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Yoga

yogawomanIf there exists such a philosophical regime that can bring a person closer to Elysium in every aspect of life—balance, health, aging—its enthusiasts argue that it is yoga.  Investigations into the complexities of this physical / mental / spiritual discipline have focused on the almost inexplicable efficacy of its practice.  That it is conjectured to effect a return to normal following a physical or mental derangement deserves at least a little attention.

The cognitive behaviors of yoga entail calorie restriction, meditation, breathing techniques and additional practices that separate it from other holistic modalities, and have a distinct affect on the function of the human body.  Research at the Albert Einstein College of Medicine, in New York, has classified yoga’s influence on human physiology into four categories that encompass humoral factors (affecting immunity), CNS activity, cell trafficking, and bioelectromagnetism (the study of membrane and action potential).  The investigators allowed that, “…yogic practices might optimize health, delay aging, and ameliorate chronic illness and stress from disability.”  (Kuntsevich. 2010)  A reductionist approach tries to explain complex matters by using the simplest of its facets and nomenclature, but this cannot address the intricacy of yoga and its long-term benefits to the whole person.

From lower back pain, arthritis and carpal tunnel syndrome, all the way to functional development in children, yoga has been an oft-visited body of knowledge.  Practicing yoga increases flexibility, strength and stamina, and can do that in the gentlest of manners using Hatha techniques, or by employing the more explosive Ashtanga form, which relies on quick movements from one pose to another.

Because lower back pain cannot satisfactorily be treated with surgery and injections, other interventions have been pursued, yoga paramount among them.  Chronic back pain has a significant impact on a person’s ability to work and perform daily tasks.  The fact that pain is non-specific makes some therapies uncertain, but the physical motions of yoga meet the need for non-invasive remediation.  (Carter. 2011)  Perhaps it is such that synovial lubrication is enhanced, or that directed movements create healing substances at the cellular level.  Whatever the reason, it works.

If yoga intensifies a person’s awareness of his body and helps him to understand his relationship to a body in pain, with the expectation of attenuating discomfort, then the discipline has been effective, particularly in changing cognitions and behaviors towards nociception.  (Tul. 2011)  Modified forms of Hatha yoga have been tested on such patients with outcomes that were not surprising.  Not only were flexibility and reach improved, but also the emotional insults that accompany refractory pain, such as anxiety and mild depression, were reduced, as reported in a study performed at the Richard Stockton College of New Jersey, providing renewed interest in additional study on the salubrious nature of yoga.  (Galantino.  2004)

Recent work at Johns Hopkins examined prior studies on yoga’s application to arthritis, and found that evidence was strong for reduced disease symptoms and disability, especially the tender and swollen joints that characterize the condition.  (Haaz.  2011)  Noting that it can be tailored to the specific needs of the geriatric population, investigators at the University of Pittsburgh concluded that yoga is among the mind-body interventions associated with reduced pain perception.  (Morone.  2007)

Executive function in a human being is that capacity to make decisions in novel situations, outside the domain of normal automatic processes.  This is tantamount to thinking outside the box, and appears to be a desirable developmental milestone in children.  Yoga is just one of the activities that can help to develop such a trait, one that telegraphs creativity, flexibility, self-control, and self-discipline.  The physical benefits are the cherry on top.  (Diamond. 2011)

It is accepted that what enters a pregnant woman’s digestive system has an effect on the neonate, as well as on the mother.  Could mind-body processes do the same?  There is evidence that improvement in perceived stress, mood, and perinatal outcomes may be realized from practicing yoga.  Not only that, but also it was found that such practices resulted in higher birth weight, less time in labor, and fewer instrument-assisted births, accompanied by lower stress and anxiety levels in both mother and child.  (Beddoe. 2008)  Good news, eh?

Other health issues that benefit from yogic practices include metabolic syndrome (Anderson.  2011), chronic obstructive pulmonary disease (Fulambarker.  2010), and essential hypertension (Anand.  1999).  Each deserves additional attention.

References

Kuntsevich V, Bushell WC, Theise ND.
Mechanisms of yogic practices in health, aging, and disease.
Mt Sinai J Med. 2010 Sep-Oct;77(5):559-69.

Carter C, Stratton C, Mallory D.
Yoga to treat nonspecific low back pain.
AAOHN J. 2011 Aug;59(8):355-61; quiz 362.

Tul Y, Unruh A, Dick BD.
Yoga for chronic pain management: a qualitative exploration.
Scand J Caring Sci. 2011 Sep;25(3):435-43. doi: 10.1111/j.1471-6712.2010.00842.x.

Galantino ML, Bzdewka TM, Eissler-Russo JL, Holbrook ML, Mogck EP, Geigle P, Farrar JT.
The impact of modified Hatha yoga on chronic low back pain: a pilot study.
Altern Ther Health Med. 2004 Mar-Apr;10(2):56-9.

Haaz S, Bartlett SJ.
Yoga for arthritis: a scoping review.
Rheum Dis Clin North Am. 2011 Feb;37(1):33-46.

Morone NE, Greco CM.
Mind-body interventions for chronic pain in older adults: a structured review.
Pain Med. 2007 May-Jun;8(4):359-75.

Diamond A, Lee K.
Interventions shown to aid executive function development in children 4 to 12 years old.
Science. 2011 Aug 19;333(6045):959-64.

Beddoe AE, Lee KA.
Mind-body interventions during pregnancy.
J Obstet Gynecol Neonatal Nurs. 2008 Mar-Apr;37(2):165-75.

Anderson JG, Taylor AG.
The metabolic syndrome and mind-body therapies: a systematic review.
J Nutr Metab. 2011;2011:276419.

Fulambarker A, Farooki B, Kheir F, Copur AS, Srinivasan L, Schultz S.
Effect of Yoga in Chronic Obstructive Pulmonary Disease
Am J Ther. 2010 Oct 22.

Anand MP.
Non-pharmacological management of essential hypertension.
J Indian Med Assoc. 1999 Jun;97(6):220-5.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Zinc Away Your Inflammation

coin-pailWhen you put your hand into your pants pocket and shake it around, you can hear the jingling of loose change. No change, no jingle. You have identified a deficit. It’s not that easy with some nutrient deficits. Zinc is one of them. Although zinc levels are low in some disorders, the most reliable method for diagnosing zinc deficiency is a positive response to zinc supplementation.  Most of the zinc in the body is held in skeletal muscle and bone, so we’re not likely to notice a shortage right away because there are no signs. Growth retardation, low insulin levels, anorexia, mental fog, rough skin, and decreased thyroid function are symptoms, but these may also be related to other causes.  Worldwide, zinc deficiency is not uncommon, though it is rare in the United States. Nonetheless, it’s a good idea to make sure your buckets are filled.

Functionally, zinc is part of more than a hundred different enzymes that catalyze important chemical reactions. Structurally, it helps to build proteins and cell membranes. In fact, there is a component call a zinc-finger that stabilizes protein complexes and helps to regulate gene expression by binding to DNA. Loss of this mineral from the cell membrane opens it to insult from oxidative damage.

What was once considered hyperbolic in promoting zinc as treatment for illnesses such as colds and related respiratory concerns is now being examined as practicable. One of the body’s protective reactions to attack by irritation, infection or injury is inflammation, characterized by redness, swelling, discomfort and, occasionally, loss of function.  Inflammation will activate platelets and attract monocytes/macrophages to swallow up harmful foreign particles. If it becomes chronic, inflammation can grow increasingly destructive of healthy tissue while it tries to heal that tissue already under attack. Out-of-control inflammation can become a threat to life.

