposure to sunlight can accelerate lupus.

    Many attemptsat effecting a remission or a cure, may have been unsuccessful as they might not have realized that lupus combines elements that are usually associated with either the young, or with the aged.

    It was with these thoughts in mind, that in 1982, an attempt was made to seek a workable solution.

    It was based on the premise that lupus was contracted by a synergistic group of precursors, that, taken as separate entities, would not, of themselves, have such a debilitaive effect. As stress levels in modern society increase, so should the rate of lupus increase.

    In trying to find a set of common factors, we started with the curious effect on serotonin related production of l-tryptophan. Perhaps the apparent low effective serotonin level in the patient might have been because the serotonin was somehow (because of an abnormality in the cerebral neurochemistry) producing an unbalance in the  l-tryptophan. Another possibiliy was the unnatural 'folding' of the DNA. By use of the corticosteroids doctors attempted to reduce some of the side effects of the irritation.

    Might these be overcome by overiding the harmfull effects by resorting to a thorogh replacement by the use of the appropriate vitamin regimen?

    These hypotheses were worth investigating!

CAUTION: As the treatment can change neurotransmitter levels on both serotonin, and MAOB inhibitors, thus increasing the level of l-dopa, caution should be exercised. As some forms of cancer cells increase the level of serotonin in the blood, the use of antioxidants is necessary to prevent adverse DNA damage or mutations. As part of the program uses folicin and vitamin B12 as well as growth hormone (GH) these cautions are especially pertinent!

As in any treatment for depression, where (serotonin) is involved in stress mitigation, Vitamin B5 and vitamin B6, it may be needed. To reduce the possibility of peripheral neuoropathy co-administration of neurotrophin-3 may be necessary.

As any treatment with l-tyrosine can cause similar effects, the same caution is applicable! The problem is how to reinforce the immune system without triggering hyperactivity. Some method  has to be developed to retain normal immune system response while preventing the patient's own immune system from attacking the patient's own body!

It was felt that investigating a child's immune system response to its mother's body, some insight could be gained! Prospective mothers who have lupus seem to be in a temporary remission during pregnancy, only to have it reappear after their baby is born.

We decided after several years of study, that perhaps the action of l-tryptophan might lead us somewhere.

(What follows, seems to fit many of the problems associated with lupus. To some extent, this might also have some application to myasthenia gravis, ALS, MS and the other autoimmune afflictions.) If we postulate that  the enzyme IDO blocks the abnormal action of l-tryptphan and the overactive t-cell production that is the consequence - perhaps this might lead to be a 'cure' for some auto-immune afflictions! AA0.1

But inspection of the literature shows a strange "linkage" between abberations in melatonin, low levels of serotonin, low levels of GH and low levels of Vitamin B6. In addition there seems to be an aberration in the hippocampus and a reversed reaction or overreaction to such SSRI drugs as Prozac.

There might be a clue in the overreaction to sulfa drugs, which in some patients, can produce a very severe skin shedding when sulfa drugs are utilized to treat Campfor Bactus. Some doctors have found the sulfa drugs can cause a flare-up in lupus.

Large (over 150 mg) Vitamin B6 may lead to a major decrease in the effects of any l-tryptophan especially when taken with zinc and vitamin B5 and Vitamin B12. Remember, that in doses over 250 Mg of B6, the minor calming effect seems to be absent although the SSRI effect increases! Much more study still remains!

Preface and commentary:

The treatment of Lupus is based on many different (and sometimes conflicting) factors. What follows does not imply that all of the various factors are present in every case of lupus. As some factors may predispose the development of lupus with varying degrees of severity, there seems to be no single condition, such as a gene, that causes the onset of lupus. Rather, lupus seems to depend on a synergistic combination. Therefore, the following discussion paper tries to indicate things that are common (in varying degrees) in many people with lupus.

Terminology can be confusing. Consider the situation with allergies. Some allergists state that patients cannot, a priori, be allergic to perfumes because perfumes contain an essential oil rather than the pollen of the flowers used in the preparation of the perfume. This is cited as a justification for the inclusion of perfume-strips in some popular magazines. This takes place in spite of reader's protests that they feel faint, nervous, or have headaches, because of the inclusion of the strips. These allergists ignore the fact that some perfumes contain synthetic organic chemicals that were selected for their stability. In many cases, these are not easily metabolized both may break-down into unexpected fractions. Because of budget limitations, not all possible side effects can be explored.

As there is not a serious "common element" present all the time, such complaints can, all too often, be ignored.

Therefore, such cases that occur, are dismissed as being psychosomatic. There seems to be a ever increasing need, among specialists in many professions, to attach labels. By doing this, experts may be presuming to know with what their dealing. Anything else can be ignored as irrelevant!

What may not be appreciated is, using the case of migraines attacks as an example, that in this instance, those perfumes are 'triggers,' in much the same way that MSG is a trigger. At low concentrations, it makes people apprehensive or nervous. At higher levels it may cause migraines 1, or, in the case of serotonin aberrations,

panic attacks. Both migraines and panic attacks have been linked to an imbalance in the level of serotonin and prostaglandin's in the brain. The serotonin in the blood platelets causes the arterial contraction and then the dilation, the prostaglandin produces the inflammation. Lack of sleep, or stress, raises the level of prostaglandin's and the lead to a condition of hyperhomocystene.

But panic attacks, could be caused by a CCK DN.00.00(cholccystokinin) neurotransmitter defect which could be linked to a malfunction in the brain's misuse of SSRI's. A possible co-factor, may be an altered succeptability to sensory overload!

In young children, the use of MSG appears to cause some cases of ADS (Attention Deficit Syndrome), asthma, and heart arrhythmia. For some of the children, even soybean protein derived milk substitutes such as Prosoyba (tm) may be counter-indicated. There may be a link to Celiac disease, Gluten and/or Yeast Intolerance! The FDA stopped the use of MSG in baby food. However even such things as some soups, some potato chips, and other basic foods, may use MSG (or autolized yeast, etc.) in their manufactured products.

There appears that no study has been made to search for any possible correlation between the use of MSG and Ritalin(tm).

A major concern is the apparent increase in the number of excitotoxins that are now a major portion of a childs diet. The so-called fast food outlets are decreasing the amounts of trans-fats and it is hoped that the number of added preservatives may also decrease. The question has to be asked, "just how many  preservatives have to be taken out of the food so that it is still save to consume - allowing for the delays for when it is produced until it is consumed?

Stress can also cause other immune system problems, by possibly decreasing the effectiveness of the blood-brain barrier, thus allowing defective DNA or the fragments to affect the brain itself. This may be why people who live in a "happy" environment seem to have less heart attacks, less strokes and less arthritis.

It also may be the reason there is about a six-month delay in the development of even disease such as pneumonia, viral attacks, and even severe depression!

Unfortunately, a lower than normal level of serotonin can cause timidity, and the inability to form close personal relationships. There is the ever-present fear of being criticized or judged.

Perhaps, some of these are even the side effects, such as hypoglycemia, of the antimalaral drugs used in treating lupus. These may have not been considered fully. As a result, any general panic or depression is regarded as a "just another cause for having contracting lupus". There does not seem to be a simple genotype which can be identified at this time. Some people seem to have an ability to "roll with the punches" of life, and others don't. Childhood stress seems to play an important part in the ability to withstand stress, and this is often overlooked by doctors, especially male doctors!

Some doctors, frequently confuse the depression in lupus, with being depressed from overwork or stress. They advise patients to change jobs. They often fail to take into account that the very thought of changing a job, can be very stressful in itself!

As another possible common factor, of the headaches of hypoglycemia, photophobia is sometimes present in severe headache attacks, as are sensitivity to loud noises, ataxia, nausea, syncope, and vertigo. Hypoglycemia CC1, especially in females, appears to be tied to a low (somatropen) growth hormone (GH) level, melatonin, sometimes lactose intolerance is present, as well as dyslexiaCC2 . Hearing function may be affected including an a apparent inability to differentiate between the sound of someone speaking and noise.

It is now increasingly accepted that a low GH level may be related to the amount of a baby's cuddling and/or the mother's apparent neglect of the child at the emotional, or "bonding" period. Children who are loved gain more weight, have less psychological "hang-ups", and adjust to life's problems much better. This may be why, pets may play an important role in emotional adjustment. Such children seem to develop an high degree of empathy to other people but they have to have it returned to almost an unnatural extent, to feel loved. Quite obviously, other children don't feel the same emotion, or don't feel it to the same degree. This is probably why getting tagged with being "sensitive" has such adverse connotations.

The consequence, is that such a child may become a "loner" and may swing back and forth between fear and dominance, in alteration, embracing first the left hemisphere's and then the right hemisphere's mode of thought (0r the reverse)! This may be have the serious consequence of increasing any latent degree of bipolarism!

As children mature, this pitfall may widen even as it grows deeper. There seems to be less reason to accept people as they are.In simple terms. And once they are classified as bipolar, the gulf deepens! Their defense mechanisms go into overdrive. In some countries "eccentrics" are not scorned. Society has apparently forgotten that many of the most brilliant discoveries have been the result of such aberrations.

But if they sense that they can never be accepted by their peers, they might become "true believers", prophets, or even zealots! They think that whatever is not totally correct, has to be totally wrong! This toggle-effect may, in time, in time, cause someone such as this, to loose all sense of humor.

The very antimalarials uses to treat lupus, as we said previously, can excaberate depression. This can lead to major psychological problems for the patient being treated for lupus. They may need more than a casual level of support. Most doctors don't realize this!

In extreme cases, the "victim of lupus" (and I mean this term), may develop the rather extreme need to abandon everything (including possessions) and run away. If they are not able to handle the extra stress of the antimalarials, they may find something inside of them, that will enable them to survive!

This, may cause them to become "control freaks" (which can result in a tendendy to 'bully' other people). In turn, they will start to become a problem with other people in the company. They try to work harder, pay unnecessary attention to minute details, and thus are constantly behind in their work! In compensation, they try to work harder, and may feel it necessary to work on weekends and even avoid holidays. The results are that they feel that their hard work is not being recognized!

This will sometimes make them want them to "try and take-over" every job, even to the point of disregarding the proven competence of others! then, like the aggressive driver, they spent too much time in "spinning-their-wheels", cutting in-and-out of other driver's lanes (jobs) and getting nowhere!

In a similar fashion, people may say they are allergic to lactose, when they mean they are lactose intolerant. Patients who suffer headaches (or migraines when they consume too much complex carbohydrates or foods containing certain prostaglandin's) may be complex carbohydrate intolerant, and may be gluten intolerant (Celiacism). It is probable that a person with lupus is serotonin deficient, perhaps because of a defect in protein conversion which can cause depression and panic attacks.

(Hint: In the Canadian Maritime Provinces someone has opened a bakery that speclizes in gluten free foods. Because the woman had a serius reaction to gluten she researched for several years and was finally able to make a host of items that tasted excellent and were all gluten free. Now she is distributing her products coast to cost in Canada and is exporting to the US.)

There may be a deficit in their body's production of vitamin B6, leading to a susceptibility to yeast infections, and/or fungus infections, which may be a link to hypoglycemia. It is also a possible link to the lower production of serotonin as well as a possible link to a l-dopa abnormality.

A yeast infection can produce a while series of side effects, such as vertigo, panic, depression, loss of short-term memory and other, unexcited side effects. The CEIA test (Candi-sphere seriodiagnosis analysis) for yeast infections should be performed.

Lactose intolerance has much the same etiology as Celiacism, so much so that a parent who is lactose-intolorant may fail to recognize the development of the adult phase in herself or himself. One common element is headaches, nausea, or even depression. these also may be linked to yeast problems. It therefore, often difficult for doctors to grasp the entire pattern of lupus!

The study of hypoglycemia has suffered because of over popularization in the 70's. In this respect it is similar to migraines. Initially, migraines fell into disrepute in the 1930's due to an ill conceived study that attempted to define a migraine personality. Those persons were presumed to have a neurosis that would respond to psychiatric care. Unfortunately, there was an element of truth. Many patients were counseled to switch to less stressful occupations 4 and some of the migraines stopped. However some migraines were caused by other more serious factors. In the case of weather related migraines, they may tied to latent or potentially active cerebral aneurysms, or more simply, a result of blood vessel constriction/dilation cycle.

Extreme cases of hypoglycemia may lower the body temperature so much that the person exhibits the classic signs of hypothermia, slow pulse, difficulty in walking, hand tremor, vertigo, slurred speech or even stuttering! Observers may even think that the people are drunk! But the same symptoms are present in yeast infections as well. Occasionally, the yeast in the body, will combine with sugars, to produce more than methane. It can produce ethanol as well. In this case, people who never touch alcohol, may have so high a blood alcohol reading, that they can be charged with drunken driving! In this case, they may have, literally, severe hangover types of headaches. Drinking a lot of water the night before, will reduce the brain swelling and mitigate, if not stop, the headache. Patient's with yeast infections, may have hypoglycemia, as the infection is fueled by sugar. When the blood sugar gets very low, the condition may remain stable! As patients with lowered immune system levels may not be able to fight off the infection.

People with hypoglycemia, may have less difficulties with classic allergies. But they can still have some problems with chemically or visually -induced triggers. On the other hand, when a patient sees to have developed allergies to a whole host of substances, a doctor should suspect a yeast infection, a fungus infection, a protozoa or even a combination!

An inspection of medication used to relieve migraines will probably show that similar medications are used for hypoglycemia, headaches, vertigo, nausea, antidepressants, tranquilizers or high blood pressure.

Even condiments or spices such as horseradish (hraine), pepper, ginger, paprika, mushrooms, mustard, chili-peppers, Tabasco sauce, Wostershire sauce and capsinin-containing foods such as Japalino peppers, may be in common use an alternative to salt. Most of these are now recognized as an anti-inflammatory agents. But they are also effective against yeast, fungus, and protozoa infections!

The search of accepted texts on hypoglycemia together with the equivalent reference texts on fungus and yeast infections will reveal too many similarities to be coincidental!

Even some gardening manuals will reveal the same so-called "cures" for moss and fungi!

The hypoglycemic patient might be lacking in a normal level of bile or stomach acid. That is why, for them, considering their possible yeast intolerance, antacids may never work. They may be especially fond of some foods or condiments (such as) pickles, because in some cases, their acidity may an aid to digestion. Frequently these people's work habits make them prone to stomach ulcers. This is why they should be tested and, if necessary, treated for e-pilorii bacteria that their marginal immune system may be unable to handle. However sulfa drugs should be used with caution.

There is a possibility for an alteration in the traditional method of dealing with pre-diabetic hypoglycemia. When, upon awakening, the body as accumulated the essential bile acids, the patient may be more able to handle a normal breakfast. As the level of available bile decreases thereafter, less food is needed If too much is food is consumed, indigestion will result!

As lipids carry the energy in the bloodstream, too few lipids can seriously affect their metabolic by-products, in such things as testosterone, prednisone, etc.

As a possible result, mild hypoglycemia became an essential for survival. (just as in the case of the Navaho and the Australian aboriginal). In the case of the first two, a near desert was involved. There may have a concentration of minerals in the desert sand. I would expect to find zinc, copper and chromium among others.

Some bacteria and fungi have the ability to extract needed nutrients such as minerals, to grow. This may be the case in "Manna" and it might also be true of certain cacti in Arizona which provided potable water. Another possible link is Aloe Vera, a desert plant, which is effective against sunburn and is thought to increase insulin production.

Another pattern is found in the use of garlic to stop fungi or moss in grass! (It is also worth making a comment upon the language of the Navaho which sounds like Hebrew).

We cannot afford to overlook anything by which we could gain insight. For example, a similar sort of story is found in England in the form of the mushroom 'fairy circles', which were revered. A fairly common problem among researchers world-wide is over specialization. The joke is that when a scientist become a specialist, soon he knows everything about nothing and looses his effectiveness.

Because of the "necessity" for peer review, new approaches to a problem are too often dismissed by the "experts".

Because inbreeding with other parallel thinkers is a survival trait, a close inspection of family names and physical characteristics may hold some unexpected surprises.

Because any people who embraced the 'legends' survived, often because of the parallel thinking (or the use of their quick wits), they were often at odds with the serial thinkers who regarded them with deep suspicion and frequently attempted to subject them to inquisitorial actions to confiscate their wealth!



        There are three main monoamine neurotransmitters: serotonin, dopamine and norandreline. Each of them is produced by a specific amino acid. Serotonin is produced by l-trypophan, while dopamine and norandrenin are produced by l-tyrosine. Cells located outside the brain, such as blood platlets and some intestinal lining cells, either use or make serotonin. Because of the blood-brain barrier, all serotonin used by the brain cells must be produced by the neurons. However, the blood-brain barrier served to protect the brain against imported toxins has a drawback; even needed amino acids are thus limited in their access to the brain. Nutrients must be conveyed to the brain using transient molocules. This creates a difficulty for serotonin. Its precursor tryptophan has to share the conveyence with five other essential amino acids: leucine, isoleucine, valine and phenoalanine.  The normal diet consists of some animal (or fish) based protiens and vegatarian protiens. The problem may be that tryptophan is the least plentiful of the amino acids in our diet. There may be a reason for this imbalance. L-tryptophan may be linked to some of the neuro-degenative diseases , such as lupus!

        Female patients who have lupus, may find that their body, during pregnency, produces a drug that alters a woman's immune system to protect thr baby's immune system against  l-tyrosine. After the baby is born, there may be a sudden reduction in serotonin. This may be linked to a sudden alteration in the hormone system (the cortisol level may alter) that makes the mother suseptable to the "flee or fight" syndrome to protect her child! As such a mother can suffer 'post partum' depression, her blood insulin level may rise even more, leading to the epiliform attacks.

        Eating a diet high in carbohydrates , is generally is a way to increase the level of of tryptophan. As such a diet may reduce some of the other essential amino acids such a diet increases the insulin level in the bloodstream. The result can be insulin seizures! They may be prevetable by the use of a (high fat) ketogenic diet.

        This may be the familial link to diabetes.

        There is a major dietary problem that ensues. As the energy is parially based on the essential lipids in the diet, the typical patient may be lacking in muscle strength and the stress level may be so high as to make the patient's  hair thin, friable. and laking in luster.

    Now, with these factors in mind, you may proceed.

Although a hereditary common factor in lupus may be rheumathroid arthritis, another hereditary item may be a family history of diabetes, heart problems, cancer, or indeed, any of the autoimmune, or neuro-degenerative diseases. All may require an unstable HPA axis and cortico-steroid unbalance.

Much has been discussed about chlorine from industrial effluents, as a possible link to breast cancer. However the chlorine used in bleaching wood pulp may not be the culprit! A more likely candidate could the bis-phenyls, especially nonyl phenyl. Racial Carson linked DDT to genetic problems in birds. But PCB's are also mutagenic. Could there be an interaction between DDT, PCB's and dioxin, where the cumulative effect is much greater than the sum of the parts? One has to wonder whether diallyl phthalate (a common plasticizer) is involved as well?

Estrogen like chemicals can be a major problem, for they may be difficult for body to convert. In other words, they may be so stable that they cannot be converted in the normal fashion, to simpler, less irritating materials. We may have encountered synthetic perfumes that resist the normal process of breakdown, and, what is even more serious, can cause unexpected side effects such as chemical sensitivities, migraines, vertigo or nausea!

Because the demands for proteins by hypoglycemia, which may break down protein to boost the drastically low of level blood sugar (glucose), the breakdown may affect all the sources for protein in the body, including the muscles, the connective tissues, the myelin sheath on the nerves (singly as in multiple sclerosis, in toto, as in myasthenia gravis, or selectively as in ALS - in the stomach or bowel, and Lupus). The consequences may include any form of arthritis!

Another possible hereditary factor for Lupus, may be a erratic level of melatonin CD01 . This could result in sleep difficulties, produce a susceptibility to autoimmune or other neurological problems, such as is the case with lupus, or depression/panic attacks, which may also be liked to a lower than normal level of vitamin B6. As a lower level of melatonin, and/or vitamin B6, may be linked to lower level of somatropen - growth hormone (GH), there is a possibility of diminished height as well. A low level of melatonin is also linked to retinitus pigmentosa CD01.01

Another common factor may be an elevated level of insulin production by the body. This could show-up in the patient's having a tendency to be overweight in spite of an overproduction of the human equivalent of Leptin CC3. This, together with an elevated level of prostaglandin's, and hypoglycemia, could a common factor in cancer, DF00.01heart attacks, or strokes, and, in addition, an increased propensity for diabetes! The patient could have problems if there was too many carbohydrates in the diet, as they might be a factor in the severity of headache attacks. In extreme cases, the patient could even be Celiac. Indeed the ratio of protein to carbohydrates may have to be adjusted in favor of an increase in protein! As too much protein may result in possible increase in intestinal cancer, unless extra foliate (folic acid+vitamin B12+vitamin B6) is supplemented in the patient's diet, this forms another hereditary factor.

The presence in the fetus of high levels of growth hormone (GH), folic acid, and vitamin B12 as well as some factor that blocks the normal action of l-tryptophan could be a clue to the apparent non rejection of fetal tissue cells. This, in itself, could pose a clue to a way to mitigate tissue rejection in transplants! Consider, what is difference in the GR reaction in males and females? As a result could a man be more likely to contract a disease where low GH was not a factor?

There may be another factor as well. Attention Deficit Syndrome (ADS) might be present. Watch for the inability to remember whether such things as , for example, a stove is off, a door locked, or even an appointment has to be kept. This type of behavior, in children, is conventionally is alleviated by the use of Ritalin. This seems to be caused by an oversentization of the hippocampus by repeated stress reactions.

A possible alternate might be to raise the patient's l-dopa level. As this presupposes a family history of a general deficiency of the B vitamins, look for either bi-polar illness or even schizophrenia where habitual smoking raised the dopamine level too much!. This may have been overcome by developing a over intense ability to focus on one aspect of a problem, to the exclusion of other, more important factors! This, in turn, might cause business problems as too much time is spent in pursuit of trivia! The patient may be addicted to chocolate, coffee, or smoking. These may help them to "maintain focus".

