With a touch from the old school...
Triage Theory of Aging, Specific Nutrient Deficiency Identification by Simple and Cheap Laboratory & Clinical Testing
The triage theory of aging proposes that a single nutrient deficiency will increase age-related diseases because vitamin-dependent proteins and enzymes needed for short term survival processes (breathing, eating, etc.) are protected at the expense of proteins needed for long-term survival processes (immunity, cellular repair, heart function, etc.). Triage comes from the French term, the process of sorting out victims, as of a battle or disaster, to determine medical priorities in order to increase the number of survivors as they live or die. So triage that! All of us have one or more vitamin dependent processes that are running us down sub-optimally. For example, magnesium inadequacy affects over half of the US population and is associated with increased risk for many age-related diseases. I will explain in my usual verbose and lengthy discussions how to diagnose these deficiencies, simply and cheaply, should you care to read on...
Professor Bruce Ames, the famed researcher for lipoic acid, presented His Triage Theory of Aging at the A4M meeting on December 9, 2010. The Triage Theory of Aging provides an ideal argument for recommending a sophisticated and individualized multivitamin/mineral supplement for slowing down the inevitable aging process. Researchers tested this theory with selenium dependent proteins and the results confirm previous evidence – that even modest selenium deficiency compromises long-term health and even results in cancer. In other words, deficiencies that are not severe enough to show obvious clinical symptoms today, will still significantly compromise cellular function if not corrected. As Carey Reams so aptly stated, triage deficient nutrition is: 'cancer on the installment plan!'
Ames review of scientific literature showed that about 50 human genetic diseases due to defective enzymes can be remedied or ameliorated by the administration of high doses of the vitamin component of the corresponding coenzyme, which at least partially restores enzyme activity. Severe deficiency of the vitamins and minerals required for life is relatively uncommon in developed nations, but modest deficiency is very common and often not taken seriously as Professor Ames points out. However, this thinking may change as so-called experts examine even moderate selenium and vitamin C deficiencies to show how damage accumulates over time as a result of vitamin and mineral loss, leading to age-related diseases. Seems the school lunch dieticians may finally wake up to the propaganda they have been wrongfully touting for so many decades ? All is not well on the three squares of fruit cups, meat and potatoes, frozen veggies, coffee or milk, and dessert (the five necessary food groups then, but we can add pizza now!).
Understanding how best to define and measure optimum nutrition will make the application of my new modality a boon, to allow each person to optimize their own nutrition with a much more realistic possibility than it is today with hap-hazzard clinical guesswork or multilevel one for all (some for none) supplementation schemes.
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For years, I have observed massive oxalates in "gravelers," patients who form sand in the kidneys, and offset this liver dysfunction with high dose vitamin B6. For years, I have given low nitric oxide producers high dose B complex, and find it to return with reduction of blood pressure and urinary excretion levels of ammonia. |
For years, I have measured Dr. Voll's SMP. Joint point, seen deviated values in the absence of joint pain, only to be neutralized with high dose vitamin C, the body's intercellular cement. Thus, we have an electrodermal measurement point for Vitamin C. What could be more useful?
Suffice it to say, we have a number of parameters upon which to estimate hereditary vitamin dependencies, it is just a matter of putting it all together into a clinical format for office efficiency. But first, let me make a bit of an explanation of all this so you can grasp the vitals...
Evolution of vitamin-dependent organisms
The word metabolism derives from the Greek word for “change.” Metabolism represents the sum of the chemical changes that convert nutrients, the “raw materials” necessary to nourish living organisms, into energy and the chemically complex finished products of cells. Metabolism consists of literally hundreds of enzymatic reactions organized into discrete pathways. These pathways proceed in a stepwise fashion, transforming substrates into end products through many specific chemical intermediates. Metabolism is sometimes referred to as intermediary metabolism to reflect this aspect of the process.
One of the great unifying principles of modern biology is that organisms show marked similarity in their major pathways of metabolism. Given the almost unlimited possibilities within organic chemistry, and the infinitely complex biologic world, this generality of metabolism would appear most unlikely. However, it’s true, and it provides strong evidence that all life has descended from a common ancestral form. All forms of nutrition and almost all metabolic pathways evolved in early prokaryotes prior to the appearance of eukaryotes 1 billion years ago. For example, glycolysis , the metabolic pathway by which energy is released from glucose and captured in the form of ATP under anaerobic conditions, is common to almost every cell. It is believed to be the most ancient of metabolic pathways, having arisen prior to the appearance of oxygen in abundance in the atmosphere. All organisms, even those that can synthesize their own glucose, are capable of glucose degradation and ATP synthesis via glycolysis. Other prominent pathways are also virtually ubiquitous among organisms.
Evolution of metabolic processes in the earliest primitive forms of life required the development of enzyme systems and hormones to catalyze the complex sequences of chemical reactions involved leading to the development of mammalian metabolism. In the beginning, the environment presumably could supply all the necessary compounds (including the vitamin coenzymes); eventually, these compounds were synthesized within an organism for necessary adaptation on land. As higher forms of life evolved, however, the ability to synthesize certain of these vitamin coenzymes was gradually lost. As sea creatures migrated onto land, the thyroid had to evolve to help with regulation of heat so as to adopt to air. As man migrated inward to lands of iodine deficient soils, cretinism arose.
Since higher plants show no requirements for vitamins altogether, or other growth factors, it is assumed that they retain the ability to synthesize them. Among insects, however, niacin, thiamin, riboflavin, vitamin B6, vitamin C, and pantothenic acid are required by a few groups. All vertebrates, including humans, require dietary sources of vitamin A, vitamin D, thiamin, riboflavin, vitamin B6, and pantothenic acid; some vertebrates, particularly the more highly evolved ones, have additional requirements for other vitamins. Humans have lost altogether our ability to synthesize vitamin C.