As an intermediary in the inflammatory process, zinc helps to control the ardor with which the body fights infections and other physiological troublemakers. Current research has learned that zinc modulates inflammation by connecting with, and impeding, the function of specific protein instigators. This work has focused on the context of sepsis, which is a systemic response to infection that can be devastating enough to cause death. This septic condition has a name—Systemic Inflammatory Response Syndrome (SIRS). What often follows is depressed organ function—Multiple Organ Dysfunction Syndrome (MODS)—and consequent death.  Nuclear factor-kappa Beta, known as NF-kB, is a protein that acts as a transcription factor, and is especially active in responses to stressors like free radicals, radiation, bacterial and viral antigens, and cytokines. The latter initiate an immune response and include chemicals such as interferons and interleukins. In NF-kB is not kept in check, it can wreak more havoc than Attila the Hun.

In the presence of adequate zinc levels, NF-kB activity is downregulated and pro-inflammatory response is controlled (Liu, 2013). This doesn’t necessarily mean that zinc is a cure-all, since its paucity will telegraph other mineral insufficiencies, as well. Laboratory animals suffering induced zinc deficiency while being exposed to sepsis have responded with systemic inflammation and subsequent damage to vital organs, resulting in predicted mortality. In these instances NF-kB was overexpressed, appearing especially active in the respiratory system. Zinc supplementation administered immediately prior to the initiation of sepsis was able to stave off morbidity and mortality (Bao, 2010).

When a pathogen attacks the body, monocytes are the first line of defense. One job is to awaken the sleeping giant and to get the immunity ball rolling. This is when NF-kB enters the nucleus and unlocks the door so zinc can cross the cell membrane. When the zinc merges with a protein ally, it calms down the NF-kB to prevent runaway inflammation. The balance of activity in this drama is delicate, meaning that more (zinc) is not necessarily better. Even a modest deficiency, though, will invite immune dysfunction and increase the chance for infection from whatever is floating around.  The medical, social and academic venues that host crowds of people, such as hospitals, churches and schools can test your susceptibility, which increases with age by virtue of failure to tend to personal needs for lack of motivation and, perhaps, wherewithal.

Though zinc toxicity can be caused by drinking from galvanized containers, it’s more likely to come from overzealous supplementation or from ingesting multiple sources that contain zinc. That includes food as well as supplements. Abdominal pain, diarrhea, nausea and vomiting are the initial signs of overdose. Chronic excess will interrupt copper metabolism and disrupt a raft of physiological functions that include making red blood cells and myelin, and regulating some gene functions. Adults need only eleven milligrams a day; forty is pushing the envelope. Half-dozen oysters provide more than seventy-five milligrams.  Even denture adhesives contain enough zinc to cause symptoms of toxicity if combined with dietary and supplement sources. Taking zinc with a quinolone or tetracycline antibiotic will reduce the absorption of both the zinc and the drug. This also will happen with some medications used for rheumatoid arthritis.  Nasal sprays containing zinc can cause irreversible loss of smell, which can be dangerous if you can’t detect a gas leak. Being stored throughout the body, zinc is a permanent resident; so once again, it’s a matter of balance.

References

Bao B, Prasad AS, Beck FW, Snell D, Suneja A, Sarkar FH, Doshi N, Fitzgerald JT, Swerdlow P.
Zinc supplementation decreases oxidative stress, incidence of infection, and generation of inflammatory cytokines in sickle cell disease patients.
Transl Res. 2008 Aug;152(2):67-80.

Bao S, Liu MJ, Lee B, Besecker B, Lai JP, Guttridge DC, Knoell DL.
Zinc modulates the innate immune response in vivo to polymicrobial sepsis through regulation of NF-kappaB.
Am J Physiol Lung Cell Mol Physiol. 2010 Jun;298(6):L744-54.

Barceloux DG.
Zinc.
J Toxicol Clin Toxicol. 1999;37(2):279-92.

Besecker BY, Exline MC, Hollyfield J, Phillips G, Disilvestro RA, Wewers MD, Knoell DL.
A comparison of zinc metabolism, inflammation, and disease severity in critically ill infected and noninfected adults early after intensive care unit admission.
Am J Clin Nutr. 2011 Jun;93(6):1356-64.

Freake HC, Govoni KE, Guda K, Huang C, Zinn SA.
Actions and interactions of thyroid hormone and zinc status in growing rats.
J Nutr. 2001 Apr;131(4):1135-41.

Lang C, Murgia C, Leong M, Tan LW, Perozzi G, Knight D, Ruffin R, Zalewski P.
Anti-inflammatory effects of zinc and alterations in zinc transporter mRNA in mouse models of allergic inflammation.
Am J Physiol Lung Cell Mol Physiol. 2007 Feb;292(2):L577-84.

Liu MJ, Bao S, Gálvez-Peralta M, Pyle CJ, Rudawsky AC, Pavlovicz RE, Killilea DW, Li C, Nebert DW, Wewers MD, Knoell DL.
ZIP8 Regulates Host Defense through Zinc-Mediated Inhibition of NF-κB.
Cell Rep. 2013 Feb 8. pii: S2211-1247(13)00016-8.

Knoell DL, Liu MJ.
Impact of zinc metabolism on innate immune function in the setting of sepsis.
Int J Vitam Nutr Res. 2010 Oct;80(4-5):271-7.

Lang C, Murgia C, Leong M, Tan LW, Perozzi G, Knight D, Ruffin R, Zalewski P.
Anti-inflammatory effects of zinc and alterations in zinc transporter mRNA in mouse models of allergic inflammation.
Am J Physiol Lung Cell Mol Physiol. 2007 Feb;292(2):L577-84.

O’Dell BL.
Role of zinc in plasma membrane function.
J Nutr. 2000 May;130(5S Suppl):1432S-6S.

Overbeck S, Rink L, Haase H.
Modulating the immune response by oral zinc supplementation: a single approach for multiple diseases.
Arch Immunol Ther Exp (Warsz). 2008 Jan-Feb;56(1):15-30.

Prasad AS.
Zinc: role in immunity, oxidative stress and chronic inflammation.
Curr Opin Clin Nutr Metab Care. 2009 Nov;12(6):646-52. doi: 10.1097/MCO.0b013e3283312956.

Sandström B.
Micronutrient interactions: effects on absorption and bioavailability.
Br J Nutr. 2001 May;85 Suppl 2:S181-5.

Vasto S, Mocchegiani E, Candore G, Listì F, Colonna-Romano G, Lio D, Malavolta M, Giacconi R, Cipriano C, Caruso C.
Inflammation, genes and zinc in ageing and age-related diseases.
Biogerontology. 2006 Oct-Dec;7(5-6):315-27.

Vasto S, Mocchegiani E, Malavolta M, Cuppari I, Listì F, Nuzzo D, Ditta V, Candore G, Caruso C.
Zinc and inflammatory/immune response in aging.
Ann N Y Acad Sci. 2007 Apr;1100:111-22.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Arthritis and Common Chemicals

arthritisMerely because something is hereditary doesn’t mean it has to be inherited unless it’s a defined, overt physical characteristic, such as eye color or hairline. Disease or propensity for disease does not have to telegraph itself through gene expression. In the belief that genetic activity can be turned on and off, more than a handful of scientists are convinced that arthritis, in this case, does not have to pass from seed to seed along the family tree. Arthritis, the osteo- kind, can be spawned from unseen environmental assaults, namely perfluorinated chemicals, which are fluorocarbon derivatives. You remember fluorocarbons. They’re part of the chlorofluorocarbons (CFC’s) once used as propellants in spray cans and in refrigerant fluids. Although they aren’t used for aerosol sprays any more, they’re still in the marketplace. When released into the atmosphere, CFC’s affect stratospheric ozone, the depletion of which is implicated in the rise of skin diseases and climate change, not to mention depressed growth in plants and interrupted photosynthesis. Photosynthesis is important only to those of us who need to eat. Fluorocarbons are bioaccumulative—they are stored in the body.

