How to stop pain, halt autoimmune destruction, turn off the ‘septic switch’ and restore cellular immunity
Exploring and Exposing Vitamin C Myths
The maligned lingual ascorbic acid test is the convenient reduced glutathione test we have sought.
How to evaluate the adaptive capacity of your patient
More than fifty years ago, Emanuel Cheraskin, MD, DDS favored and promoted the clinical use of the lingual ascorbic acid test, the timed disappearance of a metered dose of a mild oxidant in the form of a blue phenol dye dispensed in distilled water and placed on to the tongue. The blue dye is 2,6 dichloroindophenol sodium; and when it is reduced, it turns colorless.
Most people have an area on the dorsal surface of the tongue with intact pink shag carpeting of structural filiform papillae. A single drop of blue dye is dispensed from a non-threatening plastic dripper near the front of the protruded, lightly brushed, dried and tethered tongue where it can easily be observed. A gentle wiggle of the tongue with the 2X2 cotton gauze or paper towel humorously helps the wetting process and to get a consistent reading of the fading and disappearance of the dye. Someone keeps track of time.
Optimal clearing is considered 15-20 seconds, with marginal results going up to 25-30 seconds. More than 30 seconds is considered significant deficiency. This is clinical scurvy, outright vitamin C deficiency. Collagen cannot be made for healing or repair. Wrinkles and sag occur. White blood cells become sluggish. We have noted clinically that people’s gums are always excessively tender and bleed profusely in response to gentle diagnostic periodontal probing at 35 seconds or longer, unless we first recharge their antioxidant potential with a fizzy vitamin C drink (along with many other cofactors).
There is a myth that one should not take vitamin C before dental visits because the local anesthetic will wear off too fast. Most people can safely take 1,000mg of ascorbates before their visit and not even fill up their antioxidant reservoir. Emergency patients often have extended vitamin C times suggesting glutathione exhaustion and uncontrolled inflammation with hyperalgesia, an alkaline exaggerated pain state making profound local anesthesia almost impossible.
First we bring the patient into reductive balance by supplementing with vitamins C and E, lipoic acid and bioflavonoids along with other critical parts of the oxidative-reductive chain. We then wait eight to ten minutes for physiologic effect. Then a single dose of local anesthetic typically works with profound numbness and holds for appropriate length of time.
Rarely, some people clear the dye too quickly. One can overdose with way too many antioxidants and actually paradoxically cause fatigue, or even detoxify local anesthesia too quickly. Or, when sick people are in unbuffered alkaline oxidative crisis and are currently in upregulated process of melt down, they can clear the dye or detoxify local anesthesia very quickly.
We test even when people protest that they have taken their vitamins. This is how we discovered that vitamin powders spoil quickly (in a month), especially outside the refrigerator. In our office in Miami, people taking several forms of commercially available ester-C test poorly most of the time with the lingual test. Ester-C is a mixture of vitamin C metabolites. Some act as oxidants, some as antioxidants. Perhaps ester-C spoils quickly. Fresh, ‘name branded’ ester-C occasionally tests well in my patient population.
As a young Navy dentist during the Viet Nam War, I saw my first patient evaluated with the lingual ascorbic acid test in 1969. He presented as a handsome blond-haired, blue-eyed, 18 year old outwardly fit-appearing sailor. Inside his mouth, he had a nickel-sized fungating and perforating palatal lesion that reminded me of deadly squamous cell carcinomas I had seen in the cheeks of long-term habitual snuff chewers (sucking on sugar-cured tobacco) seeking treatment in the inner city hospitals of Detroit. Our horrific alternative diagnosis was the perforating palatal lesion of tertiary syphilis. Based on what I knew then, a thought fearfully flickered through my mind, “Either way, he is a dead man.”
His teeth and gums were covered with rich layers of white yeasty plaque and gingival margins were shiny red. It took only a gentle stream of syringe-delivered compressed air to make his swollen hyperplastic gums waffle in the diagnostic breeze allowing bright red blood to gush from angrily inflamed gingival crevices. It took two minutes for the blue dye to mostly clear from his tongue. A tentative primary diagnosis of scurvy (vitamin C deficiency) was made.
In scurvy, the body literally becomes unglued since its primary structural fiber, collagen cannot be manufactured. Teeth loosen, blood gushes from the gums or fingernail beds, bruising occurs anywhere, anemia results, wound healing is slowed and old scars unravel. Fatigue with irritability and pain from headache and tender gums to joint and muscle aches are hallmark signs.
White blood cells cannot protect themselves against their own oxidative burst, so cellular immunity shuts down and onboard biofilm becomes pathogenic. Humoral immunity reflexly becomes up regulated. The patient becomes hypersensitive and infected, classically dying from ‘antibiotic resistant’ infection and septic shock.
This sailor’s diet choices from his ship-bound cafeteria menu were limited to hamburgers, hot dogs and mashed potatoes (served from a vitamin-depleting steam tray). We suggested a broader diet including fruits and vegetables and prescribed a massive daily dose of vitamin C (for the era) of 500mg.
