Acetylcholine/Choline Deficiency in Chronic Illness – The Hunt for the Missing Egg

ucm278430We hear a lot about vitamins and minerals such as B12, folate, magnesium, vitamin C, and so on, but there seems very little talk these days on the importance of dietary lecithin and choline. Are you consuming an adequate amount of acetylcholine, or other phospholipids? The odds are that you are not.

A little bit about choline

The human body produces choline by methylation of phosphatidylethanolamine (from dietary sources such as lecithin and others) to form phosphatidylcholine in the liver by the PEMT enzyme. Phosphatidylcholine may also be consumed in the diet or by supplementation. Choline is oxidized to betaine which acts as an important methyl donor and osmolyte.

For those wanting to see how this relates to the methylation cycle, below is a nice graphic (courtesy of Wikipedia).

Choline metabolism

It is well known that magnesium deficiency is widespread (57% of the population does not meet the U.S. RDA according to the USDA), but the numbers for choline deficiency are even more shocking.

According the National Health and Nutrition Examination Survey (NHANES) in 2003-2004, only about 10% of the population have an adequate intake of choline. This means about 90% of the population consumes a diet deficient in choline. Furthermore, those without an adequate intake of choline may not have symptoms.

Along with folate and B12 deficiency, inadequate consumption of choline can lead to high homocysteine and all the risks associated with hyperhomocysteinaemia, such as cardiovascular disease, neuropsychiatric illness (Alzheimer’s disease, schizophrenia) and osteoporosis. Inadequate choline intake can also lead to fatty liver or non-alcoholic fatty liver disease (NAFLD).

The most common symptoms of choline deficiency are fatty liver and/or hemorrhagic kidney necrosis. Consuming choline rich foods usually relieve these deficiency symptoms. Diagnosing fatty liver isn’t as simple as running  ALT and AST since nearly 80% of people with fatty liver have normal levels of these enzymes according to a population study published in the journal Hepatology. In fact, in an experiment, 10 women were fed a diet low in choline. Nine developed fatty liver and only one had elevated liver enzymes.

For those who are genotyped by 23andMe, there is a SNP (rs7946) related to NAFLD you can look at in the PEMT gene called PEMT G523A (V175M). Caucasians with nonalcoholic fatty liver are more likely to carry the rs7946 (T), with the effect being most pronounced for rs7946(T;T) genotypes. [PMID 16051693]

If you are genotyped by 23andMe, make sure you are logged in to 23andMe and you will see your results for this SNP.


Choline, the nervous system, and the heart

Despite it’s role in the CNS and stimulating parasympathetic activity, there is very little info about choline and mental illness. However, in a large population-based study published in The American Journal of Clinical Nutrition, people with higher blood levels of choline had lower levels of anxiety – however, levels of choline did not correlate with depressive symptoms.

Despite the lack of studies, it has been clinically observed that supplementing Lecithin or putting patients on a Lecithin rich diet can lower levels of anxiety, help the nervous system by establishing balance between sympathetic and parasympathetic, and even manage cardiac dysrhthmias. The Milner Acetylcholine Protocol (MAP) uses lecithin to manage cardiac dysrhthmias.

Phospholipids and the cell membrane

The fundamental building blocks of all cell membranes are phospholipids. Lecithin consists of phospholipids such as phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, Phosphatidic acid, other minor phospholipids and glycolipids. About 50% of the mass of most cell membranes are composed of phospholipids. The plasma membranes of cells also contain glycolipids and cholesterol – which correspond to about 40% of the total lipid molecules. Adequate intake of phospholipids and glycolipids is important for the integrity of the cell membranes. Lecithin contains a balanced amount of phospholipids and glycolipids.

Phospholipid supplementation has also been shown to help with mitochondrial dysfunction in patients with diseases such as Chronic Fatigue Syndrome, chronic Lyme Disease, Fibromyalgia, and Gulf War Illness. Fatigue reduced about 40% in Chronic Fatigue Syndrome patients after lipid replacement therapy (supplementing phospholipids) according to the Journal of Chronic Fatigue Syndrome.

Adequate intake of choline and choline-rich foods

Adequate intake of choline varies by age. Here is a table by

Adequate Intake (AI) levels for choline are:


Adequate Intake (AI)
of Choline

Infants:(0-6 months)
(7-12 months)
125 milligrams
150 milligrams
Children:(1-3 years)
(4-8 years)
(9-13 years)
200 milligrams
250 milligrams
375 milligrams
Adolescents:(14-18 years)400 milligrams (Females)
550 milligrams (Males)
Adults:(19 and older)425 milligrams (Females)
550 milligrams (Males)
Pregnant women450 milligrams
Breastfeeding women550 milligrams also has a very nice graphic showing the best sources of choline. According to their chart, beef liver and egg are by far the best sources for lecithin with modest amounts in lean beef, chicken breast, cod, wheat germ, and cauliflower.
Unfortunately, not all nutrition data is the same, and for the sake of comparison, below is what Wikipedia lists as high choline foods.

Animal and plant foodsCholine (mg)Calories
32 gram sunflower lecithin syrup544250
5 ounces (142 g) raw beef liver473192
15 gram soy lecithin granules450120
A cup of wheat germ202432
Half a pound (227 g) cod fish190238
A pound (454 grams) of broccoli182158
A pound (454 grams) of cauliflower177104
Quart of milk, 1% fat173410
Half a pound of chicken150543
Two cups (0.47 liters) firm tofu142353 
A cup of uncooked amaranth135716
30 gram Brewer’s yeast (2 tbsps)120116
A cup of uncooked quinoa119626
100 grams of Soybeans dry116268
Large hardboiled egg11378
A pound of spinach113154
Two cups of cooked kidney beans108450
A cup (146 g) of peanuts77828
A cup (143 g) of almonds74822
Three cups (710 cc) cooked brown rice54649
A grapefruit19103

Since cooking eggs at high temperatures destroys the choline content, it’s best to cook the egg so the yolk is runny to preserve lecithin content. For people without egg allergies, properly cooked eggs is one of the best sources of lecithin.

In presence of an egg allergy, consuming liver or supplementing with sunflower lecithin may be the best options to ensure an adequate intake of choline. Sunflower lecithin may be a better source for lecithin than soy because unlike soy lecithin, sunflower lecithin is never derived from GMO crops. Also, soy is generally more allergenic than sunflower, so soy lecithin could potentially provoke unwanted effects in sensitive individuals.

Acetylcholine, phospholipids, autoantibodies, and a word of caution

Acetylcholine and antiphospholipid autoantibodies are seen in various autoimmune and chronic illnesses. It is well know that with Myasthenia Gravis, patients most commonly have autoantibodies against nicotinic acetylcholine receptor (nAChR). A large number of CFS patients may have acetylcholine receptor antibodies according to a study published in the International Journal of Molecular Medicine.

Dysautonomia and POTS can also be associated with autoantibodies against acetylcholine receptors. Mayo medical laboratories has a very comprehensive Autoimmune Dysautonomia Evaluation lab test that tests for autoantibodies against acetylcholine receptors and much more.

Antiphospholipid Syndrome (or Hughes syndrome) is an autoimmune condition that can lead to hypercoagulation and blood clots. Conditions such as Lupus, Sjogren’s syndrome, Chronic Fatigue Syndrome, and Fibromyalgia are often associated with antiphospholipid antibodies. Antiphospholipid antibodies can even develop in presence of chronic infections such as Hepatitis C, Syphilis, Chlamydia pneumoniae, EBV, HHV-6, Lyme disease, mycoplasma, Q Fever, and many other infections. Antiphospholipid syndrome can be tested for with LabCorp’s Thrombotic Risk Profile.

At this time there is insufficient evidence to determine if supplementing lecithin would be beneficial or harmful for those with acetylcholine receptor autoantibodies or antiphospholipid syndrome. More clinical research is needed to understand how lecithin supplementation influences the various autoimmune processes that may exist in these patients.

Whether you are a health expert with experience utilizing choline rich foods or lecithin supplements to treat chronic illness, or a patient using choline to promote your own health, please share your experience below.

By geneticgenie | October 21st, 2013 | Posted in Uncategorized |

41 Responses to “Acetylcholine/Choline Deficiency in Chronic Illness – The Hunt for the Missing Egg”

  1. Melissa Says:

    This article was particularly interesting to me as I have been diagnosed with Lyme and CFS in the past and also have Myasthenia Gravis, POTS/Dysautomnia as well as heterozygous for the MTHFR gene, which I’ve begun to suspect plays a role in my diseases and perhaps this as well. Thanks for the valuable info!

  2. Susan Says:

    Thanks for the good information. You may also want to add some information about cystic fibrosis and choline. There’s been some interesting papers from British Columbia on this topic. Thanks for the reference to the papers on chronic fatigue. Very helpful.

  3. geneticgenie Says:

    Susan – If I were to include all info there is about choline, I might as well write a book. But interesting note about cystic fibrosis. A little research shows that they can have high homocysteine and tend to have low glutathione too. And choline can improve homocysteine and glutahtione in cystic fibrosis patients. There is a lot of talk about using B12 and Folate to reduce homocysteine, with not as much talk about how prevalent choline deficiency is. Choline lowers homocysteine. And like folate, it turns into an important methyl donor when it is oxidized into betaine.

  4. geneticgenie Says:

    Interesting history Melissa. Were you ever tested for acetylcholine receptor autoantibodies or antiphospholipid antibodies?

  5. MK Says:

    I have several biggie mutations in the methylation cycle and have been on various vitamins and supplements for several years with mixed results. I started on 1 Tbsp per day of liquid soy lecithin back in the spring, and there was an almost immediate and very noticeable difference in my anxiety level, chronic constipation, and focusing issues. Despite being in the gifted program as a kid and having a high IQ, I have always been frustrated with my attention level and ability to finish what I start (didn’t finish HS on time, dropped out/kicked out of college multiple times 10 years ago). I am now taking college classes and getting all A’s. In the middle of summer semester I ran out of lecithin and kept meaning to pick some up and didn’t really make it a priority, but for the 2 weeks I was off of it I would just sit in front of the computer, unable to complete the papers I had to write. That spaciness and lack of focus went away as soon as I restarted the supplement. I’ve tried citicoline and a normal choline/inositol supplement, and they both made me nutty. Lecithin doesn’t do that. Tastes like crap and the texture is nasty but I can choke it down if it gets me through school. : )

  6. Shae Says:

    I have Dysautonomia (hyperMCAS POTS and NCS/NMH) plus a host of comorbid conditions. I am a ‘no call’ on this allele. Any suggestions?

  7. geneticgenie Says:

    Shae – A no call for that gene probably means that 23andMe had trouble genotyping that part or area of your DNA. So there are no conclusions you can draw from that.

    However, it’s just a single gene and it’s not determinant of fatty liver or choline deficiency. It just increases odds of developing fatty liver which can be caused by choline deficiency.

    I don’t give medical advice, but do you eat eggs? Some may do well with them, some potentially worse depending on autoantibodies and allergies. Nevertheless, most otherwise healthy people do not get enough lecithin as described in the post.

    POTS can be caused by acetylcholine dysregulation and acetylcholine receptor antibodies and many other things. What to do in that case isn’t clear to me, but a good POTS specialist (found at usually knows how to test for these things and what to do about them.

  8. Shae Says:

    I love eggs. Unfortunately, I’m a complicated zebra…I can’t take the typical Meds, and have unfortunate comorbidities. Kinda hosed, basically. I’m also hyperMCAS POTS (extremely rare subset of hyper POTS) as well as NCS/NMH, so it gets complicated, indeed. I know several of my COMT SNPs carry mutations.

  9. Tiffany Says:

    I got a prenatal diagnosis of trisomy 21 for my last child and read a study in a mouse model of T21 where pre- and perinatal choline improved symptoms. I started 3 g/day choline at ~20 weeks and my now 8 month old was born with no major health issues and is progressing age appropriately in terms of meeting milestones. We have continued choline during breastfeeding. I would love to find out the level of methylation on my son’s 21st chromosome as I’m sure that the high dose choline has decreased the severity of effects from the additional chromosome.

  10. melvin Says:

    the snp you named above for pemt is the one my results say is the normal one TT and shows green not red colored like the mthfr.

    Why would the wild type normal be a higher risk for fatty liver?

  11. geneticgenie Says:

    First, the wild type isn’t always beneficial. Second, it is the wild type for caucasians, but not for most other ethnicities.

    Digging a bit more before this comment, it doesn’t appear that there is universal agreement that this SNP increases risk of NAFLD. However, caucasians with NAFLD appear to be more likely to be TT. Confusing indeed!

  12. James Says:

    Great article but I think there is an error.

    We are only interested in the raw egg yolk portion of the egg which would be about 17 grams. This means there is roughly 116 mg of lecithin per raw egg yolk and not 389 mg.

  13. geneticgenie Says:

    James – thank you for your correction. Will correct the article.

  14. john Says:

    I am diagnosed with myasthenia gravis.and undergone post thymectomy. Can I use this lecithin as a supplement. Will I see any improvement in my situation. Thanks in advance.

  15. Kathrynn Says:

    I have been having some intermittent ptosis (eyelid drooping) and myasthenia gravis was suggested as a possibility. I put together several conversations about myasthenia gravis with a word I remembered from my detox report “acetylation”, so I ran my 23andme results for PEMT and I am +/+ homozygous TT for the rs7946 and also rs4646408 is +/+ TT as well. Of the rest of the PEMT there are 22 heterozygous, 10 normal, and 13 not genotyped. According to my detox report I am probably a slow acetylator since I have NAT2 R197Q rs1799930 AA +/+. Also in the detox report are CYP1B1 L432V rs1056836 GG +/+ and CYP1B1 N453S rs1800440 CC +/+ but I’m not sure if that has an impact on acetylcholine or not. Myasthenia gravis is an autoimmune disease. In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle contraction from occurring. I have autoimmune diseases already which automatically makes me susceptible to others.
    Am I correct in thinking that these gene defects regarding acetylation would mean that I have less acetylcholine in the first place? If so it would seem to me that antibodies further blocking receptors for what little there is might bring on symptoms or exacerbate them.
    I was having an episode of ptosis yesterday and I find it interesting/strange that I had a craving for fried eggs with runny yolks. I ate 5 of them. The ptosis went away later that evening. I hadn’t read your article at that time but now I wonder if it was my body craving the lecithin for the choline? Also, I happen to have choline bitartrate powder… would that be beneficial to take or not?

  16. Christi Says:

    I’m hoping to connect the dots between this and BCHE gene rs1799807, cholinesterase inhibitors, nightshade intolerance. Anne Wright has written on it.

    I’ve had a decrease in POTS like symptoms, mysthenia gravis like symptoms, CFS/Fibromyalgia, just from eliminating Nightshade foods.

    I like eggs but they seem to make me sick to my stomach, I wish I could benefit from a choline supplement I still have anxiety and memory problems.

  17. Dan Says:

    HI Christi,

    I’m not a doctor, but a patient like you. I’ve also found that I need to avoid nightshade foods big time or I get muscle cramps, twitching, and just overall overstimulation. High acetylcholine levels can cause anxiety as well due to that overstimulation.

    I recently found a study that showed a connection between B12 deficiency and low acetylcholinesterase levels, suggesting that perhaps B12 may help increase the breakdown of acetylcholine.

    The same with l-carnitine. Treatment with l-carnitine helped restore acetylcholinesterase levels in aged rats.

    Not sure if the same thing occurs in humans, but it’s worth noting that B12 levels are often functionally low, as are l-carnitine.

    Hope this is helpful in some way.