Lupus may require several factors to act together before it manifests itself. It has been argued that some cause of depression (that causes an immune system dysfunction) must be present a priori, or whether lupus itself produces the depression a posteriori. As noted, a chronic lack of sleep can weaken the immune system, as can excessive exposure to the UV rays of the sun. However, any doctor needs to recognize the side effects of antimalarials!

In a similar fashion, hypoglycemia can be inherited or self-induced. The abnormal protein present in the blood of lupus patients may be a recessive factor that manifests itself only when a person has a weakened immune system. The dry reddened skin on the cheeks and the forehead is a sign of a minor circulatory problem similar to the reddened cheeks of someone exposed to low temperatures. In cases of severe hypoglycemia where protein is lacking in the diet, the body may draw on its own protein reserves from muscles, connective tissues of cartilage. This, in turn, may be caused by a lowering of the body's coenzyme Q-10 (CoQ10). AA1

Although it seems unlikely, the presence of a genetically altered brain chemical may result in a analogue of procainamide in the brain. However, unlike procainamide itself, which can result in a form of lupus 6.4b6that might possibly be different from "true lupus". (see the comment on procaine therapy). Again, it is the presence of several overlapping factors that may cause lupus.

Because of hereditary factors, hypoglycemic's may have one lazy eye, or be legally blind in one eye. They may have been dyslexic, or just a 'slow learner,' a day-dreamer, be minororally autistic. The patient may have learned to read a language that is normally read from right to left (where it is a survival trait) or have been able to read only in columns. All these are symptomatic of hereditary hypoglycemia and all are linked with hemispheric dominance in the brain. Of course, hypoglycemia can be induced by such things as alcoholism, cancer, and work or study induced stress.

A typical Lupus patient may, as an adult, exhibit some childlike qualities, such as an unusual gift for languages, writing, art, or music, all of which require a facility for parallel thought processes.

Stress is involved in Hypothalmus-Pituitary-Andrenal (HPA) axis and cortico-steroid inhibition. Any instability in the HPA axis, may lead to elevated cortico-steroid production and consequent immune system problems that may be triggered by hypoglycemic stress.

Hypoglycemia increases susceptibility to infections, including neurological diseases which is why herpes-zoster (shingles) infections are an indication of hypoglycemic nervousness or stress whenever a patient has been infected with chickenpox. This also can be caused by an immune system that has been weakened by an exposure to some substance causing an allergic over-reaction.

Other stress related events such as heart attacks, and strokes may require a combination of high blood pressure and cholesterol to attack. All require a homeostatic (hyper homocystene) imbalance involving HPA axis problems.

As stated, hypoglycemia frequently can be induced from lack of sleep, job stress, the stress of studying, alcoholism, drug abuse, some social diseases, or several factors in common, including hereditary factors. There is no other common factor, except that induced hypoglycemic's are more likely to be linear thinkers. Hereditary hypoglycemic's are more prone to be parallel thinkers, and may as well suffer from depression, manic-depressive syndrome or panic attacks. They frequently fond themselves in professions requiring great creativity such as the arts, teaching, and sales where their parallel thinking can lead to an unusual degree of success. A GTL (glucose tolerance test) is useful.

The mild "high" of hypoglycemia can become just as addictive as alcohol. Doctors may misdiagnose it as an addiction to alcohol. This is why people can become workaholics. However it may be involuntary. Because it can lead to depression, the patient is driven to succeed and work harder rather than learning to working smarter! Frequently small mistakes will appear overwhelming and the patient could suffer a stroke or heart attack because of an elevated CRF (corticotrophin releasing factor) level!

In much the same way as an addiction to being a workaholic took place, an addiction to tobacco may have developed. MRI scans have demonstrated that Nicotine alters the brain chemistry by increasing the neurotransmitter (Dopamine) that makes smoking such a pleasure. At the same time it also inhibits the Monoamine oxidase B (MAOB ) that lowers the dopamine level AA01.7. As a high level of Dopamine seems to mitigate the severity of Parkinson's Disease, it might account for the reduction in that disease among heavy smokers! It has been suggested that treatment with St. John's Wort (Hypericum perforatum), or even selegiline, either of which are MAO inhibitors, may lessen the depression and other aspects of lupus. (Anti-depressants are often a combination of several drugs, (SSRI's) which act to raise serotonin levels, by acting as an MAO inhibitor.)

The amino acid L-tyrosine passes the blood-brain barrier and is converted by the dopamine producing neurons, to L-dopa, and then to dopamine in the brain, which accounts for tyrosine's beneficial effects - including resistance to cold, depression, stress, and hyper-active nervousness. It also is a reason to watch its use in treating depression! Researcher'sBC1 efforts, resulted in segaline (also known as depranyl). Related drugs may also find use for Alzheimer's, but they may produce the sometimes life threatening "cheese" effect and are potentially dangerous when combined with alcohol. Indeed, some non drowsy anti-histamines also have the same dangerous potential.

Consider the case of FenFluoramine in weight loss programs. It can cause serious hypertension in the lungs in a minority of patients. Several similar reactions may have been caused by antidepressants containing fluorine.

Check the patient's tolerance to cold. If it is high, there may be a risk of overdosing with vitamin B6!

However, the cigarette tobacco smoke BB1 also destroys much of the tocophrerols, cartenoids, and retinol, possibly leading to cancer because of a lessening in the natural immunology.

See also the cautionary reference to PABA - DMAE - Procaine 6 ** .

Indeed, depressed persons have less of the neurotransmitter Phelylethylamine (PEA) in their body fluids. DL-phenyalalanine (DLPA) inhibits the enzymes that destroy endorphins, as well as raising PEA levels. Vitamin B1(cobalamin), the amino acid DL-phenyalalanine (DLPA), and methionine, may prove effective. Hypericum perforatum, (St. Johns Wart) whose active ingredient is Hypercin is held in esteem in Europe as a mild non-prescription antidepressant which has less side effects than most prescription drugs. Methionone also acts to ward off fatigue by converting norandrenaline into adrenaline.

The habit of smoking may ensue even if the other needs of the body are satisfied! Formerly, people in tobacco-growing areas might have suffered from pellagra because growing tobacco depleted the soil and made it vitamin B3 deficient. Tobacco contains nicotine, related to (Vitamin B3) and the body may well come to depend on it to reduce the nervousness caused by mild overwork (mild hypoglycemia). Dopamine has also been used to reduce depression. An obvious substitute for smoking is taking nicotinic acid - niacin. Unlike tobacco smoke that contains damaging tars, niacin increases circulation and to some extent relieves the symptoms of tension by stabilizing the blood pressure.

It is not the tobacco that reinforces the craving, although a habit may ensue even if the other needs of the body are satisfied! Tobacco contains nicotine and the body may well come to depend on it to reduce the nervousness caused by mild hypoglycemia. Endorphin enhancers may be necessary as well.

A possible substitute for tobacco is nicotinic acid - niacin. Unlike smoking, niacin increases circulation and to some extent relieves the symptoms of hypoglycemia. By increasing the glucose level. It has another beneficial effect as well. Taken twice a day in 500 mg. doses (in a time release form to reduce the flush reaction) it can also cause a steady reduction in cholesterol! Taken with lecithin (in 10 grain amounts) it has been postulated as a treatment for inner ear caused vertigo - much the same as ginger. But where adult onset diabetes may be a problem, the patient may have to take chromium picolinolate as well!

Another possibility involved with MAO inhibition by nicotinamide, involves its apparent effect in switching off the gene that may cause diabetes as well as lessens the memory loss effects on people with Alzheimer's.

Women seem to suffer from SAD more often than men. It has been postulated that this may be caused by a light deficit response by the pineal that leave an excess of melatonin behind in the female brain. There may be a link to a lower level of Vitamin D as well as a low level of calcium. Remember, in nothern latitudes, the level of light may may lead to a disfunction in the pineal gland; look for a succeptibility to arthritus, ostiopina and fractures. These might be the result of the low daylight light level causing a deficiency in Vitamin D and serium calcium . Even though arthritus is a misuse of the calcium in the body, if it is too low the body will take needed calcium from the bones. The lack of Vitamin D weii excaberate this! Therefore, it may be prudent to limit the administration of oral melatonin to the late spring, summer, and early fall.

There has been an immense amount of work on the differences in DNA between women and men. The DNA in men has an increased tendency to break into smaller fragments that have a tendency to attach themselves to the ends of normal DNA. This may be why men or more susceptible to some form of diseases which can be more readily avoided in women. With men, there appears to be a more intense need for antioxidants to allay the problems of gene fractures and a propensity to have problems caused by recessive genes.

Hereditary hypoglycemia (genetic hypoglycemia) can generally be classified into two groups, high GTL and low GTL. A typical high GTL group may be descendants from Yorkshire families where the tolerance to cold may be because of a high level of tyrosine. In Yorkshire a different manisifation of Hypoglicemia may occour. Here the lowered level of glucose might be caused by a yeast related problem where any type od 'suger' is consumed by the abnomally high level of yeast. Most often this is manifested in woman, however in men having a non-acidic metabolism. A possible  clue might be a man that never suffering from heartburn. The bile level might be so low that normal digestion is difficult. The patient might think that he is suffering from a heart attack. A test may reveal that it is nothing more than a gas buildup caused by undigested food. At one time, doctors had these patients take a low level of acid. Now the treatment is taking two acidophilus capsules before meals. Unsweetened yogurt may help.

In severe cases candesis infections may result. The treatment can be very severe and might be banning all foods that contain yeast, inchuding simple carbohydrates. Sometimes a minor yeast infection might be stopped by a very dilute form of vinegar. However, a unsweetened yoghurt douch might be indicated.

In more extreme cases, a form of yeast might be encountered in acidic soils where summer vacation cottages have been built. Here the yeast spores might be inhaled with a consequent severe lung infection. This condition is so rare that it might not be propery diagnosed and death might occur.

A person with a high GTL and a high L-tyrosine level is less affected by the cold - and may suffer because of being unaware of the cold.

A person with a low GTL may be descendants of Semitic, Baltic or Mongol families. The patient might also have Thysellonic anemia (Thalaseslemia) BA1.14. In like fashion people with a low GTL may feel the cold and frequently crave a diet rich in fats. If hypoglycemia is present a basic blood sugar test will reveal it. If present a glucose tolerance test should be performed to show if the (GTL) glucose tolerance level is high or low.

If hypoglycemia seems to be overemphasized, it is because it, a HPA and cortico-steroid inhibition dysfunction, play a part in the development of Lupus. In addition, it may even be linked to hypoglycemia brought on by constant use of aspirin or any medication based on quinine. This argued for the addition of both vitamin E as well as vitamin C to the diet if cataracts are to be avoided.

In effect, in lupus, as well in the use of the treatments of lupus by using antimalarials, the normal feedback loop of Homeostasis is not functioning properly. This should not be inferred as a case for using steroids as anti-inflammitories as these can result in further loss of bone and actually increase arthritis!

Other serious problems that could occur are epiliform attacks, brought on by the low glucose level of hypoglycemia interacting with sudden changes in PO2, possibly because of sleep apnea. Another somewhat more remote possibility is a history of severe headaches resulting in ketosis. As an example with migraines, (the probability of severe migraines in a patient with a low level of serotonin is minimal), nevertheless, when the frequency of the migraines are reduced, the ketosis is reduced as well. If the seizures start about the same time, they were probably brought on by a prolonged, healthy, low fat diet resulting in absence of the ketones that accompany a loss of weight due to fat or the inability of the serum lipids to act as a source of energy! Sometimes, it is forgotten that some form of lipids are needed to carry the energy. Often, it seems as if there is a constant state of hormonal war, in a patient having lupus.

As there is a link to an increased production of insulin in the body, any epiliform attacks, or seizures may have been a form of insulin shock This may not show up on an EEG, even when flicker is used.

Thus, there is the distinct possibility of the body's over-production or insulin or corticosteroid, causing an edoctrinal imbalance that may lead to micro seizures if not seizures themselves! It may be that the ketones were inhibiting the seizures. The treatment is to substantially increase the fat in the diet, with only the proteins necessary to avoid hypoglycemia. The patient must be on a diet that will produce ketosis!

This, in children, involve a ketogenic-diet!

As parallel thinkers sometimes are subject to seizures, they may have too short a neurotransmission time, and as a consequence, may lapse into a form of positive feedback thus producing a seizure!

Because the lupus patient probably is deficient in serotonin, they are prone to panic attacks rather than migraines.

(Where there are a hereditary seizures, they may be due to a shorter path length or a faster response in the brain, suggesting a higher level of insulin as a cause of seizures. This argues for a faster response time for complex problems, or a parallel form of thinking, where there is not the buffering effect of a time lapse to prevent most of the brain's neurons from triggering at the same time! Where there is a possibility of manic-depressive thought, the entire "dual brain" triggers for epiliform atacks, may not be present as the deay might allow the triggering impuse to dampen down)

To continue, survival may have depended on a evolution over  many generations,  this may be a consequence of a subtlied altered body chemistry, there may be some foods that are preferential.

For this reason, fruits that are basic (alkaline) such as apples, grapefruit, or oranges, are frequently favorites, as they seem to aid digestion. Although they are contraindicated in diets designed for people with Celiac problems, the possible culprit is yeast, which as produces a breakdown product, produce furfuric acid which seems to act as a headache or migraine trigger, as well as produce muscle and joint cramps. Foods such as pancakes, or crumpets, which use baking-powder, rather than yeast to rise, seem not to produce any symptoms. These difficulties may occur, as the patient has a metabolism making them susceptible to yeast and fungus infections.

Triggers such as strobe lights apply to both migraines, panic attacks, and epiliform attacks. A minute number of drivers are susceptible to both migraines and, as been demonstrated in France, petit-mal seizures. Usually they are young and in good health, but over-tired from studying.

The general consequences of lupus could apply equally to people who have inherited and/or genetic hypoglycemia but have a high ACTH level for some other reason. Even the treatments for lupus may cause problems.

It has been suggested that whenever the body's state of homeostasis is severely disturbed, that host of diseases may ensue about six months afterward. This may even include the other neuro-degenerative diseases for which there may be a genetic pre-disposition (the use of genetic pre-disposition is deliberate because it is doubtful that a single birth gene defect could produce such a host of diseases later in life, were it not for gene defects, or gene alteration, possibly caused by oxidization-which in men may cause gene fragments to "splice" into the DNA-which,in turn, could lead to a statistically higher rate of neurological diseases in men) that has not been manifest. That is, when a person is young, their immune system may protect them. Various factors such as genetic defects caused by free-radicals, and pollutants such as lead, or any of the organo-phosphate chemicals may alter that protection leading to a manifestation of the disease.

The patient's eyestrain or being lazy in one eye, might be caused by the necessity of mediation between the conflicting overlapping of the different visual images that couldn't be mediated by the lateral geniculate nucleus 'stereo apparatus. This plays an increase in the body's demand for glucose. There is also a possible link between dyslexia and Meres-Irlan syndrome.

If an attempt is made to train the lazy eye this itself can cause an increase in the hypoglycemia. As it is generally recognized that hypoglycemic nervousness is a precursor or possible alternative to what would otherwise be a migraine trigger, or a trigger for a panic attack, it would seem possible to link excessive nervousness to migraines, and indeed nervous stress is a cause of both headaches and migraines. The nervousness may lead to a series of diagnostic problems, such as pituitary dysfunction, (including an overactive or underactive thyroid), or anemia (low blood iron). Indeed trace-minerals normally present in the body (such as iron, calcium, manganese, chromium, zinc, selenium and others, may require the use of supplements. See the note on Thysellonic anemia.

Stress 4or extreme panic, manifests itself in an increase CRF (corticotrophin releasing factor) level in the body (see the section on stress) together with a host of related neurotransmitters and the suppression of stress inhibitors themselves. This must be considered during any treatment. (Stress can also cause other immune-system problems, by possibly decreasing the effectiveness of the blood-brain barrier, thus allowing defective DNA or the fragments to affect the brain itself.)

Panic attacks have many physiological similarities to migraines. Blood drains from the stomach and the intestines, (in the process halting peristaltic movement,) to flood the muscles in preparation to fight or flee (in fear). As a consequence, the person has their digestive processes interrupted for a span of time that is dependent upon the duration of the attack. Adrenaline (epinephrine) floods the body to ready it for instant response. The blood pressure rises in order to increase circulation, leading to the possibility of heart attack or stroke. This results in a postponed exhaustion and often a protective loss of short-term memory, after the panic attack. It is protective in that it can lessen any delirious physiological effects.

(Hint: Be sure to develop normal sleep habits as prolonged sleep deprivation may lead to erratic behaviour, confusion, panic attacks, exteme anger, paranoia and, will eventually produce a nervous breakdown.)

This loss in short-term memory, can become habitual, and in this case, breeds' confusion and a feeling of contradiction. This may, in persons who have been able to mask the outward symptoms of anger or panic for years, to develop a feeling of chronic fatigue. The patient's mind can 'forget' the event although it remains buried in he subconscious! The patient may be left with an irrational fear of even talking about what caused the panic in the first place! This can lead to an alteration in the function of the hippocampus. This, in turn, postulated an increased need for vitamin B5, as well as a possible need for the use of vitamin B3 (niacin) to increase the circulation in both hemispheres. as this will increase the glucose level in the blood, tri-valent chromium may have to be added to increase the GTF.

Businessmen and professionals learn through experience, what is important and what is not. The major block to success in any profession is panic

The hypoglycemic exhaustion experienced after an extremely bad headache or a migraine or a panic attack, may result in a prolongation of the hypoglycemia. This may itself increase the duration of the headache, or panic attack until a person "sleeps it off"! In the case of panic attacks, recovery can be more rapid, unless the person learns to cope with the panic. This may require a change of lifestyle, profession or simply a major alteration in sleep patterns.

In some cases, doctors fail to recognize that the patient is literally 'stressed-out' for some reason, with an unstable HPA and cortico-steroid inhibition. Thus, the last thing they should receive is more corticosteroid! Because of their adverse effects to the immune system, corticosteroid are contra-indicated whenever hypoglycemia or lupus has developed!

Many doctors may remember the symptoms that they themselves experienced during the term of their residency. However they may have forgotten, they had to remain functional in spite of their hypoglycemic state. They were required to make immediate decisions in spite of how tired they felt. Many successful businessmen or professional performers are the same.

As parallel thinkers may exhibit excessive parallelism, they may be termed day-dreamers. Or they may exhibit traits such as some degree of manic-depressive behavior and may have never learned that it can be turned into an asset. Serial thinkers regard it as something to be 'cured'. In children the cure is frequently Ritalin. In adults, it may be Prozac. Indeed, if the patient cannot handle the depression by trying to stay awake, by drug or alcohol abuse, they will need treatment in a hospital.

However, when a lupus patient is in a state of panic or in a hypoglycemic condition for whatever cause, (such as the use of antimalarials, or as in the case of the anniversary of a traumatic event) they may be classified as having bipolarism, schizophrenia or some other mental illness. They may be told, "To consult with a psychiatrist before it is too late!" They are understandably, shocked, angry, or even bewildered! The implication is that the patient cased their own illness through some unwitting and/or easily avoidable excess. The patient may even, feeling the distressing effects of the hypoglycemia, have known the symptoms and may have been attempting to sleep more than usual, perhaps as much as ten hours a day. Others may have reduced their workload in a futile effort in attempting to relieve their stress.

Frequently, psychologists, who should, of all professions comprehend how suggestible a lupus patient, when any hypoglycemic state, can induce needless anxiety. The psychologists amass a standard battery of tests that they give to a patient, without understanding that in this day of hospital-based television shows, that their patient my recognize a test, to use an example, for Alzheimer's and be panicked because of it! Some doctors have only received a brief lecture about lupus in their training, and may discount the symptoms. For considering the number of organs that may be affected, it is not without cause that lupus is called "the great pretender".

Lifestyle and childhood factors on the development of lupus: Quite frequently the stress factors of childhood, play a prominent part in the onset of lupus. The parents may have made the child feel that it was unwanted or a burden. As a consequence, an intelligent child may have developed some form of escape mechanism, such a voracious appetite for reading, along with a lack of social skills. Because the treatment for lupus frequently involves the use of antimalarials which can heighten hypoglycemia, there is a n increased need to take "life one-day-at-a-time". This is a way of combating, depression, but is runs counter to running a business where an unusual amount of pre-planning may be necessary!

As an adult, there may, as a direct consequence, been a history of broken relationships for which the patient feels that the problem was the other person's fault. This may have led to a state of near chronic depression because they may have a heightened need to control other people (such bullying as their husbands). In this sense, they may be termed "control freaks".

At one time some of the north american tribes used to chew pumpkin seeds to feel better. The reason for this is the seeds are high in l-triprophan. This may be the reason for Thanksgiving's Turkey and pumpkin pie - both are high in l-triopophan.

Men and women think in different ways. Men tend to take the long-term view of life's problems, whereas women quite prefer to take life one-step-a-time". Obviously, these essential difference in outlooks, can lead to conflicts. As a result, men think of women as being almost hysterical at times, while women find that men don't want to "talk things out". As their viewpoints of life, are different, their needs are different as well! As a result, many doctors can't understand the emotional needs of their women patients, and because they think that their female patients "are crying wolf" far too often!

Where men's occupations require essentially parallel thinking, they quite often have problems caused by these professions! Acting, or comedy are typical! Some of the best comedians are men and men seem to have more problems. Often they are so insecure, they find personal relationships a major problem! The may exhibit addictive behavior patterns such as excessive drinking , or the use of drugs. All of these offer an escape from reality. In much the same way, such persons may become obsessive readers. This can be more befinecial as it can develop the ability to see the patterns in life or in a business. Their memory for names of voices can become phenomenal. These people can become excellent in acting, in teaching, or even in sales!

As most men can have less ability for parallel thought, their problems, when they occur, can be more unexpectedly disruptive to their wives! The results can be broken marriages! Because woman are less prone to "see the forest than see the trees", they are surprised by any real long-term crisis, and lash out in their vicinity! They find that their security is now threatened, forgetting that they may have been partially to blame!

