Diabetes and Omega-3’s

Diabetes, Omega-3 fatty acids Super FoodsReading, interpreting and understanding scientific literature can be tedious because the authors often find that their previous paper on the subject missed its mark or was completely wrong. Easy to do when you are blazing new trails; however, the caution they go through to cover their tracks oftentimes makes for difficult reading. Luc Djousse and his colleagues at the U of Washington reported in the May 18, 2011 edition of the American Journal of Clinical Nutrition that, “With the use of objective biomarkers, long-chain omega 3 Fatty Acids (FAs) and Alpha-Linolenic Acid (ALA) were not associated with a higher incidence of diabetes. Individuals with the highest concentrations of both types of FAs had lower risk of diabetes.”

Speed reading is absolutely out of place. Omega-3 fatty acids in the body help to control the inflammation process, which is a benefit because the start of the healing process—initiated by the omega-6 arachidonic acid—also involves the possibility of getting carried away with the exercise. Say you have a cut or abrasion. The key activity that ensues is to stop the loss of fluids – save the blood.  It is that process which tells the body to start the healing by sending white blood cells and platelets to the site of the wound and to agglomerate and close the exit door by swelling the tissues, which is also another way of looking at inflammation. To inflame can be life saving. The omega-3’s are then involved in the work of modulating the activity helping to ease the inflammation that comes with the correction process.

Fatty acids, especially those that are long and highly unsaturated, increase cell membrane fluidity and functionality. Fatty acids are essential to membrane activity at the location of hormone receptors. Insulin resistance in adult-onset diabetes is directly associated with fewer membrane enhancing long-chain fatty acids, largely due to impaired function of desaturase and elongase enzymes needed for a healthy membrane. Ruiz-Gutierrez 1993, “We have studied the fatty acid composition of erythrocyte membrane phospholipids in nine Type 1 (insulin-dependent) diabetic patients and nine healthy control subjects. Cell membranes from the diabetic patients showed a marked decrease in the total amount of polyunsaturated fatty acids mainly at the expense of docosahexaenoic acid, DHA, and arachidonic acid C20:4n6”.

Cell membrane abnormalities in lipid content are found to be related to poor metabolic control, which is a characteristic of diabetes. Diet is a very important  factor, and interventions with dietary essential fatty acids (EFAs) in the correct ratio (found to be 4:1, omega-6:omega-3), can make a difference. Decsif  T., 2002, “Reduced availability of long-chain polyunsaturates in diabetic children suggests that an enhanced dietary supply of long-chain polyunsaturates may be beneficial”. Children with diabetes demonstrate a deficit of long-chain fatty acids, so incorporating them into a child’s diet is prudent. An unspoken benefit in the application of EFA’s to diabetes treatment is the decrease in triglyceride levels, themselves striking indicators of the potential for cardiovascular issues and very often appearing in persons with diabetes.

Herein resides the prolonged physiological support of the EFAs. For those who lack the efficient conversion of the omega-3 alpha linolenic acid from plant sources (notably flaxseeds and their oil) to EPA and DHA, fish oil may be a viable alternative. In fact the the FA conversion process with diabetes is almost non-existent, but also common with aging.

For quite some time the essential fatty acids have been misunderstood. Of the types of fatty acids, the omega-3’s have received the most publicity, having been applauded for positive health effects, principally, because over the last century the general population ate little fish and had little or no n-3s in the diet. Unless they were more or less health nuts, few did not have any exposure to omega 3s as in flax, and even if they did their ability to elevate up to EPA and DHA was minimal. Fish oil was the answer but the explosion that ensued caused over-consumption and still does.

Hence the comments of Djousse et al that n-3 FAs did not increase diabetes but if both the omega 6s and the 3 s were added together there was marked improvements. There is an inference that n-3s were of no benefit and needed the balance of both EFAs, which we applaud and so should you. Balance is paramount.


Djoussé L, Biggs ML, Lemaitre RN, King IB, Song X, Ix JH, Mukamal KJ, Siscovick DS, Mozaffarian D. Plasma omega-3 fatty acids and incident diabetes in older adults. Am J Clin Nutr. 2011 May 18.

Ruiz-Gutierrez V, Stiefel P, Villar J, García-Donas MA, Acosta D, Carneado J.  Cell membrane fatty acid composition in type 1 (insulin-dependent) diabetic patients: relationship with sodium transport abnormalities and metabolic control.  Diabetologia. 1993 Sep;36(9):850-6.

