Friday, August 5, 2011
Chronic Otitis Externa can present similar to AOE, is not only long standing, but the inflammation is usually secondary to eczema, psoriasis, seborrheic dermatitis, or fungi (Candida albicans and Aspergillus). Rarely fungi only, can cause AOE. Wax in the ear can combine with the swelling of the canal skin and any associated pus to block the canal and decreases hearing. In more severe or untreated cases, the infection can spread to the surrounding soft tissues causing Malignant or Necrotic Otitis Externa. These are more likely in diabetics, immune suppression, and in the elderly. In its mildest forms, EOE is so common that some physicians have suggested that most people will have at least a brief episode at some point in life. A small percentage of people have an innate tendency toward chronic external otitis. These folks have a genetic predisposition for producing too small amount of or an inferior (too little IgA) protective wax.
Most people can avoid AOE altogether once they understand the intricate mechanisms of the disease. The skin of the bony ear canal is unique, in that it is not movable but is closely attached to the bone, and it is almost paper-thin. For these reasons it is easily abraded or torn by even minimal physical force. Inflammation of the ear canal skin typically begins with a physical insult, most often from injury caused by attempts at self-cleaning or scratching with cotton swabs, pen caps, finger nails, hair pins, keys, or other small implements. This trauma and prolonged water exposure in the forms of swimming, bathing, showering or exposure to extreme humidity, which can compromise the protective barrier function of the canal skin, allowing bacteria to flourish. Densely impacted wax, usually caused by enthusiastic use of cotton swabs, can put enough pressure on the ear canal skin to injure it and initiate infection. A sensation of blockage or itching can prompt attempts to clean, scratch, or open the ear canal, which potentially worsens and perpetuates the condition. The cotton fibers of a swab are abrasive to the thin, fixed canal skin. Self-manipulative measures to improve the condition often make it worse and are to be discouraged, in that it can result in significant injury to the ear. It is well established that the ear canal is self-cleaning. The top layer of the ear canal skin normally migrates toward the ear opening, essentially sweeping the canal on a continuing basis. In other words, a normal ear canal is self-cleaning.
Pain is the predominant complaint and the only symptom and is directly related to the severity of AOE. Unlike Otitis Media, the pain of AOE is worsened if the ear is pulled gently. Patients may also experience ear discharge and itchiness. Initially, when doctors look inside the ear with an otoscope, they observe very little abnormality. If they are astute, they may notice a decrease of the normal ear wax. However, when enough swelling and discharge in the ear canal is present to block the opening, the eardrum cannot be seen. Looking at the eardrum is very important to the doctor in that this is how the diagnosis of Otitis Media is made and to rule out a punctured ear drum. The “pus” exuding from the canal is not true pus (all white cells), but the liquid debris of wax, dead skin, and the previous drops placed within the canal for treatment.
The treatment when EOA is very mild is simply to refrain from swimming or washing ones hair for a few days, and keeping all implements out of the ear. It is a self-limiting, self-resolving condition! However, if the infection is moderate to severe, or if the climate is humid enough that the skin of the ear remains moist, spontaneous improvement may not occur.
Effective therapy for the ear canal includes acidifying and drying agents, used either singly or in combination. When severe, topical solutions (or suspensions) of eardrops are the mainstays of treatment for EOA. Effective medications include eardrops containing antibiotics to fight infection, and corticosteroids to reduce itching and inflammation. Some contain antibiotics, either antibacterial or antifungal, and others are simply designed to mildly acidify the ear canal environment to discourage bacterial growth. Some prescription drops also contain anti-inflammatory steroids, which help to resolve swelling and itching. Cortisporin (neomycin-polymyxin B-hydrocortisone), Ciprodex ear drops ( Ciprofloxacin and dexamethasone), Gentisone HC ear drops (Gentamicin and hydrocortisone), Ciproxin HC ear drops ( ciprofloxacin and hydrocortisone), Sofradex ear drops (containing Framycetin Sulphate, Gramicidin, Dexamethasone/sodium metasulphobenzoate, Phenylethanol), Kenacomb ear drops, ( triamcinolone acetonide, neomycin and gramicidin (antibiotics) and nystatin (antifungal).
Over the counter ear drops are also available, including spirit drops (alcohol solution) which dries out the ear, and drops such as Aqua Ear which contains a mixture of alcohol and acetic acid, to dry the ear and make it difficult for microbes to grow. Home remedies with half Vodka or Gin with half vinegar can also be used in a pinch. Athletes Foot OTC preparations such as a topical antifungal like 1% clotrimazole are also effective. Removal of debris (wax, shed skin, and pus) from the ear canal promotes direct contact of the prescribed medication with the infected skin and shortens recovery time. When canal swelling has progressed to the point where the ear canal is blocked, topical drops may not penetrate far enough into the ear canal to be effective. Inserting cotton (earwick) saturated with medication is frequently applied. The wick is kept saturated with medication until the canal opens sufficiently then the drops will penetrate. If the canal is significantly edematous, a foam (Pope) can be used. Antibiotic eardrops should be given for 7 days. The ear should be left open. Although the AOE generally resolves in a few days with topical washes and antibiotics, complete return of hearing and cerumen gland function may take a few weeks. Once healed completely, the ear canal is again self-cleaning. Until it recovers fully, the canal may be more prone to repeat infection from further physical or chemical insult.
Preventing acute external otitis are similar to those for treatment. Avoid inserting anything into the ear canal. (Q-tips or cotton swabs is the most common event leading to AOE.) Other measures to use after prolonged swimming in a person prone to external otitis is to dry the ear canals with a hair dryer. Alternatively, drops containing dilute acetic acid and alcohol(2:1) will do the job. Avoid swimming in polluted water. Do not wash hair or swim if very mild symptoms of AOE begin. The use of earplugs or bathing caps when swimming and earplugs while shampooing hair may help prevent EOA. Hard and poorly fitting earplugs can scratch the ear canal skin and set off an episode. A simple method of making a soft waterproof disposable earplug is with cotton balls covered with Vasoline. These coated cotton balls are NOT inserted into the ear canal, but pressed into the ear to cover the opening of the canal.
Saturday, July 2, 2011
Normal erectile function involves three synergistic and simultaneous processes: 1) neurologically mediated increase in penile arterial inflow, 2) relaxation of cavernosal smooth muscle, and 3) restriction of venous outflow from the penis.
Loss of the functional integrity of the endothelium and subsequent endothelial dysfunction plays an integral role in this issue. Pharmacological (Phosphodiesterase drugs such as Viagra) and endocrine (Testosterone) interventions help restore some function, but more is needed because of the 45% failure rate with these treatments. The incidence of ED dramatically increases in men who have endothelial dysfunction such as seen in middle age particularly those with diabetes mellitus, hypercholesterolemia, and cardiovascular disease. These diseases have in common a dysfunctional endothelium.
Penile erection is a psychoneurovascular phenomenon that depends upon cerebral stimulation, neural integrity, and a functional vascular system with healthy cavernosal tissues . It is the fit endothelium that produces the NO. Assuming the desire (libido), an intact nervous system and enough NO being produced from the endothelium, the penis will become erect and remain that way until it becomes refractory following ejaculation. Testosterone will encourage the brain if given sufficient visual and tactile clues. The intact nerves are needed not only for the brain to perceive touch, but to release the neurotransmitters to the penile arteries to dilate them. This dilatation to a large extent depends on the production of NO from the endothelium. If enough NO is released it will compensate for some lack of integrity of the neurovascularity. NO, then, is another therapy not generally used by doctors that is additive to testosterone and the phophodiesterase stimulators. Science has discovered several ways to increase NO production that will be discussed in another article.
Monday, June 6, 2011
Two doctors, three opinions are given, but the opinion that is the most important is YOURS, the patient. It is not the physician who will suffer the most if good therapies go en getting wrong, an adverse drug reaction occurs, or the operation was a success, but the patient died, but you and you family. You should be in charge of your health both preventively and therapeutically! A healing relationship with your physician is important and teamwork is key, but it should be you as the patient that is responsible for the path to take. The doctor is the knowledgeable coach or adviser, perhaps a family member, the team manager, but there is no doubt that if you are in your right mind that the decision of care should be yours! It is incumbent for you to be as knowledgeable as possible on the medical problem on hand. Information from the Internet, perhaps starting at Wikipedia, then a noncommercial website should be considered. Speaking to other patients with a similar problem, reading magazine articles or books does give a good working knowledge on your medical issue. Even getting another professional opinion from a physician who is not in cahoots with your original doc is a good idea.
Too often Primary Care Physicians function as gatekeepers; they may open the floodgates and let the patient drown in too many medical procedures and medicines. Fragmentation in medical care also is rampant today. The patient who decides what organ or area their problem lies in sees that specialist. Therefore, there is a cardiologist for their heart, a pulmonologist for their lungs, a nephrologist for their kidneys, a hematologist for their blood, and a “Big Toe doctor” for their gout. That leaves us with no one to take care of the whole person; moreover, the left hand doesn’t know what the right hand is doing. The gastroenterologist does not effectively communicate with the neurologist. If your primary care doc does not function as a knowledgeable clinical coordinator, then that responsibility by default is on you. As I try to set forth in this book, it is not how old a person is that counts, but how they feel and function when they are old. Medicine and certainly not this book alone has all the answers, but with your significant participation you will enable yourself to age gracefully and to live a full and abundant life. It is imperative then to discover THE DOCTOR WITHIN!