Women and men react differently to shopping. Women find shopping exciting and pleasurable whereas men find it stressful. Recent studies in England seem to be confirmatory. Women seem (to men) unable to reach a decision about what to choose. As a result, they overbuy and have to return things. This also extends to packing for a trip.

Men seem to be able to reach a quick decision, abut to their wives, this seems to make them impulsive!

This may have led other people to eventually break-off emerging friendships, when the realized that the patient couldn't or wouldn't do anything to alleviate their depression. Such a simple change in lifestyle as obtaining enough sleep would have seemed irrational to the patient. The result is predicable, the patient would have formed causal friendships with over avid readers, who, because they themselves were depressed, could empathize with the patient. The diagnostician should look for items such a failed marriages, divorces, loss of custody of children from a failed marriage and similar indications. There may even a number of failed friendships where the patient or the patient's friends sought to capitalize on these bonds, such as by borrowing money, or clothes, without having any thought of returning it or them. Of course this applies to people who seek a victim rather than a true friend. But, as may be appreciated, a major problem can ensue.

The patient may reach the mental state (caused depression which is heightened by lack of sleep), were they are unable to distinguish between friend and foe, and even become paranoid!

Because they themselves can become workaholics, they may demand the same of others. Anyone who says no, by their definition, is an enemy. They feel that everything must be perfect or done perfectly, which makes them poor supervisors. In patient's the quest to become buddies, they allow liberties. When these result in lack of performance, they blame the subordinate. They are literally unable to realize that relationships are a matter of give-and-take. They are inclined to be overgenerous in attempt to impress. When the other party protests, they feel attacked.

This makes marriages a problem, because the depressed patient may attribute an ulterior motive for everything the marriage partner does because, in the patient's perspective, they themselves are not deserving. They may, as a child, made to feel guilty for even existing! They may carry their propensity for guilt into adulthood. Their partner may resist control which may lead to unusual degrees of friction in the marriage. As the patient may by this time have become so self-centered, they fail to realize that their partner has some serious health problem which is real, rather than psychosomatic. As a direct consequence, any real problem can be ignored (in the false perception of the patient) until it leads to a crisis! Even so, to bolster their own lack of self-esteem, they may attempt to avoid their own guilt by transferring the blame to the other person in the relationship! (See section on female-male thought differences).

(Hint: the less processing involved in the processing of food to make it last for a long period of time, the more additives have to be added. Some of these not omly increase shelf life but accumulate in the body for the reason that their stability has an unwanted side effect. In time any mild toxic effect can contribute to health problems. Conisider the effect of cheap synthetic perfumes, they never seem to break down and are so stabile that the side effects on other people can be horrendous.) (Remember the giant pumpkins - the level of l-triptophan - growth hormone was so high that it seem to act like a cancer!)

Once again we have to remember that the use of the antimalarials may have increased the problem by increasing hypoglycemia.

Thus the lupus patient may tend to see everything in black or white; everything is perfect, or everything is wrong! All this may also make it impossible for them to act as supervisors, because, in the long term, they may seek perfection rather than excellence.

Other indications:

The patient may be simply nervous, hypertensive, or seem to be in a mild state of shock. If nervous, the he/she may have developed some of the symptoms of chronic fatigue or chronic sleep deprivation. It has been proposed that chronic fatigue syndrome 2 may be suffering from a low CRF and a ether a hyperfunctioning or hyporfunctioning of the HPA axis.

Patients who have hereditary hypoglycemia may have, as an essential survival mechanism, developed a taste for high protein foods (such as fish or meat) because they were raised on such a diet. In addition, an unusual hunger for protein may develop because of the constant nervous tension, which, in itself can produce or indicate hypoglycemia. Their low level of Coenzyme Q10 and elevated MAO level, may together interfere with their body's utilization of lipids and protein, and the under-production of the normal levels of serotonin as well as many other essentials to a leading a normal life.

Their hypoglycemic state may ensue because the body may be under stress and be metabolizing an excessive amount of glucose/glycogen. Or as is quite possible, the body is unable to use the protein or lipids on the normal fashion! While symptoms such as chronic fatigue syndrome may develop, the cause of it may be misdiagnosed as the result of nervous exhaustion caused by protracted lack of sleep and/or occupational stress! The hypoglycemia and the resultant demand for insulin, may cause the eventual development of diabetes. Again, check if there is a history of diabetes in the patient's family. As this may have a common factor in the development of lupus, and heart attacks, or indeed, a family history of other neurological problems, a comprehensive work-up may be necessary!

Stress that results in hypoglycemia, can cause a reduction in the body's immune system response. It can result in the activation of several viruses of the herpes virus group including Epstein-Barr virus, the varella-zoster virus, HSV-1, HSV-2, and cytomegaloviruses. What should be of concern to doctors, is a possible link between herpes-zoster amid other neurological diseases such as ALS and MS!

The condition, if there is a high cholesterol level and/or high blood pressure can lead to heart attacks or strokes! Some lipids in the diet are essential such as vitamin E, combined with either borage oil or Efamol. In women, phyto-estrogens in the form of flax-seed oil, with an increase in elemental calcium, are necessary to avoid developing loss of bone-mass after menopause. Insomnia can be a problem and it may be the signal to increase calcium levels! Women and men may argue that as a person grows older, they usually need less sleep. But this results in an increase in hypoglycemia!

If the predisposing cause has been allowed to mature, the sense of personal-body-space may be so altered that because of the hypoglycemia, that a feeling of disassociation (from reality) may have developed.

Where there is post-nasal drip the possibility of a chronic sinus infection exists because of the reduced immune function. This could lead to a further complication from the use of corticosteroid to reduce the inflammation. Neither viruses or yeast infections may be cured by this treatment. The use of antibiotics is worse, as if it a yeast that is involved, the medication may only allow it to run rampant! The doctor may have to resort to a medication for a problem such as candids albicans (Nystatin or Mycostatin) or one of the many prorozas such as Guardia. However, treatment for a protozoa may not be effective as the yeast that caused the problem may still be there!

Persons with a yeast infection may develop a whole host of other allergies because their immune system is struggling to cope! As a result, they may develop a persistent cough, a chemical sensitivity, or even such things as rampant dandruff or thickened toenails! There has been a suggestion that the inclusion of antibiotiotics in animal feed, may actually cause the spread of yeast infections, both in the animal's feed itself, and in the persons eating their meat and drinking their milk!

The ataxia may be combined with reduced exercise from the feeling of fatigue (hypoglycemia), to cause a reduction in pulmonary function causing bronchial complications - the patient has been reduced to a more sedentary lifestyle. Respiratory infections could be complicated by the lowered pulmonary function. Indeed pneumonia and TB has been linked to familial or stress-induced hypoglycemia. Expect increased coughing to be required to clear the bronchi of mucus.

Other related symptoms may follow, including a papery dry texture to the skin caused the hypoglycemia that compounds the skin condition of lupus. Remember the comments on yeast infections.

The change to more sedentary lifestyle, when combined with the lowered glucose level and the resulting nervousness, combined with the mild depression to trigger an increased hunger that can cause an instability in weight! Consider the role of too much insulin!

If the patient seems listless and unusually tired and, the hypoglycemic state might be increased by chronic fatigue syndrome 2or vaso-depressor-syncope 3.

If tunnel vision is combined with vertigo, the patient may have a fear of heights. The hypoglycemia may have developer to the degree that the patient may report sudden attacks of vertigo or ataxia when he/she goes out into brilliant sunlight and has to glance down, especially onto a wet or shiny surface. This itself, can lead to panic.

Other indications may be if the patient finds it hard to relax in a brightly lit area. Does the patient seem unusually at ease in rooms or areas with dim lighting? These are subtle indicators and may be due to other factors altogether. With lower lighting levels there may be much less eyestrain. Both afford the patient some relief from the distressing side effects of the lupus. Again hyperglycemic depression is a possible cause but the other factor is that as the body's immune system is very marginal, exposure to sunlight or ultra-violet radiation can produce such a fierce attack on the body's immune system, that the results are self-evident to the patient. Otherwise, when persons are diagnosed with lupus, they are cautioned against exposing themselves to prolonged sunlight, as it causes a reoccurrence!

The effect of adaptation to new eyeglasses may be present to an unusual degree in lupus patients. Typing may result in a consistent pattern of errors being made because the patient may have dyslexia. Indeed, the patient may have been unable to learn to type.

With a hypoglycemic person tries to strengthen a weak eye, the result may be an increase in their hypoglycemia. This is caused by the increase in effective visual field requiring that the brain required more glucose to function. Whenever such a person tries to use variable focal length eyeglasses, they may experience severe nausea, disorientation, and panic. All are signs of a dramatic increase in hypoglycemia!

If the patient has had alternating occurrences of constipation and diarrhea caused by a more-or-less constantly upset stomach this could indicate hypoglycemic stress causing, through insufficient bile acids, flatulence, indigestion, and stomach pain which in itself can prevent a sound sleep. When a patient compounds this by staying awake at night, or is in the habit of watching excessive amounts of TV, or listening to excessive talk-show radio, without a compensatory amount of catnaps, or sleep periods during the day, their hypoglycemia and panic will get worse!

Insufficient bile acids are implicated in asthma, pancreatic distinctions (including cancer), and lung problems. It is a consequence of the depletion of pancreatic gluthiaone which can be normalized by selenium. AA14

As stated, the development of lupus requires a combination of factors, including a lowering of the body's immune threshold, the presence of certain types of genetic material that is almost fits the template of something for which the body has already developed an immunity.

Subjective Evaluation:

Ask if the patient has had any neck pain. A history of tension headaches could be an indication that the patient had grown accustomed to holding the head rigidly. This would minimize any nausea, eyestrain, or vertigo, brought on by head movement. If the patient seems to have an owl-eyed stare; this too could confirm that the patient is attempting to hold his/her eyes essentially immobile.

Question whether any neurological symptoms are typical of right brain or left brain dysfunction; or could they be some of both? They may even alternate!

Right brain dysfunction's include; left body weakness or paralysis; difficulty with dressing; spatial tasks; perceptual deficits including poor understanding of what's being seen; quick impulsive behavior in contrast to former deliberate manner; memory flaws including difficulty in remembering dates, appointments; math; many motor skills; frequent stumbling; inability to tell whether standing upright or leaning; problems in positioning - misses buttons; unsafe driving or crossing streets; poor judgment about their own capacities - ignoring defects and displaying overconfidence; comprehension of oral communications but not visual clues; needs constant feedback to relearn tasks.

Left brain dysfunction's include: right body weakness or paralysis; a slow cautious manner in contrast to their former confidence; disarithia - difficulty in clearly articulating words; swallowing problems; disorganized way of doing familiar actions; language, reading and writing difficulties.

Patients who are hypoglycemic may have problems in brain hemisphere mediation and become either left brain dominant or right brain dominant, accounting for the cyclic nature of manic-depression. This can be 'cured' by drugs, or can, in some people can be turned into an advantage though their recognition that each hemisphere has its own unique abilities. Such a patient may be, by self recognition, have learned meditative guidelines and taught her/himself to 'plan thoroughly in depression and act carefully in manic'. Through the constant application of the meditative guidelines to their own conduct, the may be able to avoid excess in either until, they become second nature!

Otherwise they may, under extreme stress, be diagnosed as having multiple personality disorder, rather than a form of schizophrenia caused by lack of sleep, that can result in faulty hemispherical mediation or bipolar disorder.

The numerous symptoms of both left brain and right brain dysfunction's, may, when combined with the progressive nature of lupus; will result in a possibility an erroneous diagnosis of some other form of nervous system degeneration. Because of the hypoglycemia a variation in the amount of corticosteroid may be presupposed. Cushing's syndrome, or Addison's disease might be suspected.

This may indicate dyslexia or bipolarism. It may be caused by a defect in the arrival time of neural stimuli from the retina which suggests a disfunction in the lateral geniculate neuculus. A possible complication is Meares-Irlan's Syndrome.DM.00This is treated by selecting a specific color for the patient's eyeglasses by trial and error. In this manner, the bandwidth of the neural signal is limited, allowing the stress level to be diminished and the vertigo to to be controlled.

This can be seen in patient's who have been treated with lithium. However it parallel's some of the symptoms of vitanin B6 overdose. This abberation extends to treatment with hypercaria perphorai (St. John's Wart). This is sometimes combined with Ginko Bilboa.

Vertigo may be present, other possibilities for misdiagnosis to guard against - might be Méirère's disease or even a protozoic infection such as guardiasis.

Thyroid, pancreatic, or adrenal problems may indeed be involved in the low blood sugar or the hypoglycemia may be a function of more than one of them. In the case of a presupposed thyroid dysfunction, the patient's diet must be checked. Frequently, salt was avoided as the parents "knew it was bad"! Unfortunately for some doctor's diagnosis, salt was iodized for protection against goiter, of thyroid dysfunction. A common sign is a craving for shellfish to increase the iodine in the body, which has been overlooked. Kelp supplements are needed to boost the level of iodine.

Objective Evaluation:

The diagnose of lupus can be confirmed by a blood test for abnormal T-cells levels. a high SED level as well as the usual SLE cells.

An MRI might also reveal an enlarged pituitary, adrenal glands or thyroid. This may have caused the predisposition to the lupus, may have been caused by the patient's history of chronic stress 4 or be familial.

In any case, the result is the hypothalamus's demand for hormones produced by the anterior and posterior pituitary such as ACTH (corticotrophin), somatropen - growth hormone (GH), thyroid stimulating hormone (THS), prolactin (PRL), leutinizing and follicle stimulating hormone (LH/FSH). LH/FSH are vital in reproduction. As hypothalamic somostasin and dopamine inhibit the release of GH and PRL which in turn causes a deficiency in immune response. In turn their deficiency further reduces the immune system's ability to handle further stress.

An increase in the production of CRF (corticotrophin releasing factor) results in a concomitant release of a host of other hormones, such as ACTH, PRL, and LH/FSH. CRF also is implicated in stress headaches, migraines, hypoglycemia, and an increase in the body's production of corticosteroid.

Eventually the body is no longer able to attain a state of homeostasis and beneficial hormone production (GH, THS, PRL, LH/FSH) becomes severely diminished or destabilized. The result, in Lupus, is loss or thinning of the hair, loss of muscle strength, a deterioration in the connective tissues particularly in the body's joints leading to severe arthritis, and the connective tissues in the other organs of the body as well, poor blood circulation, and a further reduction in the body's immune response.

If headaches or panic attacks are a factor, it is wise to remember that migraines and panic attacks frequently trigger the vagus nerve to produce the fight or flight reaction. The lupus patient may react accordingly as the fight or flight reaction acts both centrally and peripherally. There is an enhancement of the pathways that mediate arousal, improved alertness, attention span and aggression. There is also a similar reduction in the factors involving feeding, sexual behavior, growth, and reproduction. Hypoglycemia can cause the same frequently trigger the vagus nerve to produce the fight or flight reaction.

The fight or flight reaction was a survival trait. This may indicate why it is especially well developed among parallel thinkers. In its more advanced cases, persons may be manic-depressive when they are under real or imagined stress. Stress requires a release of Glutamide from the muscles of the body. The secret is in developing ways to handle stress so that things are not perceived as always being black or white! Remember part of the art of civilization is learning to see shade of gray. It has been suggested that parallel thinkers are the product of family conflict, where the child, facing inconsistencies between the parental response, grows-up in an unstable environment that forces the child to be constantly seeking patterns. Too much instability develops only cunning rather than developing character per se.

Survival under threats (real or imaginary), and involve an increase in the heart rate, blood pressure, and respiration. They lead to recurrent stress hyperventilation whenever a real or imaginary threat is perceived and this, in turn, can result in the prolongation of the panic attack to the point of fugue.

Short-term memory becomes dysfunctional leading to difficulties in remembering if some essential action was performed. The patient wants everything done immediately because the thing, subconsciously, that the other person will forget because, under the same circumstances, they will forget. Frequently, their problem is ascribed to another member of the patient's family, a friend or friends, or a coworker at the office (transference). If the perception of stress is prolonged, chronic high blood pressure, chronic fatigue, chronic smoking, chronic alcohol abuse, and chronic overeating can result. Because of ingrained habits, what were initially minor disorders, can lead to serious problems and increased hypoglycemia. See the section on stress.


Because of the complexity of Lupus, many factors are involved in its treatment. A possible treatment is through the aggressive use of antioxidants combined with a replacement of the minerals lost to the body through the hypoglycemic's increased production of urine, or frequency of urination, together with the necessary aggressive vitamin supplementation. The use of antioxidants will prevent the proliferation of damaged cells. Depending on the amount of time lupus was first diagnosed the recovery time may vary. It obviously be a function of the development time. Lupus patients probably have arthritis because of their body's overproduction of corticosteroids, why it is not prudent to use streoidal antiinflammatory in the treatment of joint pain.

Rather, by using the patient's own overproduction of steroids, as part the treatment, when combined with DNA-damage-controlling antioxidants, the affliction of lupus may be reversed! at the same time, certain vitamins, such as vitamin B6, may not only reverse the tunnel vision brought about by anti-inflammatory drugs such as Chloroquin, DI.00 but cause muscle mass to increase as well. As B6 increases the level of serotonin, it, when combined with an MAOB inhibitor such as items linked to niacinamide, SSRI's or even tyrosine, might relieve the depression. Because too much vitamin B6 may cause ataxia, or serious nerve problems, vitamin B5 should be taken as well. There is also the possibility that an imbalance in the dopamine, may lead to schitzoidal behavior and/or extreme bi-polarism. Lithium is sometimes used as a treatment in these cases, but in some patients, it can cause extreme depression or dyslexia that requires using a reduces spectral distribution of light, in order for the patient to function almost normally.

For obvious reasons, the consumption of alcohol should be discouraged. Because the patient's depression can lead to a dependence upon alcohol , this is a major point in the treatment!

As a first step, it is essential to break the patient's dysfunctional sleep pattern. This may require such things as ensuring that the patient is so tired, that the patient goes to sleep without the recourse to things such as reading of watching TV!

It may also be remotely possible that some other neuro-degenerative diseases may be placed on hold if not placed in remission by using the same treatment technique.

If the patient had a heart condition, extra precautions may be needed as appropriate.

If the patient's heart permits it, a program of exercise is beneficial to cause an improvement in blood circulation will assist the body to rid itself of metabolic products of the stress, the accumulated bronchial mucus caused by a possible sedentary state of the months preceding the discovery of the lupus, and it may provide a psychological focus for the recovery. A great need for understanding and emotional support is vital if the feeling of panic is going to decrease.

Although the normal diagnosis might give a SSRI medication such as Prozac may be needed, the increase in serotonin level itself may could be counter-priductive by increasing the l-tryptophan thus restarting lupus!! A vitamin B-complex is a start on both the efficient use of the available serotonin, as well as imitigating the body's use of serotonin.

A deficiency in Vitamin B6, will stop or hinder the existing vitamin B6 in its ability to produce GH as well a serotonin necessary for the normal body functions. Too much Vitamin B6 can result in a overdose which can lead to ataxia and other problems. (Vitamin B5 should always be taken whenever larger dosages of vitamin B6 are given.) It can also lead to a deficiency in neurotrophin3. This may be a possible linkage to sunlight's UV devastating effect on patients with lupus.

It is now supposed presumed l-tryptophan is linked to auto-immune disease such as lupus, as well as some neurodegenerative afflictions as well. In  the newborn there seems to be some chemical that protects the infant from being rejected by the mother's body (as well as the reverse)! That chemical may be present in the placenta as well as the umbilical cord! (See comment on folic acid and vitamin B-12) As the body's normal production of niacin is derived from l-tryptophan, bi-polarism could be present!  AA0.1

It will be needed as well as other vitamins. In addition, a lupus patient's depression mihht be relived by a diet high in Tyrosine 10. During recovery, the boost in the level of SSRI effect through the use of Vitamin B6 and B-complex may not be advisable over an extended period of time as a serotonin-like tolerance may develop. In the case of serotonin enhancers such as Prozac, it seems prudent not to rely on major serotonin enhancement because of the side-effects. L-tyrosine (at the 250 mg level) may prove more effective when it is combined with B-complex 100.

A steady pace is best until the patient demonstrates accelerated capabilities. Guard against a Vitamin B6 overdose. If the patient starts to have migranes,or shows evidence of peripheral neuoropathy, lower the level, or stop the vitamin B6 immediately!

Considering the state of central nervous system depression, many apparent psychological anomalies may appear. Usually an anti-depressant is prescribed to cure the problem. It is wise to avoid treating the symptom rather than the underlying cause. In some cases, depression can the result of the hypoglycemia rather than the cause of it! As depression could be the result of a bad sleep pattern, a possible treatment might have considered - increased exposure of the patient's eye to sunlight-balanced light. Because the patient may have photophobic hypoglycemia the wouldn't be wise. A prescription for oral melatonin 8may be needed, but this may not be effective if the bi-polarism problem has not been addressed! Even the use of vitamins to assist the body to produce more melatonin may be better. Niacinimide together with vitanin B6, should increase the production of melatonin.

In sleep avoidance, not only is the body's natural sleep pattern disturbed, it disturbs the usual cyclic pattern of steady melatonin level 5 increase until, about four AM when the body's surge in cortico-steroid production causes a drop in the melatonin level, and starts the cycle over! For this reason, panic attacks usually occur upon awakening! Therefore, the patient's lack or abberent melatonin, could lead to a cortico-steroid imbalance leasing to arthritis!

Don't ever think that just because a patient has marked hypoglycemia that the patient is always suicidal! Many medical students suffer from hypoglycemia induced by the requisite long hours and the stress of the job. Businessmen face the same long hours and stress. If they are unable to handle the hypoglycemia, they find other jobs!

