Death – A Non-analytical Posting

I’m dying. Or, I seem to be dying.

Better yet, solve the following riddle:

What do you call someone who has been seriously ill for five years, unable to walk since June 2015, no longer able to sit upright (due to weakness/exhaustion), and has been told by doctors that there’s nothing that can be done for them (mainly due to the fact that the patient remains maddeningly undiagnosed, despite several batteries of tests and expert opinions)?

Well, that’s me… I think.

And since I’m lying here on a mattress, this must mean I’m on my death bed.

I think I’m too young to own and operate a death bed. And I don’t have one, but I don’t suspect a manual will help.

Anyway, I chose to wear myself out by typing this. In an hour my forearms will be painfully sore.

My Day

I awaken at 814am and lay in bed quietly.

I assess my situation, realizing things are still bad.

I check my email.

I mentally visualize each of my diagnosis/cure theories, one by one.

Ugh! My fingers on my left hand are going numb. And my left bicep is beginning to throb.

 

To be continued…

Seroquel Withdrawals – Things Get Better and Better…

Give a moment, and I shall explain my Seroquel experience in detail. On second thought, scratch that… I will instead engineer an abbreviated version much do to my current withdrawal symptoms.

During the course of 2010 I became increasingly ill with an, as of yet, undiagnosed digestive illness. Late August of that same year I had my first “smell” hallucination, which began coinciding with every bout of digestive illness from that point forward.

Two separate gastroenterologists did not believe it was possible for digestive upsets to cause my “smell misidentifications”… wherein, soap smelled like fish and my wife’s breath smelled like vegetable soup, but only after episodes of digestive distress. The clinical term for this malady is Parosmia.

Eventually the GI sent me to a counselor who sent me to a psychiatrist who put me on 50mgs of the extended release version and some amount of Lexipro (an anti-depressant).

Seeing as I wasn’t depressed, I did not take the Lexipro, but did start in on the Seroquel (10/2013). Immediately, my Parosmia (smell hallucinations) went away.

I resolved my digestive ailments on my own (10/2013), but began suffering from debilitating muscle exhaustion and fatigue… which continues unresolved.

By January 2015 I cut down to 25mgs of Seroquel. Side effects were minimal, besides an occasionally odd feeling of fear (lasting no more than an hour at a time). After a week or so I seemed to adjust to the lower dose.

In June of 2015 I cut my dose down to 12.5mgs. Within two days the Parosmia came back. My wife’s breath smelled like chemicals, perhaps, 40% of the time. Again, I experienced odd feelings of fear (lasting no more than two hours at a time). After ten days I seemed to adjust to the lower dosage.

October of 2015 I cut down further, this time taking a quarter of a 25mg pill (approximately 6.25mgs). There weren’t any notable side effects this time.

November 1st 2015: I stopped Seroquel completely.

Sleep was harder to come by for the first few days.

Also, I developed a sore throat and felt as though I was catching a cold. This symptom lasted for eleven days, but seems to be on the wane this past week.

The worst of the symptoms is related to my vision. Every day by early afternoon my eyes start failing me. They itch and burn and feel as though they are covered by a thin layer of sand. Eye drops don’t really help. And worse than that, my eyes are highly sensitive to any light source. Mostly I don a pair of sunglasses and/or wear a sleep mask.

I suspect this may have something to do with the histamine blocking function inherent to Seroquel.

 

 

How Everything is Related: A Valid Attempt at Making Sense Out of Nonsense

By Howard Neal (the patient/the impatient, as of 11/13/2015)

Theories Upon Theories…

In an act of desperation, I’m putting it all out there for readers, fellow sufferers and problem-solvers alike. I am currently unable to sit upright, and am unable to visit the doctor’s office without an ambulance delivering me (insurance won’t cover because I remain undiagnosed). There’s more, but I don’t want to get all weepy… as you know, weepy time is strictly mid-morning fare.

Basically, I do research when I am able and otherwise hope a mystery “someone” decides to help me (preferably someone from the medical or medical research community… or perhaps a millionaire billionaire type of person who appreciates that which I have to offer the universe). No doctors are treating me or are willing to push for a diagnosis/cure, because… ???