Of special concern are perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS). (Aren’t abbreviations great?) What in the world are these things used for? If what you own resists stains and water, it probably contains one of these. Ever hear of Scotchgard? How about stone or tile sealers? Got your new sofa treated against kids’ spillage? Fast food wrappers don’t leak grease, do they? Gunk doesn’t stick to dental floss, does it? Ever do any plumbing and use Teflon tape to help seal a joint? Oh, yeah, got Teflon? The oxygen atoms on these chemicals help them to bind proteins to fatty acids or hormone substrates such as albumin, and to nuclear receptors that regulate genes, such as PPAR’s (Anitole, 2007) (Cheng, 2008). Their half-life is about three years. Production of these nifty chemicals has declined for safety reasons, ahem, but exposure remains widespread.

PFOA, especially, is associated with infertility (Fei, 2009) (Joensen, 2009) and ADD/ADHD in young adolescents (Hoffman, 2010). But its association with osteoarthritis concerns us at this time. Fluorine (chemical symbol F) is a corrosive gas that reacts with practically everything else in the periodic table except the noble gases, which happen to be so noble that they don’t mix with anything. If fluorine mixes with something else, it’s now a fluoride. On teeth, from the outside, fluoride is O.K. From inside the body, it’s not. That’s why the toothpaste label says not to swallow it. Fluoride usually enters the body either by inhalation or ingestion. (Did you know that tea contains fluoride? We’ll get to that in a minute.)

F reacts with hydrochloric acid in the stomach to form hydrofluoric acid (HF), which just so happens to be the precursor to Prozac. This acid passes to the liver, but evades phase 1 detoxification, where the liver uses O2 and enzymes to oxidize toxins to make them water-soluble. This short circuit occurs because fluorine is the strongest oxidizer currently known. At this point, hydrofluoric acid passes into the bloodstream and is distributed to all body parts, including bones. Now, bones are made from calcium compounds, particularly carbonated hydroxyapatite. When an acid and a base combine, they form a salt. Hydrofluoric acid mixes with the calcium (alkaline) to form CaF2, an insoluble salt. That increases density of bone, but lowers strength. The bone is less elastic and more prone to fractures. As bone thickens, it restricts mobility. To compound matters, factors that acidify the urine increase the retention of fluoride. However, happily, the opposite is also true. Absorption of fluoride is reduced by calcium (Whitford, 1994).

Tea may pose problems for heavy tea drinkers. Being labeled a heavy tea drinker is not common in the United States unless you earn membership in the gallon-a-day club. Tea plants readily absorb fluoride—and aluminum—from soil. Therefore, the beverage will contain various levels of fluoride, depending on soil levels. Brewed black tea in the States contains about 3 to 4 parts per million (which is practically identical to milligrams per liter); commercial iced tea has between 1 and 4 (Whyte, 2006) (Whitford, 1994) (Izuora, 2011). The number of skeletal fluorosis reports has grown in recent years, but that has been seen mostly in people who consumed 20 milligrams of fluoride a day for decades. In the mean time, 5 milligrams a day (That would be about a quart a day.) can present preclinical stages of fluorosis, so what has been diagnosed as arthritis may actually be skeletal fluorosis. Though this problem is more extensive in the tea cultures of Asia, it’s still a good idea to drink tea in moderation.

Getting back to PFOA and PFOS, levels in humans vary widely. Certain occupations can increase exposure thousands of times, especially for those working in chemical, metal refining and power plants. Drinking water contaminated with these chemicals contributes to human misery as much as direct exposure. Some American states have ground water that contains either naturally occurring fluoride compounds or the wastes from industrial sources. Ohio and West Virginia are two. In areas such as these, osteoarthritis prevalence exceeds that in other regions. Though a terrible affliction for anyone, women seem to be affected more than men. Cartilage damage and inflammatory responses are part of the spectrum (Uhl, 2013).

If you start to feel aches and pains that are new to you, take a look at what you’re been wearing, where you’ve been, and what you ate and drank. Stain resistant trousers and shirts, high intake of black and green teas, and the wrappers from the fast-food joint might be the cause. (See http://www.bodybio.com/content.aspx?page=Enhancing-the-worst)  Global production of these substances has been on the wane, but leftovers still occupy the environment. Substitute compounds are no doubt in the future, but now we have to be concerned about their long-term effects. Although research is sketchy, iodine, calcium, magnesium and boron are being studied as antidotes to fluoride toxicity (Kao, 2004) (Heard, 2001).

References

Cao J, Bai X, Zhao Y, Liu J, Zhou D, Fang S, Jia M, Wu J.
The relationship of fluorosis and brick tea drinking in Chinese Tibetans.
Environ Health Perspect. 1996 Dec;104(12):1340-3.

Cao J, Zhao Y, Liu J, Xirao R.
[Brick-tea type adult bone fluorosis].
Wei Sheng Yan Jiu. 2003 Mar;32(2):141-3.

Cao J, Zhao Y, Liu J, Xirao R, Danzeng S, Daji D, Yan Y.
Brick tea fluoride as a main source of adult fluorosis.
Food Chem Toxicol. 2003 Apr;41(4):535-42.

Cheng X, Klaassen CD.
Perfluorocarboxylic acids induce cytochrome P450 enzymes in mouse liver through activation of PPAR-alpha and CAR transcription factors.
Toxicol Sci. 2008 Nov;106(1):29-36.

Czerwinski E, Nowak J, Dabrowska D, Skolarczyk A, Kita B, Ksiezyk M.
Bone and joint pathology in fluoride-exposed workers.
Arch Environ Health. 1988 Sep-Oct;43(5):340-3.

Fei C, McLaughlin JK, Lipworth L, Olsen J.
Maternal levels of perfluorinated chemicals and subfecundity
Hum Reprod. 2009 May;24(5):1200-5.

Grandjean P, Thomsen G.
Reversibility of skeletal fluorosis.
Br J Ind Med. 1983 Nov;40(4):456-61.

Hayacibara MF, Queiroz CS, Tabchoury CP, Cury JA.
Fluoride and aluminum in teas and tea-based beverages.
Rev Saude Publica. 2004 Feb;38(1):100-5.

Heard K, Hill RE, Cairns CB, Dart RC.
Calcium neutralizes fluoride bioavailability in a lethal model of fluoride poisoning.
J Toxicol Clin Toxicol. 2001;39(4):349-53.

Hoffman K, Webster TF, Weisskopf MG, Weinberg J, Vieira VM.
Exposure to polyfluoroalkyl chemicals and attention deficit/hyperactivity disorder in U.S. children 12-15 years of age
Environ Health Perspect. 2010 Dec;118(12):1762-7.

Izuora K, Twombly JG, Whitford GM, Demertzis J, Pacifici R, Whyte MP.
Skeletal fluorosis from brewed tea.
J Clin Endocrinol Metab. 2011 Aug;96(8):2318-24.

Joensen UN, Bossi R, Leffers H, Jensen AA, Skakkebaek NE, Jørgensen N.
Do perfluoroalkyl compounds impair human semen quality?
Environ Health Perspect. 2009 Jun;117(6):923-7.

Kao WF, Deng JF, Chiang SC, Heard K, Yen DH, Lu MC, Kuo BI, Kuo CC, Liu TY, Lee CH.
A simple, safe, and efficient way to treat severe fluoride poisoning–oral calcium or magnesium.
J Toxicol Clin Toxicol. 2004;42(1):33-40.