Palliatives may be needed. There will be a need for extra sleep if chronic sleep deprivation is to be prevented from developing and even that will not be enough! Frequent rest periods or 'cat naps' are a possible solution. It may be necessary to ensure that the patient gets-up immediately on awakening to restore the normal sleep cycle. The 'healing' effect of the melatonin is essential to promote normal tissue renewal and growth although its production is shutoff by the pineal by the first daylight. The patient may have to resort to the use of dark glasses to avoid excessive eyestrain during the initial stages of recovery from the lupus, remembering that the use of the patient's eyes consumes glucose and produces hypoglycemia. After six months to a couple of years, the dark glasses may no longer seem necessary. This is especially true if Aralin (Chloroquin) DI.00 was used in the treatment! If it was used, and if the patient is elderly, extra care may be needed to avoid bone-breaking falls, when descending stairs. Check for possible side effects when cortico-steroid level is high, or when they are used as an anti-inflammitory.

If stress or the treatment thereof, has resulted in some degree of photophobia, have patient use dark glasses during the day. If the patient's apparent bipolarism, is treated with lithium, several unexpected consequences are possible, especially if the depression is because of dyslexia. The patient's dyslexia may return in a particularly severe form! Often treatment with colored glasses to make the vision monochromatic, is necessary, in order to allay the patient's (Menes-Irulen syndrome) vertigo! This may have been agrivated by the use of Chloroquin or similar drugs. Even treatment with lithium can cause this problem!

As hypoglycemic stress, panic, timidity or constant anxiety, was a factor in the development of lupus, be aware that once the patient is in remission there is an excellent chance of them reverting to the same behavior pattern that initiated the development of lupus in the first place. There will be a potential problem unless the pattern of perceiving things as either totally black or totally white has never been resolved!

As an avoidance of stress plays a major role in maintaining the lupus in remission, the patient and family may need counseling.

All should be informed of a technique that can relieve stress and panic, and to some extent, it is a co-factor in the development and recovery from lupus:

  1. Some problems can't be solved so why waste time in worrying about them
  2. Some problems are easy to solve. Do them and get it over with.
  3. The rest are may be tough, but after all, did you expect life to be easy all the time?
  4. Work smarter, not harder.
  5. Strive for excellence and not for perfection.
  6. Avoid gossips as they have to maintain their own lack of self-esteem by preying on other to try to diminish other peoples self esteem! Only in this way can they bolster their own ego!
  7. Take time to smell the flowers in life and don't become a workaholic.
  8. Don't stop performing acts of kindness' for others. The act is its own reward and doesn't require acknowledgment!
Insofar as the process of recovery is concerned, remember that the body's melatonin/cortico-steroid cycle will have to be stabilized.

A physician will have to confirm what vitamins that might be of assistance during the various stages of the recovery treatment. Vitamin therapy, in itself, is not a cure. It merely assists the body in creating a state of homeostasis with minimal adverse effects.

A note on cancer - A nine year study by the US National Cancer Institute which was conducted by nutritional researchers, and assessing 35,000 people, seemed to show that Vitamins A, C, E and selenium, reduced cancer of all types by 19%, heart disease by 40%, and cataracts by 43%.

Glutamide levels in the body lower with increasing age. Stress causes a serious reduction in Glutamide. The muscle tissue has to break down to release the Glutamide needed to increase the immune system's efficiency. For this reason a L-glutamine supplement (250) may be necessary in addition to the Vitamin B6 supplementation. (See cautionary reference to PABA - DAME).

If necessary, one (250 mg) of L-Glutamine should be taken at bedtime. If the patient is celiac and on a low gluten, gluten can cause migraines. See comment on MSG.

The vitamin and mineral supplements will have to be taken in the morning, (with the exception of second dose of vitamin B5, in the evening) immediately after eating breakfast.The vitamins necessary for the treatment of lupus include; 10,000 IU of Beta-carotene, 75 to 100 mg. of a B-complex, with the addition of at least 100 mg. of vitamin B-6 are needed.

An addition, may be to take a form of Lycopene BA1.1 as a cancer preventive. A possible alternative is cranberry-juice extract in the form of capsules.

Vitamin B6 will counter retinal/eye problems caused if Alavar (choroquin) or Plaquinil (both anti-malarials) was used in the treatment of lupus. An ophthalmologist can tell, by an examination, if the retinal pigments have been affected. Vitamin B6 and B5 will, in certain cases, reverse any eye damage causing tunnel vision or blind spots. The effect of the antimalarials is dosage dependent. In the case of Alavar 400 mg seems to be the threshold. With Plaquinil, it is about 250 mg. Corticosteroids may be contraindicated it there is any family history of seizures. Indeed, some anti-malarials can induce seizures!

The use of these two vitamins will improve both the peripheral vision and the acuteness of the eyes. Vitamin B6 has, as a tradeoff, a moderate increase in any ataxia. Later the separate dosage of B6 may be decreased to 100 mg. The B-complex may be reduced to 50 mg.

There is another co-factor. The use of vitamin B6 together with the vitamin B complex also increase strength promote muscle growth. The patient's co-ordination, while walking may take time to catch up. The vitamin B6 will aid the growth hormone (GH) and seems to increase connective tissue growth as well as improve the possibility of myelin growth in addition.

The increased requirement for protein for muscle development should be allowed for in the diet, and loss of sleep has to be prevented otherwise any hypoglycemia may increase!

A typical 100 mg B-complex contains the following:

Note: Vitamin B5 is used as a treatment for hypoglycemia. During treatment , the patient may feet a high. The normal production of corticosteroids may become unbalanced.. This is why it is vital for the patient to get enough sleep. Normally, as vitamin B5, makes people sleepy, it is vital to induce the patient to avoid a routine where they get less sleep than usual, or the cycle may start over!More calcium may be needed as well as vitamin-D, as the lack of bright sunlight for a lupus patient has to be taken into account. The added calcum will also assist in a normal sleeping pattern!

The mitigation of the residual serotonin by the additional amount of Vitamin B6 will be needed to manage the patient's depression and/or panic attacks. It is suggested that 250 mg of B6 (and 250 mg of B5) may be needed for eighteen to twenty-four months. Then,a reassement should be done to avoid the effects of B6 overdosages. See the comment about l-tyrosine.

As is the case with serotonin based anti-depressants, an constant overdoseage of Vitamin B6 when combined with sleep deprivation, and a lower level of QE-10, can cause hand tremor, slurred speech, blurred vision and even ataxia!

The PABA as well as zinc, may be essential to prevent the sunlight's UV from causing a problem. (Current studies do not appear to link vitamin A, E, beta-carotene, or selenium Ref 1\BA1.11 by themselves to the UV.) What is more probable, is the level of Lycopene might be already too low to withstand any prolonged exposure to sunlight! As is it now known, the level of UV is increasing rapidly due to the depletion of the ozone layer.

PABA may also darken the patient's hair.

Always be sure to take 100 mg. of Vitamin B5 (D-calcium Pantothenate). This vitamin seems to promote healthy hair growth as well as apparently serving to calm the patient and ensuring sleep. Vitamin B5 can apparently overcome the reduced level of leutinizing and follicle stimulating hormone (LH/FSH). Taken just before going to bed, this vitamin, together with hot chocolate is very effective in promoting a restful sleep and combating the adverse effects of stress. A second B5 can be taken at the same time. Vitamin B5 also increases the formation of axial dendrites in the brain. In this way it may counteract the possible reduction in nerve fibers in the spine. However, prilonged high dosages of vitamin B6, may increas the level of peripheral neurophathy, neurithophin 3 may be needed.

Vitamin B6 Problems

Prolonged high dosages of vitamin B6 may increases the level of peripheral neuropathy, Neurithophin 3 may be needed. If anything that resembles a swelling in the joints in knee, stop administering B6 immediately. CoQ 10 has to be stopped.

Even the level of B6 in multivitamin B complex can cause the same problem.

Circulation problems might ensue. Look for increased cortisol levels.

To increase the circulation, take Niacin with a flush relieving additive such as Intositol. The pills are scored and, initially half a Niacin after breakfast and the other half after dinner. Sometimes stress levels are so high that there is the possibilities of bi-polar behavior.(Sads). Because people with Lupus are very sensitive to small amounts of UV, supplementation of Vitamin D is essential.

Another possibility is the use of Ginko Max three times a day.

Caution the patient against excessive force on the knee joints such as running up and down the stairs.

Discontinue or reduce the amount of vitamin B6 when niacin is being used, if muscle cramps become a problem! B5 together with vitamin E should solve the problem! Possibly because of lack of sleep, when this is combined with Vitamins B3, B5, and B6, it might cause the body temperature to be lowered.Be sure to use warm bedding when it's cold. See the comment on L-tyrosine, which increases the tolerance to low temperatures. This may be the signal to lower the level of B6, and substitute L-Tyrosine as well as increase the B5!

It is thought that Vitamin B6 when used together with niacinimide cause the body to produce more melatonin however I could not locate any paper on the possibilty.

Taken immediately after breakfast with the other supplements, Folic acid, 0.4 to 1.0 mg, is needed to supplement the leutinizing and follicle stimulating hormone (LH/FSH). Folic acid will also reduce the possibility of stress-induced heart attacks. The folic acid should be used with Vitamin B12 as well as vitamin B6. Together they will reduce the homocystine level DL.00, and reduce the possibility of colon cancer, stabilize the body's production of thyroid stimulating hormone (THS) and prevent anemia. Remember that a supposed healthy diet was one that was low in salt, and therefore in iodine as well! Doctor's may have forgotten that before iodized salt was in general use, hypoglycemic women used to develop goiters on their neck. Therefore, an iodine additive may have to be given! An easily found source of iodine is in Kelp capsules. Quite often some lupus patients who were on a low-salt diet all their lives may have developed thyroid problems! The patient should be assessed for pernicious anemia beforehand otherwise the Folic acid will mask the symptoms.

If nausea and/or vertigo is part of the patient's problem suspect Lactose-intolerance, Celiacism or simply problems in the digestion of complex carbohydrates. Be sure to remember that childhood lactose intolerance may have been masked in a child that was raised on a farm as the un-pasturesized milk contained lacto-bacteria, which Pasteurization killed. Frequently the lack if an enzyme to digest pasteurized milk is so minor that the digestion of many cheeses pose no difficulties. Acidolphus based yogurt's will aid in digestion. A possible indication is yeast or fungus infections which may be extended to skin outbreaks from poison ivy or poison sumac.

A supplement based on a lactobacillus acidolphus may be of use as an addition to yogurt.

Vitamin A in the form of Beta-carotene (5,000 to 10,000 U.I.) a day, is believed to be the optimal dosage. The retinoids are thought to be of benefit in leukemia and other forms of cancer. As the oil level in the epidermis may increase as the patient's health improves, some form pimples or even sebaceous dermatitis may develop if the patient delays taking beta-carotene supplement.

If the patient has Thysellonic anemia (Thyselemia), it is not advised to use iron supplements as without the attendant L-triptophan necessary to metabolize the iron they may be useless. In patients with Thyselemia), anything that increses the iron in the serum, can cause other problems.

The patient should take between 0.500 mgm and 1,000 mgm of vitamin C (a known anti-oxidant), 400 to 800 units of vitamin E, (another known antioxidant that is effective in increasing activity in the sarcoplasmic reticulum - preventing build up lactic acid in the muscles. Poor circulation causes bruising, taken together with the niacinamide in the 100 mG of B-complex, circulation will be improved and this, together with the zinc, will alleviate the bruising. Zinc causes ruptured blood vessels to heal much more quickly.

Lack of proper blood circulation will also cause cramps. Although Vitamin E has been linked to causing minor iron deficiency, as iron is also implicated in heart disease, this may be a side benefit.

Vitamin C requires the presence of flavinoids from Vitamin B2 - as well as vitamin E otherwise it will be destroyed by oxidization. Vitamin E must have selenium in order for the body to metabolize it.

Add gamma-linolenic acid, such as found in a 25 mg. capsule of oil of evening primrose, (black current oil, or borage oil) which has been reported to prevent strokes.

Add 25 mg. zinc in the form of trivalent zinc (a zinc deficiency is a co-factor in arthritis and some forms of cancer). Zinc is a powerful antioxidant and a zinc deficiency may be a factor in diabetes. To be effective, it should be taken with a in vitamin B complex. It is thought that an inbalance in the mettalloenzimes may be a factor in both rheumatoid arthritus and osteo-arthritus. See the reference to the recent study at the University of Nebraska DG.O2

The susceptibility to diabetes may be offset by the once a day chromium picolinate (or vanadium picolinate - Vanadryl). Unfortunately, rheumatoid arthritis does not sem to benefit from this treatment.

The use of Aspartame (tm) may result in an increase in the SED rate and may also lead to a diagnosis of MS!

As women grow older, more calcium will be needed in order to prevent osteoporosis or osteopina. Supplimental calcium and vitamin D will be needed. The normal level of vitamin D may prove insufficient. A possible clue may be found in a marked preference to fish. Vitamin D supplimentation of 2,000 IU may be needed. (there is a suggection that a low level of vitamine D may lead to colal-rectical cancer). It  may also be necessesary to add linseed oil as a phyto-estrogen. (See the following paragraph.) Alother supliment that is useful is the Alpha fatty acids - Omega Protect as an example. As a lupus patient is advised to aviod the UV exposure of sunlite, they will have to take a vitanin D suppliment - 2,000 IU as an example. This seems to mitigate SAD's which can strike even in summer months. This may be part of the cyclic depression.

A zinc deficiency is common where foods are grown using artificial fertilizers which are deficient in zinc. Over many years, the zinc becomes depleted in the soil. Zinc also stops the pituitary from producing prolactin (PRL). Prolactin stops testosterone from being produced. Instead, dihydrotestosterone (DHT) is produced. In men, the effect of an increase in the level of the enzyme 5-alpha-reductase which, in turn, causes a increase in dihydrotestosterone; this is the principal factor in prostate enlargement and, presumably, prostrate cancer. However, prolactin may enhance the production of new stem cells and may enhance recovery from a stroke.

In women, prolactin (PRL) plays a different role. Testosterone is also important because it is essential to the sex drive in a woman. After pregnancy, the body produces more prolactin in order that the mother can produce milk. When a mother has been nursng her baby, when it is weaned, the mother's prolactin level should diminish. Indeed, the time for the production of PRL should de reduced several months after birth in order to increase libido.But when the mother doesn't nurse, her prolactin level remains elevated, and there is an increased possibility of the woman developing breast cancer.

If there is a zinc deficiency, and/or the level of l-tryptophan increases, the Lupus may flare-up after the birth of each child disrupts the bodies immune system.

If there is, because of heredity, already sufficient testosterone to make the libido strong anyway, the absence of zinc will not have any adverse effect, other than to increase the possibility of arthritis.

Panax ginseng 11 is thought to increase the production of testosterone.

Flowers of anise (licorice flavor) can be an effective salt replacement in whole or in part. The anise plant Glycerrhizae radix 12, besides lowering cholesterol, also may reduce tumors as well as candida. However, remember that licorice contains salt!

All should be taken after breakfast in order to make their release more gradual . If the reactions are too severe, breakup the separate vitamins into two doses, the second immediatly after lunch. A caution, Eat four or five smaller meals a day. If weight-gain is a problem, the patient may have to reduce the complex-carbohydrate components and use Efamol or Priminol or to reduce the severity of any headaches as well as increase the quantity of dietary protein.

Vitamin B3 (Niacin), in 500 mg doses will also improve circulation. It may have be taken with (PABA) Para-Aminobenzoic acid (100 mg) to mitigate the irritation of the "flush." It is also used, as noted, to treat vertigo when taken with 10 grains of lecithin. It may assist the left and right hemispheres of the brain to work in conjunction by preventing circulatory unbalance. Asmaller dosage (250 mg (time release) will benfit any possible bi-polarism caused by the low level of l-tryptophan.

It was once touted that when PABA is combined with DMAE 6 (di-methyl-amino-ethanol) and L-Glutamine it provides a useful stimulant to memory, and the more beneficial sleep patterns that can reduce hypoglycemia. Together they produce procaine, and, as is the case with lidocane, seem to prevent headaches or migraines as well as being a possible life extension factor.

See the cautionary note on PABA - DMAE (Denol).

Coenzyme factor Q-10 (50 mg) and L-taurine (100 mg) should be considered as a part of the daily supplementation. QE-10 is increased by exercise. Initially, the level of QE-10 is high and seems to be only moderately affected, by the amount of exercise, but as a person passes the age or 20, the level decreases steadily. Exercise seems boost the level of QE-10. If a person has led a sedentary existence because of an affliction such as Lupus, additional QE-10 must be used in order to build up the energy reserve. In this way, an effective level of exercise can be resumed. In a similar fashion, L-taurine is needed.

PABA also may substantially decrease the loss of immune system-function to the UV-component of sunlight, a factor in the development of lupus.

Chromium picolinate (200 uG to 400 uG - depending on body weight) (or vanadium picolinate) will assist in the conversion of glycogen to glucose, as well as increase the GTF (glucose tolerance factor), and this will reduce the patient's hunger. For the same reason, it will reduce the hypoglycemia and the headaches or migraines in addition. A normal GTF is essential in protection against diabetes, a common occurrence when people have lupus or prolonged or hypoglycemia.

In these cases a natural anti-inflammatory such as horseradish, ginger7 or spices such as those containing capsainin 8 may help every time a nausea and/or vertigo attack takes place. As an alternate treatments, for vertigo alone, pressure on the acupuncture P5 point (an inch below the wrist on the inside) may also help. As the bile-acid level may be normal only at breakfast-time, and indigestion may be minimized allowing increased levels of complex carbohydrates and fats.

As mentioned, especially when the patient gets tired, (after a period working or walking in brightly sunlit areas) the fatigue coupled with a reduction in immune response, may make the patient especially prone to ataxia. Where the patient's doctor advises, natural central nervous system remedies such as ginkgo bilboa extract9 (40 mg), taken at least twice a day may also be of assistance.

The patient must be kept warm, otherwise shivering may 'burn' glucose. If the patient is too warm, open a window or set the air-conditioner for a lower temperature. Patients with hypoglycemia are prone to suffer from respiratory problems and, in seeming contradiction, may be heavy smokers because of a craving for nicotinamide6.4a1, because of its effects on depression (via increasing the dopamine level and the not-apparent need for a MAO suppressant. As (nicotinic acid is vitamin B3), it would suggest that by using either niacinamide or niacin, the smoking addiction may be more readily be broken!

  1. The patient may be suffering from extreme fatigue (although denying it) and will get tired easily. More protein must be eaten for the muscle strength to return. During the winter, they may be extremely cold and suffering from hypothermia with or without realizing it!
  2. Part way through the initial recovery, the sense of being able to move about quickly without loosing balance may suddenly improve.
  3. The patient may sense, on a periodic basis, that the color saturation of the television has increased because of the reduction in hypoglycemia. When outdoors, colors may appear more vivid. The sense of disassociation may begin to fade about this time or continue in episodic recovery.
  4. Frontal headaches will develop during the recovery, and if the patient ever had severe headaches, they may increase unless a high protein diet is adhered to. The patient should always drink plenty of water.
Caution! If The patient's GTL is high and providing that chocolate is not a headache trigger, a glass of 1% B.F. chocolate milk will have a calming effect by providing a necessary increase in glucose, some very minor simulative effect from the caffeine, the calming effect of ß-endorphin, as well as a negligble increase in the L-tryptophan (that is also used to treat hypoglycemia.) Caution! As an umbalance in l-tryptophan may be a link to autoimmune diseases such a lupus.

Although, during the recovery, While the vitamins will provide a boost, they won't make the patient into a superwoman (or superman)!

Caution the patient to be sure to get plenty of sleep! Guard against a repetition of the same work habits or conditions that possibly resulted in the development of lupus in the first place. Bad sleep habits are notoriously difficult to break! A high protein-breakfast won't use up as much insulin as a high carbohydrate meal. Even though a diet containing complex carbohydrates may increas energy levels a moderate amount is better. hey are needed to prevent depression, panic, or excessive anxiety, and to avoid being dysfunctional! Thereafter an moderate increase in the serotonin-rich complex carbohydrates may be needed; as l-tryptophan is not properly convereted to serotonin, even though there may be a craving for these foods, digestion may not function properly and gas pains can be a consequence. It may be better to make the foods containing complex carbohydrates part of breakfast rather than at supper time.

Note that there may be a link to cancer though over use of SSRI's.

Check for the consequences of sleep deprivation.Consider that they may be caused by excess in vitamin B6 as well as a major lack in calcium!

The side effects include a loss in the ability to concentrate, a need to repeat everything at least two or three times, a spaced-out quality or manner, constant annoyance or anger, the false perception that other people are angry with them, moodiness, depression and threats of suicide as a means of button-pushing other people into a desired action, a growing of lack of self esteem whenever the patient is rebuffed which, through transference, is thought the other person's real problem

A repetition of the insistence that the patient can't sleep, is a cause for immediate counciling, otherwise the hypoglycemia may erupt! Generally insomnia, might be be caused by a chronically low level of calcium in the body. Indicatations are a ostiopina, and even fractures.A simple way to promote sleep, is to take two Tums and 100 mg of vitamin D ten mintes before bedtime.

If the patient is under prolonged stress, and resorts to other anti-inflammitories, or even other antidepressants, fibrocitus-like pain may develop unless hot baths or hydromassage is used. The apparent fibrocitus/fibromyalgia, may be a sign of anti-inflammitory or antidepressant and/or B6 and/or more especially (niacin) B3 over-dosage with too low a level of folic acid and B12 to counteract the possibility of hyperhomocysteinemia.

Conversely, it may be the consequence of the use of corticosteroid or the body's own overproduction of insulin and corticosteroid through a defective sleep cycle, that have caused minor damage to the shoulder or hip joint!

During treatment, it is not unusual to expect that any trauma to the patient's body, such as a fracture or even a sprain, will cause an increased reaction in the patient's immune system such as to surprise many doctors. Expect therefore:

  1. That the patient will need more sleep than usual, at the same time that sleep is hardest to attain This difficulty in getting to sleep may be a sign that the patient may be overdosing on vitamin B6 without taking supplimental calcium .
  2. That depression may set-in, caused by the patient's own over-production of cortico steroids. Sleep and a realization by the patient that sleep is neccessary for a full recovery may be a diffiult point to make!
  3. Extra councilling may be necessary to help the patient from suffering a relapse.
  4. Anti-inflammitories may be necessary to avoid memory dysfunction
To paraphrase an old adage, "You can lead a horse to water but you can't make him think!"