Overall Synopsis (includes possible causes and contributing factors):

  • Problems digesting lactose as child/adult (long-term lingual lipase or enzyme issue?)
  • Lactose-free since 1991 (causing/contributing to nutrient deficiency?)
  • removed
  • Gluten-free since 2001 (causing/contributing to nutrient deficiency?)
  • Heavy antacid usage 2000-2004 (sodium bicarbonate) diminished nutrient absorption
  • Cigarette smoking 20 years less than ½ pack per day – Cadmium affects Zinc functionality
  • Lack of sunlight/vitamin D (graveyard shift 2004-2010 + indoors 2013-2015) causes Magnesium/Calcium/Phosphorus imbalance
  • High sugar intake (2011-12) caused Zinc absorption issues and exacerbated bloating, diarrhea with increased losses of zinc
  • Seroquel (2011-2015) further lowered WBC, blocked serotonin in intestine (Serotonin regulates gut motility)
  • Dopamine blocked by Seroquel (possible reason why no appetite past 5 years)
  • Tricyclic antidepressants may reduce levels of riboflavin (2011-2015)
  • Sodium Bicarbonate counteracts Tricyclic antidepressants
  • Sodium bicarbonate depletes potassium
  • Nutrients needed for gluten-free dieters: B6, B12, Folate, D, Riboflavin, and Thiamin
  • Diet high in rice and rice proteins inhibits zinc absorption (always lots of rice in gluten-free diet c2001)
  • Zinc deficiency decreases Calcium and Phosphorus accumulation
  • Poor or absent Gustin levels (Zinc dependent) results in impaired taste and smell
  • TRY Digestive enzymes AGAIN?

Vitamins and Minerals

Vitamin D (has been low, between 28-30, past 5 years) – deficiency can cause phosphorus absorption issues; Fanconi syndrome; muscle weakness pain; D tends to promote the absorption of both phosphorus and calcium from the intestine 

B12 (my level is [391] coinciding with high methylfolate indicating possibility of low B12 level) – deficiency can cause Parosmia, Tinnitus, hallucinations and muscle weakness

Phosphorus (8/2015 blood work indicates low @ [2.0] ) – Cadmium hinders Phosphate reabsorption; Loss of appetite and exhaustion; helps digestion; need D and Magnesium to absorb; loss of appetite; reduce the effects of lactic acid build-up in the muscles; activates many of the vitamin B-Complex vitamins, allowing them to function as coenzymes in various metabolic processes; Phosphate, from ATP, reacts with choline (Dr Leopold);

Magnesium (blood levels okay… ingesting small amounts gave some energy/bad side effects) – needs D to properly bind/absorb, needed to absorb 300 enzymes, Magnesium is the great regulator of the five major electrolytes salt, potassium, magnesium, calcium and phosphorous; Malic acid is frequently shown to be low in CFS sufferers (together with Magnesium).

Malic Acid – The administration of malic acid to rats has been shown to elevate mitochondrial malate and increase mitochondrial respiration and energy production. Surprisingly, relatively small amounts of exogenous malic acid were required to increase mitochondrial energy production and ATP formation.

  • In addition, malic acid is the only metabolite of the citric acid cycle positively correlated with physical activity. It has also been demonstrated that exercise-induced mitochondrial respiration is associated with an accumulation of malic acid….  malic acid is useful under low oxygen conditions, where “Malic acid also helps reduce lactic acid build-up in muscles.” What is not all that clear is how that works and why.
  • Shallow breathing makes the body produce lactic acid to get its energy. Some consequences are muscle pains and anxiety. Malic acid supplements, an acid found in food, in apples and other fruit, … Szent-Gyorgyi found that malic acid kicks red muscle into using oxygen to produce its energy rather than anaerobic ways of doing it. Rather than reducing the effects of lactic acid, malic acid gives a signal to the mitochondria to use oxygen to burn fat as fuel or to use oxygen to burn glucose as energy.

Zinc (zinc blood levels ok, but functionality may be diminished due to cadmium interference/intestinal issues/malabsorption) – some functionality may be replaced by Cadmium; Zinc is necessary to utilize enzymes. The presence of intraluminal factors, such as dietary phytate (white rice and rice proteins) or unabsorbed fat, may interfere with efficient reabsorption and cause essentially a “leaching” of zinc from the body. Observations consistent with this have been made in infants with fat malabsorption (Krebs et al. 1999).