  18. A Researcher Says:

    The article is appreciated. Phospholipid and Choline associated factors are utilized to produce more than Ninety Nine Percent of molecules produced by biological systems through Methionine. Phospholipids Phosphatidylcholine, Phosphatidylethanolamine, and Sphingomyelin may constitute more than 90 percent of cellular membranes. The only pathway, of the three primary and other ancillary synthesis mechanisms of Methionine, which does not produce Homocysteine is the Vitamin B12 reliant Methionine Synthase pathway. Asymmetric Dimethylarginine, Homocysteine, Trimethylamine-N-Oxide and C Reactive protein as the most indicative factors for susceptibility to sudden Adverse Health Events, including demise. These factors are also principal factors in the emergence of most aspects of Human pathology, from Plasticity Changes and other deterioration of biological structure. Particularly, however, these result in impaired vasomodulation through impaired synthesis of Nitric Oxide. Each of these may emerge as a result of Choline deficiency or Phospholipid deficiency in general, except for Trimethylamine-N-oxide which results from ingesting Phospholipids or Meats, Chicken, Eggs or Fish, without taking a Probiotic. Less than optimal Microflora may produce Trimethylamine which permeates digestive Pathway tissue to become reduced to Trimethylamine-N-Oxide by Hepatic tissue, extracting Nitric Oxide, resulting in Vasoconstriction, producing a systemic degradation molecule Trimethylamine-N-Oxide and resulting in susceptibility to sudden adverse health events until these factors are cleared from digestive pathways sometimes taking months or more than an annum. Choline deficiency, along Phosphatidylcholine, Folate, Trimethylglycine and the myriad other factors within Choline associated pathways, are almost clinically and in the research literature observed to be a requisite factor or incipient enabling circumstance to almost every Pathology. Homocysteine levels, illustratively, have been suggested by research analyses to be indicative of stage of development, phase in span of being, and indicative of level of pervasive progressive Pathology. Difference in Phosphatidylcholine synthesis levels between genders, illustratively, is about precisely Homologous to the difference in Span of Being between genders when excluding the effect of the PEMT Single Nucleotide Genetic Polymorphism which impairs one of the Phosphatidylcholine synthesis pathways. Some populations in the United States exhibit Fifty percent of some gender which exhibit such impairment homozygously and Seventy Five percent or more whom exhibit such impairment heterozygously without regard to gender. There is substantial information at AMEHSI.ORG that provides support in this regard. Imperatively, however, Choline is utilized to produce Methionine and Phosphatidylcholine. Folate is utilized to produce Methionine when Choline is not adequately exhibited. Trimethylglycine is produced from Methionine and potential from Phosphatidylcholine. Trimethylglycine is utilized to recycle Homocysteine into Choline, whereas numerous other factors potentally donate Methyl Groups to Homcysteine or Cysteine to produce Choline or Methionine.

    There is a precise cadre of factors essential to biological function exhibited at AMEHSI.ORG. These factors are included in the AMEHSI Specification which presents guidance in producing an iterative interactive cadre of Assay, Analysis of personalization of the specification to the individual and then enables the use of such capabilities to determine the precise molecular mechanisms which are exhibit differently on an individual bases to cause Pathology. The factors may be, essentially,

    Folate, and not Folic Acid
    Betaine as Trimethylglycine and not only Betaine Hydrochloride if including this Hydrochloride factor at all,
    A Probiotic which does not include the name Firmicutes or Rhamnosus, such as the Probiotic Product Align or other diverse product,
    Prebiotic factors such as live plant foods which provide a version of Methionine Synthase that is not B12 Cobalamin reliant,
    A Complete B Vitamin Complex which includes B6, B12, Methylcobalamin, Thaimine, biotin, Riboflavin, Pantothene, and Niacin,
    L-Arginine to remediate Asymmetric Dimethylarginine accumulation,
    An Amino Acid Supplement with the complete 20 Amino acids, excluding Phenylalanine if Phenylketonuria is exhibited or excluding Glycine if Non Ketotic Hyperglycemia is exhibited.
    Water, Daily, preferably in the morning and evening.
    A diverse supplement including essential other vitamins and minerals.
    A typical or managed regimen of ingestion and activity otherwise.

    If nothing else, then Olive Oil, Sugar Beets and a Probiotic, along with water in the morning and evening, may provides substantial support during most Pathology, and may potentially substantial mediate Diabetic and other Progressive Conditions.

    Always ask your physician to Assay these factors, possibly at every visit
    Asymmetric Dimethylarginine
    C – Reactive Protein.

    Always ask that your Assay results consider optimal levels, not typical levels. Typical levels are based upon increasing exhibition of such factors correlative to progressing Gerontological status and phase of being, which are based upon a presumption that demise occurs. Increased levels of these, however, result in substantial Pathology and risk of sudden Adverse Health Events, without regard to phase of development or stage in Span of Being. Normal levels for increased numbers of annum in Span of Being empirically constitute increased levels of occurring systemic degradation and increased susceptibility to Adverse Health Outcomes. Similarly, typical levels of Choline are substantially inadequate, whereas recommended levels may be logarithmically lower than that exhibited during Gestational phases which is typical the most recent instance in which Humans obtain adequate levels of Choline, except during Breast feeding which supplies most of the factors suggested as beneficial is in the posting. A substantial factor in the emergence of Autoimmune conditions is the Emergence of Thymus involution, resultant of a Choline Deficiency, in which the producer of Human T immune Cellular material degrades progressively into indiscernible Adipose tissue beginning with Choline deficiency exhibited during incipient post Natal circumstance.

    There is more information at AMEHSI.ORG.

  19. David Says:

    No discussion about choline, phosphatidylcholine or lecithin (or even L-carnitine, betaine or TMG) consumption is complete without a thorough discussion of TMAO (Trimethylamine N-oxide).

    There are several studies on this subject. Here is one:

    Gut flora metabolism of phosphatidylcholine promotes cardiovascular… – PubMed – NCBI

    As far as popular media, Dr. Oz, who used to recommend L-Carnitine supplements, has retracted that recommendation. When it comes to TMAO, there is little difference between L-Carnitine and choline supplements.

  20. Joel Greene Says:

    I have acetylcholine esterase deficiency. My C-reactive protein test was “7″. Do I have a higher level of inflammation or does this mean that a serious health telatefevent is imminent?

  21. A Research Says:

    The AMEHSI Specification at AMEHSI.ORG provides guidance regarding Trimethylamine production by less than beneficial Ingestive Pathway Microbial Factors. Trimethylamine is produced by such less than beneficial microbial factors when Choline, Trimethylglycine and L-Carnitine exhibiting nutritional factors are ingested. The precise Pathology is, then varied. Most incipiently, Trimethylamine may traverse the Intestinal Membrane, including the fluid membrane Peritoneum which encapsulates many tissues and organs, as a result of Phospholipid Choline factor deficiency, which impairs permeability of cellular material, specific permeability of cellular material which enables traversal of only particular material, as well as increased levels of TNF Alpha which impair Tight Junction or Gap Junction Protein function such that tissues become less tightly situated, including less cohesive in sharing molecular factors. Trimethylamine then becomes transformed into Trimethylamine-N-Oxide by FMO (1 and 3) within Hepatic Tissues in Particular. The N-Oxide is obtained from bioavailable Nitric Oxide within Hepatic Tissues and along gradients exhibited systemically within biological systems. This may produce a decrease in Nitric Oxide locally and potentially systemically. Such may result in vasodilatation and ephemeral Local Ischemia.*
    The ability of Hepatic Tissues to manage systemic toxicity, participate Insulin management biofeedback with Pancreas and Renal Tissue, and thus systemic levels of Toxicity and other factors may become ephemerally or persistently impaired. The context of increased levels of Homocysteine, Asymmetric Dimethylarginine, Methylglyoxyl and other factors, however, may also produce impairment of Nitric Oxide management, including directly inhibiting Nitric Oxide Synthase. When multiplicity of such factors are exhibited the ability to recover from one such circumstance may become impaired, thereby constituting exhibition of the Number 1, 2, 4 most indicative factors of susceptibility to an adverse health event. Cellular material distress may then increase, resulting in C – Reactive protein indicator increase which is associated with cellular material experience Lysis or degradation, illustrating the essential nature of assaying C – Reactive Protein. Trimethylamine-N-Oxide, however, may be transformed, again, into Trimethylamine particularly by less than beneficial Ingestive Pathway Microflora and particularly as a result of impaired permeability of digestive pathway tissues. Such Impaired permeability may enable flow of TMAO into digestive pathway from Internal Vasculature, Arterial, or other Pathways to interact again with Digestive Pathway Microflora to produce TMA. Along with progressive pathology and individuals have experience demise, a substantially pervasive phenomenon is the exhibit of Gaseous bowel discharge, which may be indicative of a role in such outcome from TMAO being transformed to TMA, resulting release exhibition of Nitric Oxide as well as Amine groups or Imino groups, which may be further metabolized upon Microbial Metabolic cycles which produce Methane Gas.*

    The Bidirectional flow of molecular factors generally across digestive pathway tissue membranes may not be typical for expansive cadres of factors such as TMA, TMAO and CA2+ Ions which may be large molecules, however, small molecular factors such as water and Potassium Ions may move across such membranes along with unidirectional flow of secreted factors which assist in digestion and perform tissue defense mechanism activity. Humans pervasively typically exhibits a Phospholipid and Choline deficiency, particularly during incipient phases of Post Gestational Circumstance when a Logarithmic 17 Fold decrease of Acetylcholine availability typically occurs. Resultant of inadequate availability of Choline, Thymus Involution begins, culminating in degradation of Thymus into disorganized Adipose Tissue. The Thymus produces T Immunological Cellular Material include narrow ranges of autoimmune activity against all molecules within biological systems, which becomes more expansive as Thymus degrades producing autoimmune conditions, become less expansive as Thymus becomes disorganized, and then enabling other factors such as the Immune Complements system and the effects of persistent local or systemic Inflammation to produce autoimmune conditions along with its degraded structural characteristics. Also, Fetal Hemoglobin transforms into Adult Hemoglobin, resulting in decreased ability to transport oxygen, decreased Hemoglobin resiliency to Basic Molecular factors, as well as being Homologous to the NKCC1 to KCC2 shift. The NKCC1 to KCC2 shift is a decrease in genetic expression of NKCC1 comparatively to KCC2, except in Auditory structures and except in the Renal Thick Ascending Loop, resulting impairment of and degradation of essential G Protein interactive pathways which assist in managing Nitric Oxide levels during gestational development. NKCC1 essentially provides a manner of systemically assuring Vasomodulative Dilatation and Constriction Homeostasis which is essential for managing systemic Ionic Gradients of CA2+, Chloride, MN2+, MG2+ and other factors. Such Homeostasis may be essential in enabling motility, migration, integration, proliferation and development of Progenitor cellular material produced in local tissues, Marrow, and obtained from Breast Milk. Thus it enables Somatic Epigenetic propagation from Maternal Host to incipient Post Natal Biophysiology as well supports reconstitution of dense tissue bases in the context of pervasive Apoptosis and Necrosis resultant detrimental environmental influences. Impairment of such characteristics enabled by NKCC1 may be essential aspects of Mesenchymal Endothelial and other cellular Phenotype transitions as well as gradients upon which Metastases move to become integrated into Distal Tissue bases, thereby constituting a principal factor in the progression of Oncology toward Human demise including 90 percent or more of Oncology associated demise. The Changes associated with the NKCC1 to KCC2 shift, as well as the other changes indicate in this analysis are delayed by Breast Feeding with Human Breast Milk*

    Similarly, detrimental environmental factors affecting biophysiology upon emergence from Maternal Host environment may result in DNA repair occurring between Twenty Thousand and 1 Million instances each day within each individual cellular material. Result of such Phospholipid and Choline deficiency with context of such ubiquitous requirement of Phospholipids and Choline associated Factors, ubiquitous tissue bases begin to have inadequate Choline to conduct DNA repair, DNA Synthesis, Genomic Replication, Genomic Translation, Protein Synthesis, production of RNA and exhibition other essential aspects of biological function. Phospholipids associated with Choline are exhibited or utilized to produce more than Ninety percent of cellular membranes, pervasive aspects of extracellular matrix and more than Ninety Nine percent of molecules synthesized by Human biophysiology. An immediate inability to synthesize enough Genomic Material emerges with Natal to Post Natal Transition. P53 becomes induced pervasively as a result o DNA impairment including being a typical aspect of replication during cellular division and also invoking myriad sub pathways which can result in G1 to G2m or S phase pause. Optimal Homologous DNA Repair which is considered Error Free typically occurs G2M or S phase. Less than optimal End Joining or Non Homologous repair typically occurs in G1 Phase. P53 may result in DNA Repair, other rescuing Genomic Repair Pathways, Apoptosis when DNA cannot be repaired, or other pathways which potentiate Necrosis when Apoptosis cannot be induced in response to irreparable DNA. Thymus degradation, correlative to the central role of Thymus in producing Immunological T Cellular material, however, results in impairment of an essential Necrotic pathway constituted of T Cellular Immunological Synapse. Thus Interleukins and TNF Alpha become essential to inducing inflammation in enablement of Necrosis, resulting in increased cellular metabolism which does not specifically produce Apoptosis or Necrosis and, however, results in something extreme occurring such as destabilization of cellular entities such that Necrosis or Apoptosis might increasedly occur. When such Necrosis or Apoptosis resultant of changed metabolism cannot occur, persistent inflammation may then become exhibited, becoming causal to Leukaemic, Lymphomic and Oncological Pathology. Particularly, unrepaired cellular material or tissue, including scarring or removed organs, may result in persistent inflammation and signaling until such impairment may be repaired or until such organs may be regenerated.*

    Specifically, however, P53 also induces P21 which also induces G1 phase pause by interacting directly within Cyclin Dependent Kinases (CDK) pathways which manage cellular cycle progression and by acting as an inhibitor (CDKI). Phospholipases also may induce cellular cycle abatement by becoming activated in response to inadequate Phospholipid and Choline availability, and by Catabolism Phospholipids from cellular membranes until enough are exhibited within Cytosol or Cytoplasm to mimic adequate Phospholipid availability. Phospholipase activity may be a substantial incipient causal factor to ubiquitous Cellular membrane Impairment associated with Pathology. Such cellular cycle pause factors thus, induce accumulation of cellular material in G1, G2M or S phase, regardless of if there may be adequate material to conduct Genomic repair or enough material to conduct Biosynthesis producing Nucleotides, RNA, DNA, or cellular membranes. The emergence of Post Natal Biophysiology from Maternal Host may be substantially detrimental and the decrease of mass in the Human biophysiology during incipient Post Natal circumstance may not only be resultant of excretion of fluid; being, instead, the result of pervasive Apoptosis, Tissue density degradation and Acetylcholine attrition. Correlatively, inadequate levels of Phospholipids and Choline associated factors, as well as exhibition of P53, p21 and Phospholipase induces a persistent susceptibility of cellular material which has typical p53 pathway Function to degraded whereas cellular material which has impaired p53 has a comparatively increased potential to be resilient. Choline deficiency inversely transforms Human biophysiological outcomes.*

    Moreover, as principle Epigenetic mechanisms affecting DNA Methylation, DNA Synthesis, Replication, Repair and Transcription, Choline associated Phospholipid factors may have substantially central causality to Genetic anomaly, regardless of if such anomaly has a Bona Fide Structural Basis or emerges during Transcription and Replication (Epigenetic). Thus, tissues with impaired P53 pathways become more pervasively exhibited and P53 impairment is exhibited as essential or central causality (Escape Mechanism) in more than 96 percent of oncology conditions. Particularly, p21, if inhibited in mammalian organisms along with provision of adequate levels of Phospholipid associated Choline factors, results in ubiquitous aspects of Human anatomy spontaneously regenerating when impaired or if such aspects o Anatomy have been removed. Such regenerative capability suggests that P21 may have emerged as an adaptive mechanism to pervasively exhibited Phospholipid Deficiency and Choline associated molecular factor deficiency. Furthermore, Decellularization is a mechanism of washing away cellular material which has emerged upon extracellular matrix. Cellular material produces Extracellular Matrix in a balance of Flux produced from Synthesis from Glycine, Phospholipids and others factors along with degradation resultant of Synthesized Metalloproteases. Such healthy flux may result healthy regeneration of Tissue and Organ supporting Extracellular Matrix and is often impaired during progressive conditions such as Cardiac, Renal, or Hepatic Glomerulization. *

    It is pervasively known, along with P21 regeneration capability, that removal of an organ from a Mammal, along with decellularization, as well as subsequent introduction of progenitor cellular material upon such Extracellular Matrix, may result complete regeneration of organs and tissues, such as Pulmonary, Cardiac and other organs, Ex Vivo. The most imperatively presented aspect of such capability is that such organs, particularly Pulmonary and Cardiac Organs, typically spontaneously exhibit biophysiological and Electrochemical activity once these have become regenerate, Ex Vivo. Essentially, the Cardiac Organ begins to exhibit a Rhythm, without a requirement of being encapsulated within the mammalian Anatomy. *