T. Decsif, H. Minda, R. Hermann, A. Kozári, É. Erhardt, I. Burus, Sz. Molnár and Gy. Soltész  Polyunsaturated fatty acids in plasma and erythrocyte membrane lipids of diabetic children  Prostaglandins, Leukotrienes and Essential Fatty Acids. 67(4); Oct 2002: 203-210

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

Milk – It Does A Body Something, For Sure

milk-carton-glassMost advertisements try to float the reader / viewer to the side of the river that hosts the heralded product. You’ll unlikely see a car salesman tell you there’s a better deal across the street.  If you know someone who tells the doctor what medications to Rx based on TV blurbs, you know the story.  It’s all in the power of the ad, truth or not.  You probably don’t know that the dairy industry has a champion called the International Dairy Journal, a highly-respected periodical that doesn’t exactly promote good old dihydrogen oxide, the most abundant molecule on the planet.  In January of 2012 there appeared in this publication a piece that addressed dairy foods and cognitive decline, commonly known as dementia, declaring that study participants who consumed dairy products at least once a day performed better on measures of cognitive function than those who rarely or never consumed dairy.  (Crichton, 2012)  What?  Did you expect something less stellar?  At least, the study candidly admits that the causal mechanisms “are still to be determined.”  Maybe there’s more to dairy than we know about if something needs to be determined.

Two years prior to this study, the same authors told us that drinking low-fat milk improves social functioning, stress and memory.  Maybe this proclamation means that low-fat milk can make you a better dancer and that you won’t worry about it if you think you are, but really aren’t, whether you forget or not.  Funny thing, whole milk has no such benefit.  (Crichton, 2010)  Yet, there’s the admission that the jury is still out.  Neither report had a definitive conclusion.  Both of these studies took place in Australia, but that shouldn’t make any difference because Australian and American cows speak the same language, except the Aussies add “mate” after “moo.”

Not to pop the milk drinkers’ balloon, despite the pleasure it might bring, but an in-between 2011 investigation performed by the Agricultural Research Service section of the USDA found that milk was less effective than meat for improving cognitive function and physical activity, but this time in a child population.  (Allen, 2011)  What this boils down to is that the stuff in meat is the same as the stuff in milk, but there’s more of it.  That would be iron, zinc, riboflavin, vitamin B12, and the rest of the nutrients for which animal products are hailed.

There is, however, another side to this coin. (Maybe “dodecahedron” would be a better metaphor because there are a few sides.)  That milk contains about four hundred different fatty acids makes it the most complex of all natural fats.  These fats come from one of two sources—the feed or the microbial happenings in the cow’s rumen.  In the olden days, back in the 1940s and early 50s, these fats floated on top of the milk because homogenization either wasn’t used or didn’t work as planned.  The kid who was the first to rise in the morning could retrieve the glass container from the front steps and eat the cream from the top of the bottle, leaving the low-fat remainder for the rest of the family.  Little did he or she realize that the goodness of butyric acid, a salutary short-chain fatty acid, was accompanied by the not-so-goodness of saturated fat and a little trans fat.  A small fraction of the beneficent essential fatty acids is in the mix, but hardly enough to make much difference.  However, there are other things in milk.  Among them are somatic cells, which some people equate with pus.  Aww, they wouldn’t allow that, would they?  Note that the job of the USDA is to promote agricultural interests, not yours.  In fact, clever inventors have devised ways to measure the somatic cells in your milk bottle with amazing precision (Tsenkova, 2001), with each state in the nation setting its own allowable levels based on regional variables.  ( and

Where does this stuff come from? The milking machine.  A cow’s udder is treated with iodine prior to being sucked dry, and both the iodine and a few of the cow’s body cells end up in the milk.  Doesn’t pasteurization kill germs?  Some.  But the dead cells are still in the milk, and besides, pasteurization is not sterilization.  The latter is intended to kill everything.  The former is intended to achieve a reduction in the number of viable organisms, reducing their number so they are unlikely to cause disease.  Milk can be pasteurized by heating to 145° F for half an hour or to 163° F for fifteen seconds.  The thermoduric bacteria that survive are held in check by refrigeration. To add insult to injury, the iodine may induce thyroid or dermatological issues over time.  That’s another story, though.