  • It is also possible that pathologic conditions that affect the gastrointestinal tract, perhaps especially in the distal small bowel, have adverse effects on zinc nutriture because of interference with the normal conservation of endogenously secreted zinc.
  • Deficiency of zinc results in a drop of metabolic rate. Zinc plays an important role in cholesterol metabolism.
  • One of the important zinc dependent proteins is Gustin which is involved in taste and smell. Poor or absent gustin levels results in impaired taste and smell (Parosmia inducing?).
  • Other important zinc containing enzymes are carboxopeptidase which helps break down protein. Zinc deficiency decreases the activity of matrix proteins, type 1 collagen and alkaline phosphatase decreasing Calcium and Phosphorus accumulation. (my phosphorous is recently low).
  • Zinc deficiency results in decreased levels of all types of white blood cells. People that sweat a lot are subject to more zinc loss, for example athletes, those in hot climate, menopausal ladies, experiencing night sweats. (I have a low WBC and always feel overheated –warm body core- past few years)
  • Cadmium- toxic levels of cadmium can inhibit zinc absorption Types of zinc supplements may remain a personal preference, although generally zinc should not be taken on an empty stomach (as it can result in nausea) should be taken with an animal protein meal, away from cereals and taken in conservative doses to increase absorption.
  • Enlarged Prostate (not enough zinc) – Also, one study found that men with benign prostatic hyperplasia (enlarged prostate) had fewer urinary symptoms when they took garlic, compared to men who took placebo. Garlic also reduced prostate size. More research is needed to see if garlic really helps men with enlarged prostate (issue seems to have resolved itself… diet?…resolving constipation issues?).

Sodium Bicarbonate (reaction started 2004 in midst of 60mgs Paxil utilization) – The normal serum range for bicarbonate is 22-30 mmol/L. [I’m at 30 – 32] Sodium bicarbonate has also been used in the treatment of tricyclic antidepressant overdose.[27] [could this cause reaction to antidepressant medication blood level when ingesting additional amounts via Nestle water and related products? i.e. counteracts efficacy?)  

  • Sodium bicarbonate works by increasing the movement of potassium from the blood into the cells. Sodium bicarbonate decreases the acidity of the blood, which then reverses the release of potassium out of the cells.
  • Disruptions in the normal bicarbonate level may be due to diseases that interfere with respiratory function, kidney diseases, metabolic conditions, or other causes. Due to greater permeability of the blood-brain barrier to hydrogen than to bicarbonate, the pH of cerebrospinal fluid may significantly decrease during sodium bicarbonate administration, which can cause mental stupor or coma [I experience confusion/paranoia after ingesting discernible levels of sodium bicarbonate]. Acute or chronic excessive oral ingestion may cause metabolic alkalosis, cyanosis and hypernatraemia.
  • Sodium bicarbonate reduces stomach acid [diminishing nutrient absorption]. Drugs that Deplete Potassium   …  Sodium Bicarbonate!

Poisons and Potions and Personal

Cadmium (ingestion via cigarette smoking 20yrs) – affects Zinc processes; mimics Zinc; toxicity can cause Parosmia; impairs D absorption; hinders Phosphate reabsorption

Parosmia (non-existent while taking Seroquel 25-50mgs – only occurs with intestinal disturbances) – Zinc loss via intestines; However not all cases of nerve damage resulting in anosmia is permanent as sometimes there is temporary irritation along the nerve pathway which will ease upon removing the causative factor. (could this mean that I am ingesting a certain food or substance that causes my intestinal nerve cells to send messages to my olfactory bulb for translation?). These observations support the hypothesis that vagal GI afferent signals regulate gastrointestinal motility, metabolic activity, and food intake.

  • *With lower levels of Seroquel (titrating down from 25mgs beginning 6/18/2015), serotonin likely increases in the intestines leading to better recognition of offending/noxious substance(s) in the intestine that may be causing afferent nerves to signal olfactory sensors causing Parosmia to return (a poison chemical smell on wife’s breath – formerly Campbell’s Vegetable Soup).