Other researchers determined that the amount retained by the thyroid gland is 6-7 milligrams, which, according to Dr. Abraham, is the optimal amount to keep the thyroid gland itself operating at peak performance. Keep in mind, though, that’s just for thyroid health.
Another prominent iodine researcher, Dr. Benjamin Eskin, determined that female breasts need about 5 milligrams of iodine per day. Add that to the amount your thyroid gland needs, and you come up with the 12.5 milligrams Dr. Abraham recommends.
Dr. Eskin also established that our thyroids “prefer” to concentrate the iodide form of iodine, while breasts concentrate iodine. Iodine and iodide are not always interchangeable: “Iodine” is the basic element, consisting of two “I” molecules bonded to each other (I-I); an excellent analogy is chlorine, which is two “Cl” molecules bonded to each other (Cl-Cl), while “chloride” is just one Cl molecule. “Iodide” is one of those two iodine molecules, and is almost always found with another molecule, such as potassium (potassium iodide, or K-I). In experimental animals, the thyroid glands and the skin concentrated more iodide than iodine, while the stomach concentrated more iodine. Based on these and other findings, Dr. Abraham recommends that iodine supplementation should include both forms: iodine and iodide.
Also Iodine can flush potentially dangerous elements from your system. Iodine, chlorine, bromine, and fluorine are in the same “family” of elements. Although very tiny quantities of fluoride are likely useful for human health, the amounts poured into most American public water supplies are much too high and have been correlated with higher risk of a rare bone cancer as well as bone fracture in older women. Bromide also carries some risks at high quantities, including impaired thinking and memory, drowsiness, dizziness, and irritability. But iodine can actually help your body get rid of these potentially harmful elements, as well as others like lead, cadmium, arsenic, aluminum, and mercury.
Following observations by Dr. Abraham, Brownstein conducted a study to test iodine’s ability to help rid our bodies of fluoride and bromide. Eight individuals had “baseline” measurements taken of their urinary output of fluoride and bromide. Each research volunteer took one 50-milligram “loading dose” of iodine and then proceeded to take the 12.5 milligram optimal daily dose from that point on. Only one day after starting iodine, their urinary output of bromide and fluoride increased significantly and continued at this higher rate for all 30 days of the study. Our Dr Robert Doenges, who holds the only patent on a salivary and urinary iodine analyzer, has never seen anyone who was Iodine sufficient.
Working with 10 female volunteers, Dr. Abraham conducted safety studies of the optimal 12.5 milligram iodine/iodide dose. He checked each woman’s blood pressure, weight, muscle mass, and body fat prior to starting iodine treatment, then again three months later. There were no statistically significant changes, although the body fat percentages did go down.
Dr. Abraham also took before-and-after measurements of several different markers of thyroid function, which included thyroid gland volume, TSH, total T4, free T4 (the active form of the thyroid hormone T4), and free T3. Although total T4 for the group declined significantly, both the “before” and “after” values were well within normal ranges, and there were no significant changes in free T4. The next part of Dr. Abraham’s safety study involved taking glucose, BUN, creatinine, sodium, potassium, chloride, calcium, total protein, albumin, globulin, bilirubin, alkaline phospatase, and ALT and AST (liver-function measurements) before and after three months. Although all values were within normal ranges before and after, there were statistically significant improvements in creatinine, alkaline phosphatase, and AST.
Lastly, Dr. Abraham measured hemoglobin, hematocrit, and red and white blood cells before and after three months. None of them changed significantly.
Despite this apparent safety record, if you decide to adopt “optimal-dose” iodine/iodide supplementation, it’s best to work closely and carefully with a knowledgeable physician to monitor thyroid function and general iodine safety. Dr. Abraham estimates that 14-15 milligrams of iodine/iodide daily is the upper limit for safe intake; that’s not much more than the optimal dose. Japanese researchers have found cases of hypothyroidism caused by excess iodine (20 milligrams daily).
It’s possible to be allergic to iodine, although it’s considerably less common than people usually think. It is the organified Iodine such as is used in radio-contrast that can cause problems. (For more details about iodine safety, see the October 2002 issue of Nutrition & Healing.) I have seen Iodine burns on the skin, but never allergy to inorganic Iodine.
In the 1820s, the French physician Jean Lugol combined iodine (5 percent) and potassium iodide (10 percent) along with 85 percent water. Since iodine kills germs, he used it for nearly any infectious disease, as well as many other problems, frequently with success. The combination quickly became known as “Lugol’s solution” and was adopted by practicing physicians throughout Europe and the Americas. Lugol’s solution was widely used until the 1920s. In fact it was the most commonly prescribed medicine for many hard to categorize and treat diseases in 1930-33. Then research began in earnest and many new drugs were marketed. Many physicians recommended two drops daily for good health and more on occasion to help kill germs. After doing the spot test, I tell folks to take between 2 and 10 drops depending on how fast the spot disappears. Lugols Solution is relatively inexpensive but does take a prescription and is available in some regular pharmacies and in all of the compounding ones.
And here's the most amazing thing about gymnema. Scientists were stunned when they discovered an increase in the number of "beta cells" in the pancreas of test subjects. That means gymnema could actually help repair and regenerate new pancreas cells that produce insulin!
This is unprecedented in the history of health sciences. Imagine, a single nutrient that can help lower blood sugar, support your body's ability to produce the insulin you need, and even repair your pancreas. Gymnema can do all this and more.
But as good as Gymnema and these other nutrients are, you'll really get the full effect when you take them in combination with this next ingredient…
Alpha-lipoic acid (ALA) is a powerful antioxidant. It regenerates other antioxidants in your body, such as vitamins C and E. And if you have high blood sugar, ALA can be a lifesaver. In one carefully controlled study, 74 patients were given ALA or a placebo. ALA boosted their ability to absorb and use blood glucose by 27%.
Another study shows that ALA improves your body's sensitivity to insulin. And your ability to burn blood sugar. ALA can also lower your fasting glucose levels and enable your cells to store more glucose for energy. Rather than having a blood sugar build-up. Astragalus, ginseng, gymnema, and ALA aren’t the only natural nutrients that can help balance your blood sugar...
The truth about cinnamon
It's no secret that eating too many sugary foods and refined carbs can cause your blood sugar to skyrocket. Over time, high blood sugar can damage and even kill off the "insulin receptors" on your cells. When that happens, your body's cells don't respond as well to insulin. So they don't absorb as much sugar into your muscles and fat cells, to produce or store energy.
Recently, scientists discovered that cinnamon could solve this problem. Researchers looked at 60 patients with high blood sugar. Half took a placebo. The other half took either 1, 3 or 6 grams of cinnamon daily. After just 40 days, the group taking cinnamon had reduced their fasting blood glucose by nearly a third.
There are plenty more studies that show the beneficial effects of cinnamon. But hold on a minute! Don't think that you can run out to the supermarket and grab any old cinnamon for these kind of results. Or that cinnamon supplements always do the trick. There's only one form of cinnamon that's been shown to work in human studies. It's called Cinnamomum cassia. That's the kind used in these studies. And the only kind of cinnamon you should ever buy to control your blood sugar. Some supplements just list “cinnamon bark extract.” This says to me that it’s not the same as the Cinnamomum cassia used in studies! So if you've tried cinnamon supplements and been disappointed with the results, that could be the reason why.
- Chromium — which has been shown to lower blood glucose levels. Chromium also reduces your cravings for sweets and carbs, so your blood sugar doesn't spike so high after a meal.
- Algimate® — a soluble fiber derived from seaweed. It sticks to the sugars in your digestive system. Research shows it can slow the absorption of both fats and sugars in the small intestine.
- Fenugreek — slows the absorption of sugars in the stomach. It stimulates insulin production. And it lowers cholesterol and triglycerides.
- Cordyceps — used for thousands of years as a tonic for lung, kidney and heart problems. Cordyceps became famous when two female Chinese athletes set new track and field event world records in 1993. Their coach attributed their success to high altitude training and a diet containing Cordyceps.
- Maitake — lowers blood glucose and improves cholesterol levels.
- Kudzu root — supports pancreatic cells and stimulate insulin production.
- Holy basil leaf — reduces both fasting and post-meal glucose levels. Holy Basil is high in antioxidants. Having high blood sugar is an inflammatory condition. Antioxidants are powerful anti-inflammatory nutrients.
- Jambolan seed — also thought to lower blood sugar, and have antioxidant and anti-inflammatory properties. One study showed Jambolan may even protect the pancreas by restoring protective enzymes such as glutathione back to normal levels.
- L-taurine — this sulphur amino acid is well known for protecting the heart. How? By reducing free radicals in blood fats. This translates into lower cholesterol and higher levels of "good" HDL cholesterol. Taurine also protects your eyes and actually regenerates worn-out retinal tissues.
- Ophiopogon — treats the fluid imbalance that causes many people with high blood sugar to urinate frequently and be thirsty.
- Chinese yam — strengthens the spleen and kidney function, combating the thirst and frequent urination associated with high blood sugar.
- Anemarrhena rhizome — decreases insulin resistance in those with high blood sugar. Yet it leaves people with "normal" blood sugar levels untouched.