The casein in milk protein yields peptides called casomorphins, with different breeds of cattle offering different peptides, totaling about thirteen variants, each of which is divided into categories known as A1 and A2.  A1 caseins contain the amino acid histidine, essential for the growth and repair of tissue, but also responsible for manufacturing histamine, the stuff that makes your nose runny in an allergic reaction or that makes you itch after a mosquito attack. Although concentration-dependent, this state of affairs is uncomfortable at best, and is blamed specifically on beta-casomorphine-7, “…a naturally occurring product of cow’s milk with opiate-like activity…” (Kurek, 1992).  A2 caseins contain proline, a non-essential amino acid that is a component of cartilage.  That casomorphins have opioid activity matters little in light of the discovery that particular A1 casein can become glycated and promote adverse immune effects (Elliott, 2006), among them diabetes.

So, what is glycation?  It’s the result of a sugar bonding to a protein or a fat without the watchful eye of an enzyme, such as might happen in a frying pan or even in the body after ingesting a sugar, resulting in a haphazard process that impairs cellular function.  This is not to be confused with glycosylation, an enzyme-controlled process aimed at a specific molecule to enable its particular function.  Glycation forms advanced-glycation-end products, or AGE’s that are implicated in neurodegenerative diseases (Li, 2012) and mitochondrial dysfunction (Hashimoto, 2003).

About 8% of infants under age one are allergic to cow’s milk (Constantinide, 2011).  This might account for the crankiness of the child who is unable to define the earache or the gastric distress that cause discomfort and pain.  Yes, a child may outgrow milk allergy, only to be bombarded with symptoms decades later, most of which arise from reactions to the foreign protein that is casein, a material once used to make paint.  Casomorphin from type A1 is believed to play a role in ischemic heart disease, while that from type A2 encourages neither heart disease nor diabetes (Kaminski, 2007).  Are you expected to test your milk to find whether it’s higher in one or the other variant?  Type A1 Beta-casomorphin-7 is implicated in several human miseries, and is especially hazardous to those with leaky gut syndrome, to this day a questionable diagnosis to the traditional medical community.  Nonetheless, BCM-7 affects GI motility and mucosal immune function (Elitsur & Luk, 1991).  Now that it’s been established that type A1 is the bad casein, here’s the list of cattle ranked according to A1 casein content, from bad to good:  Holstein (much more A1 than A2); Jersey, Ayrshire and Milking Shorthorn (these three have almost equal levels);  Brown Swiss (more A2 than A1), and Guernsey (almost a 100 x A2 than A1).  The next time you get milk from the supermarket, the neighborhood convenience store or the gas station around the corner, be sure to ask the dairy manager/clerk from which breed of cow the milk was pumped.

There is much more to deny a cow its center stage, ranging from mineral imbalances to disease promotion via shared hormones with humans, items to be addressed another time.  But if there’s cognitive benefit to be derived from milk, it comes from phospholipids (Schubert, 2011) (Lopez, 2008), the structural and functional cellular components that are better obtained, without unwanted tag-a-longs, from non-dairy sources.  Milk phospholipid and fat content depends on what the cow is fed.  Cattle feed high in flaxseed, for example, will produce milk higher in polyunsaturated fats and lower in saturated ones (Lopez, 2008).  Regardless, only about 1% of milk lipids are phospholipids.  Even if there were a higher percentage, the heat of pasteurization that destroys enzymes (It takes only 120° F to deactivate an enzyme.) also would oxidize the phospholipids to uselessness.

Cow’s milk does a body good if you’re a calf.  The ideal for humans is, well, breast milk.  If breast feeding is out of the question, there are alternatives that supply the fats an infant needs for development.  Hemp milk is one of these, but it’s expensive.  It’s loaded with omega-3 fatty acids and potassium, and enough vitamins to meet the need.  Omega-6 fats can be fortified with sunflower, safflower or evening primrose oils, and phospholipid needs can be more than satisfied with real, honest-to-goodness phosphatidylcholine.  After age four, a tot can switch to alternative milk, but the supplementary essential fats and phosphatidylcholine should stay because they definitely do a body good…all the way into old age.  It is not common for animals to drink the milk of another species.  Who chose cattle to be the source of beverage,  cavemen?  “Hey, Charlie, let’s yank on that thing hangin’ down under that animal and drink what comes out.”  One more thing:  what milk does to a prostate gland shouldn’t happen to anyone (Schmitz-Dräger, 2011)  (Tate, 2011)  (Torfadottir, 2012).