 

  • Note: I only had one smell hallucination the entire time I was taking at least 25mg of Seroquel – hallucination restarted within a few days of cutting down to 12.5mgs
  • Alpha Lipoic Acid – some recovery from their smell disorders – Alpha-lipoic acid is an antioxidant made by the body. It is found in every cell, where it helps turn glucose into energyAlpha-lipoic acid also acts as a synergist with B vitamins to help in the production of energy from the proteins, carbohydrates and fats consumed through foods …essential for aerobic metabolism
  • Lack of dopamine has resulted in documented cases of parosmia. Certain drugs can cause a decrease of dopamine in the brain. Dopamine antagonists are used to treat disorders such as schizophrenia, in which the brain produces too much dopamine (Seroquel ‘antagonist’ 4 years).
  • “Corollary discharge signals are used to define expectation, and when the sensory input does not match this expectation, the nervous system sends out a signal that says ‘there is something wrong’ (in my case, I assume this only happens when there is/are noxious food items and/or intestinal distress underway, causing the parosmia to initiate) which may be felt as pain in the phantom limb”6. Phantom limb pains, like the unpleasant scents experienced in parosmia and phantosmia, are often intense and long-lasting. Why should a person receive sensory inputs from the nose that are incongruent with the corollary discharge messages? olfactory sensory input is a result of direct interaction of neurons and molecules from the things that are smelled. http://serendip.brynmawr.edu/exchange/node/1823
  • Food Intolerance After Gastric Band Surgery – Parosmia tends to be more common in people who have had gastric bypass surgery, but it can also happen after gastric banding. Left untreated, nutritional problems can damage the nervous system.
  • Recent advances in understanding the molecular physiology of taste indicate that taste receptors able to sense such nutrients are widely distributed in the GI tract, including the oral cavity. These receptors act as nutrient sensors to trigger food digestion, the release of GI peptides and the formation of food preferences. This finding strongly supports the possibility of intercellular communication between mucosal cells and the vagus nerve (based on previous research, is there any possibility that my vagus nerve is malfunctioning?).
  • Our understanding of the sensing of nutrients by the gut is based on the “intestinal sensor cell hypothesis” originally proposed in the 1970s by Fujita et al. 34)
  • This hypothesis states that nutrient-sensing cells are distributed in the gastric antrum or duodenal mucosa and that when these cells inter-act with luminal nutrients, they release hormones in an endocrine or paracrine manner to transfer information about luminal nutrient content to other organs, including the brain, via endocrine or vagal pathways. However, the cells involved in gut nutrient perception remained unidentified for a long time.  In 1996, Höfer et al. suggested that taste-like cells similar to the taste cells in the oral cavity are distributed in the gastric and intestinal mucosa and proposed that these taste-like cells represent the unknown sensor cells (is there any way my intestinal cells are trying to transmit an important message to my olfactory sensors?).
  • Subsequently, with the development of molecular biology techniques in the field of taste research, several taste receptors that sense amino acids have been identified. We now know that metabotropic glutamate receptors (mGluRs), such as mGluR1 and mGluR4, a calcium sensing receptor (CaSR), and a taste receptor (the T1R1/T1R3 complex) are linked to amino acid sensation in the tongue. These receptors are also candidates for luminal amino acid sensors. San Gabriel et al. reported that mGluR1 is located in the glandular stomach. Their report suggested the possibility that glutamate is sensed by mGluR1, which conveys sensory information to vagal afferent nerves. 36)  (I’ve got issues with lingual lipase production… perhaps my amino acid needs are not being identified and/or I am somehow deficient
  • Although the molecule that senses glutamate in the gastric mucosa is still unknown, intragastric infusion of MSG causes a vago-vagal reflex, which increases VGE and vagal pancreatic efferent nerve activity 24) (Fig. 2).
  • In addition, using a functional magnetic resonance imaging (fMRI) technique, it has been revealed that the intragastric infusion of MSG induces activation in forebrain regions, Using a unitary recording technique in the nodose ganglion, Jeannigros and colleagues subsequently revealed the response of the vagal celiac afferent nerve to amino acid infusions in the cat small intestine in detail. Their report described many sensors sensitive to arginine, leucine and other amino acids. 39,40) (possible problems as related to Celiac disease/intolerance?)
  • Recently, we re-examined the luminal amino acid sensitivity of vagal celiac afferents in rats. Intraintestinal infusion of MSG, lysine, leucine, and other amino acids evoked excitatory responses in vagal celiac afferents. 41)
  • In contrast to these amino acids, intraintestinal infusion of glycine, methionine, and certain other amino acids led to the depression of afferent nerve activity. In addition, introduction of a glucose solution into the intestine increased vagal celiac afferent activity; the sensing mechanism underlying glucose effects has been described in another review. 44)
  • Glucose solution also suppressed sympathetic adrenal efferent activity and enhanced vagal pancreatic efferent activity. 41)
  • These observations support the hypothesis that vagal GI afferent signals regulate gastrointestinal motility, metabolic activity, and food intake (so there has to be a connection, right?).