    Such observations regarding regeneration may be imperative to introduce, because the following information may not be believed unless one understands these and explorers the nature of systems, perspectives, cognitive constructs and other aspects of the Social and Human Condition presented in material at AMEHSI.ORG. Diabetes, illustratively, essentially, as a health condition, may not exist. Diabetes associate pathology may be the result ephemeral Ischemia, tissue degradation, impaired regeneration, and Extracellular Matrix degeneration resultant of a Phospholipid associated Choline Deficiency. Such circumstance may most incipient be resultant of increased levels of Homocysteine, Asymmetric Dimethylarginine, Trimethylamine, Trimethylamine-N-Oxide and C Reactive protein. These represent the four most indicative factors of susceptibility to adverse health events, upon which epigenetic, behavioral, environmental, emotional, socioeconomic, demographic, contrived systems produced by humanity and other factors act to shape biophysiological, Social and Health status outcomes. Each of these, however, also may have direct pervasive degradative effect to Extracellular Matrix, Cellular Material, Vasculature, Arterial Pathways, Organs, and Neurological material, constituting principal causality to ubiquitous progressive health conditions including those constituting the detrimental aspects of progressing Gerontological status.*

    Illustratively, the difference in the production of Phosphatidylcholine (PC) between Genders of Humanity, adjusted by the nearly Fifty percent of Female Gender whom may typically have both strands of DNA impaired (Homozygously impaired) for Phosphatidylethanolamine Methyl Transferase (PEMT) production may be substantially homologous to the difference in typical Span of Being between Female and Male Gender. PEMT production is required for one of the several pathways in which PC is synthesized. The typically observed levels of detrimental indicators, including Homocysteine in particular, may increase as Span of Being increases. These, however, are as much causal of susceptibility to sudden adverse health events, sudden demise, progressive conditions, and Pathology associated with progressing Gerontological status, as they may be indicative of such circumstance. A comparative scenario might be constructed by considering what may occur when bringing ones automobile to a Mechanic resultant of an observed decreased in responsiveness, decrease in per Gallon of Fuel mileage, or emergence of other less than optimal characteristics resultant of inadequate levels of Lubricating Oils, Pressurization Fluids and degraded Spark Plugs. The mechanic might say, “This is typical because the Car has been utilized for an expansive duration,” and then subsequently suggest that there is nothing more that can be done. Homologously, instead of treating the causal factors as Pathology or aspects of Pathology, Homocysteine, Asymmetric Dimethylarginine, Trimethylamine-N-oxide and C Reactive Protein may pervasively not be assayed during a health services intervention and may then be suggested to be typical for a particular individual at a particular phase in their Span of Being. Such indicative factors, as both indicators and tangentially causal factors to Sudden Adverse Health Events and progressive degradation of biological systems, might instead be considered with context of their empirical causality to Pathology. Contrived systems pervasively suggest, enculturate, and participate in assuring less than optimal outcomes and demise. Often, Health services interactions may not be conducted utilizing required essential assay, may substitute indicators of health status for directly causal influences, and may perpetuate perspectives and observed circumstance in accordance with philosophical, social constructs or systemic construct produced in eras before capabilities available in this era. Imperatively, a deficiency of a particular enzyme or factor within biological systems is often not intervened by providing the precise molecular factor which is deficient. Accordingly, why is an Acetylcholine Esterase Deficiency not always being intervened with provision of Acetylcholine Esterase, Precursors to Acetyl Choline Esterase, Cofactors which induce improved expression when one strand of DNA from this is produced might be impaired (Haploinsufficiency), or intervening the circumstance which most pervasively result in Bona Fide Inherited Structural Anomaly or emergence of such structural Anomally, Phospholipid and Choline Factor Deficiency? *

    Empirically, any level of Homocysteine, Asymmetric Dimethylarginine, Trimethylamine-N-Oxide or C-Reactive protein which is dissimilar to that typically exhibited during the most optimal phase of Human development or which constitutes empirically discernible degradative effect to biological systems without associated mitigating biosynthesis, should be considered Pathology. Considerations otherwise are a substantial enabling perspective to Pathology and emergence of Demise. Although one may cursorily consider such a suggestion as rhetoric, there is compelling research which suggests that health services providers whom believe that Human demise is a requisite aspect of the Human experience pervasively have patients whom incur demise at increased levels. Roemer’s Axiom, is a public health correlate which observes that if a Health services facility is built in a particular area which becomes occupied to a particular level, and another Facility is built immediately adjacent to the first, then the second one typically becomes occupied at levels similar to that location which was most incipiently constructed. Populations which migrate to different Nations or area, typically transform to exhibit pathologies in accordance with local populations within the first or second generation of inhabiting such new area. If there is not adequate population to occupy the second constructed facility constructed adjacent to the first Health Services Facility, then populations may migrate to the area such that second edifice may be occupied adequately. Roemer’s Axiom may be pervasively observed among health services systems and among myriad other systems among Humanity. *
    Returning from a Human systems analysis to Molecular Physiology, Pathology associated with Diabetes may result from ephemeral or persistent Ischemia which prevents biofeedback mechanisms between behavior, Perception, Social or Economic interactions, influences imparted by artifacts and contrived systems, Hepatic Organ, Renal Organ, Pancreas or other tissues, as well as impaired regeneration, degradation of Extracellular Matrix, impaired Flux of Cellular Membranes and as well as degraded Flux within Extracellular Matrix. Advanced End Products (Including Glycation, Lipoxidation, Glucoxidation, Reactive Oxygen Species and others) each also may become integrated into proteins, molecules, tissues, as well as permeate membranes to affect DNA, RNA, Organelles, Membranes, vasculature, organs or tissues, resulting in persistent inflammation as RAGE and SRAGE signaling. Advanced End Products may most incipiently be enabled to potentiate Plasticity changes as a result Phospholipid and Choline Deficiency, increased levels of the highly degradative factors presented herein, and resultant impairment of rejuvenating Flux within Cellular Membrane, Extracellular Matrix, Tissues, Organs and Vasculature. Receptor for Glycation End Products (RAGE) and Soluble RAGE (SRAGE) each may also induce persistent inflammatory signaling by activating Immunological Response to Advanced End Products. These factors and circumstances represent substantial aspects of Diabetes associated Pathology as well as pervasive Gerontological associated Pathology. *

    Imperatively, again, however, may it be observed that Insulin may not typically directly interact with Glucose, Fructose or other Sugars. Insulin, instead, may typically be released responsively to exhibition of such factors within Biological fluids and resultant biofeedback mechanisms between Organs as well as behavioral and perceptive influences. Insulin induces cellular material to release accumulated Insulin and induces cellular material to increase expression of GLUT. GLUT precursors, then, may become expressed from DNA to RNA, become synthesized by Ribosome Molecular Machines into GLUT, exit the Nucleus – Endoplasmic Reticulum Complex, and migrate to the cellular membrane. Additionally, GLUT which may been enabled to be expressed by Insulin may then increases the capacity of GLUT expressed otherwise in assisting in attachment of Glucose to the Cellular Membrane, and moving Glucose across the Plasma Membrane into Cytosol where it becomes introduced into the Pentose Phosphate Pathway.*

    Glycine, obtained in its naturally occurring circumstance within Phosphatidylserine, Phosphatidylcholine and ubiquitous Phospholipids, however, also increases the capacity of Glucose Metabolism by interacting with latter aspects of the Pentose Phosphate Pathway. Here, an essential distinction emerges. P53, expressed resultant of a Choline deficiency, may also integrate into and impair the enzyme require to conduct the first step of Glucose metabolism within the Pentose Phosphate Pathway. Such integration and inhibition of the Pentose Phosphate Pathway’s incipient phase is exhibited along with impaired ability of Glycine to deplete Glucose, as both of these circumstance become exhibited along with pervasively exhibited Choline associated Phospholipid deficiency. Thus, cellular material may begin to accumulate Glucose and Glycogen resultant of a Choline deficiency. The Pentose Phosphate Pathway, then, becomes segmented between its most incipient phases and subsequent phases. Phospholipase, however, may intervene through Catabolism myriad factors from cellular membranes, including Phosphofructokinase which reconstitutes the enzyme exhibited immediately after the P53 impaired phases and introduces Phosphofructokinase which Phosphorylates myriad molecules providing energy to overcome P53, P21 and Choline Deficiency induced cellular cycle pause. Carbohydrate Responsive Element ‘Integration’ Protein (CHREBP) is increased in expression responsively to Glucose exhibition and functions by integrating with P53 such that it may have less ability to integrated with and such that P53 may have less ability to impair molecules interactive in incipient aspects of the P53 Pathway. Insulin also becomes exhibited as a response to systemic availability of Glucose and thus affects Glucose through biofeedback mechanisms. Phospholipase Catabolism of Membranes as well as CHREBP activity, however, results in progression of cellular cycle by mimicking the adequate availability of molecular factors required for essential Biosynthesis, DNA Replication, assay of Genome, Repair of Genome and Transcription of requisite molecular factors. Resultantly, cellular cycle progresses, with increased potential for emergence of Genetic Anomaly, Epigenetic Anomaly and impaired assurance of optimal pathways such as P53, p21, BRCA1, BRCA2, PTEN, MDMD2, and other factors which, when impaired, result of substantial susceptibility to emergence of atypical biophysiological outcomes. Relevantly, P21 typically induces cellular cycle pause in Hypertrophic Phases, in which cellular material may be absorbing myriad factors from environment to ready themselves for tunneling through subsequent phases with minimal or no interactivity with external environment. Choline associated Factor deficiency thus induces all manner of adaptations in which bypass of assurance of optimal Genomic, Epigenetic, RNA, Protein, Membrane, Regenerative, Biosynthesis, Degradative-Biosynthesis Flux, and Toxicity Management capabilities occurs. Thus, insulin, as it may not be required to induce GLUT, may induce increased GLUT, and may be required particularly as a result of Choline associated Factor Deficiency which impairs Glycine mediated Glucose depletion, may have emerged among myriad other adaptive mechanisms as a result of Choline associated molecular factor deficiency.*

    To orchestrate such observations into a relevant context, molecular factors may traverse Vasculature, Arterial, and Extravascular or Extra-arterial pathways. Molecules moving from such pathways typically traverse Extra-arterial or Extra-Vascular Pathways to reach cellular material as well as become absorbed by cellular material occupying the intra0arterial or intra-vascular interfacing area (Endothelial and other areas). Thus, as the layer of tissue interfacing Circulatory Pathways progresses to underlying cellular material and tissues, or as molecules progress from circulatory pathways or from capillaries to reach near and then more distance cellular entities, absorption may begin to change the bioavailability of such essential distributed factors. Thus, gradients emerge in which more distant material from circulatory pathways may have less opportunity to acquire adequate resources. Tight and Gap Junction Proteins, however, typically may assist by sharing molecules observed within one cellular material with many other to produce biophysiological and electrochemical uniformity, as well as permitting essential factors to traverse spaces between such cellular entities in a increased unimpeded manner. Gradients, however, may emerge, particularly within Factors which are deficient. *

    The Folate (Methyl) Trap is a condition in which Choline Associated Molecular Factors including Phospholipids, may be conserved for use by the most essential tissues and cellular material. Additionally, within such essential tissues and cellular material, such as Neurological tissue, such resources may be conserved for essential aspects of cellular function. Such essential aspects of function might include Ionic characteristics or Transcription and might not include DNA Repair and other Biosynthesis resulting imbalances in Membrane Phospholipid Flux as well as Extracellular Matrix Flux. Thus, Cardiac and Hepatic tissues, for instance, might have resources directed toward them to the detriment of other organs or tissues. Such redirection of essential resources might occur as a result of systemic priority, volume of utilization, size of organ, and influence of such tissues comparatively to others systemically. A useful perspective of the emergence of Neoplasm and Oncology may be that these might occur resultantly of an inadequate distribution of Choline and Phospholipid factors resultant of Gradients and opportunity based absorption as such factors become distributed. Such influences to distribution and bioavailability of Phospholipid and Choline factors may be exhibited comparatively to an increased or more pervasive systemic distribution of Glucose as a result of P53 mediated inhibition of the incipient phases of the Pentose Phosphate Pathway. Hyperglycemic Memory is an example such Phenomenon in which systemic changes to biophysiology resultant of high Glucose levels endure afterwards for substantial duration. Depletion of Choline pervasively as it is available and accumulation of Glucose as result of impaired ability to deplete it with Glycine, P53 inhibition of the Pentose Phosphate Pathway, and ephemeral Ischemia of Hepatic, Renal, or Pancreas tissues, may result in pervasive CHREBP activity which allows cellular cycle progression and increases general Adipose Lipid synthesis. Carbohydrate Responsive Element ‘Integration’ Protein (CHREBP) enables cellular cycle progression in cellular material, particularly in Hepatic Tissue, and induces Lipogenesis in non-proliferating Hepatic Cellular material. CHREBP enabled cellular cycle progressioin bypasses Choline dependent biophysiological stability mechanisms and potentiates pervasive emergence of Proliferation Anomaly, Differentiation Anomaly, as well as less than optimal Genetic, Epigenetic, Transcription, Replication and Biosynthesis outcomes. The Glucose – Choline Paradigm thus may represent compelling aspect of small cellular Pathology, whereas persistent inflammation and pathology more tangentially resultant of Choline deficiency, in which accumulation of cellular material in Hypertrophic expanding phases occurs, may be a compelling comparative perspective of non-small cellular Pathology.*

    The perspectives presented here present relevant traversal of systems to understand the factors which shape biophysiological, Anatomical, Pathology, Perceptive, Cognitive, Behavioral, Health Status and Social outcomes. Deficiency, as well as Pathology as molecular levels, may pervasively be shaped into Health status outcomes and Social Outcomes by all manner of systems including cognitive, linguistic, social, economic, nutritional, behavioral, business, entertainment, communications, education, and other systems exhibited about Humanity. Much of the unproductive behavior, cognitive associations, and perspectives, including use of Expletives, Derogatory Stereotypes, utilization of detrimental Habitual or mood changing factors, may mask molecular or biophysiological level deficiency and circumstance, persist as a result of such masking influence to these conditions, result in biophysiological manifestation of unproductive generationally propagated views, or persist as result influence to biophysiology which mimics obtainment of essential deprived factors. *

    A response to the C reactive protein test at a particular level may not be ascertainable unless one consider the results of other Assay, including many others presented by the AMEHSI Specification, those presented by one’s health services providers, some which are relevant to one’s biophysiological, behavioral, habitual, nutritional, location oriented, and other circumstance. An increased C-Reactive Protein Assay may or may not be typical. It can be indicative of impairment, repair, Inflammation, exercise and other factors. Assay of Homocysteine, Asymmetric Dimethylarginine, Trimethylamine (TMA), Trimethylamine-N-Oxide (TMAO), as well as C Reactive Protein provides a more complete perspective of susceptibility. TMA to TMAO ratio may also be indicative. It may be asserted however, that most enzymes or molecules which are deficient are obtainable as supplements, thus a deficiency of Factor A may be intervened by obtainment and instrumentation of Factor A, its precursors, or Cofactors which can induce increased expression as a result of molecular circumstance in an individual Coil of DNA is impaired (Haploinsufficiency). *

    Ingestion of Meat, Chicken, Eggs or Fish, as well as Nutritional factors with increased levels of L – Carnitine, Phosphatidylcholine and Trimethylglycine, support less than optimal Microflora and may induce cycles of TMA TMAO at increased levels. Causality, however, is not these factors. The type of Digestive Pathway Microflora may be a most causal factor. Patterns of ingesting of such factors may be a causal factor. Choline deficiency and Phosphatidylcholine deficiency systemically which produces Digestive Pathway Inflammation, ‘Leaky Gut’ Syndromes, TNF Alpha, Bidirectional Permeability of Digestive Pathways Tissues, as well as impaired cellular membrane characteristics or other causes of systemic Inflammation, may contributed to such circumstance. The condition is Clinically treated and abated by instrumentation of Prebiotic factors, Probiotics that include Microflora which do not increase TMA – TMAO production, and an intermittent (Three or four instances per annum) of a diverse coverage Antibiotic, may each individually or together provide relief of TMA TMAO Paradigm associated Pathology. Probiotics utilized should be varieties which do not increase TMA – TMAO. Versions which include Firmicutes or Rhamnosus in the name, for instance, might be avoided or might be accompanied by other varieties which do not produce TMA – TMAO, as well as potentially accompanied by versions which consume and Metabolize TMA and TMAO into out of cycle factors such as Methane. The more diverse and the more numerous the different strains which are utilized therapeutically or which are exhibited within Digestive Pathways, the more correlative these may be with optimal Health Status.*