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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.

Essential Fats Explained

fattyacid-sourceThe essential fatty acids (EFA’s) are just that—essential, meaning they have to come from the diet because the body can’t manufacture them. They might be used as fuel, but they are absolute components of the biological processes that make us work. Only two fatty acid families are vital to humans, omega-6’s and omega-3’s. It’s been shown that their ratio is more important than their volume. The parent fatty acid (FA) in the omega-6 (n-6) line is linoleic acid, abundant in many vegetable oils and ultimately responsible for the biosynthesis of arachidonic acid and related prostaglandins, which are compounds that regulate physiological activities. Alpha-linolenic acid (ALA) is the mother omega-3 (n-3) fatty acid, commonly extracted from seed oils such as flaxseed and hemp, but also found in walnuts. Nearly every aspect of human physiology is affected by essential fats, receptors for which are located in practically every cell.

The n-6 fatty acids have been denigrated in recent years because their excess has been linked to several metabolic upsets. Unbalanced diets are harmful to health, and the n-6’s that overpopulate processed foods and rancid supermarket oils have contributed to myriad health woes. What possibly started out as a 1 to 1 or 2 to 1 ratio of n-6 fatty acids to n-3 fatty acids in the human diet eons ago has become a physiological disaster of imbalance, where the ratio exceeds 10 to 1 in the typical Western diet, and may even approach 20 to 1, or worse, in personal food intake. All fatty acids go through a process of desaturation and elongation to become eminently bioactive compounds. The ultimate products of the process are beneficial to human health, especially if they are made step-by-step by the body and not forced upon it through manufactured meals, unnaturally finished meat products, stale/oxidized vegetable oils, and fossilized eggs, not to mention horrific snack foods. In a healthy body, linoleic acid is converted to gamma-linolenic acid (GLA), which becomes arachidonic acid, from which come the chemicals that control inflammation. After adulthood, the body’s ability to make those conversions is uncertain, so starting with GLA gives us a head start. However, mother linoleic acid is anti-inflammatory in its own right and even a marginal conversion to GLA has been held effective in the management of conditions as diverse as rheumatoid arthritis, eczema and ADD/ADHD.

The n-3 parent, ALA, also must come from diet because humans lack the enzymes necessary to convert it from other fats. But it’s the downstream omega-3’s that get the publicity:  EPA and DHA. Like the n-6’s, the conversion of ALA to EPA and later to DHA is an uncertain proposition in adulthood, which is why most adults use fish oil, a source of pre-made fatty acids. Even in the absence of the requisite conversion co-factors (vitamin B6, Mg, biotin, vitamin B3, vitamin C and Zn), ALA is anti-inflammatory and cardiac friendly (Pan, 2012) (Vedtofte, 2012), with recent scrutiny heralding its potential to inhibit progression of atherosclerosis (Bassett, 2011). The most readily available source of ALA is flaxseed, although chia, the newest kid on the block, is entering the marketplace.

Signs of fatty acid deficiency include a dry scaly rash, impoverished growth in youngsters, increased susceptibility to infections and poor wound healing, but are uncommon. The enzymes that convert the parent fatty acids act preferentially toward the n-3’s. By the time these enzymes deal with the omega-3 fats, some of the omega-6’s have been used for energy, hence the need to get more 6’s than 3’s, in a ratio of about 4 to 1, as evidenced by intensive research done in the 1990’s and early-mid 2000’s (Yahuda, 1993, 1996) (Simopoulos, 2002, 2008). But this ratio is based on the body’s own manufacture of the downstream fatty acids, GLA and arachidonic acid (ARA) along the n-6 line (the latter now included in products designed for infants to insure proper brain development) and EPA/DHA down the n-3 line. Deficiency of essential fatty acids sometimes strikes those suffering from cystic fibrosis or fat malabsorption issues. If patients receive total parenteral nutrition without the inclusion of EFA’s, deficit will appear in about a week or two.