http://www.researchgate.net/publication/47676090_Role_Played_by_Afferent_Signals_from_Olfactory_Gustatory_and_Gastrointestinal_Sensors_in_Regulation_of_Autonomic_Nerve_Activity

  • Olfactory and Gustatory Hallucinations: Studies approaching these subtypes from a neurobiological perspective indicate that the presence of phantageusia and phantosmia correlate with depressed levels of the GABA neurotransmitter in the central nervous system (2). The GABA levels in the CNS are proposed to have an inhibitory, as well as causal role in the expression of taste and olfactory hallucinations (2).
  • Causes & Comorbid Disorders: Approximately 2/3 of all olfactory dysfunctions occur as a result of damage to the neuroepithelium of olfactory centers (1). Damages may arise from a multitude factors, including environmental as well as psychopathological origins, resulting in the olfactory hallucinatory experiences. http://neurowiki2012.wikispaces.com/Olfactory+and+Gustatory+Hallucinations
  • Amino acid sensing in the gastrointestinal tract Ana San GabrielAffiliated withScientific Affairs, Communications Department, Ajinomoto Co., Inc. Email author
  • Ingesting Hummus seems to temporarily neutralize chemical breath odor from wife

Seroquel (taken from 6/2011-11/2015 … started 50mgs through late 2014, then 25mg through 6/2015 and titrating down to nothing on 11/1/2015) is an antagonist: serotonin, dopamine, histamine, and adrenergic α1 and α2 receptors…  are blocked… (assuming mostly histamine in relation to my small dosage)

  • α1-receptors primarily mediate smooth muscle contraction
  • α1-adrenergic receptor subtypes increase inhibition in the olfactory system, suggesting a synaptic mechanism for noradrenergic modulation of olfactory driven behaviors.[9] (that’s why Parosmia went away, correct?)
  • Note that only active muscle α1-adrenergic receptors will be blocked. Resting muscle will not have its α1-adrenergic receptors blocked (resting muscle generally okay, problems arise during/after muscle activity)
  • Approximately 90% of the human body‘s total serotonin is located in the enterochromaffin cells in the GI tract, where it is used to regulate intestinal movements. (perhaps this relates to my impression of gastroparesis and/or poor ingestion of key nutrients) Blood vessels with α1-adrenergic receptors are present in the skin, the sphincters[2] of gastrointestinal system
  • When humans smell food, dopamine is released to increase the appetite. (no appetite past five years, not sure if this applies)
  • If irritants are present in the food, the enterochromaffin cells release more serotonin to make the gut move faster, i.e., to cause diarrhea, so the gut is emptied of the noxious substance. (always told gi’s my body is trying to get rid of poison… perhaps relating to my intestinal intolerance for processed sugars, et al
  • Seroquel XR can cause low white blood cells (my count has been low past 5 years), which can be dangerous. Possible risk factors for leukopenia/neutropenia (I had both of these… with recent improvements)
  • Patients with severe neutropenia (absolute neutrophil count less than 1000/mm3) [I was 1019 in late 2014, so I wasn’t “severe” by definition) should discontinue Quetiapine and have their WBC followed until recovery. 
  • *With lower levels of Seroquel (titrating down from 25mgs beginning 6/18/2015), serotonin likely increases in the intestines leading to better recognition of offending/noxious substance(s) in the intestine that may be causing afferent nerves to signal olfactory sensors causing Parosmia to return (a poison chemical smell on wife’s breath – formerly Campbell’s Vegetable Soup). 
  • Note: I only had one smell hallucination the entire time I was taking at least 25mg of Seroquel – hallucination restarted within a few days of cutting down to 12.5mgs
  • **Discontinued Seroquel 11/1/15 – some short duration paranoia/fear lasting one week – continuing (as of 11/13/15) difficulties with intermittent low grade fever/occasional sore throat – eyes scratching and burning with light sensitivity – eye pain worsens as day progresses – eye drops do not seem to help