Two weeks later, our compliant patient’s palate was completely healed. We had neglected to provide tooth brushing instructions. His teeth and gums were still covered with thick whitish plaque. But we could not make his gums bleed, either with compressed air or physical probing. I was changed forever as a doctor. That began an educational process about vitamins, minerals and accessory nutrients and how their biochemistry affected pain, physiology, psychology and performance.
We used to think of scurvy as simply vitamin C deficiency, now we include the concept of glutathione exhaustion. Glutathione systems are human’s primary onboard antioxidants, and perhaps this system has other advantages, since the human genome has lost access coding to manufacture the enzyme necessary to make vitamin C from sugar. Onboard commensal yeast can manufacture some vitamin C, and yeast biofilm does seem to beneficently expand in our times of need. Obtained from diet or biofilm, vitamin C is a critical cofactor for collagen cross linking, acts as a general stress adaptive hormone and helps recycle glutathione, the primary hydrogen ion donor in physiology.
In the pecking order of oxidative stress, first the body uses up exogenous vitamin C, weakening structural and cellular immunities, allowing pain. When recyclable glutathiones are next wasted, the ‘septic switch’ is turned with depressed cellular immunity and heightened humoral autoimmunity accompanied by increasing pain and fatigue. When recyclable superoxide dismutases are next wasted or function is compromised by virus, unrelenting fatigue sets in due to body’s inability to protect itself from oxygen during energy production. This is the classic ‘TMJ syndrome’ patient. The precious exogenous fat-soluble gene-regulating carotenoids are saved to the end, when all hope is lost.
Clinically, the lingual ascorbic acid test is timely until reduced glutathione is exhausted. Some few subjects test adequate without any supplemental vitamin C. Range of time past 25-30 seconds suggests deepening degrees of glutathione exhaustion and significant loss of hydrogen ion reserve.
Some people have tongues that are too smooth and slick and/or are too dry and dehydrated exhibiting such a high surface tension that the drop of dye will not wet and consistently spread against their smoother shag covering of the tongue, ineffectively pooling instead in crevices. Stress induced triage allows thinning of structural filiform papillae, while preserving rounded bumps of underlying sensory ‘survival’ taste buds, fungiform papillae.
Smooth tongue tells us that these folks are trudging on exhausted, doing the best they can, with long-term stress apoptotic signaling overwhelming repair messaging. The lingual ascorbic acid test is frustratingly difficult to interpret with this exhausted sub set, that is often sleep-deprived, stubborn, depressed and apathetic, in other words, generally disinterested in, or incapable of change. We keep trying, and ask again “What did you eat for breakfast?”
The same blue dye can check urine for the doses of vitamin C necessary to fill one’s internal ascorbate tank enough to cause spillage at the kidney’s gates. Another way to test for optimal vitamin C intake, as well as to cope, cleanse and compensate for one’s individual viral and toxic load, is to: once per week take buffered C powders by the teaspoonful diluted in a couple ounces of water every fifteen minutes to ‘bowel tolerance,’ past loose bowels, until a full evacuation, an enema-like watery-whoosh results.
For the next week, replenish gut flora with probiotics, friendly bacteria or fermented foods with each meal. Optimal oral daily therapeutic dose of ascorbic acid is then three quarters of the flush dose, taken over the day one third at a time. Repeat weekly until only 5-7gms of vitamin C causes a flush.
Critics of the blue phenol dye as just a lingual ascorbic acid test are technically correct. Disappearance of the oxidant dye depends not only on vitamin C, but on reducing power in general. Reducing power is the hydrogen ion reserve and it is supported with vitamins C and E, lipoic acid and flavinoids, but depends primarily on stores of reduced glutathione and its efficient recycling. Reducing power is what we are testing on the tongue in real time. It is critical to know how it is for that patient right now in the clinical setting, before we may harm them by stressing their hydrogen ion reserves with our current chosen therapy. That is the beauty of this instantly available and immediate inexpensive ‘tissue level’ test of glutathione stores.
Glutathione is critical for building our reductive anabolic tides and protecting us from the oxidative stress of the catabolic alkaline tides. This ubiquitous tripeptide is necessary for stomach acid and other acid production and is key electron chaperone for efficient aerobic energy production and protects us from the oxidative step of glycosylation (cytochrome P450 regulated) during the formation of proteins.
Minerals are available and molecular structures are fluid and readied for excretion or structural integration during hydrolytic acidic tides. It takes alkalinity to saponify fats, oxidize toxins, waste and perceived enemies as well as to create shape of proteins. Normally recycled when detoxifying normal hormones and metabolites, glutathione is lost molecule for molecule when detoxifying xenobiotics or external toxins.
Onboard viruses and bacteria often genetically encode for glutathione production, as we do. When our microorganisms replicate in low magnesium, zinc or selenium states, they become more actively pathogenic and steal from us the very nutrients necessary for us to make glutathione. Exhaustion of available reduced glutathione is the ‘septic switch’ that shuts down cellular immunity as well as our own primary cellular defenses against auto-immune internal or external oxidative stress messaging.