- Henon bamboo — protects your eyes by fighting a nasty enzyme called aldose reductase. Aldose reductase destroys bloods vessels in your retina.
- Tiger lily bulb — which is used in traditional Chinese medicine to protect your heart and eyes.
Wednesday, May 18, 2011
To document the diagnosis, blood anti-transaminase, anti-myelysin and anti-gliadin studies are preformed. But they are only positive if the patient has significant bowel disease when the blood is drawn and he/she has been consuming gluten on a regular basis. The markers of HLA-DQ2 or HLA-DQ8 haplotype, which show the genetic predisposition can also be tested, but are more expensive and do not guarantee that the patient really does have the disease. According to Ken Fine, et al. (The prevalence and causes of chronic diarrhea in treated celiac sprue. Gastroenterology 1997; 112:1830-1837) the most cost effective test to diagnose celiac disease is an anti-gliadin stool test while the suspect is consuming gluten. This is the test we used to diagnose and follow the treatment results .
BRALY'S SIGN: A visible trait of Hashimotos Thyroid Disease which is common in Celiacs was first noted in Poland in 1953 and presented to the Western Europe by the English Gastroenterologist, James Braly, MD. The majority of Celiacs have a foreshortened 5th finger now designated as Braly’s Sign. (J Pediatric Gastroenterology and Nutrition 2000; volume 31 (Suppl.3): S29. New England Journal of Medicine, August 18, 1999). A positive sign is that the end of the fifth finger is shorter than the last joint of the ring finger. We used this external marker as a hallmark of the disease also in our study. In the combined experienced of the two of us and another colleague, Susan Solomon, a clinician in Raleigh N.C. we have found this marker positive in almost 85% of Celiacs that were either biopsied proven or had the positive genetic marker of the disease.
HYDROGEN BREATH TEST: This is an inexpensive, paid by insurance study that is a presumptive assessment for intestinal disease such as gluten intolerance. Actually, it detects bacterial overgrowth in the small intestine. This is common in intestinal diseases in which the mucosa of the intestine is compromised like celiac, but also small intestinal diverticulosis, abnormal flora, parasites and previous surgery where the usual anatomy of the intestine has been changed. An example of this is bypass surgery for weight loss. Also if the intestine cannot make the enzymes to break down food stuff it also causes abnormal gases due to the fermentation from normal bacteria. Lactose intolerance is an illustration.
Normally there should be NO hydrogen in the breath since the bacteria and the enzymes and the anatomy is doing its job. But if something is awry then hydrogen which is normally produced in minute amounts goes up. Gastroenterologist picked the cut point of 10 parts per million or more to be abnormal. The test is done by holding one's breath for 30 seconds then exhaling through a carboard tube into a special handheld device. In 20 seconds, the results are apparent.
Monday, May 9, 2011
The risk factors for AD includes family history, gluten intolerance, heavy metal excess, fever blisters, glucose intolerance, obesity, head trauma, drug, age, physical and psychological stress. Stress can not only be diagnosed, but quantified by a simple office test: Heart Rate Variation (HRV). Also, if one has a single gene Apo E4 there is a 75% chance and if a double E4 a 94% chance of the disease.
The earliest observable symptoms are often mistakenly thought to be “age-related” senior moments. The inability to acquire new memories, the difficulty in recalling recently observed facts are noted first by the individual, then by loved ones and lastly by friends. These individuals, particularly those with a high social IQ, cover up these mental lapses with believable excuses. As the disease advances, symptoms include confusion, irritability, aggression, mood swings, language breakdown, long-term memory loss and the general withdrawal of the sufferer as their senses decline. Gradually, bodily functions are lost, ultimately leading to death. Individual prognosis is difficult to assess, as the duration of the disease varies. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis. When AD is suspected, the diagnosis is usually confirmed with behavioral assessments and cognitive tests, such as a MMSE. A Psychological Inventory Test (to be covered in a later posting) that checks nine different brain areas of function also helps in diagnosis and prognosis. It is best to pick up the disease in its earliest stages when much can be done to delay or even prevent it. Often I will order a MRI to look at the hippocampus volume, and if in real doubt do a PET scan with a PIB contrast.
If Alzheimer’s is in your future, much can be done to greatly delay, or better yet, prevent it. Despite the many ways to determine if you are in harms way, there is no guarantee that it will arrive until after it is too late. Therefore, an ounce of prevention should be considered before a ton of care. One cannot change their genes (Apo E or Family History), but can certainly amend them in what is now termed epigenetic modification. The research indicates that AD is mainly an inflammatory process albeit a slow ongoing oxidative smoldering process. Involved in this process are two key moleules, Nrf2 and BDNF. Nrf2 is a master regulator molecule of the antioxidant response. This response is important to diminish our oxidative stressors. Because Nrf2 is able to induce genes important in combating oxidative stress, it activates the body’s own protective response, Nrf2 is able to protect from a variety of oxidative stress-related complications, even in situations where the administration of exogenous antioxidants (such as Vitamin C and Vitamin E) have failed. The other important player, BDNF keeps nerve cells alive and stimulaes the growth of new ones. Recent studies shows that it prevents and reverse Alzheimer’s independent of the amyloid plaque tangles. BDNF levels can be naturally boosted by heavy exercise and caloric restriction. Nutrients that also help make BDNF or protect it from declining are acetyl-l-carnitine, fish oil, blueberries, and curcumin.
There are both prescription drugs and supplements that are recommended for AD. The three drugs that are FDA approved to increase an important chemical in neuro-transmission, Acetyl Choline, are Aricept, Exelon and Razadyne. The other FDA medication is Nemanda which tries, but not completely successfully, to inhibit the neurons from “burn out” from excessive excitation. Because 90% of folks who have Alzheimers also have the Herpes Simplex-2 Virus, taking a daily antiviral, such as Acyclovir may also be prevention, although not FDA approved for this. Other prescriptions that are used in that AD which by some researchers is considered to be Type 3 Diabetes are Metformine and Actos.
A supplement representing more than 30 years of neuroscience research, is BrainSustain. This is a unique powdered drink formula, developed by Board-Certified Neurologist, David Perlmutter, MD, FACN, to enhance brain performance and health. It is usually given in a smoothie or Almond Milk Shake. BrainSustainTM improves the energy production of brain mitochondria providing generous antioxidant support to combat the damaging effects of excess free radicals. It contains the following underlined ingrediants. Broccoli Seed Extract, which is the Johns Hopkins non heated patented extract of the phytochemical in broccoli (sulforaphane glucosinolate). Extensive research demonstrates that this compound upregulates the Nrf2 system, enhancing the production of important antioxidants such as glutathione and superoxide dismutase as well as activating vital Phase 2 detoxification enzymes. N-Acetyl-L-Cysteine (NAC), a derivative of the amino acid, L-cysteine, is the precursor to glutathione, one of the brain’s most important antioxidants. The aim of oral supplementation is to augment the body’s reserve. NAC itself is a potent antioxidant shown to reduce formation of nitric oxide, a free radical implicated for a causative role in neurodegenerative disorders. Phosphytl Serine (PS), a component of lecithin, plays an important role in neuronal energy production and enhances neuronal communication. After careful examination of scientific evidence, the FDA granted “qualified health claim” status to PS, stating that “Consumption of PS may reduce the risk of dementia in the elderly”. N-Acetyl-L-Carnitine (aka ALCAR), an acetylated form of the amino acid, L-carnitine, is able to cross the blood brain barrier, where it acts as an effective antioxidant and protects brain cells from toxic chemical and stress-induced damage and deterioration. N-Acetyl-L-Carnitine enhances neuronal energy production by transporting fuel sources into the mitochondria and removing energy production waste products from them. Carnitine is readily converted into acetlycholine, a neurotransmittter essential for learning and concentration. Alpha Lipoic Acid also provides more antioxidant action and regenerates other important brain antioxidants including vitamins E, C, and glutathione. Unlike other antioxidants, alpha lipoic acid is both fat and water-soluble, greatly enhancing its ability to be absorbed from the gut and penetrate into the brain. Coenzyme Q10 measurably increases the efficiency of cellular energy production and serves as a potent antioxidant that may protect the brain from oxidative stress damage, which is believed to be partially responsible for neurodegenerative disease. A special DHA, (a2), derived from algae is not only vital to brain health, but 25% of the brain is made up of it. DHA-a2 facilitates optimal structure and functioning of the brain cell membranes.
BrainSustainTM also contains VegaProTM, XYMOGEN’s proprietary pea/ rice protein blend, as well as fat soluble antioxidants, vitamins D3 and E (as mixed tocopherols), and activated B vitamins, including 50 mg of riboflavin and folic acid (as calcium folinate). Available in Vanilla Delight, Chai & Creamy Chocolate, BrainSustainTM costs from $40 to $80 a month depending on whether an individual takes one or two scoops of this product daily. In general I advise one to prevent and two to treat Dementia.
Monday, May 2, 2011
Although Hippocrates, in 400 B.C left historical records of treatments, with the mother of aspirin from the bark and leaves of the willow tree, it was not until 1828, that Johann Buchner, professor of pharmacy at the University of Munich, isolated a tiny amount of bitter tasting yellow, needle-like crystals, which he called salicinin and Leroux had extracted salicin, in crystalline form for the first time, and Raffaele Piria succeeded in obtaining the salicylic acid in its pure state. A hundred and fifty years later (1971), British pharmacologist John Robert Vane in London, showed aspirin suppressed the production of prostaglandins and thromboxanes. For this discovery, he was awarded both a Nobel Prize in Physiology and Medicine in 1982 and a knighthood.