Tinnitus (started both ears 10/2014, now mostly right ear) – caused by possible B12 or D deficiency

Lingual Lipase (30% of the time when I chew red meat of turkey, it doesn’t break down in my mouth… assumption is that lingual lipase malfunctioning) and Its Role in the Digestion of Dietary Lipid

  • …the stomach contained very little activity, however, when saliva was excluded. Lipolytic activity was not found in the stomach wall or in the parotid, submandibular, and sublingual glands. The findings suggest that the lingual serous glands secrete a lipase which catalyzes in the stomach the conversion of triglyceride to partial glycerides and FFA. It is proposed that this reaction is the first step in the digestion of dietary lipid.
  • The most important function of lingual lipase in mouth of an infant is to digest milk fat (I’ve been lactose intolerant most of my life).
  • Therefore, a deficiency of this enzyme can adversely affect the digestion of fats. This can increase the levels of cholesterol and triglycerides in the body (my levels are elevated). This enzyme is not only required for digesting fats, but for metabolizing fat-soluble vitamins as well. So, the insufficient production of this enzyme may cause a deficiency of fat-soluble vitamins, like vitamin A, D, and E. Apart from these, it has been observed that individuals with lipase deficiency can have decreased cell permeability. Decreased cell permeability refers to the condition, where nutrients cannot enter the cells easily, and waste materials cannot leave the cells promptly (each of these could apply).

Vitamins Again and Possible Deficiencies

Riboflavin (B2) –  It is also involved in the conversion/synthesis of the coenzymatic forms of the B vitamins B6 (P5P) and B9 (5-MTHF), which are essential to methylation function.

  • Severe MTHFR deficiency is extremely rare however and can result in dangerously elevated Homocysteine levels, and virtually zero conversion of 5,10-Methylene-THF into 5-MTHF. It was only when I took 150mcg of 5-MTHF four times a day that I felt immeasurably better. The 5-MTHF supplement also muscle tested positively on me. I would therefore not really recommend regular Folic Acid as a supplement.
  • Riboflavin (vitamin B2) is part of the vitamin B group. It is the central component of the cofactors FAD and FMN and as such required for a variety of flavoprotein enzyme reactions including activation of other vitamins.  All B vitamins help the body to convert food (carbohydrates) into fuel (glucose), which is used to produce energy. Riboflavin is also needed to help the body change vitamin B6 and folate into forms it can use. (Tricyclic antidepressants may reduce levels of riboflavin in the body = SEROQUEL !!!)

Potassium Deficiency (interesting how sodium bicarbonate depletes potassium… not sure how I relate to this) – Among the many functions of potassium in the body are regulation of the heartbeat and the function of the muscles… Drugs that Deplete Potassium … Sodium Bicarbonate

  • muscle weakness or twitching or spasm
  • breakdown of muscle fibres
  • leg or other muscle cramps
  • muscular paralysis
  • shortness of breath or poor lung function, and even lung paralysis in serious cases
  • abnormal heart rhythms
  • intestinal paralysis leading to constipation.

Chloride Deficiency 

  • loss of appetite
  • muscle weakness
  • lethargy

Biotin Deficiency

  • loss of appetite
  • muscular pain
  • nausea.
  • brittle nails and hair
  • dry scaly scalp or face
  • intestinal tract symptoms like loss of appetite, nausea
  • fatigue or extreme exhaustion due to impaired energy production
  • muscle pain or cramps related to physical exertion.