Before any blood tests are taken, be sure that the patient is carrying some hard candy to use if the patient feels faint!

If the patient has ever had chickenpox, overwork could bring on shingles! This should be interpreted as a 'warning shot across the bow'!

Problems during recovery: The prolonged or excessive use of vitamin B6 (as may be the case with anything involving Serotonin) as a substitute for sleep, can increase depression and bring-on ataxia. It may make any subsequent lupus recurrences, almost impossible to treat! Try taking two Tums as well as Vitamin D to promote sleep.

Be sure that if the patient is taking niacin or at least niacinimide, to lower LDL chloresterol, that there is sufficient folic acid and 12 in the diet. Otherwise injections of B12 may be needed!


NOTE: Because of the synergistic interaction between many vitamins, minerals and amino acids, a generalised classification as to their level of importance, is sometimes difficult. I have attempted to do the best in the available time, and I apologize for any omissions or errors. Any person who attempts to follow these suggestions, is advised to consult with a doctor. There are, I think, sufficient references given, to reassure a medical practitioner. The list is based on a body weight of 70-100 kilos.

Where the references are incomplete, I have chosen to include them contrary to the usual practice, as they may suggest possible leads.


As a search in Medline will reveal, there are over 2500 published papers (in English) alone during the last several years! AAA-00

AA0.0 - Depression (refer to the Hamilton rating)

AA1Coenzyme Q10 - Partial summary: CoQ10 is a critical component of the electron transport pathway in the energy-producing mitochondria. Without it, highly reactive electrons can cause damage to the lipids, proteins, and DNA contained in the mitochondria.

CoQ10 is found in diets which are high in protein whether fish or animal. Co10 can be synthesized by the body. if follows the same path as chloresterol. It is advised that people taking chosterol-lowering drugs (such as Provostatin or Lovostatin), should consider taking CoQ10 to conteract the reduction by the body's lowered capacity to produce CoQ10.

        A counterindication for the use of CoQ10, may be an inflamation of the back of the knee!

AA2 Vitamin A (Retinol)/ Beta Carotine - Partial summary: ...studies regarding the role of Vitamin A/Beta carotene is essential as is vitamins C and E in cancer-cell biology and metabolism are of critical importance in their use in cancer treatment. These vitamins exert cytotoxic ant cytostatic effects, and may reverse the cancer cel to the normal phenotype. Interrelation of vitamins A, E, and C, with oncogenes and growth factors play an importent role in cancer-cell biology. The data presented in this review can provide new insights into the understanding of anticarcogenenic mechanisms, and a rationale for the use of vitamins A, C, and E in cancer chemo-prevention and treetment...

Abstract from Int Journ Vitamin Nutr Research; 1994.

Abstract from Amer Journ Clin Nutr; 1991The increase in cells with markers of NK cells and in the expression of IL-2 recepters was dose dependant. The plasma concentration of beta-carotene was also elevated significantly; however, there was no increase in the amount of retinol present in the plasma. this indicated that the amount of immunomodulation induced by beta- carotene may be due to the caratinoid rather than the increased amount, and hence actions, of Vitamin A. The results support the role of immunostimulation as a potential mechanism of action of beta-carotene with cancer-prevention potential....

...retenoic acid, which is derived from Vitamin A and beta-carotene, could interact with the genes which are involved in the primary liver carcogenes. In PLC patients, as is the case with patients suffering from sickle-cell anaemia, malaria, kwoshwork, or marasimus, and AIDS, the plasma levels of vitamin A, E, and beta-carotene are decreased....vitamin A and E therapy, would enance the natural defenced against the deletorious effects of the oxidative stress induced by these afflictions.

Abstract from Bull Acad Natut Med; 1992

Under selected conditions, vitamin A and the carotinoids, can both accept and donate electrons. and carotinoids can quench singlet oxugen. Thus both sets of compounds than theoretically participate in a bological antioxident network.

Abstract from Journ Nutr Sci Vitaminol

Vitamin A is a fat-soluable antioxidant stored primarially in the liver, but also in the kidneys, lungs, gonads, and andrenals, from where it is released when needed. Zinc is required for the liver to move the Vitamin A out of storage. Vitamin A, and beta- carotene are involved with cell growth, vision, protection against free-radicals damage to the lung and mucous membranes, te production of healthy sperm, and with iodine, the maintenence of a properly functioning thyroid gland. Vitamin A, and beta-carotene are powerful stimualant to the body's immune system, and in lupus it should be evident that kidney, liver, and thyroid disfunctions are frequently present.

AA3 Vitamin B1 - Partial summary: Vitamin B1 (Thiamine) is an essential factor in a minor mitigation in Alzheimer's disease (AD). This could be a consiquence of a reduced level of Adenosine Triphosphate (ATP) in the brain. ADP is needed to synthesize the thiamine precoursors.

Both thiamine and taurine may be essential towards the brain's function, as the inclusion of taurine increased the rato at which thiamine was available for use in the form of thiamine diphosphate and thiamine triphosphate.

Other double-blind studies seemed to indicate that the addition of elevated vitamin levels were consistent with a reduction of mood-disorders.

AA4Vitamin B2 (Riboflavin) - Partial Summary: Vitamin B2 Studies in deficiencies in Vitamin B2 (riboflavin), Vitamin B1 (Thiamine) and B6 suggest that lowered body weight might be an indication of riboflavin deficiency, either from the bodies inability to use it, or a dietary deficency.

AA5Vitamin B3 (niacin) - Partial summary: Vitamin B3 (niacin) is most often used to reduce the LDL cholesterol level in the blood while maintaining the beneficial HDL levels. Sd it results in an increase in blood sugars, it may have to be taken with tri-valent chroium to increase the GTF. Its use has been suggested as a meanr of increasing the blood-flow to the brain as a counter to bi-polarism. Often the so called "flush" may be decreased by drinking a glass of milk.

When it is present, along with thamin and riboflavin, its primary role is involved with the cells production of energy. A sign of niacin deficiency, can be diarrea, skin disorders, confusion, weakness and dizzyness, loss of appitite, and irratitability.

The healthy body can convert triptophan in the system into niacin. Until the FDA place l-troptophan on the restricted list, it was frequently used to combat nervousness.

Nicin is most easily found in foods high in protein, especally seafood and enriched cereals and breads.Consider yeast intolerance or Celiac disease!

As an excess of niacin can cause other serious problems, such as hyperhomocystinemia such as ataxia, it chouls be taken with folic acid , vitamin B6, and vitamin B12!

AA6 Vitamin B5 - Partial summary: Vitamin B5 (calcium pantothenate) has several functions in the body, including acting as a powerfull anti-oxident and anti-stress vitamin. Rats that had to swim in cold water, and receiving high doses of vitanin B5, were able to double their functional periods.

The increased stamina produced by Vitamin B5, results from its role as part of a key enzyme, acetyl CoA, in the energy producing Krebs or citric acid cycle. Vitamin B5 also required for the systhesis of lipids, and thus plays a part in the formation of steroid hormones. When persons are under stress, they make the so-called Hypothalmus-Pituitary-Andrenal (HPA) hormones than otherwise.

Vitamin B5 is essential for the conversion of chloine into acetylchloine. the most obvious sign of the stress inherent in lupus, is the thinning or breaking of the hair.


AA7 Vitamin B6 - Partial summary: Current studies suggest that Vitamin B6 (Pyridoxine) affects the immune system response in both the hormones, brain functions, and cell-mediated immune-system response. Both lymphocyte differentation and maturation are altered by its deficency, delayed type hypersensivity and antibody production may be indirectly impaired. Some further studies indicate that the Vitamin B6 status may affect tumor growth and disease processes.

Deficency of vitamin B6 has been associated with immunological changes in the elderly, persons afflicted with HIV, and those with uremia or rheumathroid arthritis.

It has been found that a vitamin B6 deficency impaires interluekin-2 production and lymphocyte proliferation.

It has been further suggested that smooth muscle cells (SMC) and altered structural proteins are interpreted as foreign, where they are degraded by the compliment system and by macrophages. The long-lived proteins in the ground substances are glucosiated by Amadori reactions that lead to virtually stable compounds and polymerization. This process is enhanced by high/unstble blood sugar levels found in persons with a low glucose tolerence level (GTL). Such may persons may hane a high insulin level and have a family hystory of diabetes.

The principal function of Vitamin B6 (Pyridoxine) is amino acid metabolism, and the greater part of the body's B6 is carried in the muscles (leading to the conclusion that persons where he muscle mass is deficient, may have no B6 reserves), that are associated with gycogen phosphorylase ant the vitamin has a signeficant part in the actions of steroids.

Vitamin B6 (Pyridoxine) significantly reduces the total plasma lipids and choresterol levels, where it enhances the HDL levels. Serum zinc was also significently increased by Vitamin B6 (Pyridoxine). Nevertheless, where rheumathroid arthritis is already present, as in lupus, additional zinc supplementation may be needed.

There is a critical role for Vitamin B6 (Pyridoxine) in neurogenesis and neural longivity in the neocortex. Postnatal cellular events in the neocortex, that is, neuron differentation, and synaptogenesis were altered by Vitamin B6 (Pyridoxine) deficits; higher order dendrites were reduced on stellae neurons in Layers II and pyrimidal neurons in Layer V.

"...In general, T-cell-dependent responses decline with age. (In lupus, they are vital! )In the elderly are at great for low consumption of proteins, and several micronutrients such as zinc. or Vitamins C, E, and B6, which play a vital role in the normal autoimmune function. As a consequence, the incidence of inflammitory and infectous, auto-immune disorders, cutacious pathological changes, and skin-cancers increases. Morbidity and mortality rates due to tetinus, pulmonary infection, and infuenza remain high in elderly populations. Depressing the rate of immunosenesence and restoring the normal immunocompetence in the elderly, may require improved nutrition, ..."

Fattal-German, M.; "The immunoincompetence of the elderly. "; Ann Pharm Fr; 1992; 50(1): 13-24.

Caution! Overdoses of Vitamin B6 can cause Propriorecptor problems, photosensivity as well as spinal neuruon problems.

AA7.6.0Helgren ME; Cliffer KD; Torrento K; Cavnor C; Curtis R; DiStefano PS; Wiegand SJ; Lindsay RM ; ; "Title             Neurotrophin-3 administration attenuates deficits of pyridoxine-induced large-fiber sensory neuropathy. ; J Neurosci, 1997 Jan 1, 17:1, 372-82
Chronic treatment of adult rats for 2-3 weeks with high doses of pyridoxine (vitamin B6) produced a profound proprioceptive loss, similar to that found in humans overdosed with this vitamin or treated with the chemotherapeutic agent cisplatin. Pyridoxine toxicity was manifest as deficits in simple and precise locomotion and sensory nerve function and as degeneration of large-diameter/large-fiber spinal sensory neurons. As assessed quantitatively in a beam-walking task and by EMG recording of H waves evoked by peripheral nerve stimulation, coadministration of the neurotrophic factor neurotrophin-3 (NT-3; 5-20 mg . kg-1 . d-1, s.c.) during chronic pyridoxine treatment largely attenuated the behavioral and electrophysiological sequelae associated with pyridoxine toxicity. Furthermore, NT-3 administration prevented degeneration of sensory fibers in the dorsal column of the spinal cord. These data are consistent with the evidence that NT-3 is a target-derived neurotrophic factor for muscle sensory afferents and suggest that pharmacological doses of NT-3 may be beneficial in the treatment of large-fiber sensory neuropathies.
  • AA7.1Shibata, K.,Mushiage, M., Kondo, T., Hayakawa, T., Tusuge, H.; "Effects of vitamin B6 deficency on the conversion ratio of trytophan to niacin." ; Bioscy Biotech Biochem; 1995; Nov ; 59:11; 2060-3.

  • As too much l-tryptophan may be an element in the development of lupus, possibly there may a disfunction in this process - therefore a lower niacin level may be part of the development.
  • AA7.2Parkhomets, P. K., Kuchmeroskaia, T. M., Donchenko, G. V., Chichkkovskaia, G. V., Klimenko, A. P.; '[ Role of nicotinic acid and its derivetives in the disorders of the central nervous system.]"; Ukr Biochim; 1995; Jul Aug; 167:4; 3-11.
  • AA7.3Oka, T., Komori, N., Kuwahata, M., Hiroi, Y., Shimoda, T., Oakada, M., Nantori, Y.;"Pyrodoxal 5'-phosphate modulates expression of cytosolic aspartate aminotransferase gene by inactivation of glucocorticod receptor."; J Nutr Sci Vitaminol (Tokyo); 1995; 41:3; Jun; 363-75.
  • AA7.4 Calabrese, V., Ragusa, N., Rizza, V.;"Effect of pyrrodoline carboxylate (PCA) and pyridoxine on liver metabolism during chronic ethanol intake in rats." ; Int J tissue React; 1995; 17:1; 15-20.
  • AA7.5Alvarez, F. G., Guntupalli, K. K.; "Iosonazid overdose: four case reports and review of the literature."; Intensive Care Med; 1995; 21:8; Aug; 641-4.
  • AA7.6 Sone, Y; -"Age associated problems in nutrition."; Appli Human Sci; 1995; 14:15; Sept; 201-10.
  • AA7.7Shibata, K., Musiage, M., Kondo, T., Hiakayaya, T., Tsuage, H.;"Effects of vitamin B6 deficency on the conversion rate of tryptophan to niacin."; Biosci Biotechnol Biochem; 1995; 59:11; Nov; 2060-3.
  • AA7.8Heiskanen, K.,Siimes, M. A., Salmenpra, L., Perheemtupa, J;"Low vitamin B6 status associated with slow growth-rate in healthy breast-fed infants."; Pediatr Res; 1995; 38:5; Nov; 740-6.
  • AA7.9Ellis, J. M., McCully, J. S.;"Prevention of myocardal infartion by B6."; Res Commun Mol Pathol; 89:2; 1995; Aug; 208-20.
  • AA7.10Pfeifer, S. I., Norton, J., Nelson, L., Scott, S.;"Efficiency of vitamin B6 and magnesium in the treatment of autism: a methodology review and summary of outcomes."; J Autism Dev Discord; 25:5; 1995; Oct; 481-93.
  • AA7.11Kodentsova, V. M., Uspenskiaia, I. D., Vrzhesinskaia, O. A., Kharonchik, L. A., Skol'nikov, A.A., Iakushina, L. M., Markova, I, B., Spirachev, V. B.; "[Features of B-group vitamin metabolism and criteria for children suffering from celiac disease.]"; Vopor Med Khim; 41:4; 1995; Jul-Aug; 41-5.
  • AA7.12 Kharonchik, L. A.,Kodentsova, V. M., Vrzhesinskaia, O. A.,Risnik, V. V.,Spirachev, V. B."[Redifined criteria for suplying the human body with vitamin B6.]"; Vopor Med Khim; 41:3; 1995; May-Jun; 46-50.
  • AA7.13 Curhan, G. C., Wilett, W. C., Rimm, E, B., Stampfer, M, J.; "A prospective study of the effect of vitamins E and B6, and the risk of kidney stones in men."; J Urol; 155:6; 1996; Jun; 1847-51.
  • AA7.13McAlidon, T.E., Jaques, P., Zhang, Hannan, M. T., Aliabardi, P.,Weissman, B., Rush, D., Levy, D., Felson, D. T.; "Do antioxidant micronutrients protect against the development and progression of knee osteoarithis?"; Arthritis Rheum; 29:14; 1996; Apr; 648-56.
  • AA8Vitamin B12/Folic Acid - Partial summary: They must be taken together to combat pernicious anemia, but if folic acid is taken by itself, it may mask the obvious visible effects of pernicious anemia. They are taken together by women as a prelude to childbirth to prevent nural tube defects in babies.

    But they are a necessary as part of the treatment for hypoglycemia.

    AA8Partial summary:

    AA9Vitamin C - Partial summary: Vitamin C is an essential, along with vitamin E, to prevent cataracts which may be brought on by hypoglycimia, eapecially in treatment involving quinine related antinflammitories.

    AA10Vitamin D

    It is very important in a woman recovering from lupus, as they may have been avoiding sunlight, and may be lacking in vitamin D. This why there is an increased risk of develoing osteoporosis; especially where there has been a thyroid problem!

    AA10 Vitamin D - Partial summary: Vitamin D supports thyroid function and enabled the body to use calcium more efficiently.

    AA11Vitamin E - Partial summary: Vitamin E (Di-alpha tocopherol) was thought only as a aid to the dissipation of puruvates in the sarcoplamisic reticulum. Now in combination with vitamin C and selenum, it has a syngeristic effect.

    AA12Vitamin K - Partial summary: Vitamin K is an important factor in blood clotting. Vitamins and drugs that have as a major side effect, the reduction of clotting, when combined with high blood-pressure, can cause arachnoid strokes.

    AA12 .1 --Dahlback B., Hillary, A., R; Rosen, S., Zoller, B.;"Resistance to activated protein C, the EV-Q506, allele, and venous thrombosis."; Ann Hemat; 1996; 72:4; Apr; 166-76.

    AA13 Folic Acid - see vitamin A


    AA14Arginine - Partial summary: L-arganine is a single amino acid resulting from the hydrolisis (digestion) of proteins.It causes the body to build muscle bulk and to burn fat. Argenine pyroglutimate it causes the pituitary to release the natural growth hormone somatropen (GH). Argenine pyroglutimate, in addition to increasing cognition, it is a excellent GH releaser, because argenine pyroglutimate is carried across the blood-brain barrier much better than argenine itself.

    Argenine pyroglutimate is, in Italy, used to treat senility, mental retardation, and alcoholism. It is thought that argenine pyroglutimate, is the key factor rather than l-arganine itself.

    In migraines, l-arginine is useful in the hypoglycemic loss of vision and the scintillation that accompanies this phenominon.

    Caution: The form of vasopressin that is naturally present in the human body, arganine vasopressin, (AVP). It is effective in stimulating learning and memory, but it can produce potentially dangerous side effects, such as heart abnormalties and an age-related reduction of energy!

    AA15Carnitine - Partial summary: Acetyl-l-carnitine is an aparent inhibitor to neural aging. Admistered to young rats, it seems to enhance the Neural Growth Factor (NGF). As Acetyl-l-carnitine and l-carnitine act as transport mechanims for long chain fatty acids between the cystol and mitochondria to undergo beta-oxidization, they play an essental part in the production of energy and the clearing of toxic fatty acids in the mitochondria. Acetyl-l-carnitine may be essential in reduction of senile dementia in Alzheimer type as they may be a precurser for acetylcholine.

    AA16Selenium - Partial summary: Pancreatic Glutianone, (lack of bile acids), and selenium are important.

    Selenium depletion has been implicated in hepatic disorders, hypoglycemia including pancreatic problems, increased insulin production, and diabetes as well as lung problems including asthma, tubercluosis, and lung cancer. Depletion of the red-cell glutionone peroxidase follows. In some cases, it may simply cause a predisiposition to these problems. Oxidative stress which is conteracted by vitamin C and vitamin E, reduces these risks by increasing glutianone while and high body iron stores, and lead exposure, increases the risk

    Oxidativly-altered linolic acid in blood serum, a reduction in vitamin C, and vitamin E, selenium, and a reduced level of beta-corotene are factors.

    Trace elements (TE), are especially important in cases of trauma.

    Selenium supplimentation may increase the size of the heart and skeletal muscles in selenium-depleted patients.

    Selenium supplementation also seems to improve T-cell response.

    AA17Zinc - Partial summary: Zinc is an effective antioxident. Zinc-mettaloenzymes appeat to play a major role in many aspects of cellular metabolism, including DNA replication, repair, and transcription. Depending on which zinc enzymes are "overvaluable", zinc deficiency may result in an accumulation of useless or toxic materials, malproduction of essential proteins, a neoplastic change or cell death, which could be an explation in the variability in the cellular aging pattern.

    Lower levels of lineolic acid, arachidonic and total (n-6) fatty acids, in the liver phospolipids, (especially in the phosphtidychloine), are caused by a zinc deficiecy. On the other hand, (n-3) fatty acids are higher when compared with a zinc adequate controls.

    In general, dietary defiency in zinc, appears to be responsible, at least in part, for the immunodefiency that is so regularly assciated several types of human cancers, such as epideroid cancers in the neck and neck regeon (in lupus, the face and neck are most exposed to UV ratiation)

    In aging, there is a reduction in immunodefiency that may co-orelate with the reduction in serum zinc concentration in both men and women. This may be due to a reduction in the relationsip between plasma and epidural zinc, possibly caused by a a reducion in enzyme-related activities. In part, this might account for the alteration in keratinocytes with aging. (In lupus, there may be literally a premature aging, while the rest of the patient's body is still young!)

    Zinc concentrations in the heart and lungs apprear to decrease significently with age.

    During basal state, zinc release from red-blood cells, decreased with age. During studies connected with "zinc loading", response as compared to the basal-state, in plasma zinc concentrations, zinc excretions in urine, and zinc in the liver increased with age, while fractions of the zinc taken-up by red blood cells, decreased with age.

    There is some speculation that a zinc deficiency might play a role in the development of anorexia nervosa.

    "....zinc is an essential element for growth, development, and functioning od all living cells...Zinc essentiality and the lack of a reliable index of intracellular zinc, formed the rationale for the zinc hypothesis. This hypothesis, suggests a gradual, time related zinc definiecy occuring in each living cell, making zinc less available for its mettaloenzymes. the sum of all delaterious effects resulted from the distorted function of different zinc enzymes, is later manifested as the aging process. ...zinc concentration in various different tissues decreases. Cadmium may inhibit zinc activities at many stages, interfering with zinc absorbtion, distribution to different tissues, and to transport to cells or into several intercellular structures. Therefore, it is reasonable to assume that a slowly developing cadmium may result in a time-related zinc deficiency.