Kavanagh D, Renehan J.
Fluoride in tea–its dental significance: a review.
J Ir Dent Assoc. 1998;44(4):100-5.

Kurland ES, Schulman RC, Zerwekh JE, Reinus WR, Dempster DW, Whyte MP.
Recovery from skeletal fluorosis (an enigmatic, American case).
J Bone Miner Res. 2007 Jan;22(1):163-70.

Lau C, Anitole K, Hodes C, Lai D, Pfahles-Hutchens A, Seed J.
Perfluoroalkyl acids: a review of monitoring and toxicological findings.
Toxicol Sci. 2007 Oct;99(2):366-94.

Luo Rui, Liu Ri-guang1, Ye Chuan, Yu Yan-ni, Guan Zhi-zhong
Total knee arthroplasty for the treatment of knee osteoarthritis caused by endemic skeletal fluorosis
Chinese Journal of Tissue Engineering Research. Feb 26, 2012; 16 (9): 1555-1558

Petrone P, Giordano M, Giustino S, Guarino FM.
Enduring fluoride health hazard for the Vesuvius area population: the case of AD 79 Herculaneum.
PLoS One. 2011;6(6):e21085.

Savas S, Cetin M, Akdoğan M, Heybeli N.
Endemic fluorosis in Turkish patients: relationship with knee osteoarthritis.
Rheumatol Int. 2001 Sep;21(1):30-5.

Howard Thomas
Some Non-essential Aerosol Propellant Uses Finally Banned
Federal Regulations:  43 F. R. 11301 (1978)
http://lawlibrary.unm.edu/nrj/19/1/16_thomas_some.pdf

Sarah A. Uhl, Tamarra James-Todd, and Michelle L. Bell
Association of Osteoarthritis with Perfluorooctanoate and Perfluorooctane Sulfonate in NHANES 2003–2008
Environ Health Perspect. February 14, 2013

Whitford GM.
Intake and metabolism of fluoride.
Adv Dent Res. 1994 Jun;8(1):5-14.

Whitford GM.
Fluoride metabolism and excretion in children.
J Public Health Dent. 1999 Fall;59(4):224-8.

Whyte MP.
Fluoride levels in bottled teas.
Am J Med. 2006 Feb;119(2):189-90.

Wong MH, Fung KF, Carr HP.
Aluminium and fluoride contents of tea, with emphasis on brick tea and their health implications.
Toxicol Lett. 2003 Jan 31;137(1-2):111-20.

Xiangjin Ge, Yuting Jiang, Guohua Tang, Meilie Zhang, Yurong Zhao
Investigations on the Occurrence of Osteoarthritis in Middle-aged and Elderly Persons in Fluorosis Afflicted Regions of Gaomi City with High Fluoride Concentration in Drinking Water
Preventive Medicine Tribune. Volume 12, No. 1;  January 2006:  pp. 57-58 ·57·

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

What’s A Nice Bone Like You Doin’ In A Joint Like This? (Part 1)

joint-pain-manIt hurts. It hurts when I get out of bed. It hurts when I bend down to pick up the laundry basket. Ooh, my knees! Yow, my shoulder! What’s goin’ on?

Could it be arthritis, the affliction of the musculoskeletal system that attacks the joints and is the main cause of disability among people over fifty-five years of age? Maybe so. The word comes from the Greek arthron, meaning “joint,” and the Latin itis, meaning “inflammation.”  Aha! Inflammation. Drat! Where did that come from?

Arthritis is not a single disease, but one that covers almost a hundred conditions, the most common being osteoarthritis, which generally affects older folks. Some forms, though, can strike at any age—even very young.

Of course, you know what a joint is. It’s held together by ligaments, the elastic bands that keep bones in place when you move. The surface of each bone is covered with cartilage to keep the bones from rubbing directly against each other, allowing smooth, painless movement. At least that’s how it’s supposed to work. The joint is surrounded by a kind of capsule that contains synovial fluid, which is secreted by membranes inside joint cavities, tendon sheaths and bursae (always found at friction points) to provide lubrication. If you have arthritis something goes wrong with the machinery, and what goes wrong depends on the kind of arthritis you have. It could be that the cartilage is wearing thin, or that fluid is in short supply, or that there is an infection, or that the body is attacking itself in an autoimmune response. It might even be a combination of these factors.

Of the many types of arthritis, osteo- is probably the best known and most often treated. This is where we will focus—after a brief rundown of the other types. (Otherwise, this would take lots of room. Look for separate mention in future musings.) Osteoarthritis is characterized by cartilage that loses elasticity and shock absorption. As cartilage wears down, tendons and ligaments stretch, causing discomfort. Eventually, bone rubs against bone, causing considerable pain. Symptoms start slowly and develop over time, getting worse. Stiffness, especially in the A.M., might go away with use of the joint. Sometimes spurs appear around the joint; sometimes swelling, too. Hands, knees, hips and the spine are worst hit.

Rheumatoid arthritis is downright inflammatory. Here, the synovial membrane is attacked, resulting in swelling and agony. Untreated, it can cause deformity. More common in women than men, RA usually strikes between ages 40 and 60, but young children may also be afflicted. Here, the same joints in each side of the body are painfully swollen, inflamed and stiff. Fingers, arms, legs and wrists are the most common targets. Hands may be red and puffy, and tender when touched. The smaller joints are noticeably affected first.

The signs of infectious arthritis, another type, include fever, joint swelling and of course, inflammation. Tenderness or sharp pain is common. Often these symptoms are linked to an injury or another illness. Most often, only a single joint is affected. Bacterial or viral invasion of the synovial tissue might be at the root.

Juvenile rheumatoid arthritis (JRA) attacks children under sixteen and presents as one of three types: pauciarticular, which is mildest; polyarticular, which is more severe; and systemic, which is the least common, but the worst because it can affect organs. With this form, there will be intermittent fevers that spike at night and suddenly disappear. Appetite and weight will fall. Blotchy rashes may appear on the extremities, and joints will swell and remain larger than normal.

The medications used to treat arthritis vary according to the type of arthritis. Analgesics help to fight pain, but do not necessarily address inflammation. Tylenol is one, but prescription narcotics may be recommended in some cases. Nonsteroidal anti-inflammatory drugs (NSAIDS) reduce both pain and inflammation. Ibuprofen and naproxen are available over the counter, and some require a prescription. These can cause stomach upset. Rub-on creams and ointments containing capsaicin, the component that makes hot peppers hot, are called counterirritants. Sometimes they work; sometimes not. Biological medicines are genetically engineered to target specific proteins involved in an immune response. You see ads for these on TV. Each of these different kinds of medications can have unpleasant side effects, ranging from simple gastric distress to susceptibility to serious infections to cardiac involvement. To add insult to injury, you have to stay out of the sun. So much for trips to the beach. We can’t forget steroids, such as cortisone. They can reduce pain, but they also reduce vitamin and mineral levels in the body, especially calcium.