Vitamin B1 (Thiamine) Deficiency

  • muscular weakness
  • excessive fatigue
  • loss of appetite and weight loss
  • Muscle cramps, atrophy,
  • Weakness to  excessively weak
  • Gastrointestinal disorders
  • constipation, and nausea

Folate (folic acid) Deficiency

  • fatigue
  • heart palpitation
  • higher blood levels of homocysteine and risk of heart disease
  • stomach disorders,  loss of appetite, and digestive upsets
  • pallor and sensitivity to cold
  • chronic muscular fatigue,  general weakness
  • gastrointestinal tract problems like periodontal disease, gingivitis

Nine Nutrients You May Need To Boost If You’re Gluten-Free

B6 ……….studies have shown that many people with celiac disease and following the gluten-free diet are low in vitamin B6. Start with chickpeas //// a cup will give you more than half of the vitamin B6 you need in a day….. hummus

Folate, also known as folic acid, ….. Lots of conventional gluten-containing foods are fortified with extra folate …. so if you’re eating gluten-free, you’ll need to take special care to get enough. …spinach, asparagus and brussels sprouts green peas and broccoli.

Vitamin D … if you’re eating gluten-free (and especially dairy-free, too), you may not get enough. In fact, studies have shown that people with celiac disease are especially prone to vitamin D deficiencies. Few foods naturally contain much vitamin D — exceptions include cold water fish like swordfish and sockeye salmon, which contain substantial amounts. An egg yolk contains about 10% of the vitamin D you need each day.

Vitamin B12 …  Research has shown that people with celiac disease don’t tend to get enough of vitamin B12 in their diets, although their bodies may not be low in the nutrient. Part of the reason for that low intake may be that most conventional breakfast cereals are fortified with 100% of your daily vitamin B12 requirements, and of course people who avoid gluten will need to avoid many of those cereals, as well.

  • A meal-sized portion (4 oz. or more) of salmon or trout will provide 100% of your recommended daily intake, while 6 oz. of beef will give you half of what you need.

Thiamin, riboflavin and niacin are all B vitamins, and all play a role in converting food you eat into energy. As with vitamin B12, studies have shown that people following a gluten-free diet don’t seem to get enough of these vitamins, although medical testing doesn’t indicate they’re necessarily deficient.

  • All three typically are added to conventional fortified gluten-based cereals and breads, which explains why people might get less of them on the gluten-free diet.
  • Beans tend to be a good source of thiamin – half a cup of green peas or lima beans will give you about 50% of what you need each day. Acorn squash and potatoes also contain significant thiamin.

http://celiacdisease.about.com/od/sideeffectsofthediet/ss/Nine-Nutrients-To-Boost-Gluten-Free.htm#step8

It always comes back to….  

MORE Zinc deficiency or inefficiency (potentially caused by Cadmium in body tissues – blood work indicates Zinc levels sufficient, but symptoms seem too coincidental)

… supporting statements http://www.metabolics.com/blog/a-practitioners-guide-to-zinc-supplements/

  • In the case of a severe deficiency, skin ailments such as eczema, acne, and psoriasis may also develop. …on forehead and scalp
  • … protein enhances the absorption of zinc and a phytate rich diet (from cereals, grains, corn and rice) inhibit the absorption of zinc.  ….my diet is and has been high in rice and rice proteins past decade
  • zinc plays an important role in cholesterol metabolism.  I have high cholesterol / LDL-P levels
  • One of the important zinc dependent proteins is Gustin which is involved in taste and smellPoor or absent gustin levels results in impaired taste and smell.        I have Parosmia 
  • Zinc deficiency decreases the activity of matrix proteins, type 1 collagen and alkaline phosphatase decreasing Calcium and Phosphorus accumulation. I have low phosphorous, per today’s blood work … need to research
  • Zinc deficiency results in decreased levels of all types of white blood cells. I’ve had low WBC past 5 years
  • People that sweat a lot are subject to more zinc loss, for example athletes, those in hot climate, menopausal ladies, experiencing night sweats. Despite my skin being cold to the touch, I’m always hot… perspiration greatest during the evening

Tinnitus… can be helped with zinc

Cadmium (quit smoking 3 years ago, but half-life in body = 10+ years) inhibits absorption of zinc/functionality

IBS / diarrhea (zinc lost in feces) – Diarrhoea is both a cause and result of Zinc deficiency. Too rapid movement of chyme/stool through the small and large intestine (i.e. short transit times) will result in greatly reduced levels of Zinc absorption, and indeed other nutritional elements.