More than 50 million people in the U.S. take aspirin every day to help prevent heart attacks, strokes and cancer. However, research has demonstrated that up to 25 percent of these individuals may not benefit from the anti-clotting effect of aspirin, and are more than three times more likely to die from a heart attack or stroke. So Aspirin does not have the same effect on everyone. This suboptimal response to aspirin by an individual is commonly known as aspirin resistance or insensitivity Since these individuals are at increased risk of heart attack or stroke, doctors are beginning to recognize the importance of testing for aspirin effect. On the other hand, the higher doses of aspirin, not only in some will produce a paradoxical clotting effect, but in others a hemorrhage!
Until recently, there was no quick, accurate and effective way to test for aspirin effect. An ADP adhesive study or a specific prostaglandin assay was used in research settings and not paid for by insurances. But now, with the AspirinWorks Test, we can be sure the aspirin is working with a simple no fasting urine test. The AspirinWorks Test is FDA cleared for use in apparently healthy individuals, and test samples can be collected in the doctor’s office at any time. The AspirinWorks Test determines the effect of aspirin on platelets by measuring the level of the biomarker called thromboxane B2 (11dhTxB2). The higher the levels of thromboxane B2, the stickier the blood platelets, and the less impact the aspirin is having. This crucial information allows physicians to individualize a patient’s therapy, which may be as simple as adjusting the dose.
When prescribing blood pressure or cholesterol medication, doctors routinely check the patient’s blood pressure or cholesterol to make sure the patient is getting the right dose of medication. Similarly it is important to know if the dose of aspirin you’re taking is effective. Now, when prescribing aspirin we can then decide to increase or decrease your aspirin dose or if additional medication is needed. As mentioned in my previous writings that just as important is the aspirin to prevent blood from clotting within the blood stream, acetaminophen is needed to inhibit the clot on the arterial wall!
Therefore acetaminophen (Tylenol) has been shown to work in conjunction with the aspirin. At the University of Georgia, Dr. Phillip Greenspan found that the acetaminophen is a potent inhibitor of the enzyme, myeloperoxidase. This enzyme oxidizes the LDL, modifies it in such a way that it is more delectable to the certain white cells (macrophages) that reside within the wall of our arteries. These ingest the LDL cholesterol and cause the plaque and obstruction, which is the father of atherosclerosis. In that the acetaminophen blocks the activity of this enzyme, there is less transformation of the bad cholesterol (LDL) that is available for the macrophages to ingest. This research was presented at the conference on arteriosclerosis, thrombosis and vascular biology in Denver, May 21, 2000 and in 2006 documented by John Merrill PhD at Rutgers. This can also be taken to prevent pain. Some people state it helps them to sleep, when taken at bedtime. Also a recent study at the University of Florida demonstrated that acetamenaphen elevates the mood. The bad press that Acetaminophen has recently had makes this well studied drug almost a curse word. It is true in very high doses like over 6,000 mg a day it can negatively affect the liver and perhaps the kidney, but 1000mg/day is positively healthy for all who want protect their blood vessels.
THE BOTTOM LINE-“Betwixt and between, Aspirin and Tylenol will keep the artery clean” One each 81 mg Aspirin and 500 mg Acetaminophen (TylenolR), both twice a day, will keep the heart attack and stroke away!!
Tuesday, April 26, 2011
An excellent source of information regarding iodine historical use in medicine, present day assumptions, sufficiency, safety and physiological implications is available in papers written by Dr. Guy Abraham, Dr Jorge Flechas and Dr. David Brownstein for The Original Internist publication. These papers are available from the web at www.optimox.com. Or a search in Google for the iodine supplement Iodoral will yield the same results.
We encourage the reader to acquaint themselves with the aforementioned papers. A brief summary of their work is included as follows:
Swiss physician J.F. Coindet in 1812 had success treating goiter (extreme hypothyroidism) with seaweed and reasoned elemental iodine was the primary reason for his patient’s improvement. He tried tincture of iodine at 250 mg per day with great success in 150 goiter patients. Over the last century physicians refined the iodine compounds until French physician Gene Lugol’s in 1829 devised his formula of 12.5 to 37.5 mg of iodine with potassium iodide in water as the most efficient and sufficient dose. Addition of potassium iodide increased the solubility of iodine sufficiently to be more clinically valuable.
Lugol’s formula was used very successfully until the 1930s for the treatment of hypothyroidism, hyperthyroidism and other medical conditions that demonstrated efficacy. It is noteworthy that only 0.05 mg/day of iodine is necessary to prevent goiter. This amount is available in iodized salt thereby eliminating goiter as a prevalent health concern. However 0.05 mg/day is not enough for optimal health. Iodine is the one halogen (chlorine, bromine and fluorine are the others in order of increasing oxidizing potential) the body requires for many biochemical processes.
History of sufficiency:
In the 1930s physicians started using the recently developed thyroid hormones for treatment of thyroid hypo- or hyper- activity. The assumption was that iodized salt provided iodine sufficiency. Even though the chloride in table salt is a competing halide (chlorine - halogen) there is enough uptake of iodine in iodized salt from the potassium iodide to prevent goiter. Therefore synthetic (patentable) thyroid hormone replacement was developed to increase the thyroid’s production of T4 (thyroxine).
Hintze et al (1) compared the response of patients with simple goiter to administration of I at 400 ug/day and to the administration of T4 at 150 ug/day…. Iodine was more effective by itself than the administration of the T4 hormone by itself.
Most people get iodine in their diet from seafood and iodized salt. However, only about 50% of Americans use iodized salt and because of concerns about high blood pressure, many people have reduced their salt intake. One gram of salt contains 77 mcg of iodine. Because of the high chloride content in table salt, some experts estimate that only about 10% of the iodine in iodized salt is actually absorbed. The recommended daily allowance (RDA) of iodine is 150 mcg (somewhat higher for pregnant women and certain other groups). Though 150 mcg daily may be sufficient to prevent an enlarged thyroid (goiter) and cretinism (severe iodine deficiency in babies leading to mental retardation and impaired development), these values are far short of the optimal values of 12,500 mcg (12.5 mg) recommended by Dr. Abraham. But, even using the lower values, many people still do not get the RDA and tests have shown that the average blood levels of iodine have decreased significantly over the past 30 years, in part no doubt, due to the substitution of bromide for iodide in baked goods in the early 1980’s.
A popular assumption is that physiologic doses of iodine are toxic. In the 1940s a study linked non-radioactive iodine to toxic reactions. It was plainly not true. T4 (thyroxine has 4 iodine atoms) and T3 (triiodothyronine has 3 iodine atoms) are the thyroid’s hormones that are control metabolism. Both have iodine atoms in their molecules. It is obvious that iodine sufficiency is needed for optimal metabolism.
Is there a relationship between iodine and chronic fatigue and other disorders?
Dr. Brownstein writes: “The illnesses that iodine/iodide has helped are many. These conditions include Fibromyalgia, thyroid disorders, chronic fatigue immune deficiency syndrome, autoimmune disorders as well as cancer. Most patients who are deficient in iodine will respond positively to iodine supplementation. In fact, I have come to the conclusion that iodine deficiency sets up the immune system to malfunction which can lead to many of the above disorders developing. Every patient could benefit from a thorough evaluation of their iodine levels.” (2)
Is there a probable relationship to fibrocystic breast disease (FDB)?
Mainland Japanese women have a very low incidence and prevalence of FDB and breast cancer. (13) Several investigators have proposed that the essential element I was the protective factor in mainland Japanese. (4 – 10) If indeed, the essential element I is the postulated protective factor, the administration of I to American women in amounts equivalent to that consumed by mainland Japanese women would be expected to protect them from breast cancer and improve FDB, as previously proposed by Stadel for breast cancer and confirmed for FDB by Ghent et al. (7) Based on data supplied by the Japanese Ministry of Health, the average daily I intake in mainland Japanese is 13.8 mg. (6)
The administration of thyroid hormones to I-deficient women may increase further their risk for breast cancer. In a group of women undergoing mammography for screening purposes (14) the incidence of breast cancer was twice as high in women receiving thyroid medications for hypothyroidism (most likely induced by I deficiency) than women not on thyroid supplement. The mean incidences were 6.2% in controls and 12.1% in women on thyroid hormones. The incidence of breast cancer was twice as high in women on thyroid hormones for more than 15 years (19.5%) compared to those on thyroid hormones for 5 years (10%).
Sodium – iodide symporter:
The ability of the thyroid gland to transport and concentrate iodide from blood is absolutely necessary for the synthesis of thyroid hormones. The key player in this process is the sodium-iodide symporter, an integral membrane protein that resides in the membrane of thyroid epithelial cells. As its name indicates, the sodium-iodide symporter simultaneously transports both Na+ and I- ions from extracellular fluid (i.e. blood) into the thryoid epithelial cell. Considering critical role of iodine trapping in thyroid function, it is not surprising that abnormalities in expression or function of the symporter can lead to thyroid disease.