    Fish, illustratively, utilize TMAO in order to maintain biophysiological Homeostasis and support molecular function at substantial depths within Aquatic Environment. Fish, however, exhibit such substantially beneficial molecules and influence otherwise, that although increased levels of TMAO may be obtained from its ingestions, comparatively to Microflora produced TMA from metabolism of Meat, Chicken Eggs, or Lecithin factors such as Oils and Bread, Fish may be considered similarly to these other ingested factors in potential susceptibility to Adverse Health Events. Thus, TMAO and TMAO Synthesis from TMA may induce pressurization changes as well as Vasomodulative constriction.*

    During Ischemia a substantially beneficial capability may constituted of Introducing Choline, Trimethylglycine, Phosphatidylcholine, Prebiotics, Probiotics, diverse coverage Antibiotics, L – Arginine, L – Ornithine, Citrulline(L version), Probucol, Vitamin E, Xanthones, Calcitonin Gene Associated Peptide (CGRP), Low levels of Capsaicin, Farnesoid X Receptor Agonist GW4064, N G Dimethylarginine Dimethylaminohydrolase 1 (DDAH1), N G Dimethylarginine Dimethylaminohydrolase 2 (DDAH2), Water, Nitric Oxide Synthase or other factors. Inflammation, Coagulation Cascade, and Associated Ischemia may pervasively exhibit such Vasomodulative constriction as an essential aspect of Pathology. Homocysteine, for instance, integrates with Fibronectin, deposits Fibronectin within Cardiac, Vasculature, Arterial, and other essential tissues, as well as introduces changes to Free Fibrin which changes the circumstances required for Coagulation Cascade. Pressurization, Thermodynamic, Biological Fluid Factors otherwise, as well as Ionic factors which become atypical may change the level of influence or circumstance in which Thrombosis associated or Fibrin factor associated Inflammation, as well as Leukocyte or other factors which may induce Inflammation, Coagulation, Tissue Remodeling or circumstance which can produce impedance within Circulatory Pathways (Ischemia) might occur. Each of these may be aspects of Sudden Adverse Health Events or progressive degradation of biological systems most incipiently associated with Choline associated factor deficiency and potentiated by Homocysteine, Asymmetric Dimethylarginine, Trimethylamine, Trimethylamine-N-Oxide, C-Reactive Protein, Lactic Acid (L and D version) associated Methylglyoxyl as well as other circumstance including persistent exhibition of Inflammatory Signaling or Inflammatory Cascades. *

    Interestingly, upon ingestion of the Meat, Chicken, Eggs or Fish, TMA and TMAO increase, thus inducing increased susceptibility to adverse health events which persist until such factors become completely removed from the digestive pathway. Vegetarians have decreased susceptibility when ingesting the same factors resultant of the decreased levels of accumulated remnants of such factors in their digestive pathways, and decreased accumulation of Microflora upon such remnants within their digestive pathways. The more often one ingests Carnitine, Phosphatidylcholine and Trimethylglycine, the higher the level of TMA TMAO during each such ingestion and digestion of such factors. This phenomenon may be precisely Homologous to the difference Digestive Pathway Neurological Function (Slow Wave Potential) comparative to Cardiac Function. Slow Wave Potential occurs when an individual Neurotransmitter mediated activation of a Neuron does not result in achievement of the Activation Threshold (Action Potential Achievement) of such Neuron. Neurotransmitters typical are emitted by a Presynaptic Neuron and move to a Post Synaptic Neuron, interacting with a receptor which is usually on the extracellular environment interfacing Membrane (Plasma Membrane). Activation of the receptor results in opening of an Ion Channel which allows molecules with Negative or Positive attributes to traverse the cellular membrane. If the receptor is a Transmembrane protein activation may result in a change to the shape, twist and writhe of the Transmembrane protein receptor such that the integrated molecule is moved across the cellular membrane. If the receptor is a Ligand, it then activates an intracellular signaling cascade which induces changes to DNA expression. Activation of a receptor may also induce a Phosphorylation, Acetylation or other cascade which changes or activates numerous molecules to increase and change cellular metabolism. Ionic Gradients are typically maintained between intracellular and extracellular environment producing a base level of energy and membrane turgor. Intracellular environment may typically exhibit Negative Polarity comparatively to Extracellular environment. Before the NKCC1 to KCC2 shift, which may be delayed by Breast Feeding utilizing Human Breast Milk, Neurotransmitter activation results in a decrease in intracellular Negative Polarity toward a threshold of Action Potential. After the NKCC1 to KCC2 Shift, Neurotransmitter activation results in an increase in intracellular Negative Polarity toward a Threshold of Action Potential. When an Influx or Efflux of Ions occurs, a gradient between the intracellular Location of such Influx or Efflux and the other aspects of intracellular environment is produced. Diffusion resolves such gradients and the resolution activity is utilized as a source of energy to conduct movement, activity or impart other influence to molecular inter-systems. Energy molecules such as ATP, ADP, NADP, Phosporylation and others are utilized to conduct activity in direction or manner not supported by such gradients. When an Action Potential Threshold is achieved, the Cellular Environment exhibits a substantial response, such as opening of myriad Ion Channels, Efflux, Influx, Phosphorylation, changes to DN Expression, Membrane Changes, Exhibition of an Electrochemical Influence, or other factors which may constitute biophysiological activity including a Muscle Contraction. Slow Wave Potential requires multiple, sequential, activation of a Neuron in which each activation does not become completely resolved by gradients to produce intracellular uniformity and thus Homeostasis. Each stimulation within a Slow Wave Potential activation sequence induces changes to polarity which successively become nearer and nearer to activation Threshold, until such Threshold is achieved and Action Potential becomes realized. Slow Wave Potential may be indicative of Digestive Pathway movement of Ingested Nutritional Factors (Peristalsis). *

    Tobacco Combustive utilization provides relevant perspective of the paradigm between Genetic, Epigenetic, Sudden Adverse and Progressive Adverse Biophysiological determinism. Tobacco Combustive utilization may not typically, if ever, induce an Oncological condition which is not already exhibited as a susceptibility at Genetic or Epigenetic levels. Typically, an Oncological condition exhibited by a user of Tobacco Combustive products, may have a Bona Fide Genetic Basis which is enabled by Phospholipid and Choline deficiency first, and then, perhaps, by Toxicity potentially associated with Tobacco Combustion. Much of Bona Fide Genetic Structural Anomally may be the result of Choline and Phospholipid factor deficiency. Although a distinction can be made by Bona Fide inherited Genetic Structural Anomally comparatively to an emerged de novo Bona Fide Genetic Structural Anomally within particular cellular material, Choline and Phospholipid deficiency may be substantially influential in emergence of both such circumstances. Molecular and Genetic Anthropology, Archeology and Paleontology, might suggest the nature of the emergence of many such amelioration particularly pervasive complex molecular or metabolic pathways exhibited as adaptation to Phospholipid or Choline deficiency, suggesting that some Genetic Anomally may be reversion to an earlier biophysiological status in which a particular genetic construct may not have been required, particularly when such deficiency may not have been pervasively exhibited. Imperatively, however, Tobacco Combustive utilization may directly introduce Nitric Oxide, which intervenes, incipiently, Vasomodulative Constriction resultant of increasing Homocysteine, Asymmetric Dimethylarginine, Trimethylamine-N-Oxide, Trimethylamine, D – Lactic Acid Metabolic pathway production of Methylglyoxyl and other circumstance.*

    As Choline Deficiency may be pervasive, Tobacco Combustion may provide Nicotine which is pervasively similar to Nicotinamide utilized in Energy Cycles as well as within Choline Associated Molecular Factor Pathways. The structures of Nicotine and Nicotinamide, however, may be different in a minuscule and substantially influential manner, thereby constituting a masking influence which obfuscates deficiency enough to produce a Cognitive, Perceptive and Behavioral association. Such association, however, at molecular levels, may be imprecise. Similarly, although Tobacco Combustive utilization provides Nitric Oxide, Nitric Oxide exhibition is biofeedback mechanisms which reduces the activity of Nitric Oxide Synthase, resulting in Vasomodulative Dilatation incipiently, resumption of Homeostasis subsequently, and is able to reproduce such Vasomodulative Dilatation after some duration between use of such products. Impairment of Nitric Oxide Synthesis, however, is only one of myriad aspects of Pathology associated with increased levels of Homocysteine, Asymmetric Dimethylarginine(ADMA), Trimethylamine(TMA), Trimethylamine-N-Oxide (TMAO), C –Reactive Protein (CRP), D – Lactic or L-Lactic Acid metabolism associated Methylglyoxyl. Polyamines, or molecules with more than one Amino Group, illustratively, may induce pervasive tissue remodeling. Each of these detrimental molecular factors may induce Vasomodulative dilatation, as well as systemic degradation of cellular membranes, tissues, vasculature, arterial structure and Apoptosis. C-Reactive Protein is an indicator levels cellular material degradation locally or systemically. Thus, Tobacco Combustive utilization may relieve one aspect of Sudden Adverse Health Event associated Pathology from such factors. Tobacco combustive utilization, as a result of its masking of incipient deficiency and as a result of its being substituted for obtaining such essential factors, might typically be instrumented for duration which surpasses the exhibition of its beneficial effect. Furthermore the progressive degradative influences as well as the Sudden Adverse Health Event potentiating influences of Homocysteine, TMA, TMAO, ADMA, CRP and Methylglyoxyl otherwise, may not be intervened through introduction Nitric Oxide. Thus, Tobacco combustion may circumstantially redirect typically occurring susceptibility to Sudden Adverse Health Events toward Progressive Degradative influences to biophysiology and thus produce progressive conditions of which condition such as Oncology, Leukaemic, Lymphomic, Emphysema, Glaucoma, and other Pathology may be constituted.*

    Although some of the factors introduced into biological systems support metabolic pathways, the introduction of Toxins otherwise may affect Hepatic, Renal, Spleenic, Pulmonary, and Vision tissue capacity to manage toxicity, particularly with context of pervasive deficiency of Choline. Thus Choline is utilized by cellular material to Produce Trimethylglycine. Trimethylglycine is specifically utilized at increased levels comparatively to Choline to manage toxicity within Hepatic, Renal, Spleenic, Pulmonary and Vision Tissue bases. Trimethylglycine stabilizes the shape, twist, writhe and other aspects of Quaternary Molecular structure of biophysiologically active molecules. Such stabilization may be imperative in Pulmonary, Hepatic, Renal, Spleenic and Vision tissues as a result of Toxicity management activity which can induce substantial toxicity, as well as induce substantial changes to thermodynamic, electrochemical, Ionic, PH, PK and other aspects of environment. Particularly, however, an understanding of molecular inter-systems is requisite to appreciating such benefit. Molecules from external environment as well as those produce from DNA translation into hnRNA, reduce to mRNA, and enabled by tRNA to be synthesized into proteins by Ribosome Molecular Machine, may experience substantial typical or detrimental influence from Advanced End Products, reactive molecules, pathogens, or the effects of deficiency in which complete or accurate biosynthesis may not occur. Synthesized or exhibited factors then may experience numerous interactions within a particular molecular pathway, multiple pathways, or generally. Each molecular interaction may produce a change in the molecular characteristics and structure of a molecule, including progressive changes to shape, twist and writhe which change its Quaternary structure. Molecular pathways which result in biological function or biological structure, thus, are influenced in myriad manner by molecular or other systems ranging from Nucleus and Sub Quantum levels to structural levels and external environment. Interactions and Influences, including integration of other molecules and segmentation may occur in a particular order such that a particular characteristics of segmentation, integration, shape, twist, writhe, Electrons comparatively to Neutrons, Free Electrons in the outer layer, as well other circumstance may be achieved. Such may then constituted a particular instance in which a molecule may have most substantial propensity to exhibit a particular molecular interaction, constituting a particular phase of a particular series of interactions. Each phase such interactions may require such specific circumstance, as well as less or more specific circumstance. Each molecular interaction within such series of interactions (Molecular or Metabolic Pathway) may exhibit several interactions at the submolecular level as intermediaries. Particularly, however, it is the environmental characteristics such as density of Hydrogen, Oxygen, Water, Other molecules, Ions, Free Electrons, PH, PK, Thermodynamic, Pressurization or other characteristic which also produces the shape, twist and writhe of molecular factors. A change in such environment may also change the available of molecules which have an affinity for unobscured aspects of a complex biologically active Protein with many Folds comparatively to the affinity of factors within the encapsulating environment which have an affinity for obscured extents (Domains) of the same molecule, thereby inducing changes to shape, twist and writhe. *

    Correlatively, molecular inter-systems which affect such circumstance include all factors in the environment external to biological systems. Human biophysiology may readily adapt to changes in density of molecular factors in external environment, extracellular internal environment and intracellular locations. Molecular changes to environment may typically result in some change to the exhibition of such factors within internal environment, being managed by the Complements Innate Immunological System which attaches molecules to such factors to enable their degradation, as well as by T Immunological cellular capability.*

    Cellular material exhibits Classes of reporter molecules which are expressed from DNA, then typical become integrated with generally occurring molecules, producing a complex which migrates to the Extracellular environment interfacing Plasma Membrane. Autophagy, Ubiquitylation, and Lipophagy each constitute a manner of attaching indicator molecules to other molecules within intracellular environment which enable these to be degraded into constitutive Amino Acids or Micromolecules for recycling into Proteins, as well as potentiating encapsulation of such prospectively degraded molecules into Vesicles which migrate to Cellular membrane for excretion. Incompletely degradation of molecules as well as Reporter Class molecules which integrate with molecules generally results in integration with and movement of such factors to the Cellular Membrane for Antigen Presentation. Antigen Presentation may be Constitutive of such Reported or Undegradable molecules being moved to the Plasma Membrane, becoming exhibited among Antigen Presented Complexes typically comprised of one or T Cellular specific receptors aggregated as motile Lipid Rafts, and subsequent interaction with a T Immunological Cellular Entity. The T Immunological Cellular Entity interaction with the Reported Molecule results in a Ligand activation with the T Immunological Cellular Entity in which the Reported Molecule’s sequence of Proteins are then produced inversely within its DNA. The type of DNA repair which enables a T or B Cellular entity to change its DNA to represent such Reported Molecules is indicated as V(D)J recombination in which multiple variable aspects of Genome are changed randomly or specifically in response to environment. The Antigen Competent T Cellular material may then migrate to Thymus, Proliferate, or Migrate to many areas exhibited Lymph or other tissue, such that the Antigen may be presented again to such tissue. This subsequent presentation of Antigen to other T or B Immunological cellular Material results in Proliferation Cascade of T and B Immunological Cellular Material as an aspect of Inflammation. Such DNA Repair and Proliferation requires Phospholipids and Choline associated factors and when atypical, such as in accumulation B Cellular material in immature development phases resultant of deficiency (Leukemia), over proliferation or under proliferation of T or B Immunological Cellular Material, or atypical differentiation and atypical proliferation of Hematopoietic Cellular Material emanated from Skeletal structure marrow (Lymphoma). The Pathology of each such conditions, if analyzed thoroughly, can occur independent of an inherent Bona Fide Genetic Structurally anomaly as a result of Phospholipid deficiency or Choline associated factor Deficiency. *

    Returning to the relevance of such analysis to molecular inter-systems, molecules which become exhibited at substantially changed levels may result in changes to Immunological Function, with an Incipient Immunological response, and after pervasive extended duration exhibition of such newly introduced molecules at a substantial levels a persistent sustained T Immune response may emerge within a Narrowed range similar to that exhibited towards molecules produced from DNA. Resultantly, such molecules may become typically reported by Report Class molecules and presented on the extracellular interfacing aspect of the Plasma membrane, such that Antigen Presenting T Cellular material, as well as Cytotoxic T versions and Cytotoxic B versions may interact with these. The Cytotoxic versions may induce Apoptosis and Cellular Lysis, increasing C Reactive Protein Levels, and inducing increased Electrolytes within Biological Fluids. Such Newly integrated molecules then may began to have an abated Cytotoxic response as a result of the substantial propensity for detrimental outcomes from such persistent Cytotoxic activity. The 1918 Influenza, illustratively, was characterized by exhibition of one the least Pathogenic Viral Harpoon structure of any other Modern instance of Influenza, along with an ability to permeate cellular membrane to affect Viral activity without such capability and as a result of being able to interact with intracellular receptors or cellular replication machinery. Resultantly, the 1918 Influenza was able to induce substantial Cytotoxic response in which the principal cause of Pathology and demise was the Immunological Response instead the Virions themselves. Such factors produced an inversion of typical outcomes in which most incipiently Post Natal Emerged populations along with those of most progressed Gerontological circumstance exhibit comparative increased susceptibility to detrimental outcomes, into a comparatively increased susceptibility to detrimental outcomes being exhibited among populations which typically had optimal functioning immunological systems. Particularly, molecules from environment may become readily integrated into internal molecular inter-systems, may become managed just as endogenously produced molecules, may affect DNA, RNA and Proteins, as well as potentially producing changes to Genome or Genetic expression. *

