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Let’s face it…unless you’ve lived under a rock for the past ten years, you already know that over 60% of Americans are overweight or obese. On the basis of statistics alone, two out of every three people reading this page are struggling with their weight – maybe more, if you consider the bias introduced by internet search engines.

Everyone who is overweight has also already heard the party line: In order to shed those extra pounds, you have to cut down on your calories and get off the couch; you can’t lose weight unless you burn more energy than you consume; and so on, and so forth…

What many people don’t know, and what is still unsettled in the minds of scientists who study the obesity issue, is how much influence our immune systems have on weight gain…and, by default, on weight control.

Enter the “hygiene hypothesis.” This theory postulates that many of our modern-day health issues – from asthma and allergies to rheumatoid arthritis and fibromyalgia – are rooted in our lack of exposure to a sufficient number of germs when we are very young. Such a notion flies in the face of conventional thinking, which holds that improved sanitation, antibiotics, and other trappings of contemporary living are the main reasons we’re all living to be 80 instead of 35.

But our sanitized surroundings may actually be contributing to some health problems along the road to that golden “fourscore-and-then-some” milestone. There’s some pretty compelling evidence that our immune systems first learn to not only protect us from our environment when we are in infancy; they also develop the critical state of balance that prevents them from beoming our antagonists later in life.

Apparently, a great deal of our “immune education” requires the existence of a robust population of probiotics in our intestinal tracts, which leads in turn to an ample supply of immune messenger molecules in our bloodstreams.

Probiotics are “friendly bacteria” that live in our environment – most of them exist in the soil – and their colonization of the human gut stimulates the type of immune response that keeps us healthy throughout our lives. Proponents of the hygiene hypothesis contend that most infants in industrialized nations do not receive their requisite “dose” of probiotic organisms at a time when it will do them the most good.

How does this relate to obesity? Well, research has already demonstrated that obese individuals exhibit highly unusual responses to immune challenges:

  • People who are overweight are much more likely to succumb to certain infections due to impaired immunity (abnormally low activity of T cells and NK cells).
  • Obesity interferes with the production of cytokines that serve as immune messenger molecules; hence, an appropriate response to an infectious organism or suppression of a hyperactive immune system does not occur in a timely fashion.
  • Obesity dampens the effects of hormones that usually trigger immune responses. Thus, infections can gain a foothold – or a revved-up immune response can continue unchecked – before the immune system’s “damage control” function can intervene.

Conversely, several recent studies have demonstrated that obesity – and many of its consequences – may actually be driven by inappropriate activities within our immune systems. In short, obesity (like coronary artery disease) is an inflammatory disorder.

It is probably premature to assume that immunomodulation (i.e., therapies aimed at balancing the immune system) will become a mainstay in the treatment of obesity. However, a great deal of scientific effort is being directed at this very idea; I have no doubt that there will soon be medications on the market for individuals whose obesity can be partly or wholly attributed to immune imbalance (although tests designed to detect the specific immune derangements that cause obesity aren’t widely available).

In the meantime, we should include a good probiotic supplement in our daily routines; no one knows for sure if reestablishing a normal population of bacteria in the gut will “repair” an unbalanced immune system, but it’s certainly reasonable to assume that it will help. Live-culture yogurt is one way to acquire some probiotics, but the number and viability of organisms in yogurt cannot be ensured. Individuals who are immunocompromised should use probiotics with caution.

Additionally, people who are trying to lose weight – particularly those whose best efforts aren’t yielding the expected results – should really consider adding some immune-balancing messenger molecules to their programs. The only such preparations that are available to the general public (and that have sufficient scientific support for their use) contain transfer factors. Transfer factors were discovered over 60 years ago, and hundreds of scientific articles attest to their effectiveness.

Only one company, 4Life Research, has the expertise – not to mention the worldwide marketing rights – to ensure the quality of transfer factor products. They’ve even coined a phrase for their preparations: “Transferceuticals®”  

Specifically, take a look at Transfer Factor Tri-Factor Formula, Shape-Fast Ultra (for people who want to improve the caloric burn) and NutraStart. All of these formulas contain healthy doses of transfer factors.

Good luck in your weight-control efforts, and don’t give up!!

Our daughter got her driver’s license yesterday. As she completed the requisite forms, she checked the box that designated her as an organ donor. But it wasn’t just a matter of ticking the square and moving on. In our state, a resident can opt to donate any needed body part or limit donation to specific organs or tissues; one can prohibit the use of an anatomical gift for certain purposes (i.e., therapy, research, or education); and one’s gift of tissues or organs can be limited to use only by non-profit procurement entities (i.e., the nearest “organs-for-sale” outlet cannot harvest your body parts).

If that whole process seems a bit convoluted, its complexity pales in comparison to the organized chaos that befalls a donated organ in the unfortunate event of a driver’s death. Before an organ or tissue takes up residence in another human being, its compatibility for its new home must be determined.

To simplify a very intricate process isn’t always easy, particularly when the only language available to describe it is rooted in scientific jargon; relatives who voluntarily donate tissues for loved ones often get mired in the “technospeak” that surrounds organ donation. Hence, it’s worth the effort to clarify the methodology – and the underlying science – that surrounds organ and tissue transplantation.

The Major Histocompatibility Complex and the Human Leukocyte Antigen System

Every human being possesses a unique combination of immunologic markers that coat the surfaces of their cells. Like fingerprints, these markers help each person’s immune system differentiate what is “us” from what is “not us.” These markers – they’re like molecular Braille protruding from a cell’s membrane – consist of long protein-like molecules that our immune cells can read and recognize.