The dry weight of the brain is about 80% lipids, the highest of any organ. The long-chain polyunsaturated fats, especially the n-6 and n-3, are crucial in modulating neural function. They occupy as much as 30% of the brain’s dry weight, making their influence on neural membrane dynamics profound. The shift away from EFA’s in the Western—typically American—diet parallels a rise in mental disorders. The need to address EFA supplementation is real and current, with the inclusion of omega-6 fats a necessity, since GLA, the downstream scion of linoleic acid, has held its own in mental health studies (Vaddadi, 2006). Together, the n-6’s and n-3’s cooperate in a number of cellular functions that affect membrane fluidity, allowing the passage of food and energy into the cell and wastes out. Arachidonic acid is a precursor to signaling molecules in the brain and is a key inflammatory intermediate, while EPA and DHA work to support the cardiovascular system, and the brain and retina.

It is arachidonic acid that supports membrane fluidity in the hippocampus, the part of the brain that directs memory, spatial relations and inhibition (Fukaya, 2007). It is arachidonic acid that protects the brain against oxidative stress and activates proteins in charge of the growth and repair of neurons (Darios, 2006). There is conjecture that ARA supplementation during the early stages of Alzheimer’s disease may slow its progress and stave off symptoms (Schaeffer, 2009). That’s a pretty good promise for something that’s been spurned…for lack of knowledge. Of the n-3’s, EPA may be effective in addressing depressive conditions and behavioral anomalies, besides being able to reduce inflammation (Brind, 2001) (Song, 2007). There had been some concern that EPA adversely affects clotting factors and fibrinogen concentrations, increasing the likelihood of bleeding. That is not so (Finnegan, 2003). It does, however, improve blood viscosity and red blood cell deformity, which allows red cells to adjust their shape to squeeze through narrow blood vessels, like capillaries. Downstream from EPA is DHA, a major fatty acid in sperm, brain phospholipids and the retina of the eye, and found to lower triglycerides. But its claim to fame is its rapid accrual in the developing brain during the third trimester of pregnancy and early postnatal period (Auestad, 2003) (Wainwright, 2000).

You can safely bet the farm that endogenous (made by the body itself) substances are more tightly regulated than exogenous. For example, the arachidonic acid your body makes from linoleic acid is more respectable than that from a haphazardly slaughtered steer, which may or may not be completely lifeless before the abattoir starts to dress it. In fear and pain, the animal releases a torrent of adrenal hormones throughout its flesh, confounding the integrity of its innate fatty acids. Endogenous fatty acids are, therefore, more wholesome.

How do we acquire the parent fatty acids?  You could buy oils that boast omega-6 and omega-3 fatty acid content from the supermarket, but it’s almost guaranteed that the balance will be too far out of whack to deliver a benefit, and the purity of the oils is possibly iffy. In fact, they might upset the apple cart. An overabundance of n-3’s can shut the immune system down for lack of guidance by the n-6 inflammation directors. On the other hand, BodyBio Balance Oil is a blend of organic, cold-pressed sunflower and flaxseed oils that are purposely geared to supply a 4 to 1 ratio of fatty acids that the body needs to initiate the cascade to longer chain fats that present vibrant physiological activity. Just the anti-inflammatory properties of the mother fatty acids, linoleic from sunflower and alpha-linolenic from flax, are enough to warrant using the oils to bolster the body’s well-being and to work out some metabolic kinks. Used to make salad dressings or to dress vegetables in place of butter, Balance Oil has the potential to set straight that which is awry, and the essential fatty acid metabolites can help to clear the brain fog on a hazy day. Cerebral lipids, especially the long-chain fatty acids, have significant direct and indirect activity on cerebral function. Not only do they affect the membranes, but also many are converted to neurally active substances. There is good evidence that mental challenges are related to EFA depletion, the supplementation of which can ameliorate the most defiant state of affairs.


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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’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).


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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.

Statins And Diabetes: Why Didn’t They Tell Me?

heart-measureCan you tell when you’ve eaten too much ice cream? Does the eructation shake your table lamps after too many sodas? Sometimes we learn what enough is by having too much. Too bad it isn’t the same with drugs. A hundred-pound lady doesn’t need as many aspirins to get rid of a headache as a two-hundred-pound guy. And for those who take a statin because the doctor said so, why does everybody start with the same doses? With Zocor, everybody starts with 40 mg. Doesn’t anybody think that maybe 5 mg could do the trick? Hey, if one quart of white semi-gloss will cover the bathroom walls adequately, why buy a gallon unless you have a use for it elsewhere? You gonna paint those walls until the gallon is empty?

