Can advances in technology actually be advancing joint disease in our young? Why is Joint Disease prevalent today in our children and our young companion animals?
Professor Franco Cavaleri BSc NB Nutraceutical Biochemist
Original post: July 23, 2010
We know osteoarthritis to be a disease of the old but more and more we’re seeing joint disease creeping into our young. Statistics show that osteoarthritis is on the rise and the easiest explanation is that our North American human population is now bearing the ripened baby boomers. However, closer investigation of the statistics reveals that the joints of our young aren’t standing up either and they’re making up a surprisingly large portion of the arthritic.
The rickety trend in our human populations is being mirrored by the same in our canine companions lending us another opportunity to pinpoint the cause. Is our environment contributing to the problem? In a way it is but its more about the lifestyle we’re choosing and even being forced to take. Despite our advances in health care and nutrition the cause is, in a sense the technology; or more accurately the by-product of our technology. Research is linking this joint phenomenon closely to nutrition and it has less to do with glucosamine than once thought.
Joint disease takes many forms ranging from autoimmune conditions to osteoarthritis which is associated with the wear and tear of time. Time; or aging is closely linked to oxidation. It’s no secret that oxidation plays a huge role in tissue degradation and disease. Oxidation or free radical activity is known to advance the production of inflammatory hormones known as prostaglandins and it does so through acceleration of specific enzymes. The uncontrolled free radical (oxidation) accompanied by the incremental inflammation literally ages our tissues and slows down our cells, including those of the joints. Our new age environment, our processed foods and our fast paced lifestyles fuel literally oxidize our cells and slow them down.
Uncontrolled oxidation contributes to inflammation. Inflammation, in turn propagates oxidation; a cyclic phenomenon that fuels itself. Oxidation accelerates the very enzymes that drugs like Aspirin (ASA) or other non-steroidal anti-inflammatory drugs (NSAIDS) block to reduce inflammation and pain. Is the prolific use of NSAIDS required simply because of our ever-escalating oxidative foods and environment? Research is starting to confirm this to be so.
The incremental inflammation has an obvious degenerative effect on joint and general health. But research shows that there’s an even more sinister influence by the free radical at the genetic level and it’s not as clear cut as mutation or damage. Unlike the acceleration effect on the inflammatory hormone production, oxidation on the chondrocyte inhibits the genetic activity responsible for production of collagen. This slows down or simply turns off the gene to ultimately turn off the production of collagen.
Oxidation has two compounding influences that advance joint disease. It prevents the in-built restorative system from keeping up with the daily breakdown of cartilage and does so without mutating the gene but rather slowing its pace. On the other hand, this oxidation accelerates production of inflammatory hormones that contribute to the symptoms of arthritis.
We also know that the body’s natural restorative activity slows down with age and recent research is also relating this age-related decline to oxidation and lack of antioxidant activity in the elderly. The damage and wear in cartilage day after day adds up to a significant problem in those latter years. Once this worker cell begins to sow down, no amount of supplemental glucosamine can get it to work and rebuild fast enough to make a difference. Glucosamine supplementation may provide some temporary anti-inflammatory relief but it can’t be used by these frozen cells to rebuild. As a result the condition simply progresses despite the symptomatic relief by glucosamine until one day nothing works.
Maintaining the condition and function of this worker cell before the development of disease is a logical way to maintain joint health. The right antioxidants with an affinity for the joint tissues block the oxidative influence to allow the cell to do its job in youth, adulthood and senior years. Just like the body of our companion canines, our human cells produce antioxidants designed to protect these systems, cells and tissues but the production of these internal (endogenous) antioxidants declines with age to diminish the inbuilt protection.
This internal antioxidant decline is one reason we and our companion animals become more vulnerable with age to oxidation and the associated inflammation. We experience this as non- specific stiffness, loss of flexibility, slower recovery from physical work and exercise and that common advancement of osteoarthritis. Maintaining antioxidant status in the body keeps these cells and maintenance systems in the ON position despite time or age; and it keeps them running in pace with natural wear and tear. Age is not about time. Joint disease is not an age- related or time-related dis-ease. How is this dynamic affecting our young children and canine companions?