    An analysis of molecular inter-systems, thus, may require introduction of the essential nature of assured levels of Phospholipids and Choline. Deficiency of such factors produces substantial impairment of Cellular Membranes, impaired Neurological Synapse, Ionic Characteristics, Immunological and other membrane receptors, as well as intracellular molecular signaling, including permitted Influx and Efflux of detrimental Advanced End Products or Pathogens. An essential aspect of Immunological Synapse may be non-specific permeability of the Outer aspects of the Plasma membrane in which myriad factors may integrate with or traverse such outer structure, along with Specific Permeability of the Inner structure of the Plasma Membrane in which only particular molecules traverse into the Cytosol. Resultantly, myriad Factors within extracellular environment Traverse outer structure of Plasma Membrane and then become impeded by the Inner Aspect of the Plasma Membrane, becoming trapped, becoming reported by Reporter Class Molecules, integrating into receptors and aggregated Lipid Rafts, and reported to T Cellular Material through Antigen Presentation. Phospholipid and Choline deficiency, therefore, produces impaired general permeability and impaired specific permeability which enables molecules which might optimally be Trapped to not become come Trapped, as well as producing circumstance in which molecules traverse directly into intracellular environment (Tunneling). Moreover, the Fluid Membranes which encapsulate many essential tissues and organs (Peritoneum) may also exhibit such paradigms of impaired Permeability, resultant of Choline and Phospholipid deficiency. *

    These may produce ancillary outcomes which can be most indicative of Pathology. HIV for instance, may often be reduced analytically to persist resultant of Latent cadres of Virions within obscure cellular material within Immunological T Bases, as well as being suggested as a Savvy, intelligently elusive Pseudorganism. The ability of HIV to elude immunological function, however, may be substantially happenstance and substantially result of inherent aspects of Biological Function. Impaired membrane permeability, illustratively, may be substantially causal to incipient intracellular exhibition of HIV as well as impairment of immunological Synapse which may induce HIV specific Cytotoxicity. The Human Genome may regularly and pervasively exhibited substitutions of Uracil for Thymine, although Uracil substitution for Thymine may be typical of RNA. Such substitution may be a defense Mechanism which disrupts Pathogen DNA which has become integrated into Genome. The Human Genome exhibits substantial aspects of Myriad integrated Pathogen DNA, some of which may possibly be actively translated and utilized in biological function, much of which may be inactivated by substitutions or through deactivating Epigenetic Methylation Patterns. HIV Transactivating Protein (TAT) may also compete with Cyclin Dependent Kinase activators by actively dePhosphorylating CDK2. CDK2 when deterministically activated results in cellular cycle progression out of G1 Phase. CDK2 may Phosphorylated and dePhosphorylated as the culmination or ancillary outcomes many different pathways and may result in progression of cellular cycle from G1 phases to subsequent stages when CDK2 may be prevalently Phosphorylated to a deterministic level for deterministic duration. G1 Phase Pause may be induced by P53, P21 and Phospholipase mediated Cellular Membrane Catabolism associated Phospholipid Flux. Thus, HIV Latency may be being produced by TAT mediated deactivation of CDK2. TAT, however, may also occupy substantial levels of Phosphate Groups, producing a substantial degraded Energy Balance, affecting Biosynthesis, Changing cellular Metabolism, impairing pervasive aspects of Immunological Response, and producing Gradients in which affect tissue prevents Marrow, and other essential sources or regenerative Progenitor material from exhibiting typical function. Imperatively hour as early as the latter aspect of the 1990’s, integration of an artificial Membrane Permeating Sequence of Proteins, constituted of repeating Arginine Sequences, to TAT, along with integration of an Apoptosis Cascade Molecular Pathway Domain (Caspase 3) was observed to induce Apoptosis pervasively within cellular material. The exhibition of Caspase 3 as an individual segmented and activated factor was conditional upon exhibition of HIV Proteases which segment the Caspase 3 domain from TAT domain resulting of utilization of TAT to produce Viral Material. The conundrum latency, however, was considered a impedance although applied management of CDK2 Phosphorylation, Phospholipases Activity, P53 and P21 might have provided benefit. Attaching a highly conserved Domain of the Viral Protein, however, was observed to induce activation of Latency exhibiting Virally affected cellular material, such that the now myriad developed Transduction domains, including the Arginine repeating structures, along with TAT and Caspase 3 may have been substantially effective capability which would only affect cellular material exhibiting such Pathology. Such circumstance, however, may not have been instrumented. In the latter aspects of the incipient Decade of the 21st Century, however, it was discovered that In Vivo eradication of Cellular material affected by HIV could be achieved by attaching Cytotoxic Oncological therapeutics to the highly conserved HIV Protein Domain, thus inducing Apoptosis or Necrosis specifically and only in all cellular Material affected by such Pathology. *

    The essential consideration presented by these assertions may be that Human demise exhibited since the incipient Public availability of such intervention, the latter aspect of the Nineteen Nineties, Clinical Studies utilization such factors may not have been exhibited or might not have been considered a priority. Particularly, again, may be the observation that systems may enculturate and assure the incurrence of adverse outcomes , including Demise. These may be particularly permitted in contexts of cursorily determinable inaction and particularly with context of presumed ability to attribute outcomes to the perception and behavior of victims. The paradigm of systemic introduction of perspective, cognitive artifacts, artifacts specifically designed to impart detriment to Humanity may be a pervasive occurrence in systems exhibited about Humanity. Humans may emerge to incipient post Natal Circumstance without any aspect of Anatomy which is more for imparting detriment to others than such aspect of Anatomy may be useful for obtaining sustenance and assisting others among Humanity in community with one another. Consider a factor which is ingested by an individual and then another factor which is ingested subsequently which produces an adverse health status or behavioral outcome. Consider, then, all of the constructs introduced from incipient Post Natal Circumstance through development, including a dependency upon financial instruments, Education, Interactions, Systems, Business, Economics and other factors to obtain the bases of the Social and Human condition. Analyze the influences entertainment, information distribution, and other influences which enculturate less than optimal outcomes which induce associations in which unproductive biophysiological, cognitive or behavioral constructs become associated with these. Introduce into these nature in which incipient deficiency and deprivation of the bases of the social and Human condition may be shaped by all manner of influences into outcomes which non among Humanity may have empirically shaped using intrinsically originated conscious direction. Introduce, also, circumstance in which much of Human inclination may be constituted of shaping such incipient deficiency into outcomes, perceived satisfaction of biophysiologically deficient pathways, as well as masking of such deprivation by actions, activity or outcomes which redirect conscious cognitive context away from these factors, although such factors may inherently progress to pervasive Human Pathology regardless of the manner in which such obfuscation may be exhibited. Perspective of the manner in which unproductive biophysiological, social and systemic outcomes may be being produced through introduction of influences which prevent autonomy in choosing manner of masking such circumstance, prevent obtainment of the factors which most empirically represent such deprivation, introducing associations which potentiating detrimental outcomes, enabling artifacts specifically designed to impart detriment to be exhibited about humanity, and assuring that propensity to experience deprived socioeconomic or biophysiological status may be a pervasive possibility among populations, is, thus, presented. The requirement to attribute causality of biophysiological or social outcomes to individuals for circumstances which have occured generationally, which pervasively do not occur in Nature, which occur again and again cyclically after such individuals’ own incurrence, may pervade systemic perspectives, instead of simply assuring that the bases of the Human and social condition may achieved by all among civilization.*

    Illustratively organs of Kingdom Animalia may engage in detrimental interactions which substantial impair each other’s biophysiological function. Such detrimental impairing interactions, however, once completed, do not result in generational animosity, do not produce Post Traumatic Syndrome, may not result in persistence of such circumstance by contrived systems, and may not be specifically induced by contrived systems which benefit from incurrence of detrimental biophysiological or social outcomes. Thus, constituent organisms of Animalia as well as pervasive organisms otherwise may not exhibit the manner of biophysiological and social outcomes sometimes exhibited with context of contrived systems of Humanity. Such outcomes, thus, may not be compelling attributed to Human Nature. Moreover, such systems with each construct of deprivation may be inducing Humanity to turn upon itself, such that systems ubiquitously may endure more expansive than Humanity, thus assuring a priority of and generational persistence of systems. Nearly every unproductive outcome potentiated by Humanity may benefit some aspect of Contrived Systems, whereas any detrimental outcome by any of Humanity may impart detriment to all among Humanity, individually, plurally and generationally. Thus the exhibition of activity which imparts detriment to another, or enables unproductive biophysiological or social outcomes, may not only be introduced by contrived systems and influences which pervasively have not bases within Natural systems. Such circumstance may, by its occurrence, as well as a result of the myriad aspects of detrimental outcomes which might result from such occurrence, may be substantially indicative of undue influence, pervasive cultivating of constructs which potentiate such outcomes, as well as exhibiting the requisite nature of such occurrences such that systems may be sustained in activity and sustained in perspective. Humanity, however, may be compelled interact about such systems as result of contrived intersystems, influences regarding obtainment of the factor supportive of the Human and Social condition, as well as the possibility that others might utilize such systems more pervasively to the detriment of themselves or Humanity. Thus an essential or useful analytic