Parosmia / smell hallucinations… loss of zinc attributed

Zinc needed for methylfolate activation/B6 – per blood work, genetic predisposition for B6 issues/utilization problems

Randomness  

Fanconi syndrome (do not have this but seemingly many similarities) is a disease of the proximal renal tubules[1] of the kidney in which glucose, amino acids, uric acid, phosphate and bicarbonate are passed into the urine, instead of being reabsorbed. Fanconi syndrome affects the proximal tubule, which is the first part of the tubule to process fluid after it is filtered through the glomerulus. It may be inherited, or caused by drugs or heavy metals.[2]

  • Different forms of Fanconi syndrome can affect different functions of the proximal tubule, and result in different complications. The loss of bicarbonate results in type 2 or proximal renal tubular acidosis. The loss of phosphate results in the bone disease rickets (even with adequate vitamin D and calcium), because phosphate is necessary for bone development.[3]
  • It is possible to acquire this disease later in life.

Krebs Cycle (no sunlight 2 calendar years) – sunlight generates Fumaric Acid necessary for cycle

Calcium (blood levels normal) – Phosphorus and D necessary to absorb calcium

Methylfolate – have genetic mutation (per Dr Zeragoza’s office) making folate absorption difficult

Lyme disease – many similar symptoms … geographically unlikely – tested negative late 2011 –

Dimished State / Vitamin D / Magnesium

So, as you may have guessed, I’m in some sort of limbo right now. And my limbo consists of ears ringing loudly and extreme fatigue at 5am on a Monday. There are other symptoms, too. Please read the previous entries as needed.

Eh, never mind… my forearm muscles are aching. Sometimes fatigue sets in before I can accomplish much of anything. I’ll try again later if and when I’m still around. Please keep in mind my level of coherence is down.

Eleven hours later, and my respiration continues. Frustration is on the wane.

Back in August I was hospitalized for several days. The hospital people were able to determine that my Vitamin D was still somewhat low, and my phosphorus was also low.

For a time the low phosphorus revelation held hope.

The hospital people transferred me to a nursing home for rehabilitation.

“Rehabilitation from what?” you may be asking yourself. And you’d be asking yourself the right question.

My stay in the nursing home began in the middle of August and last until October.

I asked the staff if I could get a phosphorus supplement. Staff said they needed additional blood work to determine if I was actually Phosphorus-depleted.

Ten days later, the results came back. My phosphorus level was elevated and they refused to provide me with a supplement.

So, how could this be? How could my Phosphorus level increase in such a way?

My blood was drawn at 4am. The mobile phlebotomist whisked away my sample, before drawing blood from up to 200 other nursing home residents (I suspect not everyone donated but there’s no way of knowing for certain).

What I was told is that these mobile phlebotomizers go nursing home hopping picking up samples here there, and everywhere, before returning back to the ranch.

So my blood was “run” at approximately 11am.

Here’s the issue. With Phosphorus, the longer it takes to “run” the blood work through the lab, the more the Phosphorus level increases.

The doctors on staff did not seem to buy into my theory. I did, however, take 50,000iu’s of Vitamin D. And this one-time dose caused extensive after-effects. My tinnitus multiplied in intensity, and I felt intense pressure in both ears, lasting several hours.

What I’ve come to learn is that ingesting Phosphorus supplements can be dangerous (arrhythmia/tachycardia), and intense ringing in the ears after taking a large dose of Vitamin D may be related to a Magnesium deficiency.

Long story short, I took several varieties/combinations of Magnesium and experienced negative side effects.

At the beginning of October I was discharged from the nursing home due to my lack of progress in physical therapy for an illness that remains undiagnosed.  Plus, insurance would no longer cover the expense. And now I am back home, bedridden… worse off than before but mostly grateful to still be alive.