Are there alternatives to drugs? Yes. The one most often used is glucosamine, often accompanied by chondroitin. Glucosamine works by stimulating the metabolism of chondrocytes—the cartilage cells—and the cells that make synovial fluid. Chondroitin is found in cartilage tissue, where it serves as the substrate for the joint matrix and works to pull water into the joint. When money is available for research, integrative therapies may be tested against allopathic treatments and placebos. Some results are real eye-openers, while others are ho-hum. Not only is glucosamine alone, as well as combined with chondroitin, well-tolerated, but also as effective as commonly used pharmaceutical interventions, and faster acting than any placebo (Lopes, 1982). A characteristic of natural treatments for an ailment is that, since they come from plants or animals as opposed to chemicals, they take longer to evoke a positive response. In a head-to-head comparison with ibuprofen, glucosamine did a better job of ameliorating pain after eight weeks of treatment than did the drug (Lopes, 1982), and did so for a larger group of people (Pujalte, 1980). As the quality of most merchandise varies from maker to maker along the continuum, so does the quality of supplements, realizing that cost is not the best indicator of grade (McAlindon, 2000). But, in the long run, glucosamine seems to be an ally in modifying the course of osteoarthritis (Reginster, 2001) and in maintaining (and even improving) structural integrity of knee joints (Bruyere, 2004). Drugs come with caveats, but so, too, do alternatives. It is not a good idea to take a supplement without at least a little guidance from someone who knows the territory, such as an integrative dietitian, a holistic-oriented physician, or some other credentialed practitioner. People don’t generally know that glucosamine could increase eye pressure in those with glaucoma. That’s the last thing they need (Murphy, 2013). And if you take a blood thinner or an aspirin a day, be careful about taking chondroitin because its chemistry is close to that of heparin and that could increase bleeding risk (Rozenfeld, 2004).

SAM-e, S-Adenosyl Methionine, is a naturally-occurring molecule distributed throughout the body that diminishes as we get older. It plays a role in more than a hundred biochemical reactions involving methylation, where it contributes to hormones, neurotransmitters, nucleic acids, proteins and phospholipids. In an early study of SAM-e effectiveness in treating osteoarthritis of the knee, hip and spine, patients found relief from morning stiffness, pain at rest and pain at movement in the first few weeks of the trial, which lasted for twenty-four months. No adverse effects were reported and none of the subjects dropped out (Konig, 1987). Mild nausea may occur with SAM-e, but that inconvenience is more bearable than the effects of drugs like Indomethacin (Vetter, 1987). What’s more, SAM-e has virtues beyond arthritis treatment. Remember that we mentioned the slowness of natural substance results. In a test at the University of California, it was learned that SAM-e is equal to celecoxib (Celebrex®) in the management of knee osteoarthritis, but slower in onset of action (Najm, 2004). If there is a problem with SAM-e, it’s the cost. However, the result is worth the outlay.

Prostaglandins are chemicals in the body that regulate several functions, including inflammation and vascular permeability. Some can start the inflammation ball rolling, while others can interrupt it. The activity of these proteins can be modulated by essential fatty acids in the omega-3 family, notably EPA, a component of fish oil and the downstream product of the alpha linolenic acid common to flaxseed oil. We know that essential fatty acids are just that—essential, meaning they must come from food or supplements because the body cannot make them. Decades-long studies have pronounced the efficacy of omega-3 fats in the management of arthritis—and other inflammatory conditions—by virtue of their capacity to tone down the pro-inflammatory and to lift up the anti-inflammatory substances that alleviate pain (Hurst, 2010) (Zainal, 2009).  A Welsh study performed at the beginning of the century noticed that n-3 fats, in a dose-dependent manner, were able to abolish the expression of pro-inflammatory mediators via a mechanism different from that of other polyunsaturated fatty acids (Curtis, 2002). Later study, also in the British Isles, found that n-3 fats reduced arthritic disease in laboratory animals inclined to suffer it (Knott, 2011). When glucosamine and n-3 fats were combined, the positive results were declared superior (Gruenwald, 2009).

Avoiding sugary foods and refined grains, and limiting red meats can do much to ease arthritic discomfort. Losing weight also helps by reducing stress on knees and hips, where the extra pounds squeeze cartilage into oblivion. Although moderate alcohol consumption is associated with decreased risk of arthritis, especially rheumatoid, it’s not recommended as a treatment. Nor is it a reason to start drinking (DiGiuseppe, 2012).

References

Bruyere O, Pavelka K, Rovati LC, Deroisy R, Olejarova M, Gatterova J, Giacovelli G, Reginster JY.
Glucosamine sulfate reduces osteoarthritis progression in postmenopausal women with knee osteoarthritis: evidence from two 3-year studies.
Menopause. 2004 Mar-Apr;11(2):138-43.

Curtis CL, Rees SG, Little CB, Flannery CR, Hughes CE, Wilson C, Dent CM, Otterness IG, Harwood JL, Caterson B.
Pathologic indicators of degradation and inflammation in human osteoarthritic cartilage are abrogated by exposure to n-3 fatty acids.
Arthritis Rheum. 2002 Jun;46(6):1544-53.

Daniela Di Giuseppe, Lars Alfredsson, Matteo Bottai, Johan Askling, Alicja Wolk
Long term alcohol intake and risk of rheumatoid arthritis in women: a population based cohort study
BMJ 2012;345:e4230

Delle Chiaie R, Pancheri P, Scapicchio P.
Efficacy and tolerability of oral and intramuscular S-adenosyl-L-methionine 1,4-butanedisulfonate (SAMe) in the treatment of major depression: comparison with imipramine in 2 multicenter studies.
Am J Clin Nutr. 2002 Nov;76(5):1172S-6S.

Gruenwald J, Petzold E, Busch R, Petzold HP, Graubaum HJ.
Effect of glucosamine sulfate with or without omega-3 fatty acids in patients with osteoarthritis.
Adv Ther. 2009 Sep;26(9):858-71.

Hedbom E, Häuselmann HJ.
Molecular aspects of pathogenesis in osteoarthritis: the role of inflammation.
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Hurst S, Zainal Z, Caterson B, Hughes CE, Harwood JL.
Dietary fatty acids and arthritis.
Prostaglandins Leukot Essent Fatty Acids. 2010 Apr-Jun;82(4-6):315-8.

Knott L, Avery NC, Hollander AP, Tarlton JF.
Regulation of osteoarthritis by omega-3 (n-3) polyunsaturated fatty acids in a naturally occurring model of disease
Osteoarthritis Cartilage. 2011 Sep;19(9):1150-7.

König B.
A long-term (two years) clinical trial with S-adenosylmethionine for the treatment of osteoarthritis.
Am J Med. 1987 Nov 20;83(5A):89-94.

Laudanno OM.
Cytoprotective effect of S-adenosylmethionine compared with that of misoprostol against ethanol-, aspirin-, and stress-induced gastric damage.
Am J Med. 1987 Nov 20;83(5A):43-7.

Lopes Vaz A.
Double-blind clinical evaluation of the relative efficacy of ibuprofen and glucosamine sulphate in the management of osteoarthrosis of the knee in out-patients.
Curr Med Res Opin. 1982;8(3):145-9.

Maccagno A, Di Giorgio EE, Caston OL, Sagasta CL.
Double-blind controlled clinical trial of oral S-adenosylmethionine versus piroxicam in knee osteoarthritis.
Am J Med. 1987 Nov 20;83(5A):72-7.

McAlindon TE, LaValley MP, Gulin JP, Felson DT.
Glucosamine and chondroitin for treatment of osteoarthritis: a systematic quality assessment and meta-analysis.
JAMA. 2000 Mar 15;283(11):1469-75.

Müller-Fassbender H.
Double-blind clinical trial of S-adenosylmethionine versus ibuprofen in the treatment of osteoarthritis.
Am J Med. 1987 Nov 20;83(5A):81-3.

Ryan K. Murphy, DO, MA; Lecea Ketzler, DO; Robert D. E. Rice, MD; Sandra M. Johnson, MD; Mona S. Doss, MA; Edward H. Jaccoma, MD
Oral Glucosamine Supplements as a Possible Ocular Hypertensive Agent
JAMA Ophthalmol. 2013; May 23:1-3.