  22. A Researcher Says:

    Thus an essential or useful analytic Monte Carlo supposition which may accompany a presumption that Human Biophysiology and Span of Being may be indefinitely sustainable, may be that systems might optimally and imperatively not be enabled to be causal influences to impairment of Biophysiology and detriment to Span of Being particularly as a result of the generationally observed circumstance in which Humanity may turn upon itself to affect such outcomes if systems might be so enabled.*
    Similarly, Humans may pervasively exhibit systemically originated Cognitive Constructs, which exhibit priority of systems comparatively to Humanity. Humans may pervasively introduce the conundrum of a perceived inability to provide Nutritional factors to all of Humanity if instrumenting capabilities which assure indefinite sustainability of biological systems. Interestingly, after Nutritional factors has been Produced, only a small percentage makes it to the ingestion setting, much of that presented at the ingested setting becomes discarded, and substantial aspects or produce products are discarded from the Market Place. Humans may suggest that the population of Western Civilization may be less than sustainable when most Western and Eastern European Nations are in decline, have been in decline for some duration or would be in decline if not for movement of populations from other aspects of the Biome to such locations. Furthermore, it may also be suggested that as aspect of Dark Material and Biomass that Human populations may be less than sustainable, although Human Span of Being has progressed beneficially most indicatively correlative to increased exhibition of Human constituting of Biomass within Biome, particularly when such increases have been exhibited by Humanity which may be living in community with one another. Thus, Humanity may have emerged to become, perhaps, the only organisms in the Universe to consider its own success in population level achievement, as well as success in achieving duration of Span of Being, as a detrimental outcome. Such perspectives, however, illustrate the pervasive manner in which cognitive constructs prioritizing systems have supplanted priority of Humanity by Humanity. Consider the manner which Humanity may impart detriment to one another in circumstance associated with Financial Instruments, whereas financial instruments may only exhibit benefit in obtainment of essential bases of the social and Human condition, thereby illustrating a pervasively exhibited Psychosis induced by systemic, cultural and other influence. Such analyses enable one to believe that it is possible to find Choline associated factors, in Literature and Information sources, being utilized in directed Health services practice since the latter aspects of the Nineteenth Century, including being utilized as a therapeutic for impairment produced by Radiological Material. Such analyses may pervasively vindicate all among Humanity, regardless of circumstance, and exhibits the pervasively essential requirement that Systems, particularly contrived systems, be directed toward the benefit of all among Humanity, individually, plurally, ubiquitously and inclusively.*
    Thus, perspective of progressive culminating degradation of biological systems might include Choline and Phospholipid deficiency, Degradation of Ionic Characteristics, Degradation of Thymus, Impairment of the ability to regenerate pervasive aspects of Anatomy, increasing Homocysteine Levels, Increasing Asymmetric Dimethylarginine, increase of Trimethylamine and Trimethylamine-N-Oxide levels, as well as pervasive Apoptosis or Pervasive Necrosis. Additionally, occurrence of Higher C – Reactive Protein levels associated with Apoptosis and Necrosis, increasing Cellular Lysis with Electrolytes being exhibited within Biological Fluids, Pervasive Ischemia potentiating Sudden Adverse Health Events and degradation of rescuing interactions between Organs Systemically, and myriad manner of Oncological Leukaemic Lymphomic associated Pathology as a result of transformation of Thymus to adipose tissue along with persistent Inflammatory signaling. Occurring also may be Glucose and CHREBP Mediated bypass of already impaired Genomic management capabilities may occur, supportive of Oncological Leukaemic and Lymphomic circumstance. Resultant of such circumstance, otherwise less than impairing circumstance produces substantial detriment to biological systems, including pervasive administration of therapeutics with occupy Hepatic, Renal, Vision, Pulmonary and Spleenic toxicity management capability, potentiating Hepatic Oncology and degradation. Impairment characteristics of biological Fluids, cellular membranes and tissues may then communication between Neurological Centers and Neurological cellular material pervasively exhibited with tissue. Biophysiological may become dysfunctional and intermittently become without function. Acute Phase factors intermittently or persistently become exhibited, inducing changes to Coagulation, Thrombosis and Fibrin Factor associated Inflammation, as well as pervasive activation of Leukocytes. Biological Fluid, which inherently exhibits factors which may respond to particular environment characteristics, may produce Inflammation, Coagulation and other Cascading changes. Pyruvate, Lactate, Free Hydrogen Ions, L Lactic Acid and D – Lactic Acid may then begin to accumulate producing Metabolic Acidosis. Such Metabolic Acidosis may be similar to conducting physiological activity to the instance in which one cannot conduct any additional activity, particularly with context of Muscular contraction associated exercise using resistance. Such Metabolic Acidosis, however, may become exhibited systemically, without requirement of biophysiological activity, and may impair Neurological level function essential to for Organ electrophysiological characteristics. Paralysis of Organs, Tissues and Neurological material may then become exhibited. Such Paralysis may be essential in permitting the transformation of pervasively beneficial molecular factors, resultant of Metabolic Acidosis, into detrimental factors which produce Catabolism of cellular material and Lysis as well as tissue degradation inclusive of Neurological cellular entities and Neurological centers. Pervasive Capabilities may be useful in preventing, impeding and reversing each of these circumstances including instrumentation Glycine, Acetylcholine, varieties of Choline such as Citicholine and Phosphatidylcholine as well as Carbi-Carb (NaHCO3 and Sodium Carbonate NA2CO3), Dichloroacetate which may increase Pyruvate Dehydrogenase (PDH), Pyruvate Dehydrogenase or factors which induce its expression, and Pyruvate Carboxylase or factors which induce its expression. Benefit may be obtained from Alanine Transaminase or influences which improve its bioavailability, CDP Choline which enables Mitochondrial ATPase and Ionic ATPase (Na+ and K+), as well as Phospholipids or Choline versions such that A2 Phospholipase function be beneficially affected. Additionally Reconstituting the Choline, Folate, Betaine (as Trimethylglycine and not Betaine Hydrochloride which is version of Chloride), Methionine, B12, B6, Thiamin, Riboflavin, Niacin, Biotin, Pantothenic molecules and Phosphatidylcholine associated molecular pathways which may enable intervention of such circumstance at their bases. Similarly, myriad Neuroprotectants which prevent degradation of tissues bases durin such circumstance are presented within the AMEHSI specification information bases, particularly associated atypical cellular proliferation circumstance. The centrality of such factors may be imperative, particularly with context of the pervasively ability to regenerate biophysiology and Anatomy.
    Regarding testing and assay, atypical biophysiological characteristics, particularly regarding a particular molecular factor, should be assayed by conducting several levels of assay. The AMEHSI Specification provides useful perspective in this regard. Assay can be useful in determine, as precisely as possible, the molecular, Genetic, bioavailability or structural anomalies which may be causal of a health condition (Escape Mechanism). Determination of any type of deficiency or atypical characteristics, particularly when it can determine that such atypical factor may have central causality to the divergence of biological function from typical circumstance which produces Pathology, might then be intervened by providing the precise molecular factor which is atypical, with typical molecular structure and with typical bioavailability. Pervasive divergence of biological systems from optimal and pervasive divergence of biological systems from typical may be most incipiently the result of five factors introduced pervasively in these analyses, particularly those associated with Phospholipid and Choline Deficiency.
    Relevantly, Clinical studies obfuscatively presume that Pathology may have pervasively similar causality within populations. Each individual exhibits different characteristics at molecular, Genetic, biophysiological, environment, behavioral and other levels. In many instances, a successful Therapeutic in a clinical study may be one that effects substantial aspects of a population beneficially, instead of effecting very few or one to completely remediating health status outcome. Similarly, a substantial factor in successful molecular therapeutics or other therapeutic influence may be the manner in which these provide aspects of Phospholipid associated molecular pathways as well as the manner in which these affect aspects of biophysiology produced by such pathways. Moreover, Clinical Studies may not often empirically ascertain the precise molecular or submolecular bases of a successful or less than successful outcome among participants. Essentially, if only one among myriad study participants exhibits beneficial outcomes, or none of such participants exhibits outcomes, then determining the precise molecular bases of such outcomes may be much more beneficial to practicing health services providers, as these may provide better information, be utilized in very specific circumstance and enable production of highly individualized therapeutic regimens which are correlated precisely to circumstance at molecular levels. A Clinical study of 1, accompanied by thorough Assay, interactively during progression of health status and instrumentation of therapeutics may be of substantially more benefit that very large studies in which unconsidered habitual or environmental factors may induce variance. Particularly, many studies include instrumentation of Placebo or a non-effective Therapeutic, as well as Nocebo in which particular segments of the Study Population receive no Therapeutics. Traditionally, Placebo may have constituted of a Sugar Capsule, which change Genetic Expression through changing Aminoglycoside Characteristics, as well as include Gelatinous material produced from Laccaic Acid, which is a substantially effective DNA Methyltransferase inhibitor.*
    Many therapeutics utilized as Placebo or which have been approved for use within Populations, may have been inducing substantial changes to Genetic Expression, thus potentiating the pervasive Clinical Studies may have been inaccurate in their presumptive bases. Such circumstance illustrates the essential nature of understanding thoroughly the molecular bases of Clinical Study outcome or Therapeutic Intervention outcome as it manifests itself as changes to biophysiological characteristics. Nocebo also exhibits similar characteristics resultant of the observed ability of health services consumers to exhibit improved health services resultant of simply being observed by a health services provider, particularly providers which do not believe that demise is a requisite aspect of Span of Being. The Placebo affect may be pervasively observed Phenomenon which has Bona Fide Biochemistry and Biophysics bases. Illustratively, the Uncertainty Principle proposes that are particular aspects of any system which have indeterminable outcomes, not as a result of uncertainty itself; however occurring as a result of the inability to precisely determine all of the factors which produce all aspects of every outcome. Thus, uncertainty increases as the ability to observe or individually discern aspects of a system increase, presenting the essential nature of highly capable technology in observing factors at molecular systems level, presenting a most efficient convergence of submolecular systems with supramolecular systems. Observable Pathology, before such emergence of Technological capability, numerous inferential indicative factors may have been utilized to reduce possible biophysiological statuses to few potential health conditions, although these may pervasively persist in use along with such technological capability. Thus, health services may pervasively observe that Health Services Consumer exhibit changes to health status without precisely determinable causality, although such causality might increased determinable if considering myriad levels of intersystemic influences included in sophisticated systems of system analyses. The standard for accepting a therapeutic or practice as beneficially may often be a requirement for such prospective capability to produce benefit to biological systems more consistently and more prevalently comparatively to Placebo or Nocebo. Optimally, however, each participant in a Clinical Study might have the precise changes to molecular level function which enable or prevent a prospective outcome, regardless of such enabling or preventative influence may be of Universes level, Sub quantum level, or somewhere in between. *
    Such information presented, herein, may be substantially indicative of the substantial research and capabilities presented within the AMEHSI Specification. The substantial capabilities, herein, as the resources exhibited within the AMEHSI specification information base may be indicative of the Logarithmically more extensive capabilities and research which may be aggregated into iterative instrumentation of the specification and guidance. Thus, the information herein, although substantial and perhaps so voluminous as to be impractical in the context of these discussions, present a compelling perspective the possibility that 1.5 Million individuals each Annum since 1900 may have incurred a most substantial detriment to their Civil Liberties, might have incurred demise which was not requisite, and might have avoided incurrence of Adverse Health Events altogether if they were provided Olive Oil, Sugar Beets and a Probiotic which does not include Firmicutes or Rhamnosus versions within reasonable proximity to emergence of such outcome. It is thus presented that if systems may produce outcomes in which such less than complex capabilities may not be applied to the benefit of Humanity, then systems pervasively may require Humanity to transform them such that their benefit to Humanity may be assured. Endeavoring upon such a path, however, requires an abdication of the inclination to attribute to causality to any among Humanity to such outcomes, acknowledge the influence of systems in producing ubiquitous biophysiological and Social outcomes of detrimental and Beneficial nature, as well as understand the nature of any system which persist for more expanse duration than its constructors to become transformed to prioritize itself and to transform Human events to presumptive bases which sustain itself. These, with context of more among Humanity in the preceding epochs and centuries, as well those whom may have conducted their being in eras which are to emerge, may present a most compelling vindication of Humanity, individually, plurally, ubiquitously and inclusively.
    Thus, central assertions may include the following. Why are these factors not assayed in every Health Services Intervention? Since these factors are most indicative of and causal to both Sudden Adverse Health Events and Progressive degradation associated with Gerontological Status, why isn’t increased levels of such factors considered to be Pathology instead of being obscured by a psychological inversion of these to be Indicative of Pathology? If Health services systems do not ubiquitously considered progressive impairment as pathology and permit pervasive susceptibility to Adverse Health Events resultant of molecular circumstance intervenable with less than complex pervasively available factors, then what other aspects of systems may exhibit similar paradigms? If these four or Five most indicative Factors to sudden adverse Health event may have potentially averted Millions of adverse Health Events since the Nineteenth Century, and literature exhibits individuals in health services practice using such pathways during such epochs, as well as these being intervenable with factors which may have been available since incipient exhibition of Civilization, what aspects of pervasive Human Impairment may be the result of Philosophical and Systemically persisted perspective regarding Span of Vital Being? Imperatively, locate any individual exhibited in the Span of the Human Experience, determine the Pathology which may have cause such individuals to not be exhibited in this era, research the pathology with Priority to Phospholipids and Choline associated factors, and it may become determinable that the principle causes of such circumstance may have pervasively been deficiency Phospholipids and Choline. The inability to acknowledge the molecular bases of such health conditions may be Homologous and perhaps caused by similar circumstances in other systems exhibited about Humanity in which perspectives and Philosophical bases which suggest that demise may be a requisite aspect of the Human experience have shaped the exhibited Span of Being of Humanity in subsequent epochs, regardless of pervasive capabilities in which biophysiology may be sustained, repaired and regenerated.
    How are the perspectives of the provider with which you interact affecting Health Status? What can you do determine if the provider entities with which you interact and to whom you may be directed do not believe in Human demise, do not ignore pervasive ability to regenerate biological function and Structure, as well as understand the nature of Progressive degradation of biological systems which can be prevented, impeded and reversed? How does one, regardless of their role in health services, manage interactions to efficiently, effectively and standardly move toward empirical determination of causal factors to less than optimal biophysiological, perceptive, cognitive and behavioral outcomes which can be remediated by reconstituting optimal and typical characteristics regarding such impaired factors?
    Assay Which May be Imperatively Included in Each Health Services Intervention
    Asymmetric Dimethylarginine
    C – Reactive Protein

    Permutations of Assay which may be conducted to Determine, as Precisely as is Possible, Molecular Bases of a health Condition.
    To reiterate that’s each iteration of Assay Includes the following Activity
    A. Biopsy of the actual specific cellular material exhibiting Pathology or Neoplasm.
    1. Genetic Structural Anomaly
    2. Molecular structure anomaly
    3. Atypical levels of relevant factors, increased or decreased.

    B. Assay of the Tissue Local to the area of Pathology.
    1. Genetic Structural Anomaly
    2. Molecular structure anomaly
    3. Atypical levels of relevant factors, increased or decreased.

    C. Systemic level assay such as biological Fluid from Vasculature or Arterial Pathways.
    1. Genetic Structural Anomaly
    2. Molecular structure anomaly
    3. Atypical levels of relevant factors, increased or decreased.

  23. A Researcher Says:

    Please don’t let the format of the text prevent consideration of the material. The volume of information produced to some inconsistencies in formatting and the review capability was not active on the submittal interface.

  24. A Researcher Says:

    ADIPOSE Hepatic Health Conditions most typically result pervasively exhibited Choline deficiency. Genetic anomoly within Cholinergic Pathways may change the distribution of Enzymes and Molecular pathways, as well as potentially produce behavioral changes manifested as Habitual, Ingestive, Life Style or other changes. There is a substantial possibility that supplementation within the Choline associated pathways may induce substantial and pervasive changes in ones biophysiology, perception, social outcomes, migration behavior, inclination, habits, cognitive outcomes and other circumstance.

  25. A Researcher Says:

    Acetylcholine may be so pervasive during gestational phases that it accumulates without detriment systemically. Post gestational circumstance may result in logarithmic decreases of Acetylcholine, thus, possibility of excess enzymes which Metabolize Acetylcholine may emerge. Similarly, there may be overproduction of Acetylcholine interactive Immunological factors resultant of such logarithmic reduction. Thymus typically mediates narrow ranges of automimmune function for all molecular factors, including endogenously produced molecules. The Pathology of Thymus degradation, resultant of Choline associated factor deficiency, toward becoming disorganized Adipose tissue may typically be incipiently be exhibited as increased Automimmunological activity, and then progress toward impaired ability to produce T Immunological Cellular Material, and then persistent Inflammatory signaling as it attempts to signal for replenishing cellular material originating from Skeletal Struture Marrow. Choline deficiency however also result in impaired Skeletal Ossification, Marrow characteristics, as well as production typical Progenitor cellular material. Resulantly such signaling in Thymus, Lungs or other tissue may induce migration of cellular material which has experience Endothelial Mesenchyml Transitions, Motility Phenotype and thus may be considered Metasteses. Adipose Cellular Material may also exhibit such Transitions and Constitute Metasteses. Ionic Gradients upon which Motile Metastesis cellular material may move may the circumstance most constitutive of susceptibility to the most Pathogenic outcomes. The degradation of Thymus and logarithmic decrease of Acetylcholine may be substantial influences in exhibition of Immunological factors which interact with Acetylcholine.

  26. A Researcher Says:

    Insulin may also induce L-Arginine mediate Nitric Oxide production.

  27. A Researcher Says:

    I very relevant factor regarding how such capabilities can be observed comparatively to less than correlative outcomes may be explained by Placebo, Nocebo, Pervasive Systemic Influences and Beliefs, which may all potentiate exceptional outcomes as well as potentiate substantial detrimental influence to outcomes.

    A Monte Carlo Hypothesis is base supposition upon which research, Clinical Study or Health Services Practice may be founded. Many instances of these present an assumption of the requisite Nature of Human demise within the Human Span of Experience. Other instances, however, present that these might be observed and may not be requisite. Other instances may be presented in which such outcomes are considered to be ubiquitously atypical. The latter two of these may be perspectives which one might optimally incur within their Health Services Providers Perspective and Practice. Regardless of if a provider entity may be consciously aware, if applied Therapeutics regarding Phospholipids (90% or more of Cellular Membranes with Phosphidylcholine at Fifty, Phosphatidylethanolamine at about Thirty and Spingomyelin at Ten), Choline associated Molecular Pathways (99.5 percent of more of molecules produced within Biophysiology), as well Assay of Homocysteine, Asymmetric Dimethylarginine, Trimethylamine, Trimethylamine-N-Oxide, and C – Reactive Protein are not included in every health services intervention, including perspective that any divergence from the most optimal circumstance regarding such factors as Pathology, then there may be an inherent acquiescence to Demise which may be foundationally shaping practice as well as outcomes.

    A foundational premise of the AMEHSI specification may be that any participant, including Providers, Health Status Managers, Consumers, Ancillaries, Pharmacists, Message Therapists, Friends, those whom are related to the consumer, Payer Organizations, or other, may instrument a Manageable Efficient Health Services Instrumentation capability which iteratively considers that any divergence from optimal biophysiological status or exhibition of factors causal to such divergence, are Pathology. Otherwise, the instance at which outcomes which Traditional Health Services perspectives might consider Pathology may emerge, particularly regarding susceptibility to sudden adverse health events, might not be adequate.

  28. A Researcher Says:

    Although such pathways suggest an empirical basis indicative of indefinitely sustainable biophysiology at optimal levels of function, disparities between observed outcomes and such potentiate outcomes may typically be the factor which result in clinician and practicing health services providers diverge in perspective and practice. Until R Zeisel Et Al at the University of North Carolina at Chapel Hill illustrated compellingly and conclusively that Choline deficiency along may result in Myriad Pathology and Demise, deficiency was pervasively not acknowledged as cause of health conditions. Research methods, however, may now utilize deficiency of Choline, Methionine, Folate, and other Phospholipid Metabolism associated factors, along with supplementation of particular Amino factors, as one of the most persistently effective models of inducing Hepatic Oncology as well as pervasive Pathology resultant of such circumstance progressively. The resources which resolve such disparities are readily available, however, requiring first being introduced to Choline and Phospholipid pathways, compellingness of these as most incipient factors in Human development or Pathology, as well as availability of adequate available research capacity to reduce these to empirical levels. Health services providers, being compensated pervasively through point of service reimbursement reliant upon volume, cannot allocate months of research to empirical levels iteratively in response to the changing biophysiology of a consumer through therapeutic regimens or through progression of Pathology. The manner in which health services are paid, the requirement of organizations to obtain adequate resources to provide for employees and expenses, as well as the persistent requirement of financial instruments with which to sustain the vital being of individuals within such organizations, represent substantial impasse to achieving such empiricism. Such influences may be pervasively exhibited in civilization and reflect the pervasive manner in which systems about humanity may be assuring demise and propagating characteristics of Human Vital Span of Being observed in antecedent eras such that biophysiological outcomes and social outcomes adhere to these in these subsequent eras regardless of the exhibition of technology potentiating substantial improvement.

    The conundrum of HIV, being able to eradicated by Arginine Repeats of TAT Protein which has been conjugated to Caspase 3 factors and a highly conserved aspect of the HIV encapsulating Protein Coat, along with the ability to conjugate such highly conserved Domain to virtually any Cytotoxic Oncology Therapeutic, represents unfielded capability that might have eradicated HIV as persistent or demise potentiating health condition as early as the central aspect of the Nineteen Nineties or antecedently. Such represents a precise instance in which populations have been managed to complacency by permitting the detrimental status of an at risk population to have causality of their biophysiological outcome attributed to behavior. Permitting such outcomes, regardless of the causality, may be wholly unproductive, as it provides a precedent which systems pervasively enculturate such that humanity may observed and accept detrimental social and biophysiological outcomes. Similarly, such Behavior may be shaped by systems pervasively upon incipient molecular and biophysiological circumstance. Each of such perspective, however, represents the manner which Humanity may be caused to turn upon another segment of Humanity, and not instrument a capability which might have been, with adequate priority, able to be refined within context of weeks in order enable applied instrumentation. Instead an obfuscative requirement for development and iteratively expansive Clinical Studies may have become presented as a requisite activity requiring decades, comparatively to an empirical clinical study constituted of few individual along with empirical assay of the precise affect at molecular or biophysiological levels which such few participants may have incurred. Prolonged, decades duration Clinical Studies may be systemic constructs which encourage acceptance of Human demise particularly with context of the technological capability to determine, empirically, the precise molecular bases of the affect which prospective therapeutics have to a cadre of few individuals at molecular and biophysiological levels. Expending resources, duration, and activity upon highly level Clinical Studies among expansive populations without such empirical level determination of successful or unsuccessful outcomes may be wholly unproductive, and may have become as causal to the persistent exhibition of health conditions in the modern era, as the health conditions themselves may have been antecedent to modern technological era. Moreover, such Clinical Studies may obfuscate the pervasive convergence of Human pathology within Phospholipid associated pathways, other essential factor deficiency, as the manner in which these converge with influences from Universes level to sub quantum levels in the molecular basis of Human biological function or biological structure.