    Comment: Zinc is thought to assist the production of interleuken.

    Bin, Q. C., Garfinkle, C.; "The cadmium toxicity hypothesis in aging: a possible explanation of the zinc deficiency hypothesis in aging."; Med Hypothhesis; 1994; Jun; 42(): 380-4. the most efficient chelating agent is aluminum (alum), it seems reasonable to assume this might be related to Alzheimers. This might also why chelation therapy is held in such disrepute. There may have not been sufficient time or doses of the essential minerals during or after the treatment to replace those essential for normal body function.

    ".....Zinc is an needed for growth and development, DNA synthesis, neurosensory functions, and cell-mediated immunity. " in aging people "Their mean dietary zinc intake was 9.06 mg./day, whereas the recommended dietary allowance is 15 mg./day. Zinc supplimentation corrected zinc defiency and normalized plasma copper levels. Serum thymulin activity, IL-1 production, and lymphocyte ecto-5' nocleotidase increased significantly after supplimentation. Improvement in response to skin-test antigens, and taste acuity was observed after zinc supplimentation. A mild zinc defieiency appears to be a signifcant problem in free-living elderly people...."

    Prasad, A. S., Fitzgerald, J. T., Hess, J. W., Kaplan, J., Pelen, F., Dardenne, M.; "Zinc deficiency in elderly patients."; Nutrition; 1993; May-Jun; 9(3): 218-34.

    AA18gamma linolenic acid - Partial summary: Gamma-linolenic acid, such as found in a 25 mg. capsule of oil of evening primrose, (black current oil, or borage oil) which has been reported to prevent strokes.

    AA20 Chromium or Vanadium picolinate (Tri-valent chromium or vanadium)

    1.0Migraines - Historical & Brief Current Viewpoints

    1.1-- Ashdown, A. M.; "A Complete system of nursing." ; Temple Press, Letchworth, England; 1939: 384.

    1.2 ------ : "The Migraine Handbook";


    2.0Chronic fatigue syndrome


    4.0 Chronic stress

    5.0Meletonin - SAD The effects of the syndrome are now so well known that I have not included them in this summary.


    6.0PABA & DMAE


    6.4cParkinson's disease and nicotinamide as for MAOB inhibition

    6.4c2 Nicotinamide and potential infections in diabetes

    6.4d Niacinamide

    7.0Ginger - Partial summary: In Europe ginger is widely prescribed for inner-ear problems, for nausea, for use as an anti-inflammatory and it is reputed to lower cholesterol and decrease the risk of cancer.

    8.0Capsainin: Partial summary: Derivitives of capsanin have been used to treat shingles as anti-viral agents.

    9.0Ginko Bilboa - Partial summary: If you look back through the wealth of written materials on ginkgo in the popular press, you will notice that many articles end by saying "In the future, everyone will use ginkgo," or "We will see that ginkgo will be as popular asprin". Authors express these sentiments because they believe that ginkgo offers legitimate benefits to users; benefits that were discovered not only through personal experience, but that have been validated in controlled studies and research.

    Is ginkgo becoming the herb of choice? Well, not quite yet in the United States or Canada, although the use of ginkgo, and other herbs, is increasing. A special market report in the spring 1996 issue of Herbal Gram magazine states that in a selection of U.S. health food stores, ginkgo was the fifth-best seller, after echinacea, garlic, goldenseal, and ginseng (1994 figures).

    Europe, however, is another matter. There, ginkgo is the most prescribed (yes, prescribed) herb, with retail sales in Germany coming in at 280 million dollars (1993 figures). Indeed, ginkgo is among the herbal products deemed "safe and effective" by a German federal health commission, and it has been used in Germany and France for cerebral insufficiency since 1965. (Cerebral insufficiency is a general term for a collection of symptoms that include difficulties of concentration and memory absentmindedness, confusion, lack of energy, tiredness, decreased physical performance, depressive mood, anxiety, dizziness, tinnitus, and headache.) These symptoms have been associated with impaired cerebral circulation and are sometimes thought to be earlv indications of dementia..)

    Why do people speak so highly of ginkgo? There is folklore-based on ginkgo's traditional medicinal uses-as is the case with many herbs, but there is also "science." Modern research on ginkgo dates back to the late 1950s when Dr. Willmar Schwabe of the Schwabe Company in West Germany worked to create an extract from the leaf. His results led to what is today considered the "standard" ginkgo: a concentrated extract of 24 percent flavoneglycosides and 6 percent terpenoids.

    Ginkgo research took off in the early 1980s when French scientists showed that the herb interferes with platelet activating factor (PAF), which is the chemical responsible for the clumping of blood platelets; in other words, blood clotting. This was exciting news, because PAF is involved in many biological processes, including arterial blood flow, asthma attacks, and organ transplant rejection, and its inhibition could have major health benefits. Indeed, this aspect of ginkgo has been one that North American researchers have paid attention to: in 1988 Dr. Elias J. Corey of Harvard University isolated and synthesized ginkgolide B, an active substance in ginkgo that interferes with PAF.

    While North Americans focused on PAF inhibition, European researchers looked hard at much more. In 1988, Springer-Verlag, a German scientific publishing company, released an English translation of 36 ginkgo studies titled Rokan (Ginkgo Biloba): Recent Results in Pharmacology and Clinic. It initially attracted little attention, and died a quiet death. However, a few people did read this book, and gradually those interested in alternative health began to hear about its content through the herbvine. It opened eyes and sparked an interest in ginkgo.

    What do the studies say?

    Early ginkgo studies in the Rokan collection and others, reported what were apparantly amazing properties for ginkgo. Here are some of the topics:

    Cerebral Insufficiency: Studies published in the 1970s and 1980s by Vorberg (Clinical Trials Journal; 22:2); Gessner (Arzneimuttelforschung 35); Choussat, et al (Geriatrie 2); and Michel, and Weltbrecht and Jansen (In Effects of ginkgo Biloba Extract on Organic Cerebral Impairment, John Libbey Eurotext Ltd.) all pointed to the effective use of ginkgo for cerebral insufficiency. A 1992 report in the British Journal of clinical Pharmacology looks at reports on 40 trials on cerebral insufficiency, and the authors state that, "Positive results have been reported for ginkgo biloba extracts in the treatment of cerebral insuffici- ency." It should be noted that the authors only considered eight of the trials well- performed. However, many of the shortcomings noted consisted of incomplete descriptions. Vascular integrity-Ginkgo has been shown to affect peripheral arterial insufficiency (this often results in cramps). A 1984 report by Baur (Arzneim-Forsch 34:716-21) and a 1990 summary by Pizzorno and Murray of three reports indicated increased pain free walking and maximum distance. A 1992 report on ginkgo in The Lancet noted that there had been 15 controlled trials for the intermittent claudication (lameness). Although the authors note that some of the trials were flawed, they report that, "all trials indicated positive effects."

    Platelet Activating Factor: A 1987 study published in Prostaglandins (Vol. 34, No. 5) stated that in an eight subject double-blind trial, ginkgo "significantly inhibited response to the allergens." In 1988, the New York Times reported that British researchers had found positive results when using ginkgolide B for asthma and allergic inflammations, both of which are influenced by PAF. Pierre Braquet provides a synthesis of the information related to PAF and ginkgolides in Drugs of the Future (Vol. 12, No. 7). He states that ginkgolides act in humans as a PAF antagonist.

    Macular Degeneration: A French study published in Rokan: Recent Results in Pharmacology and Clinic (Springer-Verlag, 1988) examines the effect of ginkgo extract on macular degeneration. This double-blind clinical study was conducted with 20 patients over 55 years of age who were diagnosed with senile maculopathy.

    Ten of the patients received 80 mg of ginkgo extract a day for 6 months, while the other 10 received a placebo. After 6 months of treatment, the ginkgo group showed "significant improvement" in acuity of distance vision.

    Antioxidant: According to a 1992 Lancet report, in vitro studies show that ginkgo has free radical scavenging properties. In the 1993 book, Ginkgo Biloba Extract (EGb 761) as a Free Radical Scavenger (Ferrandini, Droy-Lefaix, and Christen, editors) the authors state that ginkgo extract is an effective antioxidant in the brain, retina, and cardiovascular system.

    Impotency: A 1989 study reported in the journal of Urology (Vol. 141) indicates that a long-term use of ginkgo biloba extract may be helpful for this problem.

    Organ transplants: Reports from Georgetown University Medical School suggest that a highly purified ginkgo extract (not the commercial extract used in the other ginkgo studies) prevents organ rejection more fully-and with less toxicity-than the standard anti- rejection drug, cyclosporine.

    Recent studies

    More recent studies confirm the earlier ones. A 1994 study published in Phytomedecine (1:9-16) shows that regular administration of ginkgo extract has a positive influence on subjects with cerebral insufficiency. The study concentrated on "long-term and short- term memory, concentration power, maximum stress, mental flexibility, family problems, and general satisfaction of the patient with his or her life." None of the subjects exhibited any pseudodementias (defined as dementia symptoms due to depression), nor were they using any substances that affected blood vessels.

    Another 1994 study (in Human Psychopharmacology) reports on the use of ginkgo for senile dementia of the Alzheimer type. A review of this study in Herbal Gram magazine says that, "Accumulating evidence suggests that free radical oxidation and platelet- activating factor (PAF) play important roles in the cognitive decline noticed in dementia. GBE's [ginkgo biloba extract] antioxidant, PAF-inhibiting, and neuronal-protective properties make it one of the clinician's most useful tools for slowing down cognitive decline in the elderly."

    Julian Whitaker, M.D., writing in the August 11, 1995, issue of Human Events magazine, notes that a 1995 issue of the American journal of natural Medicine reported that in nine double-blind, random clinical trials of people with intermittent claudication (lameness), ginkgo extract increased the distance of pain-free walking by 75 percent to 110 percent, and increased maximum walking distance by 52.6 percent to 119 percent. Finally, the February 1996 issue of the Harvard Women's Health Watch says that, "Several small studies have indicated that it [ginkgo] stimulates circulation in the limbs and improves memory and concentration, presumably by increasing blood flow to the brain. It also appears to be an antioxidant, like vitamins C, E, and beta-carotene, and thus might help prevent atherosclerotic plaque."

    The Brain: Blood flow in the brain decreases as we age. This means less food and oxygen for brain cells. European studies show that ginkgo increases blood flow in the brain, ensuring that the brain receives the food and oxygen it needs to function.

    The Heart: Ginkgo also improves blood flow to the Heart. Because it inhibits PAF, ginkgo can reduce the possibility of blood clots forming in coronary arteries.

    The Legs: Ginkgo's antioxidant capabilities may help reduce the transformation of cholesterol to plaque and the "next step" of narrowed and hardened arteries. This could have a hand in preventing intermittent claudication (lameness), pain, and cramping.

    The Eyes: Blood flow to the retina decreases with age. This means that the eyes may not get the nutrients they need. Retinal deterioration may lead to macular degeneration, a leading cause of adult blindness. Again, ginkgo's blood-circulating properties could help.

    The Ears: Again due to decreased blood flow with age, the nerves of the inner ear do not get sufficient blood. This could result in cochlear deafness, a leading cause of age- related hearing loss.

    The Active Ingredients

    Researchers have isolated two main groups of active substances in ginkgo, flavoneglycosides and terpenoids. The flavoneglycosides include kaempferol, quercetin, and isorhamnetin with glucose or rhamnose. The terpenolds include ginkgolides A, B, and C, and bilobalide.

    According to Kleijnen and Knipschild, writing in the November 7, 1992, issue of The Lancet, the ginkgolides, in particular ginkgolide B, are responsible for the PAF inhibition. The flavoneglycosides are responsible for the antioxidant abilities, which can stimulate relaxation of contracted blood vessels.

    The ginkgo extract used in clinical trials is generally standardized to a 50:1 ratio (fifty pounds of leaves to one pound of extract), 24 percent flavoncglycosides, and a minimum of 6 percent terpenoids.

    10.0 L-tyrosne: Partial summary: L-tyrosine is not an essential amino acid in that the body synthesises it from phenalanalyne. Like phenalanalyne, it is one of the important neurotransmitters, epinephrine, norepinephrine, and dopamine.In the laboratory, animals subjected to stress, have reduced levels of norepinephrine, unless they have been treated in advance with l-tyrosine.

    The U.S. Army, mindful of these findings, established double-blind experiments in ehich soldiers were subjected to various forms of stress, including rapid ascent to 15,000 feet. Under this condition, there is increased stress, as well as lowered oxygen supply to the brain. The group that had been pre-treated with l-tyrosine, performed significantly on such tests.

    It has been suggested that l-tyrosine may be effective in cases of depression.

    The action of l-tyrosine has been found to stimulate the production of dopamine, and norepinephrine. Tyrosine kinase activity is essential for the transduction throuch the T- cell antigen receptor. It is also involved in the body's use of insulin.

    Tyrosine through a complex form of biosynthesis, produces Co-Q 10. However, if any of the precursors are missing, a problem could ensue.

    11.0Panax ginseng - Is believed to lower stress, and stimulate better mental functioning.

    12.0 Glycerrhizae radix

    12.1 Robert Bradford, Director, Bradford Research Institute BA1Lycopene --Partial summary: Lycopene, which is what makes the tomato red, is one of the phytochemicals, which also include sulphuraphane, which is, in turn, a polyphenolic chemical. Polyphenolics are strong anti-oxidents. See the reference to green tea - gunpowder tea.

    BB1 Cigarette smoke

    CB1 Parkenson's Disease

    CB1-- Moussa B. H. Youdim and Peter Reiderer ; "Understanding Parkenson's disease."; Scientific American; 1997; Jan; 52-59.

    CC1 Hypoglycemia: Partial summary: Low blood glucose has been linked to, in part, to pancreatic disorders, diabetes, cancer, liver disfunction, heart attacks, depression and many other problems brought about by immune system disfunction. It may be treated by tri-valent chromiun, tri-valent vanadium or the sulfonureas (which themselves can cause hypoglycemia).

    CC2Dyslexia. Partial summary: Dislexia is more of a problem in right-eye dislexia. It can cause problems in arithmatic. reading, writing, speech (stuttering), and motor coordination. The stress of life may cause chronic fatigue, exhaustion, and hyperglycemia, leaving patients with a lowered immune response. Gerswind's hypothesis is an attempt to correlate dylexia, with motor defects, reading problems, and a lowered immune response in attention deficit hyperactivity disorder.

    There is a possible link between dyslexia and Meres-Irlan Syndrome.

    CC3 Leptin. Partial summary: Leptin is thought to be the substance that regulates weight. In studies on animals, adding leptin to the diet of obese test animals, produces a reduction in weight untis a normal weight is acheived. Unfortunatly, this does not seem to aply to human beings! A considerable amount of research is needed to locate the gene that seems to prevent leptin from acting in the same way.

    CC4 Micronutrients - general - see also DG.O2 Mettaloprotinase

    Partial summary: Micronutrients in the form of trace elements are essential to the proper functioning of the body and brain.


    CC5Growth hormone (GH) abberations -

    Partial summary: An excess of growth hormone can cause agromeglic giantism. CD01Melatonin Retinitus pigmentosa linked to low levels of melatonin DE 01 Allicin (Garlic) The action of garlic is based on Allicin, diallyl sulphide-oxide which is a systemic vasodilator. It is thought to be a scavanger of .OH, and as a result, is an antioxident. It is thought to have anti-cancer and anti-tumor and cytotoxic attrbutes. there is little evidence that garlic is able to reduce chlorestorol, and its antioxident activity may be the source of its effect on choloresteol stabilization under conditions of stress. (see also AA7.6.0, DF.01, and DF.02)

    DG.01 Neurotroropin-3 - Partial summary: This seems to be an essemtial neurological buiding block. As Myotropin may be essential to revent ALS, neuotropin may be the missing link in stopping MS.

    Additional studies on neurotropin 3 suggest that there may be a link between neurotropin 3-4 and skin melanomas.

    DG.O2 Mettaloprotinase - Partial summary: Trace amounts of non heavy metals (with the exeption of aluminum which as a efficient chelating agent may actually bind other essential metals), may increase the body's ability to fight cancer. there is a theory that as cancer cells cannnot be "seen electrically", they may be able to grow. DH.00Hot flashes - Partial summary: vasimotor instability - triggered by hot temperatures, caffeine, alcohol and stress, thinner womem are more affected than others as the exrea adipose tissue has the ability to tranform androsterodnol to esterone and estranol. Alternative therapies such as vitamin E, primrose oil, dong quai, and black colash have some anecdotal support. A history of smoking may also be a factor. DH.01Natural and synthetic estrogens Phyto -estrogen --consider the possible role of zinc in preventing prolactin from causing oxidization or hydolizaton of estrogen. DI.00Chloroquin: Partial summary: It once was the anti-malarial drug of choice. Because of its benificial effect on reducing connective-tissue destruction, it was used in the treatment of lupus. It had the side-effect of causing tunnel vision. When the U.S. Navy tried to use it an an antimalarial drug on carrier pilots, even the slight reduction in their peripheral vision led to serioud accidents.

    Even when private or commercial pilots take are inclined to asprin for headach relief, they are supposed to ground themselves until the sude effects abate!

    DJ.00 Antimaralials - Partial summary: As it can be reference to some of these papers, antimalariels have some possible and serious side effects.

    DK.00 Mefloquin: Partial summary: Manufactured by Hoffman-LaRoche as an antimaralial, it was studied and withdrawn because of serious side-effects in one out of one hundred and fifty patients on which it was tested. These side effects were the possibility of triggering severe depression, especially when combined it with a corticosteroid. In some other countries where malaria is endemic, Mefloquin's serious psychotic side effects are recognised. But this did not prevent its in use in Somalia, where these were ignored! As it was administered because of its extended period of protection, it was 'the drug of choice' for tourists. It's half life is about 20-30 days which means that any serious psychotic episodes may be present for two to three months.
      DL.00 Homocystine: Partial summary : Niacin (vitamin B3 - pyridoxine) can cause elevated levels of homocystine which can cause problems unless the niacin is taken along with folic acid, vitamin B12 and vitamin B6. DM.00 Colour and eye movement in Dyslexia and Meres-Irlan Syndrome  
    Most studies of dyslexia have involved investigation of visual, auditory or higher cognitive function. Oculomotor control has received less attention, although Pavlides (1981) reported that there appeared to be some alterations in saccades and there is also evidence that binocular control may also be disordered (Stein 1989). Recently, however, new oculomotor testing paradigms have been developed which allow the examination of the cognitive processing underlying eye movement. The application of these to dyslexic subjects has produced some intriguing results. In the gap paradigm, a short temporal gap (200ms) is introduced between the extinction of a central fixation target and the illumination of an eccentric target towards which subjects are instructed to make a saccadic eye movement. In normal subjects mean saccade latency decreases in gap conditions, in a gap-duration dependant manner. Furthermore, the distribtion of saccade latency is alterred such that the unimodal distribution normally observed, become bi-modal in gap conditions. The saccades which make up the first peak in this distribution have a latency of approximately 100ms, and are now termed express saccades.

    Fischer and colleagues (1993) have reported that dyslexic subjects can be divided into two groups based on the effect of the gap paradigm on saccades. Short latency express saccades occurred more frequently under gap conditions in some of the dyslexic subjects compared with normals. However conversely the gap effect was noted to be absent in other dyslexic subjects. There was no distinction made as to whether any of these subjects had Meares-Irlen syndrome in addition to their dyslexia and this is something which requires further investigation.

    Recently the gap paradigm has been used to examine another type of eye movement -smooth pursuit. In normal subjects it has been found that there is a gap effect on smooth pursuit latency i.e. smooth pursuit latency is reduced in gap conditions compared to conditions with no gap. (Knox 1996). There have as yet been no studies of the gap effect on smooth pursuit eye movements in subjects with dyslexia or Meares-Irlen syndrome. It would be of interest to know whether the abnormal gap effect on saccades observed in a proportion of dyslexic subjects can be generalised to both saccades and pursuit.

    We have conducted a short series of pilot studies on a small group of patients who benefited from the use of

    coloured overlays. Using both gap saccade and gap pursuit tasks we have found that the gap effect is normal in some, but for others is asymmetrical, absent or reduced (Northway & Knox 1997).

    The figure shows the relationship between smooth pursuit latency (regression lines and 95% confidence limits) for leftward and rightward pursuit in a subject who benefited from and routinely used coloured lenses. The marked asymmetry in the 'gap effect' is very different from that observed in normal subjects, where there is a gap duration dependant reduction in pursuit latency in both directions.

    We are seeking to extend these experiments to examine the effect of the coloured overlays, in both subjects who report benefits from them, and subjects who apparently derive no benefit. We also wish to investigate the effect of colour on the oculomotor responses of normal subjects. It is hoped that results from this study will provide an explanation for the effectiveness of coloured overlays in Meares-Irlen sufferers and perhaps other groups.



    The only paper I could find was a doctorial thesis.

    Naslond, Eric.; "Upper gastrointestinal motility, gut hormones and food intake, a study in normal weight and obese humans"; Doctorial Thesis; 1997; May 23rd; Division of Surgury, Danderyl Hospital and Section of Gastroenterology and Hepatology, Department of Internal Medicine, Korolinska Hospital, Korolinska Institute, Stockholm, Sweden.

    Lab Tests Common for Lupus
    Blood Tests
    Test Normal Values Comments
    Alanine Aminotransferase (ALT, SGPT, GPT) Normal Range: Laboratory-specific U/L Intracellular enzyme involved in amino acid and carbohydrate metabolism. Present in large concentrations in liver, kidney; smaller amounts in skeletal muscle and heart. Released with tissue damage.  Increased in: Acute viral hepatitis (ALTAST), biliary tract obstruction (cholangitis, choledocholithiasis), alcoholic hepatitis and cirrhosis (ASTALT), liver abscess, metastatic or primary liver cancer; right heart failure, ischemia or hypoxia, injury to liver ("shock liver"), extensive trauma. Drugs causing cholestasis and other hepatotoxic drugs.

    Additional: ALT screening of donor blood used in blood banks to exclude non-A, non-B hepatitis. 