The sodium-iodide symporter is most highly expressed in thyroid epithelial cells. Lower levels of expression can be detected in mammary gland, salivary gland, stomach and colon, but none of these tissues is known to organify iodide. The presence of the symporter in mammary gland leads to secretion of iodine in milk, which is probably important for thyroid function in neonatal animals. (18 – 22)
One atom of iodine is transported into the cells for every 2 atoms of sodium via the sodium/iodine symporter (NIS). There is also a chloride/iodide symporter called pendrin. Normal saliva/serum iodide ratio is approx. 42. Less than 20 may be due to toxins or very high levels of bromine/fluorine binding to the symporter.
- bromine (from fruit fumigants and processed bakery products)
- chlorine (chloramine byproduct from drinking water chlorination)
- ammonium perchlorate (rocket fuel found in tap water)
- fluorine (naturally occurring in well water plus drinking water fluoridation)
- thiocyanate (from cigarette smoke)
can bind to the NIS (receptor) and damage it preventing iodine from entering the cell. The receptor can possibly be repaired with vitamin C (3000 mg/day) and Celtic (unrefined) sea salt. (16)
The basil membrane of the thyroid cell has the specific ability to pump iodine into the interior of the thyroid cell. This is called Iodide Trapping. In a normal gland the iodine pump concentrates the iodide to about 30 times the concentration in blood. The rate of trapping is influenced by TSH in a negative feedback control method. (17)
For clinical experiences the following references are useful.
Fibrocystic Breasts by Jonathan V. Wright, M.D., Published in “Nutrition & Healing” – July 1995
David Brownstein, MD., Iodine. Why You Need It Why You Can’t Live Without It. 2nd Ed. 2006
Saliva iodine significance:
There is ample evidence of renal iodine clearance in the literature in Dr. Abraham’s references and some evidence of salivary uptake from other sources. According to Mr. Zareba under a NASA grant, the mean correlation coefficient ( r ) between iodine elimination for blood/saliva was 0.99, for blood/urine, 0.95, and for saliva/urine, 0.97. The absolute value of iodine concentrations in urine revealed marked variability, which was corrected by adjusting for creatinine levels. (15) That is, with normal symporter there is excellent correlation between the iodine concentration increase in serum and saliva. However, the timing is different.
From Bruger and Member, thyroxine was not concentrated from the blood to saliva but elemental potassium iodide (KI) was from 5 to 7 times that of the blood. The maximal amount of iodine concentrated in the saliva occurred 1 to 2 ½ hours after ingestion of KI peaking to 1200 times the initial salivary iodide. The salivary/blood iodine ratio in the control period was 6 and reached a maximum of 28, 8 hours after ingestion of the iodide. (18) Obviously measuring salivary iodide within several hours of supplementation will result in a very high unusable reading. This effect has been verified by our own tests. Note that normal iodide trapping in the thyroid is about 30 times that in the blood.
The hypothesis is that since the salivary iodide uptake from the interstitium and thyroid trapping iodide from the blood is approximately the same order over time, the saliva uptake can be a rough indication of thyroid uptake. If this is true then the saliva/urine ratio can be a rough indication of thyroid iodide sufficiency. There is some anecdotal evidence from non-traditional research to suggest this relationship. Examples are as follows:
J was supplementing Iodoral® (7.5 mg KI + 5 mg Iodine per tab) at the rate of 50 mg/day for nine months (without adverse effect) encouraged by the idea of clearing mercury toxicity (a dental assistant) and tested at 25 PPM saliva and 60 PPM urine iodide. One would expect that after nine months supplementation at this dosage, iodine sufficiency would have been reached. The saliva/urine ratio of
< 1 suggests this conclusion.
Dr. T supplementing for many years with an organic bound iodine in seaweed extract tested 17 PPM saliva and 15 PPM urine. The supplementation will continue but one would expect sufficiency with this long term supplementation. Again the ratio approached 1.
B supplementing 6 months 12.5 mg/day Iodoral® tested 9 PPM saliva and 6 PPM urine suggesting a higher dosage could be used to approach higher residual levels and a lower ratio suggesting sufficiency as not reached. The 24 hour urine iodine loading test would be appropriate.
M was not supplementing but ate substantial amounts of seafood and mostly Mexican foods but very little US produced processed foods. M’s saliva tested 17 PPM and urine 15 PPM.
20 other subjects were tested who were not supplementing except for iodized salt and multivitamin tabs with iodine in the 100 ug range. None were consuming substantial ocean dwelling foods. Usual tests were 1 PPM saliva and 0.1 PPM urine. The absolute values are very low and the ratio is 10. Again a 24 hour urine loading tests would probably support this conclusion.
Testing was performed in the morning with no fast required. It is recommended that a 12 hour fast, 8:00 PM to 8:00 AM for example, be required in order to minimize the effects of hydration.
The QFA 1500 analyzer does not purport to provide sensitivities less than 0.1 mg/L (PPM) but is sensitive enough to measure the uptake effects of iodine supplementation whether in Lugol’s formula (as Iodoral® of 7.5 mg potassium iodide and 5 mg elemental iodine) or other organic form such as kelp, dulse or seaweed extract.
The hypothesis of measuring the ratios of saliva vs urine iodine as a measure of sufficiency and blood vs. urine as an indicator of availability of iodine for the tissues (iodine symporter) is unproven except from anecdotal information. Nevertheless a good body of information will be obtained through this simple test coupled with other observation to arrive at conclusions outside traditional expensive and sometimes inaccurate or incomplete medical studies.
1. Hintze, G., Emrich, D., Kobberling, J., Treatment of endemic goitre due to iodine deficiency with iodine, levothyroxine or both: results of a multicentre trial. European Journal of Clinical Investigation, 19:527-534, 1989.
2. Brownstein, D., Clinical experience with inorganic, non-radioactive iodine/iodide. The Original Internist, 12(3):105-108, 2005
3. Eskin B., Bartuska D., Dunn M., Jacob G., Dratman M., Mammary Gland Dysplasia in Iodine Deficiency, JAMA, 200:115-119, 1967.
4. Eskin, B., Iodine Metabolism and Breast Cancer. Trans. New York, Acad. of Sciences, 32:911-947, 1970.
5. Funahashi, H., Imaj, T., Tanaka, Y., et al, Suppressive Effect of Iodine on DMBA-Induced Breast Tumor Growth in the Rat. Journal of Surgical Oncology, 61:209-213, 1996.
6. Ghent, W., Eskin, B., Low, D., Hill, L., Iodine Replacement in Fibrocystic Disease of the Breast, Can. J. Surg., 36:453-460, 1993.
7. Derry, D., Breast Cancer and Iodine, Trafford Publishing, Victoria B.C., 92, 2001.
8. Vishnyakova, V.V., Murav’yeva, N.L., On the Treatment of Dyshormonal Hyperplasia of Mammary Glands, Vestn Akad Med Navk SSSR, 21:19-22, 1966.
9. Cann S., Netten J., Netten C., Hypothesis: Iodine, selenium and the development of breast cancer, Cancer Causes and Control 11:121-127, 2000.
10. Ghandrakant, C., Kapdim MD, Wolfe, J.N., Breast Cancer. Relationship to Thyroid Supplements for Hypothyroidism. JAMA, 238:1124, 1976.
11. Epstein, S.S., Steinman, D., Breast Cancer Prevention Program. Macmillan, NY, 1998, pg 5.
12. Waterhouse, J., Shanmvgakatnam, K., et al, Cancer incidence in five continents. LARC Scientific Publications, International Agency for Research on Cancer, Lyon, France, 1982.
13. Stadel B., Dietary Iodine and Risk of Breast, Endometrial, and Ovarian Cancer, The Lancet, 1:890-891, 1976.
14. Ghandrakant, C., Kapdim MD, Wolfe, J.N., Breast Cancer. Relationship to Thyroid Supplements for Hypothyroidism. JAMA, 238:1124, 1976.
15. Grazyna Zareba, Elsa Cernichiari, Lowell A. Goldsmith, and Thomas W. Clarkson., Biological Monitoring of Iodine, a Water Disinfectant for Long-Term Space Missions. (1) Center for Space Environmental Health, (2) Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642 USA, (3) Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642 USA16.
16. David Brownstein, MD., Iodine. Why You Need It Why You Can’t Live Without It. 2nd Ed. 2006
17. Guyton & Hall, Textbook of Medical Physiology 10th ed.:858, 859)
18. Maurice Berger, Samuel Member, On The Excretion of Iodine in the Saliva, From the Research Laboratory, Department of Medicine, New York Post-Graduate Medical School and Hospital, Columbia University
19. De la Vieja A, Dohan O, Levy O, Carrasco N: Molecular Analysis of the Sodium/Iodide Symporter: Impact on Thyroid and Extrathyroid Pathophysiology. Phys Rev 80:1083-1105, 2000.
20. Dohan O, De la Vieja A, Paroder V, etc: The sodium/iodide symporter (NIS): Characterization, regulation and medical significance. Endocrine Reviews 24:48-77, 2003.
21. Fugiwara H, Tatsumi K, Miki K et al: Congenital hypothyroidism caused by a mutation in the Na+/I- symporter. Nature Genetics 16:124, 1997.
22. Spitzweg C, Heufelder AE: The sodium iodide symporter: its emerging relevance to clinical thyroidology. Europ J Endocrinol 138:374, 1998.