The ever-growing popularity of fast foods and processed convenient meals simply contributes to the underlying cause of osteoarthritis by failing to challenge oxidation. It does so because the antioxidant activity of processed foods is lower than that of whole foods. Antioxidants in food are vulnerable to light, heat and oxygen exposure. Processing of food is a perfect deactivator of the precious antioxidant activity. In addition, the biochemical by-products of processing carbohydrate and protein foods together, known as advanced glycosylated endproducts (AGEs), enter the body to promote elevation of internal oxidation.
In other words, processed foods are not only commonly deficient in antioxidant activity they also can contribute to it through the damaged nutrition. Our dog’s bagged foods are processed even more intensely than most of our human foods. This presents a compounding problem that’s made even worse when they are older. As our canine companions’ cells begin to slow down their production of internal antioxidants, the negative effects of processed bagged foods have an exponentially negative influence.
This is one of the reasons our companion canines seem to age at much faster rates in their latter years than they do when they’re younger. Think about your canine’s rate of aging for a moment; the rate of aging from year one to age six is typically much slower than the rate of change seen from the next six years to age twelve. In those early years internal antioxidant production might be sufficient to help the animal cope with the extremely processed dry food. The absence of this internal protective activity in those golden years allows the bagged food`s oxidation to ravage unchallenged. As a result the body ages at a faster and faster rate as time passes.
How does this dynamic affect our young children and canine companions? Nutrient damage of processed foods is even deeper the food’s antioxidant. Vitamins are easily damaged by high heat and oxygen exposure. Minerals can complex with each other in the food mix forming indigestible and non-absorbable mineral complexes that pass right through our pets. In other words, the nutrients might be presented on the food bag’s label but the bioavailability or biological value to your pet is not good to non-existent. This is no different from how foods may present for our children.
These vitamins and minerals are essentially required by the cells to build the internal antioxidants and without them even those young cells cannot make the required antioxidants despite the inbuilt ability to do so. Without these building blocks antioxidant levels in our youth begin to reach lows like those in our seniors and the systems that need protection including the joints simply begin to function at rates of the elderly. The body then fails to keep up with daily wear and tear earlier in life. The result is premature joint disease that may begin to show signs at age five, seven or nine years instead of late into the fourteenth or even sixteenth year of age.
The same nutrient damage occurs with the food’s protein content and essential amino acids like the critically required lysine and cysteine. These amino acids are essential for tissue construction and their complexing or damage by heat and oxidation causes serious immune, structural and antioxidant deficiencies. Cysteine is typically the limiting factor in the internal production of creatine and the unequivocally important glutathione. Glutathione is a crucial antioxidant (in the form of glutathione peroxidase) throughout the body and plays a monumental role in immunity and liver detoxification.
Nutrition plays a huge role in health and disease. Lack of quality nutrition simply allows biological age in all cells and tissues to advance prematurely. Supplementing the food supply with active antioxidants empowers the body to offset the decline in the cells as our children and pets age. It also makes certain that our young have the tools in their vigorous cells to stay healthy, vibrant and antioxidant saturated to prevent premature aging of joints and general health.
As this internal decline if antioxidant status advances with age, the oral source (exogenous) of antioxidants must be increased from the lower doses that are needed by the young. This helps the cells maintain youthful activity despite chronological time; it reduces the rate of biological aging; and keeps the joints in tip top youthful condition. Not only should antioxidants be part of the general supplement program, connective tissue-specific antioxidant activity must accompany the right blend of glucosamine, chondroitin and MSM for cases of progressed joint disease in order to facilitate glucosamine use to build collagen.
Recommended addition to glucosamine and chondroitin: Grapeseed extract (95% Proanthocyanidins) Vitamin C (as magnesium ascorbate and ascorbic acid) Boswellia Serrata (65% Boswellic acid)
Green Tea extract (80% polyphenols&EGCG) Methylsulfonylmethane
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