Vitamin requirements vary according to species and even down to the individual. Further, since cells are constantly generating ATP on a 24 hour basis (a typical male weighing 70 kg uses about 2000 kcal per day of which approximately 70 and 80 kilograms of ATP daily are required to provide so much energy), vitamin needs will shift constantly based on the daily diet. It is not uncommon in rapidly growing school children to see upon microscopic examination their RBC's mixed with microcytosis and macrocytosis (anisocytes), meaning at least one daily meal is junk food. As the bone marrow churns out RBC's, depending upon the iron, folate, and vitamin B12 available from the daily diet, some RBC's come out microcytic (iron deficient), and some macrocytic (B12 deficient).
The amount of a vitamin required by a specific organism could be difficult to determine because of the numerous factors (e.g. genetic variation, relative proportions of other dietary constituents, environmental stresses). Clinical applications has proven that there is no uniform standard for the human requirements of vitamins, and the recommended daily vitamin intakes (RDA's) are sufficiently discredited to account for individual variation, digestive capacity, illness, and normal environmental stresses.
Therefore, the only clinical answer would be to determine as best as possible the current metabolic status of the individual, determine which enzyme systems need boosting, and target dosage to near optimal usage, storage and excretion values. You should by now be getting the picture.
Setting the Scene
To set out to determine specific vitamin deficiencies, a number of clinical parameters must be addressed.
Inadequate intake of a specific vitamin results in a characteristic deficiency disease (hypovitaminosis); and the severity of the disease depends upon the degree of vitamin deprivation. Symptoms may be specific (e.g. functional night blindness of vitamin A deficiency) or nonspecific (e.g., loss of appetite, failure to grow). All symptoms for a specific deficiency disease may not appear; in addition, the nature of the symptoms may vary with the individual.
In order to address these factors, we need two sets of data:
1. A thorough dietary history, both long and short range; and
2. A thorough sign/symptom survey.
A comparison of dietary intake with the individual's signs and symptoms would begin to target specific nutrient deficiencies. For example, if the individual is on a relatively cooked food diet, we would target the heat liable vitamins as suspects in comparison to their signs and symptoms. If the patient is on the typical BAD (Basic American Diet) plan, we look at carotenoid daily consumption (vitamin A) and exposure to sunlight (vitamin D) right from the start.
Back to Basics
The nutritional status can be viewed as a flow system of nutrients IN and metabolic wastes OUT. Between the IN flow and OUT flow is the biological terrain or metabolic state of enzyme pathways. The efficiency of digestion and metabolism can be readily discerned by basic laboratory tests. How one views these complex events determines the laboratory tests required. The medical doctor will order such tests as blood chemistries, the CBC (complete blood count), urinalysis, etc. The nutritionist will consider mineral analysis of hair, salivary hormones, blood chemistries, etc. Most all of these tests require outside laboratory, delay in treatment, and cost burdens on both practitioner and patient.
Would not a series of saliva, blood and urine chemistries, reduced to their utter simplicity, and ran in-house for a few dollars within minutes offer the clinical solution?
For example, one can discern a lot about calcium metabolism from an ordinary index of salivary and urinary pH and exposure to sunlight. Further, if the patient complains of reflux esophagitis, we can assume much of the dietary calcium reaches the toilet before the bone, meaning stomach acid is too weak to disassociate calcium as an ion, and the patient is on the road to osteoporosis. All of this is further verified by a simple sulkowich test for calcium urine excretion.
Consider these simple laboratory features:
- Digestive efficiency of proteins by three simple urine reagents and a spot of blood. One test is also a pre-screening for predilection to the cancer diathesis!
- Digestive efficiency of carbohydrates: detection of hypoglycemia and diabetes is straight forward, but the early signs are just as important as well as how much saccharo-butyric putrefaction occurs as an index of inefficiency and bacterial (bowel) autotoxemia.
- Digestive efficiency of fats is not as much an issue as is its mobilization once in the system, and thyroid efficiency to help burn it.
- Putrefaction: a loosely used term, however most do not understand it, let alone how to analyse it and treat it. The indican test will only show the most gross cases from obstipation but my putrechrome reaction (PCR) will detect ordinary as well as insipient bacterial dysbiosis. The test only requires 3 ml of urine and 3 drops of reagent.
- Sodium: by understanding the eternal dual between sodium and potassium, and by understanding that most ingest excessive amounts of salt, the urinary index makes evident the need for dietary reform. Sodium is our junk food index.
- Calcium: by understanding Vitamin D and sunshine, and calcium loss due to excessive sodium intake, by taking both calcium ion and sodium urinary excretion ratios, proper dosage and hydrochloric acid efficiency becomes evident.
- Iron: A single drop of blood tells all.
- Iodine: understood from studies in evolutionary biology, assume deficiency until proven otherwise but a spot test is revealing.
- Magnesium: foot odor and vegetable intake is simple enough, urinary excretion index shows more. But I have found the ECG reading in the third lead the most revealing.
- pH: The power of hydrogen reveals the mineral deficiencies as well as a most potent source - autointoxication from saccharo-butyric, bacterial putrefaction.
- Vitamin deficiencies: everyone knows about it but few have ways of objectively monitoring needs and dosages.
- Trace Mineral Deficiencies: since they run so many enzyme systems, in tandem with vitamins, they could be hard to detect, but my Taste Test makes it easy.
COST OF ALL THESE TESTS? About one dollar!
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March 13-17: Upcoming Events For Health Care Professionals
5 Day Course, Nevis West Indies: The Complete Rural Laboratory & Vital Sign Stations Workshop
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