Destructive humoral immunity with its allergies, sensitivities and autoimmune ‘friendly fire’ is then switched on by reflex at the same time our cellular glutathione defenses are down. Glutathione production is compromised by enzyme blocking heavy metals such as arsenic, lead and mercury or low vitamin C or E, low lipoic acid, diminished methylating B vitamins, low zinc, magnesium or selenium, or poor protein digestion providing low taurine, methionine or cysteine.
Glitches in glutathione production frees up glutamine (glutamate) cysteine’s other amino acid cofactor necessary to make this universal hydrogen-proffering tripeptide, along with ordinarily plentiful glycine. Now more abundantly available neuroexcitatory glutamate (which was normally linked with cysteine and glycine to make glutathione) and/or neuroexcitatory aspartate trigger ‘brain on fire’ response with even more unbridled inflammatory and premature apoptotic destruction of nerves via up regulating N-methyl-D-aspartate (NMDA) receptor activity leading to depression, bipolar behavior, anxiety, schizophrenia, cognitive dysfunction, ADD, ADHD, Alzheimer’s, ALS, Huntington’s, Parkinson’s and epilepsy.
In the lungs, similar NMDA pathways create the life-threatening anxious hyper reactive airways of asthma or the pain and nausea of vascular pain including angina and migraine. Expression of similar NMDA receptors have been found in many cancer cell lines and leads to cellular proliferation.
Ion channel inhibitors such as glycine, GABA, taurine, magnesium, essential fatty acids and use of a glutamate-inhibiting herb such as Sophora flavescens should reduce membrane irritability as well as slow the spread of cancer. It is traditionally used as diuretic to dispel heat, dry dampness, expel wind, and eliminate intestinal parasites. It is thus administered in formulas for dysentery and jaundice (damp-heat syndromes), edema and dysuria (dampness syndromes), and eczema and itching (damp-heat-wind syndromes). It is commonly used for the treatment of viral hepatitis, cancer, viral myocarditis, gastrointestinal hemorrhage and skin diseases (such as vaginal inflammation, psoriasis and eczema). Its roots contain quinolizidine alkaloids, including matrine and its oxide that interfere TNF-alpha and IL-6, suggesting that oxymatrine may inhibit the expression of the above pro-inflammatory cytokines. Matrine also inhibited expression of Substance P and NK-1R in a human model of skin inflammation, as well as acting as an agonist at mu and kappa opioid receptors. Quinolizidine alkaloids are secondary compounds found in seeds of many species of plants, cat’s claw, bilberry, blue cohosh, possibly protecting them against pathogens and seed predators.
Perhaps instead of lingual ascorbic acid test (LAAT), a more appropriate and accurate name might be the HIRT or hydrogen ion reserve test or the HIRTT, the hydrogen ion reserve tongue test. Potential advertising might be, “If you hurt, try the HIRT.” Another suggestion is FHIRT for functional hydrogen ion reserve test, although some think that acronym may also suggest hydrogen sulfide rotten-egg smell presence (which incidentally, often occurs when glutathione is exhausted). Figure out your own promotional phrases for FHIRT.
Others may market it as THIR, or tissue hydrogen ion reserve or THIRT, tongue hydrogen ion reserve test. Another name might be the glutathione exhaustion lingual test or GELT. “Nobody turns down a bit more GELT.” How about FOSTT, for functional oxidative stress tongue test? “Get it FOSTT.” Then there is metered oxidative stress tongue test or MOSTT. “What could be better than MOSTT?” As a reductive capacity test, it could be RECAT, and that is no dog.
Steven N. Green, DDS, 305-273-7779
August 25, 2008
1) When a patient is in crisis, the underlying physiology exhibits varying degrees of glutathione exhaustion.
2) The LAAT is best used as routinely a clinically relevant and useful functional HIRT (hydrogen ion reserve test) giving us a real-time clinical measure of glutathione exhaustion.
3) The invisible load that eventually overwhelms balancing allostatic compensatory stress mechanisms comes from inappropriate lifestyle patterns, creating messaging to our genes that muddies or reverses daily anabolic (reductive) tidal flows and accentuates catabolic (oxidative) tidal flows, altering dynamic metabolic set points best based on light and proper patterns of eating sustaining foods.
4) Overwhelming stress necessitates triage of cells, allowing structure to wane, such as muscles, bones, skin, teeth, nails and the normally shaggy filiform papillae of the tongue. Stressed ‘survival’ cells live on. Fat cells are ultimate survival cells. Flab survives along with nerve cells and inflammatory white blood cells. Inflammation becomes chronic rather than acute, since activated white blood cells no longer die by programmed cell death or apoptosis. Osteoclasts live on, chronically dissolving bone leading to osteoporosis. Stresses defective cells, programmed to eliminate themselves, paradoxically live on to become cancerous. Fungiform taste buds remain as the filiform papillae fade. First the tongue displays a red tip, and then with unrelenting daily stress, the fungiform papillae begin to stand out like ‘strawberry spots’ on a denuded tongue.