    The essential detrimental aspect of such studies may be that these may mimic manner of health services practice, in which iterative assay of factors regarding indicators of stability of biological systems, indicators of pathology and precise determination of escape mechanisms which are causal to emergence or progression of pathology may not be ubiquitously instrumented. Instead, indicators or biomarkers may be assayed which suggest the nature of a health condition or health status, subsequently then being intervened by application of a cadre of therapeutic or supportive capabilities, which may not relevant, which may be imprecise, and that, through iterative instrumentation followed by assay of outcomes, potentiate beneficial effect. Essentially, such may produce a circumstance in which the health condition, the Human biophysiology and the Human cognitive context may be required to compete to determine which may endure. Often, before therapeutics achieve the accurate context of affect, the Human biophysiology or the Human Cognitive context, may abdicate. Thus, the imperative nature of empirical assay may be illustrated.

    A most essential aspect of such disparity between empirically determinable ability to improve health status and the outcomes which practicing Clinicians might be able to achieve may be the emerged compolexity of molecular and metabolic biophysiology, particularly resultant of adaptation to Choline factor and Phospholipid factor deficiency. Pervasively, such defiency may inversely transform Human biophysiology. Deficiency of Phospholipids and Choline may produce impaired General Permeability as well as impaired Specific Permeability. Resultantly molecules may pervasively be able to Tunnel through membranes at Tissue levels, Cellular Plasma membrane levels and between aspects of intracellular environment. Permeability, however, impair directed management of availability of molecules, degraded Ionic and Turgor Characteristics, as well as susceptibility to systemic Gradients. Illustratively, an active Musculature, Pathology exhibited in particular tissue base, increases in require Toxicity management, or other factors might consume requisite factors at levels which exacerbate already systemically deficient resources such as Phospholipids and Choline associated factors. Similarly, such factors may be already be being redirected systemically and within intracellular environment toward the most essential activity, typically the sustainment of biophysiological and electrophysiological function. Illustratively, the comparative exhibition of Phosphatidylcholine, Phosphatidylethanolamine and Sphingomyelin, may be a substantial determinant in the ability of cellular membranes to exhibit concerted Electrophysiological function, including Cardiac or Pulmonary Rhythm as well as Peristalsis.

    Improvement of such membrane characteristics, which may occur ephemerally with instances of improved Nutrition or during an instance of obtaining adequate levels of such factors, however, may not resolve such deficiency. Molecular and Metabolic inter-systems provide an illustrative perspective of deficiency. Pervasive aspects of the Human Genome are not translated into functional molecules. There is a substantial possibility that the progressive decrease in aspects of DNA which become expressed may have been the result of a Choline deficiency generationally and cumulatively through the Span of Vital Being, as well as detriment to Genome which occurs during such progression. The reduction in Genomic expression is logarithmic when compared to the 17 fold reduction in Acetylcholine bioavailability upon incipient transition to Post Natal Circumstance. DNA is translated to hnRNA by Ribosomal Molecular Machines, utilizing Biosynthesis requiring Choline as well as recycled molecules when Choline is not adequately available.

    Methylation upon DNA typically activates, deactivates or changes expression. Methylation upon DNA at atypical locations can prevent or increase expression. Unrepaired DNA can also accumulate Methyl Groups. Impaired availability of the Methyl Groups, particularly resultant of a Choline and Phospholipid associated factor deficiency, can also result in atypical Methylation. Genetic or Epigenetic impairment of DNA Methyltransferases, which can impair Methylation and deMethylation of DNA, producing less than optimal expression and replication outcomes. DNA replication, however, may be considered the only Phase of the cellular cycle in which DNA become unMethylated, illustrating the detrimental effect of p53, Phospholipase, p21 and HIV TAT mediated dePhosphorylation associated impairment of cellular stability. DNA may also become deMethylated systemically during particular phases of Gestational development.

    Diffuse Intrinsic Pontine Glioma, for instance, may occur as a result of substitution of Methionine and Arginine into particular areas of Cholinergic Enzyme expression. Additionally, pathology typically occurs in pattern which is relevant to progression beginning at post Breast Feeding stages to incipient phases of Maturity. Choline and Phospholipid deficiency, however, may result in substantially pervasive changes which potentiate such outcomes. Myriad aspects of such pathology, upon analysis, occur precisely as a result of Choline deficiency independent of such Pathology. Imperatively, however, each instance in which Humanity may experience new stimuli, produce cognitive associations, incur learning or adaptive influences, Frontal areas of the Cranium Encapsulated Neurological Centers exhibit auto-segmentation of DNA within cellular material. Segmentation of DNA is a substantial aspect of learning and development, requiring Choline and Phospholipid associated factors. Diffuse Intrinsic Pontine Glioma may also be characterized by an inability of particular aspects of DNA which require Methylation becoming unable to Methylated as a result of Acetylation. Acetylation may induce deCondensation of DNA which may be wrapped upon structures indicated Histones such that it may be Read by DNA and RNA Polymerases, whereas deactivation produces reCondensation of DNA. Histones have a natural affinity for Phospholipids until particular Molarity of such factors is reached or until DNA becomes exhibited upon Histones. Phospholipases change the Molarity of Phospholipids artificially with context of actual deficiency. Acetylation of DNA upon Histones or upon Histones prevents Trimethylation in areas nearby. Trimethylation is molecular signal which may induce activity upon Histones.

    Such interactions may illustrate the nature of pervasive Neurological degeneration, such as Alzheimers and other conditions. Homocysteine, Asymmetric Dimethylarginine, Trimethylamine, Trimethylamine-N-Oxide, C Reactive Protein, Diabetes, deficiency of Phospholipids, Choline associated factors, Trimethylglycine, and other factors exhibit adequate factors to conduct regeneration as well as inadequate factors to conduct repaired, along with ephemeral Ischemia or progressive persistent Vasomodulative Constriction which prevents essential factors from reaching particular areas as required. Thus, such deficiency and detrimental molecules may not only be affecting Gerontological populations, not prioritizing such factors may be placing Humanity at risk beginning at incipient aspects in the Span of Being. Such may illustrate the Nature in which Political, Social and Economic factors should not be determinants in the availability of health services, empirical research, and factors essential to the Social Condition as well as factors essential to the Human Condition.

    hnRNA, comprised of sequences of three Nucleotides arranged in the Genetic Code, then has some Sequence Translated into mRNA (Exons), and disregards extensive cadres of sequences (Introns). hnRNA becomes reduced to mRNA and tRNA assists in Ribosomal Molecular Machines’ synthesis of Proteins by producing and attaching together sequences of Proteins which are homologous to the sequences within mRNA. During such activity, expressed molecules, Epigenetic molecular systems, deficiency, as well as molecules from external environment may all effect, impede, change or impair synthesis, replication, translation, Protein function and the duration of which proteins are exhibited before being recycled.

    Particularly, however, molecules may exhibit progressive changes and interactions through a series of interactions (Pathways) which culminate in an interaction constitutive of biological function or an interaction which results in production of as well as integration into biological structure. Such interactions may also occur as molecules move to extracellular environment, effecting other cellular material, tissues and organs. Each interaction within such pathway may include of Enzyme interactions with Substrates, as well as or non-enzyme molecular factor interactions. Non-Enzyme interactions can be detrimental as these are not mediated by Genetic expression. Advanced Glycation End Products, for instance, may be resultant of the progressive condensation and Crystalization of Glucose exhibited in Plasma, similar to the manner in which Rock Candy may be produce. Glucose can, in some manner, be exhibited within Biological fluids for weeks or months, illustrating a requirement for it to be Endocytosed and maintained within intracellular environment. Enzyme interactions with Substrates, however, may be inefficient. A Phenomenon indicated as Michaelis Factor or Constant, observes that when particular Enzymes become saturated by available substrate, Enzymes become unable to become Freed from the exhibited interactions such that the any additional interactions become delayed or prevented. The interaction may then be indicates as Rate Limiting.

    Choline associated pathways may be diverse and expansive. There may be substantial Rate Limiting Phases. Thus, an inclination to produce Supersaturated biophysiology, as exhibited with Super saturation by Acetylcholine during Gestational status, may result in accumulation of Substrate within intracellular or extracellular environment. Thus obtainment of excess levels of Choline may not be harmful, however, potentiating become aggregated in particular phases of Metabolic and Molecular pathways. Thus, persistently available small amounts of as many factors within Cholinergic pathways as is possible, may produce the most optimal biophysiological and regenerative outcomes.

    Furthermore, as Phospholipids are comprise pervasive membranes, cellular membranes, extracellular matrix and other structural factors, these may readily traverse such aspects of biophysiology. Topical administration of such phospholipids can become highly therapeutic systemically. A known capability of inducing increased bioavailability of an Nutritional factor is to include it with Eggs and Egg Yolk for ingestion. Eggs with Egg Yolk may exhibit considerable levels of Phosphatidylcholine which comprise 50% or more of Membranes. Those familiar with Exercise Physiology are typically familiar with the systemic Vasomodulative Dilatation produced by L-Arginine ingestion, and may be aware of the ability to include these with Phospholipids, Choline, Phosphatidylcholine and Trimethylglycine for topical administration. Topical administration of such factors may produce an almost immediate Vasomodulative Dilatation, and there may be some question of why such capability is not utilized to reverse Ischemia which produces impaired biological function.

    Vasomodulative Dilation, however, which reduces reintroduction of Circulatory Flow (Reperfusion) may produce degradation of Neurological, Vasculature and other tissue as Leukocytes, T Cellular, and other factors exhibit Catabolism. Neuroprotectants, including Choline, Phosphatidylcholine, Trimethylglycine and numerous other factors, may prevent such Catabolism and induce regenerative influence to tissue pervasively. There is a substantially possibility that most instances in which Ischemia produces impaired biological function and impaired consciousness may immediately benefited by instrumentation of the Factors presented in these discussions, particular Choline Factors, Phospholipids, Trimethylglycine, L – Arginine, Nitric Oxide Synthase, Ornithine, Citrulline and other factors.

    Regarding availability of B Vitamins, Folate (Supplantively of Choline), Choline, Phosphatidylcholine, Trimethylglycine, Bacterial Vectors as well as Ionic influence, Clothing, Shoes and other factors may provide substantial impedance to otherwise persist interaction of Dermis with Plants, Earth, Environment, Aquatic influence or other factors which might constitute persistent obtainment of such factors. Illustratively, B Vitamins may pervasively enter the Nutritional Pyramid from the Earth as well through Nutritional Factors obtained from the earth such as Sugar Beets.
    Thus, providing the factors provided in these discussions, as well as conducting assay of the few factors introduced, may be only the beginning. Deficiencies of other Factors, Genetic or Epigenetic status, Environment, Behavior, other conditions, Nutritional status and other circumstances, may require consideration once such less than pervasive factors are provided. Next, it may become require to provide small amounts of each molecule within each pathway, successively, perhaps then simultaneously, and along with monitoring of Homocysteine, ADMA, TMA, TMAO, C Reactive Protein, Vital indicators, Cognitive Function, Perception, Perceived Circumstance, impaired tissues or organs, Pathology or other. The objective may be continuous improvement toward optimal biophysiological statuses, including regenerative outcomes. Such an objective may have been achievable in many permutations of preceding generations. Such an objective, however, may become less obfuscated if a presumptive basis of practice and presumptive bases of systems affecting health status begin to exhibit the Monte Carlo Hypothesis that Human Span of Vital Being may be indefinitely sustainable.

  29. A Researcher Says:

    Hopefully, the information provided may be compelling enough to illustrate the much of the outcomes and circumstance exhibited herein may most incipiently be the result of diverse pathology resulantat most empirically of a Choline associated molecular factors and Phospholipid deficiency.

    If one is enable to consider such pespective empirically, then one may be able project such circumstance into any health condition and ascertain such incipient deficieny as enabling, causal or constitutive of such Pathology.

    Regardless of ones biophysiological status, level of impairment, level of conciousness, indicated Pathology or circumstance otherwise, instrument the AMEHSI Specification, explore the Choline Associated and Phospholipid associated Pathways, with Perspective of the Inherent ability of biological systems to be regenerate, repaired and reconstituted, including from one individual cellular material being introduced upon extracellular matrix outside of Human biological systems.

    Find health services do not require that Human biophysiologly exhibt progressive degradation and susceptibility to demise. Extricate oneself from falsely ideological directives and associations in which Humanity may be enourage to consider demise, Adverse Health Statuses and outcomes, as well as obfuscation of the emperical bases of biological function.

    Obtain an incipient glimpse of the Potential of the Human Experience and Social Condition.

    Involve ealth services providers and those whom affect health status in a Manageable Efficient Health Services Instrumentation, such that together, it might be empricially determined and applied to the benefit of oneself or others, the inherent capabilities exhibited within Human biophysiology.

  30. Researcher Says:

    At some instance, it will be possible to enable spelling and grammatical review in the submittal page. Please excuse the grammatical and spelling anomalies in the submitted information.

  31. Researcher Says:

    A particular Clinical Study examined the effects of Choline Deficiency and Choline dependency upon health status and social outcomes among Female Gender. Phosphatidylcholine is synthesized in 3 more Pathways which utilized difference precursors and sometimes different distributions of types of Adipose Acid molecules. Phosphatidylethanolamine Methyltransferase may be a requisite aspect of such varying synthesis pathways, enabling Phosphatidylcholine to be produce from Phosphatidylethanolamine as a result of transferring of a Methyl Group between precursor molecules. Phosphatidylethanolamine, comprising 25% or more of cellular membranes, and Phosphatidylethanolamine, comprising Fifty Percent or more of Cellular membranes, require particular comparative ratios such that typical electrochemical characteristics of cellular material become exhibited. The difference in Phosphatidylcholine synthesis between Female and Male Gender, presumably as a result of requirement of women to conduct biosynthesis associated with Gestational status and Breast Feeding, is suggested to represent homologues to the difference in typical span of being between Genders with Female Gender exhibiting more expansive duration correlative to increase in Phosphatidylcholine production.

    Female gender at pre Menopause status comparatively to Female Gender at Post Menopause status, were placed into three sub groups, PEMT Typical, PEMT Individual Coil of DNA Impaired Heterozygous Single Nucleotide Polymorphism, and Phosphatidylethanolamine Methyltransferase Both Strands of DNA impaired Homozygous Single Nucleotide Polymorphism. Choline factor dependency is considered to be an increased dependency upon obtaining Choline from exogenous factors resultant of genetic impairment, metabolic impairment or deficiency in factors affecting Cholinergic Pathways.

    The outcomes produce may have been one of the defining verifications of Reomer’s Axiom and exhibition of the manner in which Characterisitics of Choline associated pathways emerge upon cultural, systemic, enculturative, social, economic and other systems into biophysiological as well as social outcomes.

    Increasing in certainty, respectively, according to level of genomic repairment of PEMT from Unimpaired to Heterozygous and then to Homozyous Single Nucleotide Polymorphism, researchers were able to induce Non – Alcoholic Hepatic Steatosis, Adipose Hepatic Tissue, Oncological status and pervasive aspects of ancillary pathology by inducing Choline associated factor deficiency within each subgroup. The most essential comparison, however, may have been between pre Menopausal Homozygous Impaired groups comparatively to Post Menopausal Homozygous Impaired participants. The pre Menopausal group exhibited such susceptibility to Pathology and progression that the induced Choline factor deficiency required abatement as the participants expediently incurred risk to Vital Being. The other subgroups exhibited less Pathogenic susceptibility.

    The Post Menopausal Homozygously Impaired sub group, however, presented a challenge which required the Clinical study to be abated. The eligibility requirements for PEMT were constructed such that participants required being known, accessible, health status adequately representing a pre deficiency baseline, and not have the affects of the study obfuscated by other circumstance. The study was not able to produce more than one participant. PEMT represents such substantial affect to Biophsyiological Outcomes and Social Outcomes that the participants at post Menopausal circumstance were inaccessible presumably as the result demise, dependency upon factors with which sanctions are associated, progressed pathology, having incurred systemic deprivation of self determination or were dependent upon therapeutics to maintain Span of Vital being to such level that such populations were unable to be included. In some areas, as Fifty percent or more populations, particularly Female populations, may be Homozygously impaired for PEMT, whereas Seventy Percent may be Heterozygously impaired.

    The research at AMEHSI.ORG is imperative in that it orchestrates several other studies such these may be applied analytically and compelling to a Health Services, Cognitive, Social or Systemic context, illustrating the manner in which systems shape outcomes among Humanity.

  32. Researcher Says:

    Regardless of health condition, it can be presumed that a Choline deficiency may be the most incipient cause of susceptibility, regarding Pathogens, or most incipiently causal to Pathology otherwise. The levels of Choline factors required for optimal biological function may be substantially increased correlative to typically recommended levels, particularly as result of typically recommended levels potentially being based upon a presumption of the requisite nature of progressive degradation of biological systems culminating in Demise. In the next few posts, one may find substantial population affecting conditions which have either Choline associated factor basis, resolution or resolution otherwise which may be supported by such factors.