Najm WI, Reinsch S, Hoehler F, Tobis JS, Harvey PW.
S-adenosyl methionine (SAMe) versus celecoxib for the treatment of osteoarthritis symptoms: a double-blind cross-over trial. [ISRCTN36233495].
BMC Musculoskelet Disord. 2004 Feb 26;5:6.

Pujalte JM, Llavore EP, Ylescupidez FR.
Double-blind clinical evaluation of oral glucosamine sulphate in the basic treatment of osteoarthrosis.
Curr Med Res Opin. 1980;7(2):110-14.

Reginster JY, Deroisy R, Rovati LC, Lee RL, Lejeune E, Bruyere O, Giacovelli G, Henrotin Y, Dacre JE, Gossett C.
Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomised, placebo-controlled clinical trial.
Lancet. 2001 Jan 27;357(9252):251-6.

Roush JK, Cross AR, Renberg WC, Dodd CE, Sixby KA, Fritsch DA, Allen TA, Jewell DE, Richardson DC, Leventhal PS, Hahn KA.
Evaluation of the effects of dietary supplementation with fish oil omega-3 fatty acids on weight bearing in dogs with osteoarthritis
J Am Vet Med Assoc. 2010 Jan 1;236(1):67-73.

Soeken KL, Lee WL, Bausell RB, Agelli M, Berman BM.
Safety and efficacy of S-adenosylmethionine (SAMe) for osteoarthritis.
J Fam Pract. 2002 May;51(5):425-30.

Towheed TE, Anastassiades TP, Shea B, Houpt J, Welch V, Hochberg MC.
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Towheed TE, Maxwell L, Anastassiades TP, Shea B, Houpt J, Robinson V, Hochberg MC, Wells G.
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Vetter G.
Double-blind comparative clinical trial with S-adenosylmethionine and indomethacin in the treatment of osteoarthritis.
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Zainal Z, Longman AJ, Hurst S, Duggan K, Caterson B, Hughes CE, Harwood JL.
Relative efficacies of omega-3 polyunsaturated fatty acids in reducing expression of key proteins in a model system for studying osteoarthritis.
Osteoarthritis Cartilage. 2009 Jul;17(7):896-905.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

The Rumors on Rheumatoid Arthritis

hands-jarAunt Martha’s mother was the kindest, gentlest soul you’d ever meet. She went out of her way to make you feel at home. Food and drink were hallmarks of her cordial greeting. But she couldn’t open a package, twist open a jar or cut a cake. Her fingers were so badly gnarled that no two pointed in the same direction. Some of the joints formed the letter “Z.” Yet, despite the pain she must have borne, her loving smile prevailed. She was victimized by rheumatoid arthritis (RA) in an era when research was in its infancy, barely crawling.

This nefarious disease causes pain, swelling, stiffness and loss of function in joints— mostly hands and fingers, though it can strike any. It hits women more often than men, starting between ages twenty-five and fifty-five, though some statisticians start at forty. Unlike osteoarthritis, RA is an autoimmune condition that can affect body parts besides joints, such as the eyes, mouth and lungs. Nobody knows the cause. It could be genes, maybe the environment, or maybe hormones that direct the immune system to attack the body’s own tissues. Whatever it is, RA afflicts more than a million Americans, a sizeable fraction being kids.

The inflammation of RA can reach to the tendons, ligaments and muscles in some patients. Its chronic nature causes degradation of cartilage, bone and the ligaments that bind bones, causing deformity. Active disease presents with fatigue, appetite loss, low-grade fever, muscle and joint aches, and stiffness, the last being most notable in the morning or following periods of inactivity. Because RA is a systemic ordeal, its malevolence can inflame the glands around the eyes and mouth, causing Sjögren’s syndrome. RA-induced pleuritis is the inflammation of lung lining that causes pain with a deep breath. Because the number of red blood cells is reduced, anemia occurs, while a drop in white cells can be associated with an enlarged spleen and increased risk of infection.

Following examination of inflammatory blood markers and other criteria, the doctor can make a proper diagnosis, at which time medications probably will be prescribed. Cortisone and aspirin have been first-line drugs for decades because they act quickly. The slower ones are called disease-modifying anti-rheumatic drugs—DMARD’s—and include some heavy duty chemistry, not all of which is anti-inflammatory, but most of which has truly nasty side effects, many you have learned from television ads. What may not be realized is that some drugs destroy the substances your body needs to work the right way. The package insert that comes with the drug doesn’t tell you this, so you’ll think the absence of pain has all the bases covered. This is sufficient reason to visit an integrative dietitian or holistic-minded physician, the rare one who knows about nutrition.

Keeping your physician in the loop, you may opt to explore integrative measures to deal with RA. The good news is that there are recognized mediators of inflammation-induced bone damage (Nanjundaiah, 2013). Because of space constraints, we’ll address those with a pretty reliable track record, starting with gamma linolenic acid (GLA), an omega-6 fatty acid found in borage and evening primrose oils. While it is true that borage contains almost twice the levels of GLA as evening primrose, it is also true that borage contains pyrrolizidine alkaloids that can tax the liver. Though possibly in non-toxic amounts, these alkaloids are nonetheless there.  For that reason, EPO is often a preferred source of GLA. On the other hand, borage oil is used in clinical and observational studies because of its higher GLA values, thus requiring a smaller dosage (that may influence subject participation) and reducing cost. A University of PA study done in the early 90’s found that patients who took borage oil capsules for three months experienced reductions in pro-inflammatory prostaglandins and leukotrienes, leading to noticeable clinical improvement in RA symptoms (Pullman-Mooar, 1990).

Supplementing GLA at 3.0 and 6.0 grams a day enhances its conversion to the anti-inflammatory dihommo-gamma-linolenic-acid (DGLA), causing neutrophils to synthesize less pro-inflammatory leukotriene and platelet-activating factor (PAF—a major trigger of thrombosis), thereby attenuating discomfort (Johnson, 1997).  Compared to placebo in a six-month trial in Philadelphia, GLA was found to reduce the number of tender joints by more than a third and swollen joint count by more than a fourth, in a study from which no one withdrew (Leventhal, 1993).

Not to be outdone by its omega-6 counterpart, omega-3 fish oil flexed its anti-inflammatory muscle in trials that included non-steroidal anti-inflammatory drugs (NSAIDS) as part of the treatment. Swelling index and duration of early morning stiffness were used as markers for RA severity, and were found to have improved in subjective assessment by virtue of a decrease in pro-inflammatory leukotrienes (van der Tempel, 1990). Patients who received fish oil in combination with naproxen fared better in similar assessments than those without the fish oil or with placebo oil in studies carried out in Norway (Kjeldsen-Kragh, 1992) and New York (Kremer, 2000). A Canadian meta-analysis of seventeen n-3 studies concluded that morning stiffness and number of tender joints were reduced in those who used n-3 PUFA’s (Goldberg, 2007). Those who supplemented their OTC medications with omega-3’s from cod liver oil were able to reduce their dependence on NSAIDS (Galarraga, 2008).

In early reports, Danish scientists found that RA patients were deficient in the only mineral with anti-oxidant properties—selenium. They noted that those with the most active disease had the lowest values, and that there is significant correlation of selenium status with the number of affected joints (Tarp, 1985). Almost a decade later, the same researchers confirmed their initial findings, but also found that some subjects lack the physiological wherewithal to convert selenium to functional anti-oxidant enzymes, a state that can be overcome by supplemental mineral (Tarp, 1994).

From frankincense through ginger, to the resveratrol of grapes, science is takinga deliberate look at additions to the arsenal of RA treatments.