Monday, April 25, 2011
A sprain or strain typically occurs when people fall and land on an outstretched arm, slide into base, land on the side of their foot, or twist a knee with the foot planted firmly on the ground. This results in a overstretch or tear of the tendon/muscle or ligament(s) supporting that joint. Strains can be acute or chronic. An acute strain is caused by trauma or an injury such as a blow to the body. Improperly lifting heavy objects or overstressing the muscles can also cause it. Chronic strains are usually the result of overuse injury (prolonged, repetitive movement of the muscles and tendons).
Although all joints can potentially be sprained or strained, the most common is the ankle the second is the shoulder, and the third, the ankle counterpart in the upper extremity, the wrist. The ankle is most commonly severely injured in professional, recreational sports and even in ordinary activities like walking. Most ankle sprains happen when the foot abruptly turns inward (inversion) or outward (aversion) as athletes run, turn, fall, or land after a jump. One or more of the lateral or medial ligaments are injured but a tendon and its attached muscle can also be hurt.
The usual symptom of a muscle/tendon strain or a ligament sprain is pain, and the signs are swelling, bruising, and the loss of function (the inability to move and use the joint). Sometimes people feel a pop or tear when the injury happens. The signs and symptoms can vary in intensity, depending on the severity of the sprain.
The severity is graded one, two and three. A grade I (mild) is overstretching or slight tearing of the tissues with no joint instability. A person usually experiences minimal pain, swelling, and little or no loss of function. Bruising is absent or slight, and the person is usually able to put weight on the affected joint. A grade II (moderate) causes partial tearing and is characterized by bruising, moderate pain, and swelling. There is some difficulty putting weight on the affected joint and there is some loss of function. An x-ray or rarely an MRI may be needed to document both the diagnoses and stage. A grade III (severe) results in a complete tear or rupture. Pain, swelling, and bruising are significant, and the patient is unable to put weight on the joint. An x-ray is usually taken to rule out a fracture in the adjacent bone. Type III injury often requires immobilization and possibly surgery. It can also increase the risk of the person having future problems in that area.
Contact sports such as soccer, football, hockey, boxing, and wrestling put people at risk for strains. Gymnastics, tennis, rowing, golf, and other sports that require extensive gripping can increase the risk of hand and forearm strains. Elbow strains a type of repetitive syndrome occur in people who participate in racket sports, throwing, contact sports and work. The latter in occupations such as carpentry that requires hammering. Two Common Elbow Strains are Tennis Elbow (lateral epicondylitis) and Golfer’s Elbow (medial epicondylitis).
The healing time varies with the severity of the injury with mild and only a few fibers have been damaged. Healing occurs within two to three weeks. With moderate injury with more extensive damage to the fibers, but the tissues is not completely ruptured. Healing occurs within three to six weeks. But with a severe injury and a complete severing of the bundle. It is another story. This may require surgical repair of the tissue and the healing period can be up to a year!
Tendons, muscles, and ligaments are capable of healing and recovering from injuries in a process that is controlled by the fibers and their surrounding extracellular matrix. However, the healed tendons and ligaments never regain the same mechanical properties as before the injury. Muscle have a good blood supply, which is impart why they are red heal far faster and better than the anemic white tendons and ligaments. The three main stages of healing are inflammation, repair ( proliferation), and remodeling. Nature does a good job with these processes, but doctors can help patients to augment the rapidity of healing.
Most current treatments for the joint supportive structures are neither evidence-
based or effective. Typically Doctors recommend RICE- Rest, Ice, Compression, and
Elevation. They also give anti-inflammatory such as Ibuprofen which may help with
the pain, but delays the healing in that inflammation itself as noted above is part of
the healing process. In some cases immobilization may be helpful, but in others in
which there is no associated fracture, it delays healing in that it decreases the
natural growth factors that are stimulated with joint movement.
Molecular processes underlying joint structure healing are now being elucidated.
Metalloproteinase enzymes are thought to have a key role in the regulation of the activity of tendon cells and matrix remodeling in both normal and pathologic structures. The potential roles of neuropeptides, inflammatory mediators and mechanical strain (either too much or too little) acting on the resident tenocytes are noted to stimulate the intrinsic healing G-Proteins. Excessive or inappropriate activity of destructive matrix-degrading enzymes might be a novel therapeutic target for tendinopathy. Tenocytes in the tendon actively synthesize components as well as enzymes such as matrix metalloproteinases . Bone morphogenetic proteins (BMPs) can induce bone and cartilage formation as well as tissue differentiation, and BMP-12 specifically has been shown to influence formation and differentiation of tendon tissue and to promote fibrogenesis.
Now avant guarde physicians give Enzymes such as Bromelain and Papain early in acute trauma, don’t use inflammatory suppressants but pro-inflamants (prolotherapy), early or no immobilization, even irritating the structures such as the “aggravating technique” in tennis elbow, and a cellular level, nitroglycerin (NTG)!
The rational that NTG could be used pharmacologically to accelerate repair in injured tendons has been well documented. Gambito E, "Evidence on the effectiveness of topical nitroglycerin in the treatment of tendinopathies: a systematic review and meta-analysis" (Arch. Phys. Med. Rehabil. 2010;91:1291-305). In a more recent study from the University of Toronto (JAMA.Feb 23;2011) Jamal found that nitroglycerin ointment increased both bone density and strength in postmenopausal women. The mechanism for tendon and bone repair is speculated to be enhancement of a group of connective tissue enzymes, the metalloproteinases and a cytokine, specifically Il-17.
Bearing the above in mind, I have used NTG ointment on over thirty patients with tendon/cartilage injuries to include rotator cuff, hip, knee, and neck with good results. In the past, I have also used a topical muscle relaxant (Flexeral), an antinflamatory (Ketoprofen), an analgesic (Lidocaine) separately or together in an absorptive matrix. I have since added them to NTG to augment the earlier healing liniment and have had even better results. This combination of salubriants must be obtained at a compounding pharmacy. Many medical insurances do pay for these prescription. For more information call Chris Schiller at Economy Pharmacy (918-994-5804).
Sunday, April 3, 2011
Telomeres are sections of DNA at the end of each chromosome whose primary function is to prevent chromosomal “fraying” when a cell replicates. As a cell ages, its telomeres become shorter. How much shorter is governed by genetic factors and environmental stressors. Eventually, the telomeres become too short to allow cell replication, the cell stops dividing and will ultimately die which is a normal biological process. The more of our cells die, the older and frailer we become until we ourselves die. If our reserve is depleted, we succumb to disease or just old age. The Telomere Test can determine the length of your telomeres in relation to the chronological age. The Telomere Score is calculated based on the telomere length on white blood cells (T-lymphocytes). This is the average compared to telomere length on lymphocytes from a sample of the American population of the same age. The higher the telomere score, the “younger” the cells and the longer and better that person will live. Yearly, the test can be repeated and one can work harder or do other interventions that will enhance their score and their life.
Although we cannot change our genes we now can modify their expression by Lifestyle. In a study published in Nature this January scientists found the body activates a gene (P 53) that under stress shuts down our cells' normal growth and division cycle by controlling the telomere length. Diet plays a large role in this process. Micronutrients have been shown to have epigenetic effects by methylation of our DNA. The best but the most difficult is becoming a CRONI, (Caloric Restriction Optimal Nutritional Intake) to the point of just sustenance, a step away from starvation with just nutrient dense foods. Far easier and almost as good is eating correctly for your Apo E type, going easy on meat, with eating whole nutrient dense foods, as raw as possible, consumption of Omega 3s, and staying away from grains and processed foods. According to a study in the January 20, 2010 issue of JAMA, increased telomere and survival rates occurred among individuals with high dietary intake of marine omega-3 fatty acids and established cardiovascular disease. In this 5-year study, the researchers found that individuals with the lowest DHA+EPA experienced the most rapid rate of telomere shortening, whereas those in the highest had the slowest rate of shortening. Levels of DHA+EPA were associated with less telomere shortening before and after sequential adjustment for established risk factors and potential confounders. For each 1-standard deviation increase in red cell Omega 3 levels was associated with a 32 percent reduction in the odds of telomere shortening! Although both EPA and DHA are healthy, it seems that DHA is better. So consuming Tuna or Calamari Oil, which has a 4 to 1 ratio of DHA to EPA, is superior than any of the marine oils. What we eat and supplement today becomes the biology of our future.
Minimizing emotional (psychological) and physiological (infections, trauma and surgery) stress will keep your telomeres longer and you healthier. Additionally, increasing antioxidants slows telomere shortening. Physical exercise with adequate antioxidants will also give longer telomeres. Common sense dictates that decreasing cardiovascular risk factors (Lipids, Homocysteine, Blood Pressure, Hs-C Reactive Protein, Glucose etc.) and correcting micronutrient deficencies such as Vitamins, Minerals, and Glutathione will preserve the telomere length. Periodically getting rid of our poison buildup by colonic, and liver cleanses and from the skin by sweating (artificially by sauna or by heavy exercise) and minimizing the toxins in our water, air and food will go a long way in keeping our telomeres longer. Keeping our hormones (Thyroid, Sex and Adrenal hormones) in balance and not getting sick also keeps our telomeres longer. To not get sick means keeping our immune system healthy to include the consumption of Pre and Probiotics. Surgery should be only for life saving problems and not for elective procedures since the operation and the anesthesia shortens the telomeres. Staying out of harms' way for bodily damage in our daily pursuits such as not over indulging in alcohol and dangerous sports and occupations will keep our telomeres and our lives longer.