Over the last few years, the cholesterol model of cardiovascular disease is steadily being replaced by the inflammation model of CVD, putting statin drugs on the back burner because cholesterol, it is realized, has never caused a heart attack. In fact, half the scary cardiac events happen to people who have what are deemed ideal cholesterol numbers (Sachdeva, 2009). Yes, it is true that statins interfere with cholesterol manufacture by the body, not only in the liver, but also in the brain, where cholesterol is vital to the machinery of thought and function. Low cholesterol can lead to serious health issues when that machinery is interrupted.  Low cholesterol levels are associated with high total mortality, even in patients with coronary heart disease (Behar, 1997) (Krumholz, 1994).

Differences between young and old, and between male and female, are recognized in the cholesterol arena, too. The impact of total cholesterol as a risk factor for heart disease decreases with age (Waverling-Rijnsburger, 1997) and for women, whose moderately elevated cholesterol may actually be beneficial (Petursson, 2012). The age cutoff for both genders is fifty (Anderson, 1987). If this information regarding age was known ten years ago, why are TV ads so adamant about getting cholesterol values below a hundred?

The personal experiences of at least one NASA astronaut have attested to the nasty effects of statins, including transient global amnesia, impaired cognition, personality changes, myopathy, neuropathy and neuromuscular degeneration. The root of all these maladies is the inhibition of Co-enzyme Q 10, a physiologically necessary substance that is blocked by Lipitor, Zocor, Crestor and the rest of the gang. Without CoQ10, mitochondria don’t work their magic at cell metabolism, where they get to burn food for energy, oxidize fatty acids, and use the electrons supplied by CoQ10 for a host of other essential activities. The pathway that makes cholesterol also makes CoQ10 in the body. Stopping one stops the other. This is so well known that statin prescriptions in Canada—for Mevachor®, Pravachol® and Lipitor®— contain a warning about CoQ 10 depletion. Merck even filed two patents for a statin-CoQ 10 combination, no. 4,933,165 and no. 4,929,437, which expired in May and June of 2007 (Koon, 2013). And you thought the drug companies had your best interest at heart, eh? The cholesterol issue is a complicated one and now, to add to the quagmire of hits and misses, is the notice that statins are implicated in the risk of developing diabetes. The endearing stars in this drama are atorvastatin (Lipitor), rosuvastatin (Crestor) and simvastatin (Zocor), brought to you by Pfizer, AstraZeneca and Merck. Atorvastatin was found to be the most influential of the three at elevating blood glucose, followed by rosuvastatin and simvastatin, in a recent Canadian study carried out at the Toronto General Hospital (Carter, 2013). From this work it may be drawn that pravastatin (Pravachol) is the safest drug related to diabetes onset. Regardless of drug of choice, or rather the physician’s choice, dose intensity also seems to make a difference in diabetes risk. Intense doses, especially at 80 mg of Zocor, increase the odds of all statin-induced adverse events (Silva, 2007), extending diabetes risk to almost ten percent of the medicated population (Preiss, 2011).

For all the hoopla that accompanied statins’ debut forty years ago into the pharmaceutical world, recounting their anti-cholesterol beneficence, it’s been discovered that their real claim to fame is being anti-inflammatory. That characteristic, it’s claimed, is more important to their raison d’etre than disrupting the cholesterol (and CoQ 10) pathway (Antonopoulos, 2012) (Mora, 2006) (Weitz-Schmidt, 2002). If so, then anti-inflammatory substances that have zero side effects might be considered. In this list will be simple things with complex mechanisms, like ginger, curcumin (from turmeric), capsaicin (from hot peppers), garlic, fish oil, bromelain (from pineapples), flaxseed oil, and zinc, among others. Aside from an allergic reaction which you already would know about, the only side effects of these ingredients are possibly foul breath (that would be the anti-vampire action) and stomach upset from too much of a good thing.

The mention of CoQ10 needs at least a little thought. Natural stores of this enzyme diminish with age. The fact that it donates electrons to multiple body processes bespeaks its importance to full function. It’s comparable to using the correct gauge extension cord with an electric weed trimmer. If the cord can’t carry the voltage, the trimmer will not work to its potential. Adding CoQ 10 to the daily regimen is a prudent decision whether taking a statin or not. Why?  It helps to control blood glucose (Kolahdouz, 2013) (Mezawa, 2012).


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