References

Astorga G, Cubillos A, Masson L, Silva JJ.
Active rheumatoid arthritis: effect of dietary supplementation with omega-3 oils. A controlled double-blind trial.
Rev Med Chil. 1991 Mar;119(3):267-72.

Galarraga B, Ho M, Youssef HM, Hill A, McMahon H, Hall C, Ogston S, Nuki G, Belch JJ.
Cod liver oil (n-3 fatty acids) as an non-steroidal anti-inflammatory drug sparing agent in rheumatoid arthritis.
Rheumatology (Oxford). 2008 May;47(5):665-9.

Goel, F. J. Ahmad, R. M. Singh, and G. N. Singh
3-Acetyl-11-keto-β-boswellic acid loaded-polymeric nanomicelles for topical anti-inflammatory and anti-arthritic activity
Journal of Pharmacy and Pharmacology, vol. 62, no. 2, pp. 273–278, 2010.

Goldberg RJ, Katz J.
A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain.
Pain. 2007 May;129(1-2):210-23.

Johnson MM, Swan DD, Surette ME, Stegner J, Chilton T, Fonteh AN, Chilton FH.
Dietary supplementation with gamma-linolenic acid alters fatty acid content and eicosanoid production in healthy humans.
J Nutr. 1997 Aug;127(8):1435-44.

Kjeldsen-Kragh J, Lund JA, Riise T, Finnanger B, Haaland K, Finstad R, Mikkelsen K, Førre O.
Dietary omega-3 fatty acid supplementation and naproxen treatment in patients with rheumatoid arthritis.
J Rheumatol. 1992 Oct;19(10):1531-6.

Knekt P, Heliövaara M, Aho K, Alfthan G, Marniemi J, Aromaa A.
Serum selenium, serum alpha-tocopherol, and the risk of rheumatoid arthritis.
Epidemiology. 2000 Jul;11(4):402-5.

Kremer JM.
n-3 fatty acid supplements in rheumatoid arthritis.
Am J Clin Nutr. 2000 Jan;71(1 Suppl):349S-51S.

Lau CS, Morley KD, Belch JJ.
Effects of fish oil supplementation on non-steroidal anti-inflammatory drug requirement in patients with mild rheumatoid arthritis–a double-blind placebo controlled study.
Br J Rheumatol. 1993 Nov;32(11):982-9.

J. H. Lee, H. Jin, H. E. Shim, H. N. Kim, H. Ha, and Z. H. Lee
Epigallocatechin-3-gallate inhibits osteoclastogenesis by down-regulating c-Fos expression and suppressing the nuclear factor-κB signal
Molecular Pharmacology, vol. 77, no. 1, pp. 17–25, 2010.

M. Lei, S. Q. Liu, and Y. L. Liu
Resveratrol protects bone marrow mesenchymal stem cell derived chondrocytes cultured on chitosan-gelatin scaffolds from the inhibitory effect of interleukin-1β
Acta Pharmacologica Sinica, vol. 29, no. 11, pp. 1350–1356, 2008.

Leventhal LJ, Boyce EG, Zurier RB.
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Ann Intern Med. 1993 Nov 1;119(9):867-73.

S. A. Levy, O. Simon, J. Shelly, and M. Gardener
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D. O. Moon, M. O. Kim, Y. H. Choi, Y. M. Park, and G. Y. Kim
Curcumin attenuates inflammatory response in IL-1β-induced human synovial fibroblasts and collagen-induced arthritis in mouse model
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Morinobu, W. Biao, S. Tanaka et al.,
 (-)-Epigallocatechin-3-gallate suppresses osteoclast differentiation and ameliorates experimental arthritis in mice
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Nanjundaiah SM, Astry B, Moudgil KD.
Mediators of inflammation-induced bone damage in arthritis and their control by herbal products.
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Pullman-Mooar S, Laposata M, Lem D, Holman RT, Leventhal LJ, DeMarco D, Zurier RB.
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M. L. Sharma, S. Bani, and G. B. Singh
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Tarp U, Overvad K, Hansen JC, Thorling EB.
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Tarp U.
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van der Tempel H, Tulleken JE, Limburg PC, Muskiet FA, van Rijswijk MH.
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G. Xuzhu, M. Komai-Koma, B. P. Leung, et al.
Resveratrol modulates murine collagen-induced arthritis by inhibiting Th17 and B-cell function
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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

What Gets YOU Inflamed?

knee-inflammationAre you an adult? Would you prefer the pound(s) of cure to the ounce of prevention? One of the sad commentaries about adulthood is that we don’t take care of ourselves until something hurts, the detection of which relies on the nervous system. The nervous system is plastic, meaning that it exhibits a wide range of responses according to different conditions. The perception of pain depends on more than one factor, the environment included. With inflammation, however, there exists a hypersensitivity state that makes us aware of what’s going on. This realization is called nociception, involving a network that identifies a noxious condition that evokes responses ranging from mild to severe. Once the pain message is recognized by the nervous system it registers as an “ouch.” The greater the intensity of the stimulus, the greater is the perception of pain. In some cases, no external trigger is needed, such as one would experience with arthritis pain.

Inflammation is the body’s attempt at self-protection, the intention of which is to remove the harmful stimuli, including damaged cells, irritants or pathogens. If the stimulus comes from outside, it can be removed, although pain may linger. If it comes from inside, the body is left to its own devices. In either instance, tissue repair is the ultimate goal. To our dismay, inflammation may beget further inflammation in a self-perpetuating cascade. This occurs because of cellular alterations that cause mediator chemicals to be released and certain white cells, called macrophages, to become activated. The job of the macrophage is to swallow (-phage) the debris that comes from, or causes, tissue damage. Without inflammation, infections and wounds would never heal. In fact, too much anti-inflammatory medication, such as cortisone, slows wound healing (Goforth, 1980). The innate immunity with which we were born is always at the ready to start the inflammatory cascade and to bring healing.

Signs of overt inflammation include pain, redness, immobility (as in loss of function), swelling, and heat (more blood to the area makes it feel warm). Covert inflammation, occurring with internal organs, does not necessarily present with all these signs. Pain arises when swelling pushes on nerves, but sometimes the brain gets used to it and ignores the stimulus. The risk for inflammatory conditions rises with weight gain, as determined by an increase in white blood cells. Regardless of body mass index, C-reactive protein and homocysteine are markers for the presence of inflammatory state, which is at the center of many disorders, from arthritis, through Crohn’s disease, to various allergies and vitamin deficiencies.

Treatment for inflammation abounds in the world of allopathic medicine. Most of us know about NSAIDS, non-steroidal anti-inflammatory drugs, among which Tylenol is not, but aspirin, naproxen and ibuprofen are. Then, there are the corticosteroids—or just plain steroids—that are naturally made by the body in the adrenal glands. But these guys, given as drugs, prevent phospholipid release, and that undermines the activity of eosinophils, which are designed to fight back against allergy, for example, by releasing histamine.

Of the alternative modalities to address inflammation, ginger has accrued quite a following. For hundreds of years it’s been used to treat gastric distress, including dyspepsia and constipation. Recent research points to ginger’s role as an anti-inflammatory agent in the prevention of colon cancer, where inflammation has been identified as a precursor to the disease (Zick, 2011), the markers of which are pro-inflammatory prostaglandins—primarily PGE2—produced by cyclooxygenase (COX) as an early event in the course of the condition (Jiang, 2012).