Although it is far better to live a healthy life style, there are drugs that also have been shown to decrease our telomere shortening. The antihypertensives, Angiotension Converting Enzyme drugs such as Lisinopril and the Angiotension Recepter Blockers like Lorsartan have been shown to extend our telomeres. Likewise so has the Cholesterol lowering Statins. These drugs should be used judiciously, not to lower our lipids too much and to take concomitantly CoEnzyme Q 10. Also the diabetic medicine, Metformin, has been shown to be antiaging. But with this drug many physicians recommend using B12 too. Age is how old we are, but old is what our body is biologically. In reality it is not how old you are, but how you are when you are old that counts!
Monday, March 7, 2011
D.D. Palmer founded chiropractic in the 1890s and his son B.J. Palmer helped to expand it in the early 20th century. It has two main groups: "straights", now the minority, emphasize vitalism, innate intelligence and spinal adjustments, and consider vertebral subluxations to be the cause of all disease; "mixers" are more open to mainstream and alternative medical techniques such as exercise, massage, and nutrition. With the advent of X-Ray and the noise of a joint going back into the proper position, Chiropractic is here to stay! The so called pop is caused by the tendons or in the back the apophyseal joint causing a vacuum as it is pulled and suddenly let go-in physics called a cavitation.
The premise of chiropractic assumes a vertebral subluxation or spinal joint dysfunction interferes with the body's function and its Innate Intelligence. This vitalistic concept states that all life contains Innate Intelligence and that this force is responsible for the organization, maintenance and healing of the body. Removal of the interference to the nervous system spinal adjustment so that when the spine is in correct alignment, Innate Intelligence can act, by way of the nervous system, to heal disease within the body. However, until 1987 Chiropractic was considered a cult by the AMA of which I was a member. My experience though with the profession was that it greatly helped folks with back problems and I frequently referred patients to them.
In 1975, I was approached by the Missouri State Medical Board that my license was at stake if I continued using chiropractors as part of the “healing profession”. I was incensed that I could not practice what I thought was best for my patient. Most MDs then thought that if time and physical therapy did not work, then give heavy pain meds or sent them to orthopedic surgeons. Many were operated on and suffered a “failed back”. I was so disturbed by this that I testified in Chicago in 1976, with Chester Wilk and four other chiropractors against the AMA and several nationwide healthcare associations. This was finally resolved in 1987 after a second trial that Chiropratic did help folks indeed and in need.
The triad of Innate Intelligence, Force, and Matter espoused by Palmer a hundred years ago has gone by the wayside. Modern chiropractors study these principles in college and these ideas are seen as historical references to early chiropractic philosophy and pseudoscience. Chiropractors in Australia, England and Germany are Medical Doctors (M.D.s) who specialize in spinal manipulation and many of the techniques used by their American counterparts. A profession that originally did similar healings, the Osteopaths, but now do very little Osteopathic Manipulative Therapy took some of the slack here up. They mostly practice what we as MDs do. After four years of postgraduate (Chiropractic School) training, the student is awarded a Doctorate in Chiropractic- a D.C. Until recently most schools were privately funded, but now they are beginning to see them as part of Universities. Chiropractic is here to stay in America and I feel it is part of the holistic movement of good patient care.
Sunday, February 27, 2011
DO YOU KNOW MPO
We all have the enzyme myeloperoxidase, (MPO), in our bodies. But as plaque inside our blood vessel walls becomes more likely to rupture, we produce even more MPO at that site. The increased amounts of MPO, which can be measured in the blood causes erosion of the plaque. When the plaque in the blood vessel erodes enough, it ruptures. There a micro-clot forms to patch the weak spot. Platelets (formed elements) in the blood cells flowing by the clot start participating in growing and firming up this coagulated mass. If that clot blocks blood flow to the heart or brain, a heart attack or stroke usually occurs. A high level of MPO is a signal that a person is in risk of having a catastrophe. This is so even though the cholesterol levels and blood pressure are perfect as in almost fifty percent of these incidents. The MPO oxidizes the LDL cholesterol, modifying so it is more delectable to the certain white cells (macrophages) that reside within the wall of our arteries. These ingest the LDL particles, get sick, die and spill their fatty guts thus enlarging the existing fatty streaks to form an inflammatory plaque. This is the generator of all atherosclerosis. Unbeknownst to most doctors is that Acetaminophen blocks the activity of MPO and stops the transformation of the bad cholesterol (LDL) that is available for the macrophages to ingest.
And Aspirin stops the platelets in our blood from getting sticky, preventing the clump. The basis for the use of low dose aspirin lies in its unique inhibitory effect on a key enzyme, COX-1 (cyclooxygenase-1). In low doses, 81 mg (a child’s aspirin) twice a day, the platelets are less tacky and not as likely to coalesce together to coagulate. However, in higher amounts such as 650 mg (2 adult Aspirins) it affects the arterial walls making them sticky and more likely to initiate a clot on the rough plaque.
A personal friend of mine, Professor Gary Merrill, of Rutgers' department of cell biology and neuroscience, demonstrated significant improvement in acetaminophen-treated hearts compared with non-treated hearts following periods of induced ischemia (reduced blood flow) attributed the rapid post-ischemia recovery of heart muscle and circulation to the antioxidant properties of acetaminophen. This research as part of a growing body of evidence supporting the positive effects of acetaminophen on the cardiovascular system. His findings, together with those of Dr. Addison Taylor of Baylor College of Medicine, Houston, and Professor Phillip Greenspan of the University of Georgia College of Pharmacy, indicate that acetaminophen prevent the damaging effects of LDL cholesterol. Taylor and Greenspan separately conducted investigations showing acetaminophen may protect against the life-threatening condition, hardening of the arteries. The bad press that Acetaminophen has recently had makes this well studied drug almost a curse word. It is true in very high doses like over 6,000 mg a day it can negatively affect the liver and perhaps the kidney, but 1000mg/day is positively healthy for all who want protect their blood vessels.
After the discovery, the Cleveland Clinic, through Cleveland Heart Lab started doing the MPO test. Blood samples, are overnighted to them from the doctors offices, for MPO and four other valuable markers. They include urinary Isoprostain and Microalbumin; a pro-oxidant and an arterial disrupter, HsCRP; indicating lining damage, and Plac2; a predictor of plaque rupture. Many insurance companies and Medicare now cover the test. And for those who don't have coverage, the cost is relatively inexpensive: $189 for MPO and the other tests conducted with it.
If none of the above makes sense to you, still do yourself a favor. Betwixt and between Aspirin and Acetominophen will keep the artery clean-and YOU healthy! If you are a male over the age of 45 or a female over 50-PLEASE take one each of 81 mg Aspirin and 500 mg Acetominophen (Tylenol), both twice a day, it will keep the heart attack and stroke away!!
The increased amounts of MPO can be measured in the blood. If greater than 723 pmol/L, there is a 5-fold increase of a catastrophic event even in the absence of other cardiovascular risk factors. But if other risk factors are present a high value makes it much more dangerous. MPO is also used clinically in the Emergency Room to determine if the acute chest pain that the patient is having is a heart attack or not. Another emerging use is that it predicts the severity of heart failure (inability of the heart to pump enough blood) and the prognosis. It is also used to determine the rate of narrowing of the carotid arteries.
Statins decrease MPO levels and Acetaminophen blocks its activity, which stops the transformation of the bad cholesterol (LDL) that is available for the macrophages to ingest. This important test can be done by the Cleveland Clinic, through Cleveland Heart Lab by a special arrangement with a local physician. Blood samples, are overnighted to them for MPO and four other valuable markers. They include urinary Isoprostain and Microalbumin; a pro-oxidant and an arterial disrupter, HsCRP; indicating lining damage, and Plac2; a predictor of plaque rupture. Many insurance companies and Medicare now cover the test. And for those who don't have coverage, the cost is relatively inexpensive: $189 for MPO and the other tests conducted with it.
Monday, February 21, 2011
Not only does age, sex, weight, intestinal flora, general health, liver and kidney function alter a patient's response to drugs, but genetic factors must be considered. This information is crucial. Prescription Drug Fatality is the fourth leading cause of death after heart disease, cancer, and stroke. The major determinant involved in the metabolism of drugs, toxins and our hormones is the Cytochrome (CYP) P450 enzymes. The most important of these are CYP2D6, CYP2C9, CYP2C19, NAT2, UGT1A1, DPD, 5HTT, and CYP1A2. The'CYP's is a host of enzymes that use iron to oxidize organic molecules, as part of the body's preparation to dispose of potentially harmful substances by making them more water-soluble. The capital letter indicates the superfamily, and the number before and after, the subfamily.
In humans, CYP3A represents one of the most important subfamilies of the P450 superfamily. The CYP3A subfamily is the most abundantly expressed P450 in human liver, and CYP3A is involved in the biotransformation of approximately 50% of drugs that are metabolized. As a result, drug-drug interactions associated with modulation of CYP3A-mediated metabolism can be of substantial consequence. In the past, it was a trial and error of the dose and the drug we would use. To err could cause not only great harm, but even death of a patient. With this new tool, doctors can take the guess work out of prescribing and do it scientifically.