    Albumin Normal Range: 3.4-4.7 g/dL Major component of plasma proteins, influenced by nutritional state, hepatic function, renal function, various diseases.  Increased in: Dehydration, shock, hemoconcentration. 

    Decreased in: Decreased hepatic synthesis (chronic liver disease, malnutrition, malabsorption, malignancy, congenital analbuminemia [rare]). Increased losses (nephrotic syndrome, burns, trauma, hemorrhage with fluid replacement, fistulae, enteropathy, acute or chronic glomerulonephritis). Hemodilution (pregnancy, CHF). Drugs (eg, estrogens). 

    Additional: Serum albumin gives an indication of severity in chronic liver disease. Useful in nutritional assessment if no impairment in production or increased loss. 

    Alkaline Phosphatase Normal Range: Method and age dependent  Alkaline phosphatases are found in liver, bone, intestine, placenta.  Increased in: Obstructive hepatobiliary disease, hepatotoxic drugs, bone disease (physiologic bone growth, Paget's disease, osteomalacia, osteogenic sarcoma, bone metastases), hyperparathyroidism, rickets. Benign familial hyperphosphatasemia, pregnancy (3rd trimester), GI disease (perforated ulcer or infarct). 

    Decreased in: Hypophosphatasia. 

    Additional: Normal in osteoporosis. Alkaline phosphatase isoenzyme separation by electrophoresis or differential heat inactivation is unreliable. Use g-glutamyl transpeptidase (GGT), which increases in hepatobiliary disease, to infer origin of increased alkaline phosphatase (ie, liver or bone). 

    ANA (Antinuclear Antibodies) Normal Range: < 1:20  Heterogeneous antibodies to nuclear antigens (DNA and RNA, histone and nonhistone proteins). Antinuclear antibody is measured in patient's serum by layering serum over human epithelial cells and detecting the antibody with fluorescein-conjugated polyvalent anti-human immunoglobulin.  Elevated in: 1/3-3/4 of patients over age 65 (usually in low titers), systemic lupus erythematosus (98%), drug-induced lupus (100%), Sjšgren's (80%), rheumatoid arthritis (30-50%), scleroderma (60%), mixed connective tissue disease (100%), Felty's syndrome, mononucleosis, hepatic or biliary cirrhosis, hepatitis, leukemia, myasthenia gravis, dermatomyositis, polymyositis, chronic renal failure. 

    Additional: A negative ANA test does not completely rule out SLE, but alternative diagnoses should be considered. Pattern of staining of ANA may give some clues to diagnoses, but since the pattern also changes with serum dilution, it is not routinely reported. Only the rim (peripheral) pattern is highly specific (for SLE). Not useful as a screening test. Should be used only when there is clinical evidence of a connective tissue disease. 

    ANCA (antineutrophil
    cytoplasmic antibodies),
    P-ANCA (perinuclear)
    C-ANCA (cytoplasmic)
    Normal Range: none present Tests are on the blood serum. C-ANCA is most seen in Wegener's granulomatosus. C-ANCA suggests a systemic vasculitis disease, and is rarely seen in patients with lupus. P-ANCA is most seen in necrotizing, crescentic glomerulonephritis and polyarteritis nodosa. P-ANCA is found in some lupus patients.
    Normal Range for anti-IgG: 0 - 20 GPL
    Normal Range for anti-IgM: 0 - 10 MPL
    Anticardiolipin antibodies are a subset of a group of antibodies which react with negatively charged phospholipids. Antibodies to cardiolipin have been associated with an incresased incidence of vascular thrombosis, thrombocytopenia and recurrent fetal loss in patients with SLE. Increased in: SLE, some connective tissue diseases, and in Antiphospholipid Syndrome.

    Additional: Patients with acute and chronic infections (including syphilis, HIV, Lyme disease) may also have increased anti-cardiolipin antibodies.

    Anti-DNA Normal Range: < 1:10 titer  IgG or IgM antibodies directed against host double-stranded DNA.  Increased in: Systemic lupus erythematosus (60-70%, specificity 95%). Anti-ds-DNA antibody is not found in drug-induced lupus. 

    Additional: High titers are seen only in SLE. Titers of anti-ds-DNA correlate well with disease activity and with occurrence of glomerulonephritis. 

    antibodies (anti-RBC)
    also known as Coombs test
    Normal Range: non present The direct Coombs test measures the presence of antibodies that are bound to the surface of circulating RBCs. Indirect Coombs measures *free* anti-RBC antibodies. The sensitivity of this test is in question--but it remains the standard for detection of autoimmune anemia.
    Antineurofilament antibodies Normal Range: non present Limited studies have been done with this test. Antibodies against neurofilaments in blood serum. 60% of diffuse NP lupus patients have shown this antibody.
    Antineuronal antibodies Normal Range: non present Most specifically, this is IgG neuron-reactive antibody radioimmunoassay performed on the cerebrospinal fluid. In the general lupus population, 75% with neuro-psyciatric (NP) lupus are detected, as compared to 10% without NP lupus--*false positive*. Highest titers are found in patients with diffuse NP lupus (seizures, organic brain syndrome)--90%. 40% of focal NP are positive (stroke, cranial neuropathy, transverse myelitis).
    Anti-ribosomal P Normal Range: Negative Antibodies to ribosomal P protein from blood serum. 80 - 90% positive in NP lupus that manifests with psychosis or depression.
    Anti-Ro/SS-A Normal Range: Negative Autoantibody against acidic nuclear ribonucleoproteins that is found in patients with some connective tissue diseases, especially Sjogren's syndrome.  Positive in: Primary Sjogren's syndrome (70%), SLE (40%), rheumatoid arthritis (10%). 

    Additional: Anti-La/SS-B is another antibody against acidic ribonucleoproteins that is less sensitive for Sjogren's (50-60%) and SLE (10-15%). Patients with antibodies to SS-A may have a negative ANA test. 

    Aspartate Aminotransferase (AST, SGOT, GOT) Normal Range: Laboratory-specific U/L Intracellular enzyme involved in amino acid and carbohydrate metabolism. Present in large concentrations in liver, skeletal muscle, brain, red cells, and heart. Released into the bloodstream when tissue is damaged.  Increased in: Acute viral hepatitis (ALTAST), biliary tract obstruction (cholangitis, choledocholithiasis), mononucleosis, alcoholic hepatitis and cirrhosis (ASTALT), liver abscess, metastatic or primary liver cancer, myocardial infarction, myopathies, muscular dystrophy, dermatomyositis, rhabdomyolysis, ischemic injury to liver ("shock liver") or hypoxia. Hepatotoxic drugs (eg, isoniazid). 

    Additional: Test not indicated for diagnosis of myocardial infarction. 

    Bilirubin Normal Range: 0.1-1.2 Direct (conjugated to glucuronide) bilirubin, 0.1-0.4 mg/dL (< 7 &micro;mol/L); Indirect (unconjugated) bilirubin, 0.2-0.7 mg/dL (< 12 &micro;mol/L) mg/dL Bilirubin, a product of hemoglobin metabolism, is conjugated in the liver to the mono- and diglucuronides and excreted in bile. Some conjugated bilirubin is bound to serum albumin, so-called D (delta) bilirubin. Elevated serum bilirubin occurs in liver disease, biliary obstruction, or hemolysis.  Increased in: Acute or chronic hepatitis, cirrhosis, biliary tract obstruction, toxic hepatitis, congenital liver enzyme abnormalities (Dubin-Johnson, Rotor's, Gilbert's, Crigler-Najjar syndromes), fasting, hemolytic disorders. Hepatotoxic drugs. 

    Additional: Assay of total bilirubin includes conjugated (direct) and unconjugated (indirect) bilirubin plus delta bilirubin (conjugated bilirubin bound to albumin). It is usually clinically unnecessary to fractionate total bilirubin. The fractionation is unreliable by the diazo reaction and may underestimate unconjugated bilirubin. Only conjugated bilirubin appears in the urine and it is indicative of liver disease; hemolysis is associated with increased unconjugated bilirubin. Persistence of delta bilirubin in serum in resolving liver disease means that total bilirubin does not effectively indicate time course of resolution. 

    Blood Urea Nitrogen (BUN) Normal Range: 8-20 mg/dL Urea, an end product of protein metabolism, is excreted by the kidney. BUN is directly related to protein intake and nitrogen metabolism and inversely related to the rate of excretion of urea. Urea concentration in glomerular filtrate is the same as in plasma, but its tubular reabsorption is inversely related to the rate of urine formation.  Increased in: Renal failure (acute or chronic), urinary tract obstruction, dehydration, shock, burns, CHF, gastrointestinal bleeding. Drugs with renal toxicity, eg, gentamicin. 

    Decreased in: Hepatic failure, nephrotic syndrome, cachexia (low-protein and high-carbohydrate diets). 

    Additional: Urease assay method commonly used. BUN/Cr ratio (normally 12:1-20:1) decreased in acute tubular necrosis, advanced liver disease, low protein intake, following hemodialysis. BUN/Cr ratio increased in dehydration, GI bleeding, increased catabolism. 

    C3 Normal Range: 64-166 mg/dL The classic and alternative complement pathways converge at the C3 step in the complement cascade. Low levels indicate activation by one or both pathways. Most diseases with immune complexes will show decreased C3 levels. Test as usually performed is an immunoassay (by radial immunodiffusion or nephelometry).  Increased in: Many inflammatory conditions as an acute phase reactant, active phase of rheumatic diseases (rheumatoid arthritis, SLE, etc), acute viral hepatitis, myocardial infarction, cancer, diabetes, pregnancy, sarcoidosis, amyloidosis, thyroiditis. 

    Decreased by: Decreased synthesis (protein malnutrition, congenital deficiency, severe liver disease), or increased catabolism (immune complex disease, membranoproliferative glomerulonephritis [75%], SLE, Sjogren's, rheumatoid arthritis, disseminated intravascular coagulation, paroxysmal nocturnal hemoglobinuria, autoimmune hemolytic anemia, gram-negative bacteremia) and increased loss (burns, gastroenteropathies). 

    Additional: Complement C3 levels may be useful in following the activity of immune complex diseases. The best test to detect inherited deficiencies is CH50. Levels can confirm specific C3 defect. 

    C4 Normal Range: 15-45 mg/dL C4 is a component of the classic complement pathway. Depressed levels usually indicate classic pathway activation. Increased in: Various malignancies: not clinically useful. 

    Decreased by: Decreased synthesis, increased catabolism (SLE, rheumatoid arthritis, proliferative glomerulonephritis, hereditary angioedema), and increased loss (burns, protein-losing enteropathies). Congenital deficiency. 

    Additional: Low C4 accompanies acute attacks of hereditary angioedema, and C4 is used as a first-line test for the disease. C1 esterase inhibitor levels are not indicated for the evaluation of hereditary angioedema unless C4 is low. Congenital C4 deficiency occurs with an SLE-like syndrome. Test as usually performed is an immunoassay and not a functional assay. 

    Calcium Normal Range: 8.5-10.5 mg/dL Level of ionized calcium is regulated by parathyroid hormone and vitamin D. Serum calcium equals the sum of ionized calcium plus complexed calcium and calcium bound to proteins (mostly albumin).  Increased in: Hyperparathyroidism, malignancies secreting PTH-like substances (especially squamous cell carcinoma of lung, renal cell carcinoma), vitamin D excess, milk-alkali syndrome, multiple myeloma, Paget's disease of bone with immobilization, sarcoidosis, other granulomatous disorders, familial hypocalciuria, vitamin A intoxication, thyrotoxicosis, Addison's disease. Drugs: antacids (some), calcium salts, chronic diuretic use (eg, thiazides), lithium, others. 

    Decreased in: Hypoparathyroidism, vitamin D deficiency, renal insufficiency, pseudohypoparathyroidism, magnesium deficiency, hyperphosphatemia, massive transfusion, hypoalbuminemia. 

    Additional: Need to know serum albumin to interpret calcium level. For every decrease in albumin by 1 mg/dL, calcium should be corrected upward by 0.8 mg/dL. 

    CH50 Normal Range: Laboratory-specific U/mL The quantitative assay of hemolytic complement activity depends on the ability of the primary complement pathway to induce hemolysis of red cells sensitized with optimal amounts of anti-red cell antibodies. For precise titrations of hemolytic complement, the dilution of serum that will lyse 50% of the indicator red cells is determined as the CH50. This arbitrary unit depends on the conditions of the assay and is therefore laboratory-specific.  Decreased with: 50-80% deficiency of primary pathway complement components in congenital or acquired deficiency.

    Normal in: Deficiencies of alternative pathway, complement components. 

    Additional: This is a functional assay of biologic activity. Sensitivity to decreased levels of complement components depends on exactly how the test is performed. It is used to detect congenital and acquired severe deficiency disorders of the primary complement pathway. 

    Chloride Normal Range: 98-107 meq/L Chloride, the principal inorganic anion of extracellular fluid, is important in maintaining normal acid-base balance and normal osmolality. If chloride is lost (as HCl or NH4Cl), alkalosis ensues; if chloride is ingested or retained, acidosis ensues.  Increased in: Renal failure, nephrotic syndrome, renal tubular acidosis, dehydration, overtreatment with saline, hyperparathyroidism, diabetes insipidus, metabolic acidosis from diarrhea (loss of HCO3), respiratory alkalosis, hyperadrenocorticism. Drugs: acetazolamide (hyperchloremic acidosis), androgens, hydrochlorothiazide, salicylates (intoxication). 

    Decreased in: Vomiting, diarrhea, gastrointestinal suction, renal failure combined with salt deprivation, overtreatment with diuretics, chronic repiratory acidosis, diabetic ketoacidosis, excessive sweating, SIADH, salt-losing nephropathy, acute intermittent porphyria, water intoxication, expansion of extracellular fluid volume, adrenal insufficiency, hyperaldosteronism, metabolic alkalosis. Drugs: aldosterone, chronic laxative or bicarbonate ingestion, corticosteroids and ACTH (alkalosis), diuretics. 

    Cholesterol Normal Range: Desirable < 200 Borderline 200-239 High risk 240 mg/dL Cholesterol level is determined by lipid metabolism, which is in turn influenced by heredity, diet, and liver, kidney, thyroid, and other endocrine organ functions. Total cholesterol (TC) = LDLC + HDLC + TG/5 (valid only if triglyceride [TG] < 400). Since LDL cholesterol (LDLC) is the clinically important entity, it is calculated as LDLC = TC - HDLC - TG/5, and this is valid only if specimen is obtained fasting (in order to obtain relevant triglyceride and HDL levels).  Increased in: Familial or polygenic hyperlipoproteinemia, familial dysbetalipoproteinemia, familial combined hyperlipidemia, hyperlipoproteinemia and hyperalphalipoproteinemia, hyperlipoproteinemias secondary to hypothyroidism, uncontrolled diabetes mellitus, nephrotic syndrome, chronic hepatitis, biliary cirrhosis, obstructive jaundice, hypoproteinemia, glomerulonephritis, chronic renal failure, gout, malignancy (pancreas, prostate), pregnancy, alcoholism, glycogen storage diseases types I, III, IV, anorexia nervosa, GH deficiency, dietary excess. Drugs: androgens, chlorpropamide, corticosteroids, oral contraceptives, phenytoin, progestins, thiazides, others. 

    Decreased in: Acute hepatitis, alcoholic cirrhosis, Gaucher's disease, hyperthyroidism, acute infections, anemia, malnutrition, alphalipoprotein deficiency (Tangier disease), malignancy (liver), severe acute illness, extensive burns, COPD, rheumatoid arthritis, mental retardation, intestinal lymphangiectasia, apolipoprotein deficiency. 

    Additional: It is important to treat the cause of secondary hypercholesterolemia (hypothyroidism, etc). National Cholesterol Education Program Expert Panel has published clinical recommendations for cholesterol management.

    Creatinine Normal Range: 0.6-1.2 mg/dL Endogenous creatinine is excreted by filtration through the glomerulus and by tubular secretion. Clinically, creatinine clearance is an acceptable measure of glomerular filtration rate but sometimes overestimates GFR. For each 50% reduction in GFR, serum creatinine approximately doubles.  Increased in: Acute or chronic renal failure; urinary tract obstruction, nephrotoxic drugs. 

    Decreased in: Reduced muscle mass, possible drug effect. 

    Additional: In alkaline picrate method, substances other than Cr (eg, acetoacetate, acetone, b-hydroxybutyrate, a-ketoglutarate, pyruvate, glucose) may give falsely high results. Therefore, patients with diabetic ketoacidosis may have spuriously elevated Cr. Cephalosporins may spuriously increase or decrease Cr measurement. Increased bilirubin may spuriously decrease Cr. 

    Differential Neutophils
    Large unstained cells
    Normal Range:  1.8-6.8 K/mL 
    0.9-2.9 K/mL 
    0.1-0.6 K/mL 
    0-0.4 K/mL 
    0-0.1 K/mL
    0-0.2 K/mL 
    White blood cell differentials are now done on automated flow cytometry instruments in order to provide reproducible data. 10,000 wbcs are classified on the basis of size and peroxidase staining as neutrophils, monocytes or eosinophils (which are all peroxidase positive) and as lymphocytes and large unstained cells (which are peroxidase negative). These large unstained cells (LUC), larger than normal lymphocytes, may be atypical lymphocytes, myeloperoxidase deficient cells or peroxidase negative blasts. Basophils are identified using two angle light scattering, based on their singular resistance to lysis. There will also be an indication of more immature neutrophils (commonly called a left shift) based on the ratio of mono/polymorphonuclear white cells (lobularity index). A left shift usually suggests infection (rarely leukemia). The reproducibility of 100 cell manual differentials is notoriously poor, because of statistical error in counting and observer variation, however, review of blood smears is useful to visually identify rare abnormal cells, blasts, nucleated rbcs, morphologic abnormalities e.g., hypersegmentation, toxic granulation, sickle cells, target cells, spherocytes, basophilic stippling, and to look for rouleau (stacking of red cells due to increased globulins) and clumped platelets. White blood cell differential is unlikely to be abnormal with a normal wbc count or to be changed if the total wbc count is unchanged.  Increased neutrophils: suggests infection (bacterial or early viral, rarely leukemia), acute stress, acute and chronic inflammations, tumor, drugs, DKA.
    Decreased neutrophils: suggests aplastic anemia, drug-induced neutropenia (e.g., chloramphenicol, phenothiazine, antithyroid drugs, sulphonamide), folate or B12 deficiency, Chediak-Higashi syndrome, malignant lymphoproliferative disease, physiologic in children up to 4 years.

    Increased lymphocytes: viral infection (especially, infectious mononucleosis, pertussis), thyrotoxicosis, adrenal insufficiency disease (ALL, CLL), chronic infection, drug and allergic reactions, autoimmune disease. 
    Decreased lymphocytes: immune deficiency syndrome. Comments: 

    Increased monocytes: inflammation, infection, malignancy, TB, myeloproliferative disorders. 
    Decreased monocytes: depleted in overwhelming bacterial infection. 

    Increased eosinophils: allergic states, drug sensitivity reaction, skin disorders, tissue invasion by parasites, periarteritis nodosa, hypersensitivity response to malignancy (e.g. Hodgkin's disease), pulmonary infiltrative disease, disseminated eosinophilic hypersensitivity disease. 
    Decreased eosinophils: acute and chronic inflammation, stress, drugs: steroids. 

    Increased basophils: hypersensitivity reactions, drugs, myeloproliferative disorders (CML, polycythemia vera), myelofibrosis. 

    Erythrocyte Sedimentation Rate (Sed Rate, ESR) Normal Range: Male: < 10 Female: < 15 Erythrocytes in plasma usually settle slowly. However, if they aggregate for any reason (usually because of plasma proteins called acute phase reactants, eg, fibrinogen), they settle rapidly. Sedimentation of RBCs occurs because of their greater density than plasma. ESR measures the distance in mm that erythrocytes fall during 1 hour.  Increased in: Infections (osteomyelitis, pelvic inflammatory disease [75%]), inflammatory disease (temporal arteritis, polymyalgia rheumatica, rheumatic fever), malignant neoplasms, paraproteinemias, anemia, pregnancy, chronic renal failure, GI disease (ulcerative colitis, regional ileitis). 

    Decreased in: Polycythemia, sickle cell anemia, spherocytosis, anisocytosis, hypofibrinogenemia, hypogammaglobulinemia, congestive heart failure, microcytosis, drugs (high dose corticosteroids). Low value of no diagnostic significance. 

    Additional: There is a good correlation between ESR and C-reactive protein, but ESR is less expensive. Test is useful and indicated only for diagnosis and monitoring of temporal arteritis and polymyalgia rheumatica. The test is not sensitive or specific for other conditions. ESR is higher in women and older persons. 

    Gamma-Glutamyl Transpeptidase (GGT) Normal Range: Laboratory-specific U/L GGT is an enzyme present in liver, kidney, and pancreas. It transfers C-terminal glutamic acid from a peptide to other peptides of L-amino acids. It is induced by alcohol intake and is an extremely sensitive indicator of liver disease, particularly alcoholic liver disease.  Increased in: Liver disease: acute viral or toxic hepatitis, chronic or subacute hepatitis, cirrhosis, biliary tract obstruction (intrahepatic or extrahepatic), primary or metastatic liver neoplasm, alcoholic hepatitis, mononucleosis. Drugs (by enzyme induction): phenytoin, barbiturates, alcohol.

    Additional: Useful in follow up of alcoholics undergoing treatment. Test sensitive to modest alcohol intake. Test positive in 90% of patients with liver disease. Used to confirm hepatic origin of elevated serum alkaline phosphatase. 

    Glucose Normal Range: 60-115 mg/dL Normally, the glucose concentration in extracellular fluid is closely regulated so that a source of energy is readily available to tissues and no glucose is excreted in the urine.  Increased in: Diabetes mellitus, Cushing's syndrome (10-15%), chronic pancreatitis (30%) Drugs: corticosteroids, phenytoin, estrogen, thiazides 

    Decreased in: Pancreatic islet B cell disease with increased insulin, insulinoma, adrenocortical insufficiency, hypopituitarism, diffuse liver disease, malignancy (adrenocortical, stomach, fibrosarcoma), infant of diabetic mother, enzyme deficiency diseases (galactosemia, etc). Drugs: insulin, ethanol, propranolol, sulfonylureas, tolbutamide, other hypoglycemic agents. 