  33. Researcher Says:


  34. Researcher Says:

    Oncological, Leukaemic and Lymphomic status may pervasively be the result of Choline and Phospholipid deficiency. Myriad studies associate increased susceptibility and decrease in optimal outcomes correlative to Choline increases, obfuscatively. In many instances the clinical studies have been designed to utilize prediagnosis susceptibility based upon survey to indicate detrimental correlates toe Choline and then exhibit post diagnosis assay which reverses such Correlation which considered independent of the such survey.

    Similarly, although Phospholipid deficiency, Epigenetic, Genetic, and then environmental behavioral factors may most respresent susceptibility, it is Homocysteine, Asymmetric Dimethylarginine, Trimethylamine, Trimethylamine-N-Oxide, C-Reactive Protein and pervasive systemic degradation which produce such Oncological, Leukaemic and Lymphomic outcomes. Moreover, the associated of Choline with less than optimal outcomes may be associated with Oncology in locations reasonably near to Digestive pathways, suggesting substantially causality of Trimethylamine, Triemthylamine-N-Oxide, and Free Amines which traverse inflamed tissue membranes and induce pervasive tissue remodeling. Similarly, impairment of Vasodilitation may produce substantial levels of Ischemia systemically, Hepatically, and Renally, inducing Advanced End Products with context of impaired regeneration such that Choline may not become widely distributed.

    The AMEHSI Specification Instrumentation Guidance provides precise analytic perspectives of these. The complete Cadre of factors presented in the AMEHSI specification are, thus, requisite.

    A substantially detrimental outcome can be produced by typical therapeutic Regimines which induce individual factors supportive of health status iteratively until each one becomes unable to provide its incipiently exhibited beneficial effect. Such approaches result in cumulative degraded affect of therapeutics until a binary circumstance is exhibited in which few functional pathways may be available. Typically, a change in Nitric Oxide can degrade such few available functional pathways resultantly of otherwise clinically unaffecting influence.

    Thus, it is may be essential to transform perspectives ubiquitously toward producing regenerative outcomes instead of introducing regimens which prolong Span of Being toward a culmination in demise.

    Similar research has been presented which has delayed the instrumentation of essential capabilities with regard to HIV or other less than optimal Health Statuses. One should regard any research which suggests that Choline associated factor supplementation may individually and principally be casual of degraded Health status or outcomes. Linking of articles may not be useful here as the principle most readily presented research may be obfuscative enough to produce substantially detriment to individuals, Clinicians and researchers.

  35. Researcher Says:

    Harvoni, (Sofosbuvir, Lepadisvir), Ribavirin, Peginterferon, Betaine, S-adenosylmethionine, and possibly Choline, Folate, B Vitamins, and Methylcobalamin, may have Ubiquitous Application to Hepatitis C Conditions.

    “Sofosbuvir for Previously ‘Un-intervened’ ‘Persistent’ Hepatis C ‘Conditions’.” N Engl J Med. 2013.

    “S-Adenosyl Methionine Improves Early Viral Responses and Interferon-Simulated Gene Induction in Hepatitis C Non-Responders.” Gastroenterology. Volume 140. Pages 830 – 839. 2011.

    FDA Approves ‘Incipient’ Combination ‘Therapeutic’ to ‘Intervene’ Hepatitis C. FDA News Release. The Food and Drug Administration. United States Department of Health and Human Services. October 10, 2014.

    “Increased ‘Neoplasm Inhibition’ Effiacy by the ‘Co-Administration’ of Swainsonine and Cisplatin in Vivo.” Phytomedicine. July, 2013.

  36. Researcher Says:

    “Elimination of HIV-1 Infection by Treatment with a Docorubicin-Conjugated Anti-Envelope ‘Antigen Interacting Molecular’.” AIDS. Volume 20. Number 15. Pages 1911 – 1915. 2006.

    HIV, illustratively, requires activation of the Inositol 1 4 5 Triphosphate Receptor (IP3R), resultant cellular CA2+ Influx, Phospholipase C (PLC), as well as interactions of the L Domain Motifs of HIV GAG Protein such as P7TAP with the TSG101 domain of ESCRT. Particularly, Phospholipid Flux mediated by Phospholipase enhances HIV Virion Budding, whereas GAG L Domains, ESCRT and CA2+ signaling may constitute requisite causally linked factors to HIV Virion Budding.

    “ESCRT Machinery Potentiates HIV1 Utilization of the PI(4,5)P(2) PLC IP3R CA(2+) Signaling Cascade.” J Mol Biol. Volume 413. Number 2. Pages 347 – 358. October 21, 2011. requisite causally linked factors to HIV Virion Budding.

    “Phosphorylation of HIV 1 TAT by CDK2 in HIV 1 Transcription.” Retrovirology. Volume 3. Number 78. 2006.

  37. Researcher Says:

    Similar specific information may provided regarding virtually any health condition or less than optimal health status. Such information suggests compelling that pervasive detrimental health services and social outcomes since the Nineteenth Century were of substantially less than requisite nature. Moreover, producing Peer Reviewed research may have come to reflect or supplant Geopolitical interactions of an unproductive nature, similarly to obfuscative Clinical Studies which have delayed, without requirement, pervasively beneficial health services capability instrumentation.

    A substantial transformation of the Human experience may have resulted from these less than beneficent and unproductive nuances of the health services capability development. These may have been permitted to persist as a result of pervasively introduced, enculturated and cultivated presumptive base that demise may be a requisite aspect of the Human experience. Such circumstance prevents transformation of the Millenia of trauma which may have pervaded the Human experience, preventing that progression of Humanity in transcendence of such less than optimal experience, place generation upon generation in cycles of unresolved impasse to the bases of the Social and Human Condition.

    Particularly, as all of Human events may most compellingly presents homologues to biological systems and the circumstance of Humanity at such levels, all of contrived systems, Human events and activity, may have been directing Humanity upon such path of resolution or transcendence. It may be that systems of Liberty, most foundationally aligned with assured Self Determination, Opportunity, Vital Being and Vital Span of being, have represented the instantiation of the progression of Humanity at a particular instance, such that the next phases in such progression might emerge in a most unencumbered manner. The nature of systems founded upon Liberty, may have been abled such that Humanity might be encouraged to illustrate compellingly and institute as prevailing and persist constructs, a priority of Humanity within contrived systems. The Transformation of pervasively considered Ideals, into constructs which prevent systems from depriving the bases of the social and Human condition, as firming of the foundations of Liberty improving its ability to be cast further along the path of benefit to Humanity. The impasse presented in these discussions, may be among the defining courses of Humanity, such that a Glimpse of the potential of Humanity might incipiently be achieved. Certainly, however, regardless of one’s affiliations or foundational perspective, these capabilities represent an ability to abate the most pervasively exhibited source of detriment to the Human biophysiology, psyche, social condition and experience otherwise.

    Thus, it may be the objective of Humanity now, in these contexts, to observe and acknowledge the circumstance of all who may have come before and all who may have already come to be exhibited in eras not yet emerged, convergently in adjudicative permutations to a locality of Distance, Space and Time. For now, regardless of the instance in which it may be exhibited, represents the most optimal opportunity to shape all of the Span of Human experience to the Hopes, aspirations, and benefit of Humanity.

  38. Researcher Says:

    If any individual, group, organization, health services provider, Provider Entity, or someone with knowledge of another, has incurred a condition, an area of health service practice, research, analyses, program, project, product, or other in which Vital being, Vital span of Being, quality of such factors, requirement of regenerative outcomes or incurring relevant deprivation, the AMEHSI.ORG website has contact information where assistance may be requested. Similarly for individuals or health services providers, assistance in implementing AMEHSI specification enabled practice or care management improvements, as well as an informatics database application has been developed which may provide the ability to analyze outcomes such that practice improvements may be supported by informatics. Particularly, however, may be exhibited the opportunity to assist in determining the empirical molecular bases of a less than optimal health status, including a AMEHSI specification enable continuous determination such bases as progressively or as therapeutic changes become exhibited.

  39. Researcher Says:

    Again, disregard the spelling and grammatical anomaly. Assistance in conducting such analyses for individuals, groups, researchers, organizations or providers is available at the AMEHSI internet site.


  40. Researcher Says:

    I have had interesting path in more than two decades of experience in health services information technology, research and development. Virtually, most of the Education and activities otherwise incurred have been in resolving circumstances in many different systems which are homologous to Human Pathology. BTW, the manner in which this information is being communicated now is not typical. IT is the result of having to simplify myriad topics and assertions such that pervasive presumptions may no longer impart detriment to Humanity, regardless of level of education, linguistic familiarity, Jargon experience or comprehension levels.

  41. Researcher Says:

    Quite a bit of information has been presented. This has been beneficial, resultantly of the potential that not many would visit the site, navigate to the specification Presentation and then Navigate to the AMEHSI instrumentation guidance which is highly outcomes directed analytic document which assists in an iterative traversal of an interactive health services interaction spanning multiple visits and progressively ascertaining as precise the causal factors to divergence from optimal health status as is possible. Correlatively, suggesting that this may be requisite to meeting the standard of care may not be believed unless one might be able to conceptualize what might be done with such precision.

    The causal factors which contribute to or are most tangentially causal to emergence of the most incipient exhibition of Pathology, or which are causal to progression, persistence or emergence of ancillary causality, are indicated as Escape Mechanisms. This is decidedly constitutive of Jargon, however, evoking a decidedly useful perspective. Escape mechanism may be the Gene within DNA, Epigenetic Factor, Produced Molecule, Molecular Interaction, biological function to a molecular or metabolic pathway or biological structure which is atypical and thus causes divergence from optimal Biophysiological outcomes. Such circumstance may include deficiency which, although potentially being somewhat asymmetric to other Escape Mechanisms, results in such varied Pathology that it may be somewhat impossible to consider such varied pathology individually or separately from deficiency.

    Detrimental influences such Tobacco combustive utilization, Radiation, deprivation, Nutrition, Behavior or other factors may not be considered Escape Mechanism although these may be causal, resultant of the trillions upon trillions of oscillating mechanisms within biological systems which are intended to managing such influences, absorb such influences, or remove the affects of such influence through regeneration and repair. Much the higher level aspects of biological function such as Cognitive context, memory, cognitive function, perception, speech, mobility, Neurological integration into such outcomes, expression and behavior, may be substantially constituted of detriment being imparted to biological systems, subsequently followed by biological systems transforming such detriment to the benefit of biophysiology. Learning, illustratively, or incurring any new experience requires substantial levels auto-segmentation of both strands of DNA with the Frontal aspects of Cranium Encapsulated Neurological Centers. Genome, however, requires adequate levels of Phospholipids to become repaired using optimal repair Pathways. Thus deficiency produces substantially pervasive and inascertainable detriment which may be incipient factors enabling emerging of Pathology such as impaired lineages of cellular material. Systems about Humanity illustrate similar requirement or characteristics in which Human events, regardless of how much or how far these may have progressed upon unproductive paths, to be transformed to the Hope and benefit of Humanity.

    Relevantly, Escape Mechanism may occur as anomaly upon DNA, Epigenetic Pathways during Translation or Transcription, Produced Epigenetic Factors such as RNA or influences such as Acetylation, Methylation, and Phosphorylation. Produced Proteins, molecules from outside of biological systems, as well as the series of interactions and changes that these experience upon the path to producing a particular outcome which deterministically produces biological function or biological structure might also exhibit Anomaly. Such amelioration might occur within Organelles within cellular material, other areas of intracellular environment, within membranes, at extracellular levels, within tissue membranes, vasculature, arterial pathways, organs, glands, Neurological material or Neurological Centers.

    Thus, these provide imperative levels of assay. Such anomaly might be exhibited at Systemic levels such as that resultant of an Inherited Anomaly. Such might be exhibited within intracellular, extracellular, or biological fluids as a result Epigenetic level changes after accurate or typical DNA has been read. Pervasive Bona Fide Genetic Changes may be the result of Epigenetic influence or may be the result of changes to Histones, Methylation, Acetylation, or other factors, including those produced by deficiency.

    Anomaly might also be exhibited as increased or decreased levels of a particular molecular factor as well as atypical structure upon an particular aspect of a molecular factor.

    Anomaly might emerge within particular cellular material and then emerge into lineages produced from these. Local tissue and systemic exhibition of molecules produced by such cellular specific anomaly might be produced, move to other aspects of local tissue through diffusion, Gap Junction Proteins or affect biological systems systemically such that cellular material might not be required to exhibit such atypical circumstance in order to have its biological function changed toward a Pathology outcome. Immune function typically changes cellular metabolism such that if Necrosis or Apoptosis pathways are impaired, then the increased metabolism results in increased production of the impaired biologically functional molecules which constitute escape mechanism. Adjacent cellular entities, Local tissue or systemic tissues may then be effected.

    It is thus imperative to conduct Assay of Genetic Constructs as DNA, Epigenetic Factors such as Methylation and Acetylation, Levels of molecules, as well as structure of exhibited molecules. These assay contexts should be conducted at Systemic Levels such as within Biological Fluids, within tissue local to an area of Pathology and as a biopsy of tissue or cellular material constitutive of Pathology.

    There are published typical levels of most relevant factors which differentiate between System, local area or biopsy levels. One should, however, regularly regard the optimal levels exhibited without regard to ones Span of being as comparative baselines such that divergence from such optimal levels might be considered indicative of or represent susceptibility to Pathology. Otherwise, practice and assay may come to constitute, persist and promote progression of biological systems toward degradation and demise.

    The imperative nature of such three or more contexts of assay being conducted at such three or more levels, are that once any atypical factor might be determined, then it is possible to reconstitute typical characteristics of such factors. Illustratively, if an Aspect of DNA might have bona Fide Structural or Epigenetic emanated anomaly, then the molecule which would have been produce if such circumstance was not exhibited may be obtained as a supplement or instrumented by a health services provider. The atypical molecule might also be inhibited with an inhibitor. If a molecule is exhibited a levels lower than typical, then the molecule may be obtained and provided such the typical or optimal levels become reconstituted. Excessive levels of a typical molecule might also be inhibited.

    Thus, if iterative assay of relevant factors are not conducted with every health services intervention to determine as precise the molecular basis of emerged Pathology as is possible, then it is not possible to have conducted or to have provided care which meets the technological capability available standardly to health services providers.

    These are imperative because these progressively eradicate uncertainty in producing and assuring therapeutically effective outcomes, particularly because each determined escape mechanism can be ascertained, impeded, prevented. reversed, as well as having typical characteristics reconstituted.

    Thus, as Neoplasms pervasively may exhibit impaired cellular membranes, plasticity Changes, impaired biosynthesis and Immunological Synapse, accumulation of Advanced End Products, Persistent Changes resultant of inflammation, and other circumstance, Assaying the Neoplasm for such anomaly and then providing typical levels or typical structured versions of molecules constituted of such Pathology along with Choline, Phosphatidylcholine, TNF alpha inhibitors or other relevant factors may be tangentially in remediation, thereof. Hypodermic administrative of the precisely relevant factors into the neoplasm or local tissue might be conducted differently from factors instrumented at systemic levels. Systemic level factors instrumented simultaneous to such precise factors might be conducted with factors correlative to remediating systemic susceptibility. These may differentially, for instance, provide Choline, Folate, Trimethylglycine, Prebiotics, Probiotics, and other factors at systemic levels simultaneous to providing only the precisely determined atypical factors at the local area of Pathology or biopsy level.

    Walking the DNA repair, Genomic Stability, Apoptosis or Necrosis pathways form beginning to conclusions with successive hypodermic administration of molecules within such pathways and which have been found to be atypical, might be pervasively beneficial. Supporting Hepatic, Renal, Circulatory, Organ and other function may be typically achieved by reconstituting the Cholinergic pathways, particularly in preventing therapeutics from impairing Renal, Hepatic or other tissue.

    Thus, the AMEHSI specification provides iterative assay which progressively assists in determining as precise the causal influences to emergence of Pathology and Escape Mechanism causal to such pathology, such that the precise atypical factors may be determined, remediated, and reconstituted as typically exhibited.

    Reconstituting the Phospholipid and Cholinergic associated pathways along with other essential factors, as well as assay of Homocysteine, Asymmetric Dimethylarginine, Trimethylamine, Trimethylamine-N-Oxide and C – Reactive Proteins systemically, may be substantial incipient activity which may progress to more expansive and more specific assay, iteratively.

    Within each of these levels it is

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