In addition to our hereditary, the CYPs can be both up-regulated (induced) or down-regulated (inhibited) by other chemicals making it on occasion a complexed proposition for drug deposition. When several competing drugs are use for the same CYP enzyme an Adverse Drug Interaction occurs. At times there are multiple CYPs that work on a drug. For example, adding a hydroxyl group to a medication is the body's strategy to get rid of it and is often followed by joining them to other molecular groups such as glucuronide to increase the solubility even further. Most of the CYP in man is found in the liver, the main organ involved in drug and toxin removal, but a fair amount is also in the small intestine. CYP usually is found in the 'microsomal' part of the cytoplasm (endoplasmic reticulum).
We determine the dose and interaction of not only prescribed drugs, but OTC (over-the-counter) and herbal medicines including those used to treat depression, anxiety, seizures and psychoses; heart disease, cancer, diabetes, and pain. These include medications as Coumadin (warfarin), Prozac, Zoloft, Paxil, Effexor, hydrocodone, Amitriptyline, Claritin, Cyclobenzaprine,, Metoprolol, Tagamet, Tamoxifen, Valium, Carisoprodol, Dilantin, Premarin, and Prevacid (and the over-the-counter drugs, Allegra, and the several NSAIDS).
Almost half of us have genetic variations that affect how we process these drugs. There are four different types of metabolizers, and we all fall into one of these categories for the unpredictable pathways in Cytochrome P450 system. The first type which is the norm, and therefore that person would be an NORMAL Metabolizer and medications prescribed in the usual doses will be handled well by your body. The second type, you would be an INTERMEDIATE metabolizer. This means that you to metabolize the medications more slowly. In this case a lower dosage is needed, and there is a chance of medications building up in your system causing adverse effects. It is especially important to monitor medications if you are in this category. Intermediate metabolizers through the 2C9 pathway, for instance, have an increased risk of bleeding incidences when taking the common blood thinner Coumadin or warfarin. For this reason, screening for CYP2C9 variants may reduce the risk of adverse drug reactions in these patients. The third type is a POOR metabolizer. This type of metabolizer is potentially very dangerous, as there is a great chance for the medication to build up in your system making one very sick, or even death.For example, a poor metabolizer of phenytoin, a common antiepileptic would not be able to process the drug and would actually have toxicity if prescribed this drug. The fourth type of metabolizer is ULTRA EXTENSIVE. In this instance, one would very rapidly excrete the medication. If you were an Ultra Extensive Metabolizer through the 2D6 pathway and one were prescribed a narcotic, there may not be any pain relief because the medication would be metabolized so fast that it would have little or no effect.
PHARMACOGENETIC EFFECT OF CYTOCHROME GENOTYPES
A. PM poor metabolizer, absent or greatly reduced ability to clear or activate drugs. B. IM intermediate metabolizer. Heterozygotes for normal and reduced activity genes. C. EM EuMetabolizer or the Normal Metabolizer. The expected result. D. UM Ultra Metabolizer. Greatly increased activity accelerating clearance or activation.
POPULATION FREQUENCY OF CYTOCHROME P450 (CYP) GENOTYPES
Gene PM IM EM UM
CYP2D6 10% 35% 48% 7%
CYP2C9 2-4% >35% ~60% N/A
CYP2C19 2-20% 24-36% 14-44% 30%
Currently Available Tests:
CYP2D6(cytochrome P450 2D6) acts on one-fourth of all prescription drugs, including the selective serotonin reuptake inhibitors (SSRI), tricylic antidepressants (TCA), betablockers such as Metoprolol and many of the antiarrhythmics. Approximately 10% of the population has a slow acting form of this enzyme and 7% a super-fast acting form. Thirty-five percent are carriers of a non-functional 2D6 allele (half of the gene), especially elevating the risk of ADVERSE DRUG REACTION when these individuals are taking multiple drugs. Drugs that CYP2D6 metabolizes include Prozac, Zoloft, Paxil, Effexor, hydrocodone , amitriptyline, cyclobenzaprine (Flexeril), Coreg, Tagamet, Tamoxifen, and the over-the-counter diphenylhydramine (Benadryl) drugs, Allegra and Claritin. CYP2D6 is responsible for activating the pro-drug codeine into its active form and the drug is therefore inactive in CYP2D6 slow metabolizers.
CYP2C9(cytochrome P450 2C9) is the primary route of metabolism for Coumadin (warfarin). Approximately 10% of the population are carriers of at least one allele for the slow-metabolizing form of CYP2C9 and may be treatable with 50% of the dose at which normal metabolizers are treated. Other drugs metabolized by CYP2C9 include Amaryl, Isoniazid,, Amitriptyline, Dilantin, Hyzaar, THC (tetrahydrocannabinol), NASAIDS, and Viagra.
CYP2C19(cytochrome P450 2C19) is associated with the metabolism of Carisoprodol (Soma), Aprazolam, Dilantin, and Prevacid.
CYP1A2(cytochrome P450 1A2) is associated with the metabolism of Amitriptyline, Resperone, Duloxetine(Cymbalta), Theophylline, Caffeine, Diazepam, Sex Hormones Tamoxifen, and Cyclobenzaprine. Amongst other problems these folks have arrhythmias or get jittery when drinking coffee. Lycopene found in tomatoes reduces the effect of the above drugs and hence need more of a dose.
NAT2(N-acetyltransferase 2) is a secondary drug metabolizing enzyme that acts on Isoniazid, Demnerol, and Azulfidine. The frequency of the NAT2 "slow acetylator" in various worldwide populations ranges from 10% to more than 90%.
DPD (Dihydropyrimidine dehydrogenase) is responsible for the metabolism of Fluorouracil (5-FU), one of the most successful and widely used chemotherapy drugs.
UGT 1A1 (UDP-glucuronosyltransferase) variations can lead to severe even fatal reactions to the first dose of Camptosar (irinotecan).
5HTT (Serotonin Transporter) helps determine whether people are likely to respond to SSRIs, a class of medications that includes Citalopram(Celexa), Fluoxetine(Prosac), Paroxetine(Paxil) and Sertraline
With this tool, no longer is it a trial and error proposition as to what drug and its dose to prescribe, We can now do it scientifically with a much better outcome for the patient. Since our CYP genes do not change, this study is done only once in a lifetime. Although, there are several labratories that do this work. the best and the one that we use is the Seattle based GENELEXR . The test is paid for by most medical insurances and archived on a computer registry to be use with the patient’s permission by their current and future doctor and pharmacist. As a doctor with this science, 21st Century medicine can be practice with a far better outcome than the primitive approach we had taken in the past. Please embrace this technology; it can save your life!
Monday, February 14, 2011
Also azodicarbonamide (ADA) is added to most bread flour. It’s a pesticide from China that’s added to speed up the bleaching process. Pesticides are linked to cancer, reproductive and developmental problems, and nerve damage. It also causes coughs, headaches that can last for days, shortness of breath, wheezing, swollen nasal cavities, burning throat and breathing problems. The United Kingdom, Singapore, Australia and most of Europe ban ADA. The FDA and World Health do not think it a problem yet.
To add insult to injury bread is fortified with iron. Unless you are deficient in this mineral, it increases the incidence of liver cancer and causes hardening of the arteries. To make matters even worse most commercial breads contain high fructose corn syrup, which raises triglyceride levels, leads to obesity and diabetes, and elevates uric acid levels causing hypertension and cardiovascular disease.
GlycoMark® is a blood test, FDA approved in 2003, and now available. It is a new generation test that specifically targets glucose response above the renal threshold (about 175) over one to two weeks to give a window on postprandial (after-meal) glucose peaks. That is critical information! This knowledge can improve patient care by targeting the spikes with specific treatments that also have become available. This will prevent dangerous cardiovascular complications in patients who had previously these undetected postprandial serum glucose spikes. It allows patients to seek medical intervention in a more timely manner and when to start or change therapy, empowering them to achieve and maintain control of their disease. . The currently available markers, A1C and fructosamine (like A1C but a two week window) only reflect average glucose, potentially missing the most important hyperglycemic (high blood sugar) excursion that is balanced out by normal or slightly low sugars. The GlycoMark is an alternative marker that acurately reflects postprandial elevations. It is these sudden spikes of glucose that hit hard the sensitive endothelium (lining) of our blood vessels damaging them to form plaque. It is the plaque that not only narrows the vessel but encourages clot formation.
The test uses a natural “in serum” molecule, 1,5-anhydroglucitol (Glycomark) which like glucose, we ingest, is obviously in our blood. During normal blood sugars, the Glycomark is maintained at constant steady state level due to a large body pool and unlike glucose is not metabolized. Normally, in the kidneys, the Glycomark is filtered and completely reabsorbed and therefore neither raised or lowered in our blood under normal conditions. However, with elevated serum glucose concentrations (about 175 – the average renal threshold for glucose), glucose is not completely reabsorbed by the kidney, and serum Glycomark unlike glucose falls due to competiton of renal tubular reabsorption by glucose. Therefore the change in Glycomark depends on both the duration and amount of glucosuria (sugar in the urine). The Glycomark has been shown to reflect daily glycemic excursions in patients with A1Cs at or near goal. Even though the A1C has been validated as marker of risk of both micro- and macrovascular complications, the Glycomark is even better.