    Additional: Diagnosis of diabetes mellitus is consistent with a fasting plasma glucose 140 mg/dL on more than one occasion. Hypoglycemia is defined as glucose <50 mg/dL in men and <40 mg/dL in women. 

    Hematocrit Normal Range: Male: 39-49 Female: 35-45 Age-dependent The hematocrit represents the percentage of whole blood volume made up by erythrocytes. Laboratory instruments calculate the Hct from the erythrocyte count and the MCV, ie, Hct = RBC x MCV.  Increased in: Hemoconcentration (as in dehydration, burns, vomiting), polycythemia, extreme physical exercise. 

    Decreased in: Anemia: macrocytic (liver disease, hypothyroidism, vitamin B12 deficiency, folate deficiency), normocytic anemia (early iron deficiency, anemia of chronic disease, hemolytic anemia, acute hemorrhage) and microcytic anemia (iron deficiency, thalassemia). 

    Additional: Conversion from hemoglobin to hematocrit is roughly Hgb x3 = Hct. Hematocrit reported by clinical laboratories is not a spun hematocrit. The spun hematocrit may be spuriously high if the centrifuge is not calibrated, if the specimen is not spun to constant volume, or if there is "trapped plasma." 

    Hemoglobin Normal Range: 
    Male: 13.6-17.5 
    Female: 12.0-15.5 
    Hemoglobin is the major protein of erythrocytes and transports oxygen from the lungs to peripheral tissues. It is measured by spectrophotometry on automated instruments after hemolysis of red cells and conversion of all hemoglobin to cyanmethemoglobin. Hemoglobin is increased in: Hemoconcentration (as in dehydration, burns, vomiting), polycythemia, extreme physical exercise, heavy smoking (due to presence of nonfunctional carboxyhemoglobin). 

    Hemoglobin is decreased in: Anemia: macrocytic (liver disease, hypothyroidism, vitamin B12 deficiency, folate deficiency), normocytic anemia (early iron deficiency, anemia of chronic disease, hemolytic anemia, acute hemorrhage) and microcytic anemia (iron deficiency, thalassemia). 

    Additional: Hypertriglyceridemia and very high WBC counts can cause false elevations of Hgb. 

    Immunoglobulins (IG) Normal Range: IgA: 78-367 mg/dL IgG: 583-1761 mg/dL IgM: 52-335 mg/dL IgG makes up about 85% of total serum immunoglobulins and predominates late in immune responses. It is the only immunoglobulin to cross the placenta. IgM antibody predominates early in immune responses. Secretory IgA plays an important role in host defense mechanisms by blocking transport of microbes across mucosal surfaces.  Increased in: IgG: Polyclonal: Autoimmune diseases (eg, SLE, RA), sarcoidosis, chronic liver diseases, some parasitic diseases, chronic or recurrent infections. Monoclonal: Multiple myeloma (IgG type), lymphomas or other malignancies. IgM: Polyclonal: Isolated infections such as viral hepatitis, infectious mononucleosis, early response to bacterial or parasitic infection. Monoclonal: Waldenstrom's macroglobulinemia, lymphoma. IgA: Polyclonal: Chronic liver disease, chronic infections (especially of the GI and respiratory tracts). Monoclonal: Multiple myeloma (IgA). 

    Decreased in: IgG: Immunosuppressive therapy, genetic (severe combined immunodeficiency, Wiskott-Aldrich syndrome, common variable immunodeficiency). IgM: Immunosuppresive therapy. IgA: Inherited IgA deficiency (ataxia telangiectasia, combined immunodeficiency disorders). 

    Additional: IgG deficiency is associated with recurrent and occasionally severe pyogenic infections. Most common form of multiple myeloma is the IgG type. 

    Iron Normal Range: 50-175 &micro;g/dL Plasma iron concentration is determined by absorption from intestine; storage in intestine, liver, spleen, bone marrow; rate of breakdown or loss of hemoglobin; rate of synthesis of new hemoglobin.  Increased in: Hemochromatosis, hemosiderosis (eg, multiple transfusions, excess iron administration), hemolytic anemia, pernicious anemia, aplastic or hypoplastic anemia, viral hepatitis, lead poisoning, thalassemia. Drugs: dextran, estrogens, ethanol, oral contraceptives. 

    Decreased in: Iron deficiency, nephrotic syndrome, chronic renal failure, many infections, active hematopoiesis, remission of pernicious anemia, hypothyroidism, malignancy (carcinoma), postoperative state, kwashiorkor, drugs. 

    Additional: Used in evaluation of iron deficiency (see TIBC and Ferritin). 

    Iron Binding Capacity Normal Range: 250-460 &micro;g/dL Iron is transported in plasma complexed to the metal-binding globulin, transferrin, which is synthesized in the liver. Total iron binding capacity is calculated from transferrin levels measured immunologically. Each molecule of transferrin has two iron-binding sites, so its iron binding capacity is 1.47 mg/g. Normally, transferrin carries an amount of iron representing about 16Ð60% of its capacity to bind iron, ie, % saturation of iron binding capacity is 16-60%.  Increased in: Iron deficiency anemia, late pregnancy, infancy, hepatitis. Drugs: oral contraceptives. 

    Decreased in: Hypoproteinemic states (eg, nephrotic syndrome, starvation, malnutrition, cancer), chronic inflammatory disorders, chronic disease, chronic liver disease. 

    Additional: Increased % transferrin saturation with iron: in iron overload (iron poisoning, hemolytic anemia, sideroblastic anemia, thalassemia, hemochromatosis, pyridoxine deficiency, aplastic anemias). Decreased % transferrin saturation with iron: in iron deficiency (usually saturation <16%). Transferrin levels can also be used to assess nutritional status. 

    Lactate Dehydrogenase (LDH) Normal Range: Laboratory-specific LDH is an enzyme that catalyzes the interconversion of lactate and pyruvate in the presence of NAD/NADH. It is widely distributed in body cells and fluids and since its RBC/plasma ratio is high, it is spuriously elevated in plasma/serum following hemolysis.  Increased in: Tissue necrosis, especially in acute injury of cardiac muscle, RBCs, kidney, skeletal muscle, liver, lung, skin. Commonly elevated in various carcinomas and in Pneumocystis carinii and B cell lymphoma in AIDS. Marked elevations occur in hemolytic anemias, vitamin B12 deficiency anemia, folate deficiency anemia, polycythemia vera, acute (but not chronic) hepatitis, cirrhosis, obstructive jaundice, renal disease, musculoskeletal disease, CHF. Drugs causing hepatotoxicity or hemolysis. 

    Decreased in: Clofibrate, fluoride (low dose). 

    Additional: LDH is elevated after myocardial infarction (2-7 days), in liver congestion (eg, in CHF) and in Pneumocystis carinii pneumonitis. LDH is not a useful liver function test and it is not specific enough for the diagnosis of hemolytic or megaloblastic anemias. Its main diagnostic use is in myocardial infarction in which the CKMB elevation has passed. With the availability of specific LD1 measurements, the total LD level may no longer be useful.

    Magnesium Normal Range: 1.8-3 mg/dL Magnesium is primarily an intracellular cation (second most abundant, 60% found in bone). In extracellular fluid, it influences neuromuscular response and irritability. A magnesium deficit may exist with little or no change apparent in serum level.  Increased in: Dehydration, tissue trauma, renal failure; hypoadrenocorticism; hypothyroidism. Drugs: aspirin (prolonged use), lithium, magnesium salts, progesterone, triamterene, vitamin D (renal failure). 

    Decreased in: Chronic diarrhea, enteric fistula, starvation, chronic alcoholism, chronic liver disease, total parenteral nutrition with inadequate replacement, hypoparathyroidism (especially post-parathyroid surgery), high-dose vitamin D and calcium therapy, acute pancreatitis, delirium tremens, chronic glomerulonephritis, hyperaldosteronism, diabetic ketoacidosis, SIADH, pregnancy. Drugs: albuterol, amphotericin B, calcium salts, cisplatin, citrates (blood transfusion), cyclosporine, diuretics, ethacrynic acid. 

    Additional: Mg2+ concentration is determinated by intestinal absorption, renal excretion, and exchange with bone and with intracellular fluid. 

    Mean Corpuscular Hemoglobin (MCH) Normal Range: 26-34 pg MCH calculated from measured values of Hb and RBC; ie, MCH = Hb/RBC. A low MCH can mean hypochromia or microcytosis or both. A high MCH is evidence of macrocytosis.  Increased in: Macrocytosis. 

    Decreased in: Microcytosis (iron deficiency, thalassemia). Hypochromia (lead poisoning, sideroblastic anemia, anemia of chronic disease). 

    Mean Corpuscular Hemoglobin Concentration (MCHC) Normal Range: 31-36 g/dL MCHC describes how fully the erythrocyte volume is filled with hemoglobin and is calculated from measurement of hemoglobin (Hb), mean corpuscular corpuscular volume (MCV) and red cell count (RBC); ie, MCHC = Hb/MCV x RBC.  Increased in: Marked spherocytosis. Spuriously increased in autoagglutination, hemolysis (with spuriusly high Hb or low MCV or RBC), lipemia. Cellular dehydration syndromes, xerocytosis. 

    Decreased in: Hypochromic anemia (iron deficiency, thalassemia, lead poisoning), sideroblastic anemia, anemia of chronic disease. Spuriously decreased in high WBC (with spuriously low Hgb or high MCV or RBC). 

    Mean Corpuscular Volume (MCV) Normal Range: 80-100 fL Average volume of the red cell is measured by automated instrument, by electrical impedance or by light scatter.  Increased in: Liver disease, megaloblastic anemia (folate, B12 deficiencies), reticulocytosis, newborn. Drugs: phenytoin. Spurious increase in autoagglutination, high WBC.

    Decreased in: Iron deficiency, thalassemia; decreased or normal in anemia of chronic disease. 

    Additional: MCV can be normal in combined iron and folate deficiency. In patients with two red cell populations (macrocytic and microcytic), MCV may be normal. 

    Partial Thromboplastin Time Normal Range: 25-35 (range varies) Panic = 60 seconds Patient's plasma is activated to clot in vitro by mixing it with phospholipid and an activator substance. Screens the intrinsic coagulation pathway and adequacy of all coagulation factors except XIII and VII. PTT is usually abnormal if level of any factor falls below 30-40% of normal.  Increased in: Deficiency of any individual coagulation factor except XIII and VII, nonspecific inhibitors (lupus-like anticoagulant), specific factor inhibitors, von Willebrand's disease (may also be normal), hemophilia A and B, disseminated intravascular coagulation. Drugs: heparin, warfarin. 

    Decreased in: Hypercoagulable states, DIC. 

    Comments: PTT is the best test to monitor adequacy of heparin therapy. Test not always abnormal in von Willebrand's disease. Test may be normal in chronic DIC. Very common cause of prolongation is spurious presence of heparin in sample. 

    Phosphorous Normal Range: 2.5-4.5 mg/dL The plasma concentration of inorganic phosphate is determined by parathyroid gland function, action of vitamin D, intestinal absorption, renal function, bone metabolism, and nutrition.  Increased in: Renal failure, massive blood transfusion, sarcoidosis, neoplasms, adrenal insufficiency, acromegaly, hypoparathyroidism, hypervitaminosis D, phosphate infusions or enemas, osteolytic metastases to bone, leukemia, milk-alkali syndrome, healing bone fractures, pseudohypoparathyroidism, diabetes mellitus with ketosis, malignant hyperpyrexia, cirrhosis, lactic acidosis, respiratory acidosis. Drugs: eg, anabolic steroids, ergocalciferol, furosemide, hydrochlorothiazide and others. 

    Decreased in: Hyperparathyroidism, hypovitaminosis D (rickets, osteomalacia), malabsorption (steatorrhea); malnutrition, starvation or cachexia; GH deficiency, chronic alcoholism, severe diarrhea, vomiting, nasogastric suction, severe hypercalcemia (any cause), acute gout, osteoblastic metatases to bone, severe burns (diuretic phase), respiratory alkalosis, hyperalimentation with inadequate phosphate repletion, carbohydrate administration (intravenous), renal tubular acidosis and other renal tubular defects, diabetic ketoacidosis (during recovery), acid-base disturbances, hypokalemia, pregnancy, hypothyroidism; prolonged use of thiazides, glucose infusion, salicylates (toxicity). Drugs: eg, phosphate-binding antacids, anticonvulsants, estrogens, isoniazid, oral contraceptives.

    Platelet Count Normal Range: 150-450 X 10 3/uL Platelets are released from megakaryocytes in bone marrow, and they are important for adequate hemostasis. Platelet counting is done by flow cytometer based on size discrimination using either electrical impedance or electro-optical systems.  Increased in: Myeloproliferative disorders: polycythemia vera, CML, essential thrombocythemia, myelofibrosis, after bleeding, postsplenectomy, reactive thrombocytosis secondary to inflammatory diseases. 

    Decreased in: Decreased production: bone marrow suppression or replacement, chemotherapeutic agents, other drugs, eg, ethanol. Increased destruction or removal: splenomegaly, DIC, platelet antibodies (ITP, posttransfusion purpura, neonatal isoimmune thrombocytopenia, drugs (eg, quinidine, cephalosporins). 

    Potassium Normal Range: 3.5-5.0 meq/L Potassium is predominantly an intracellular cation whose plasma level is regulated by renal excretion. Plasma concentration determines neuromuscular and muscular irritability. Elevated or depressed potassium concentrations interfere with muscle contraction.  Increased in: Massive hemolysis, severe tissue damage, rhabdomyolysis, acidosis, dehydration, acute or chronic renal failure, Addison's disease, renal tubular acidosis type IV (hyporeninemic hypoaldosteronism), hyperkalemic familial periodic paralysis. Drugs: potassium salts, potassium-sparing diuretics (spironolactone, triamterene), non-steroidal anti-inflammatory drugs, beta-blockers, ACE inhibitors. 

    Decreased in: Low potassium intake, prolonged vomiting or diarrhea, renal tubular acidosis (types I, II), hyperaldosteronism, Cushing's syndrome, osmotic diuresis (eg, of hyperglycemia), alkalosis, familial periodic paralysis, diuretic therapy. 

    Additional: Spurious K+ can occur with hemolysis of sample, delayed separation of plama from erythrocytes, prolonged fist clenching during blood drawing, tourniquet placed for prolonged periods, and very high white cell or platelet counts. 

    Protein Normal Range: 6-8 g/dL The plasma protein concentration is determined by the nutritional state, hepatic function, renal function, and various disease states and hydration. The plasma protein concentration determines colloidal osmotic pressure.  Increased in: Polyclonal or monoclonal gammopathies, marked dehydration. Drugs: anabolic steroids, androgens, corticosteroids, epinephrine. 

    Decreased in: Protein-losing gastroenteropathies, acute burns, nephrotic syndrome, severe dietary protein deficiency, chronic liver disease, malabsorption syndrome, agammaglobulinemia. 

    Additional: The serum total protein consists primarily of albumin and globulin. Hypoproteinemia usually means hypoalbuminemia, since albumin is the major serum protein. Globulin is calculated as total protein minus albumin. 

    Prothrombin Time Normal Range: 11-15 seconds PT screens the extrinsic pathway of the coagulation system. It is performed by adding calcium and tissue thromboplastin to a sample of citrated, platelet-poor plasma and measuring the time required for fibrin clot formation. It is most sensitive to deficiencies in the vitamin K-dependent clotting factors II, VII, and X. It is also sensitive to deficiencies of factor V. It is insensitive to fibrinogen and not affected by heparin. It is used to monitor warfarin therapy.  Increased in: Liver disease, vitamin K deficiency, intravascular coagulation, circulating anticoagulant, massive blood volume replacement. Drugs: warfarin. 

    Additional: In liver disease, the PT reflects the hepatic capacity for protein synthesis. PT responds rapidly to altered hepatic function because the serum half-lives of factors II and VII are short (hours). Routine preoperative measurement of PT is unnecessary unless there is clinical history of a bleeding disorder. Efforts to standardize and report the prothrombin time as an INR (International Normalized Ratio) depend on assigning reagents an International Sensitivity Index (ISI) so that INR = [PT patient/PT normal]ISI. However, assignment of incorrect ISI by reagent manufacturers has in fact caused a greater lack of standardization. 

    Rheumatoid Factor Normal Range: Negative (<1:16)  Heterogeneous autoantibodies usually of the IgM class that react against the Fc region of human IgG. Positive in: Rheumatoid arthritis (75-90%), Sjogren's (80-90%), scleroderma, dermatomyositis, SLE (30%), sarcoidosis, Waldenstrom's macroglobulinemia. Drugs: methyldopa, others. Low titer can be found in healthy older patients (20%). 1-4% of normals and in a variety of acute immune responses (eg, viral infections, infectious mononucleosis, and viral hepatitis), chronic infections (tuberculosis, leprosy, subacute bacterial endocarditis) and chronic active hepatitis.  Additional: It can be useful in differentiating rheumatoid arthritis from other chronic inflammatory arthritides. However, a positive RF test is only one of several criteria needed to make the diagnosis of rheumatoid arthritis.
    Sodium Normal Range: 135-145 meq/L Sodium is the predominant extracellular cation. Serum sodium level is primarily determined by the volume status of the individual. Hyponatremia can be divided into hypovolemia, euvolemia, and hypervolemia categories.  Increased in: Dehydration (excessive sweating, severe vomiting or diarrhea), polyuria (diabetes mellitus, diabetes insipidus), hyperaldosteronism, inadequate water intake (coma, hypothalamic disease). Drugs: steroids, licorice, oral contraceptives. 

    Decreased in: Congestive heart failure, cirrhosis, vomiting, diarrhea, excessive sweating (with replacement of water but not salt); salt-losing nephropathy, adrenal insufficiency, nephrotic syndrome, water intoxication, SIADH. Drugs: thiazides, diuretics, ACE inhibitors, chlorpropamide, carbamazepine. 

    Additional: Spurious hyponatremia produced by severe lipemia and hyperproteinemia if sodium analysis involves a dilution step. Sodium falls about 1.6 mmol/L for each 100 mg/dL increase in blood glucose. Hyponatremia in a normovolemic patient with urine osmolality higher than plasma osmolality suggests the possibility of SIADH, myxedema, hypopituitarism, or reset osmostat. 

    Uric Acid Normal Range: Males: 2.4-7.4 Females 1.4-5.8 mg/dL Uric acid is an end product of nucleoprotein metabolism and is excreted by the kidney. An increase in serum uric acid concentration occurs with increased nucleoprotein synthesis or catabolism (blood dyscrasias, therapy of leukemia) or decreased renal excretion (eg, with use of thiazide diuretics or renal failure).  Increased in: Renal failure, gout, myeloproliferative disorders (leukemia, lymphoma, myeloma, polycythemia vera), psoriasis; glycogen storage disease (type I); Lesch-Nyhan syndrome (X-linked hypoxanthine-guanine phosphoribosyltransferase deficiency); lead nephropathy. Drugs: antimetabolite and chemotherapeutic agents, diuretics, ethanol, nicotinic acid, salicylates (low dose). 

    Decreased in: SIADH, xanthine oxidase deficiency, low-purine diet. Fanconi's syndrome, neoplastic disease (various, causing increased renal excretion), liver disease. Drugs: salicylates (high dose), allopurinol (xanthine oxidase inhibitor). 

    Additional: Sex and age affect uric acid levels. The incidence of hyperuricemia is greater in some racial groups (eg, Filipinos) than others (Whites). 

    White Blood Count (WBC, Leukocyte count) Normal Range: 3.4-10 K/&micro;L Measure of the total number of leukocytes in whole blood. Counted on automated instruments using light scattering or electrical impedance after lysis of RBCs. WBCs are distinguished from platelets by size.  Increased in: Infection, inflammation, hematologic malignancy, leukemias (AML, ALL, CML, CLL), lymphoma. Drugs: corticosteroids. 

    Decreased in: Aplastic anemia (decreased production), B12 or folate deficiency (maturation defect), sepsis (decreased survival). Drugs: phenothiazines, chloramphenicol, aminopyrine.

    Additional: Spurious increase: with high number of nucleated red cells. 

    Courtesy and Copyright © 1999 Management Techniques Incorporated.

    Preliminary Draft copy - for discussion purposes only. -- (This paper was started on Feb 16, 1986) -Now it is Revision 1.65--- Aug 22nd, 2009

    Suggested vitamins and minerals


    This represents a listing of the daily dosage that has ben found useful to put one person having lupus for fifteen years, into remission. At the time lupus started to be treated with a combination of vitamins and minerals, the patient had tunnel vision and pigmentation damage to the eyes from being treated with 400 mg of chloriquin to subdue the periodic outbreaks. the joint damage was so severe, the patient had to use a cane to walk, and could use stairways only with extreme pain. Within a year and a half of the new treatment, the patient is free of arthritis, is no longer subject to severe bruising, is able to lift heavy objects (much heavier than persons of the same body weight), and is able to run.

    Recent additions: Anti-inflammitories:

    Blueberry capsules: Two in the morning an two at night - Webber- 500mg-36:concentrate-2.5%anthocyanins
    They seem to reduce pain almost dramatically.

    Cranberry capsules: One in the morning and one at night - Jameson  - 500 mg - They may lower prostate or yeast problems.

    Warning: Avoid Aspartame as the Mayo Clinic cautions patients that it might increase the SED rate and may cause some people to exhibit the symtoms of Miasthenia Gravis, MS or Lupus.

    Links to aspartaime disease



    The latter paper is very important as it is a perfect example of how mony can cause total disregard of the abberant side effects that excitetoxins can have on people!

    Both MSG and Aspartaime are classed as excitetoxins and may cross the blood brain
    barrier, in times of stress.

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