In a British examination of pain studies, those suffering from osteoarthritis, dysmenorrhea, and acute muscle pain had been administered ginger as the sole treatment. Though additional rigorous trials are anticipated, these subjects reported a reduction in pain, as cited on subjective assessment tools (Terry, 2011). Even before interest in alternative medicine was accelerated to its present status, scientists scrutinized ginger’s reputation in the Ayurvedic community among people treated with the herb for rheumatic concerns, finding efficacy that paralleled traditional interventions (Srivastava, 1989). Applying oral powdered ginger to generalized musculoskeletal discomfort, Danish physicians realized that the safety factor of ginger far exceeded that of any known drugs, while presenting significant efficacy in the relief of pain and swelling via the inhibition of pro-inflammatory prostaglandins (Srivastava, 1992).

By sequestering these incendiary prostaglandins (PG’s), ginger proves itself to be on a par with NSAIDS, minus the concerns of adverse side effects. Similar to prostaglandins in promoting physical aberrations are leukotrienes, products of an enzyme called lipoxygenase (LOX), like COX an offspring of arachidonic acid metabolism. Leukotrienes generally work within the immune system, while PG’s almost always play a role in pure inflammation and pain. (There are beneficent PG’s, by the way.)  Leukotrienes are signaling molecules that call immune cells to the site of infiltration, as from airborne allergens. Bluntly, ginger suppresses the synthesis of leukotrienes (Grzanna, 2005), a property that separates it from NSAIDS. Other of ginger’s attributes point to an anti-oxidant character in the interruption of free radical generation (Ali, 2008), which is helpful in the fight against allergens and pain.

Nitric Oxide (NO) is one of the few signaling gases in the body. The smooth muscle that lines blood vessels is told by NO to relax, thus dilating the vessels and lowering blood pressure. In excessive concentrations, though, NO becomes a pro-oxidant as a naturally unstable free radical, especially when made by white cells (monocytes and macrophages)  during their battle against an infective agent. One logistician that maintains regulation of NO is ginger, where it was shown to control white cell activation as part of its job as an anti-inflammatory vehicle (Shimoda, 2010). Modulating inflammation is what ginger does, and not so gingerly, at that.

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Drozdov VN, Kim VA, Tkachenko EV, Varvanina GG.
Influence of a specific ginger combination on gastropathy conditions in patients with osteoarthritis of the knee or hip.
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Frondoza CG, Sohrabi A, Polotsky A, Phan PV, Hungerford DS, Lindmark L.
An in vitro screening assay for inhibitors of proinflammatory mediators in herbal extracts using human synoviocyte cultures.
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Grzanna R, Lindmark L, Frondoza CG
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Jiang Y, Turgeon DK, Wright BD, Sidahmed E, Ruffin MT, Brenner DE, Sen A, Zick SM.
Effect of ginger root on cyclooxygenase-1 and 15-hydroxyprostaglandin dehydrogenase expression in colonic mucosa of humans at normal and increased risk for colorectal cancer.
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Levy AS, Simon O, Shelly J, Gardener M.
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Lu H, Huang D, Saederup N, Charo IF, Ransohoff RM, Zhou L.
Macrophages recruited via CCR2 produce insulin-like growth factor-1 to repair acute skeletal muscle injury.
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Ramji, Divya; ho, chi; Huang, Qingron; Rafi, Mohamed; Huang, Mou
Isolation of gingerols and shogaols from ginger and evaluation of their chemopreventive activity on prostate cancer cells and anti-inflammatory effect on 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced mouse ear inflammation
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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Soda And Heart Risk: And We Thought It Was Only Teeth We Had To Worry About

soda-glassDid your mother ever say, “If you know what’s good for you, you’ll…?” Know what the matter is?  Even as adults who know what’s good for us, we drop the ball as if we didn’t know what’s good for us. Some of us even put the ball down on purpose from time to time. Hey, if we don’t know what’s good for us, how are we supposed to know what’s bad for us?

Catch this newsy tidbit. A lady in Monaco (you know, the place where Grace Kelly used to hang out) made her way to the ER with a palpitating heart that played syncopated rhythms. Intermittent fainting spells were included…free. After all was said and done, it turned out that the only thing she drank for the previous sixteen years was soda—a half-gallon a day, cola at that. If you’re thinking she got her 8 x 8 (eight, 8-ounce glasses of fluids a day), she really got more than she bargained for. The water part of soda is good; the other part isn’t so good.

Ingredients in soda are basically useless. The caramel color comes from heating corn or cane sugar until it reaches the desired color. Desired? By whom? The amount of sugar in a can of regular, non-diet, soda can reach twelve teaspoons. Would you let your child eat even ten spoons of sugar right from the bowl? If a person opts for diet soda, aspartame or some other fake sweetener is in the mix. That earns a chapter of its own. Phosphoric acid adds tang and tartness, but the label doesn’t say it also erodes tooth enamel (Brown, 2007), borrows calcium from bones, and is associated with kidney problems. “Natural flavors” don’t turn soda into health food. Caffeine, we are told, is added to enhance flavor, even to non-colas. Funny thing…a panel of trained tasters couldn’t tell the difference between caffeinated and non-caffeinated colas (Keast, 2007). It adds a slight bitterness and, of course, acts as a stimulant. Soda does, however, contain less caffeine than a cup of coffee.

Caffeine is a diuretic. You well know that a cup of coffee after, say 7 PM, is gonna make you get out of bed at three in the morning. A cola nightcap might do the same thing. Excess urine production—and maybe even diarrhea—will flush potassium from the body. That’s what seems to have happened to the Monaco Miss—potassium deficit. Well, now, does that make any difference? Let’s see what potassium is all about. It’s the number one positively charged ion in the fluid inside a cell, having a sodium counterpart on the other side of the membrane. Their concentration differences create an electrochemical gradient known as membrane potential, which allows a cell to work like a battery to provide power for its function. Simply, sodium tells your fingers to pick up a pencil; potassium says to let it go. Sodium contracts, potassium relaxes. If potassium is in short supply, muscle—including the heart—keeps trying to contract without being relaxed. Not good, right? Right. It’s bad enough that most of us are potassium shy because we fail to get the 4700 milligrams a day that we need, but it’s worse that soda can dissolve what’s left. Potassium helps the heart maintain a regular beat; deficiencies cause irregularities (Poole-Wilson, 1984).

Additional concerns about caffeine intake involve weight loss “miracles” that propose to suppress appetite and increase energy. Most of us are unaware that supplements can contain caffeine without it being listed on the label. A Brazilian tea that is marketed as an energy enhancing beverage, guarana, actually has twice the caffeine of coffee. While that can zoom you up, it can also induce seizures and blurred vision (Pendleton, 2012). O.K., so caffeine keeps you awake, that is, if you’re not accustomed to it. But it is related to sleep-disordered breathing if it comes from soda, though not coffee or tea (Aurora, 2012).

Through a process called osmotic diuresis, glucose and water are eliminated in urine. The kidneys normally reabsorb water and glucose, but excess sugar interferes with normal kidney function. The extra sugar attracts water, which has to go somewhere…the drain…and it takes potassium with it (Packer, 2008) (Sharma, 2013). And then there’s the likelihood that fructose will elevate uric acid levels and cause gout (Choi, 2008). Gosh, heart trouble or arthritic agony?  Choices, choices.

If you’ve been a heavy soda drinker for years, it only takes a week to set things straight. The CDC says that fewer than two percent of us get enough potassium (Cogswell, 2012). Potassium-rich foods aren’t that hard to find. Sweet and white potatoes, beet greens, tomatoes, bananas, orange, prune and tomato juices, spinach, sunflower seeds and molasses are some of the foods to consider. Keeping soda to less than a pint a day could keep you out of the ER. There are some places you really don’t need to be.

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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.