A cell’s machinery for producing these markers is located on one chromosome (chromosome 6, for those who are interested); hence, every cell that has a nucleus – or that ever had a nucleus – possesses its own allotment of markers. The impressive array of markers that can be generated among the human population arises from variations in the genes — called the major histocompatibility complex (MHC) – which reside within a small region on this single chromosome.

Many animals possess a MHC (it’s one of the things that differentiates one species from the next); in humans, the various types of genes that represent the MHC are collectively called the human leukocyte antigen (HLA) system.

Yes, it’s complicated, but let’s continue wading together, and we’ll eventually get to dry ground.

It is the job of the MHC to present specific markers to our leukocytes – specifically, our T lymphocytes – so immune integrity can be maintained and all foreign antigens (things that are “not us”) can be eliminated. Two major types of MHC markers have been described:

  1. Class I MHC markers are present on the surfaces of all nucleated cells and platelets. These markers are generated from HLA genes at three different locations on chromosome 6. T lymphocytes that recognize class I markers tend to be CD8 (cytotoxic) cells. CD8 cells are instrumental in killing other cells that are infected with viruses or those whose markers have changed (i.e., cancer cells)
  2. Class II MHC markers are found on the surfaces of cells that present antigens to other immune cells: B cells, macrophages, NK cells, dendritic skin cells, and Langerhans’ cells “capture” antigens that are present within their respective environments and “show” them to immune cells that can either confirm the antigens as “self” or initiate the immune cascade that eventually destroys a foreign invader.

Other types of MHC markers – mostly inflammatory molecules – also exist, but class I and II MHC markers play the lead roles in immune compatibility.

Whenever a tissue or organ is introduced to an immune system that recognizes it as a foreign antigen, that tissue or organ will be promptly rejected. “Near misses” – transplants whose MHC markers match most of the recipient’s markers – can often be tolerated if the recipient’s immune system is suppressed with medications, but any tissue with too many disparate markers cannot be safely transplanted.

In summary, then, HLA testing is used to determine if a donated organ or tissue will match the immune system of someone who needs a transplant. HLA compatibility is essential if a transplanted organ is to survive within the recipient; conversely, HLA incompatibility usually signifies that the potential recipient must wait for a different donor.

       

 

In one form or another, tea tree oil (Melaleuca alternifolia) has been used for its medicinal benefits for thousands of years. The Bundjalung aborigines of Australia revered a lagoon near present-day New South Wales – where Melaleuca leaves fell into the water and decayed for generations – as a site with phenomenal healing powers.

In 1930, the first modern reference to tea tree’s properties appeared in The Medical Journal of Australia, wherein a surgeon reported the successful treatment of surgical wounds with Melaleuca oil, which cleared skin structure infections as efficiently as carbolic acid (the most popular antiseptic of the time) without injuring the surrounding tissues.

Furthermore, due to its effectiveness as a disinfectant, tea tree oil was included in the first-aid kits carried by all Australian soldiers and sailors during World War II. Indeed, the Australian government exempted Melaleuca growers from military service because the industry was deemed critical to the war effort.

Tea tree oil is effective against multiple bacteria, several fungi, and some viruses, and it may even exert a limited antiparasitic effect (it has demonstrated activity against Sarcoptes scabiei, the mite that causes scabies).

It probably shouldn’t be surprising then – given tea tree oil’s spectrum of potential benefits – that Melaleuca’s advocates would attribute it with healing properties that reach beyond current scientific evidence. One such claim revolves around Melaleuca’s ability to enhance the human immune response.

To cut right to the chase, there are no convincing data to support claims that Melaleuca stimulates the immune system.

According to the American Cancer Society:

“Although no one claims tea tree oil can prevent or treat cancer, some proponents claim the oil can boost the immune system (this might tempt some people to assume that Melaleuca helps fight cancer). Some herbalists claim that tea tree oil can be used as a ‘lymphatic recharge’ for a ‘sluggish’ lymphatic system. Available scientific evidence does not support these claims.” (Italics are mine)
One 1999 study frequently quoted as evidence of tea tree oil’s immunostimulating properties compared terpinen-4-ol (Melaleuca’s active ingredient) with crude oil as a catalyst for white blood cell differentiation. After all, anything that leads to white cell differentiation and activation is technically an immunostimulant, right?
Unfortunately, both the crude oil extract and terpinen-4-ol produced the same degree and type of differentiation in the white cell line – specifically, monocytes – being studied. Hence, it appears that any immunostimulation attributable to tea tree oil is identical to that conferred by introducing monocytes to any other foreign substance: essentially, a nonspecific and innate response to a new antigen.
Alas, most experts believe that tea tree oil’s antimicrobial properties (which are impressive in their own right) stem from the direct actions of its chemical constituents on cell walls and growth characteristics of various microorganisms.
So, although tea tree oil displays activity against a variety of potentially nasty microbes, and even though its pharmacologic attributes make it a useful topical antiseptic, it should not be used as an immunostimulant. In short, Melaleuca has no place (for now) in the prevention or treatment of cancer.

Besides, as little as a few teaspoons of tea tree oil, taken internally, can cause fatal poisoning.        

If we want to understand the myriad and mysterious ways of our immune systems, sometimes we have to connect the dots. For practitioners of Western medicine, that occasionally means throwing off the shackles of dogma and embracing a new concept.

Way back in the 1990s, while performing autopsies on individuals who died following heart attacks, scientists discovered bacteria in the walls of some victims’ coronary arteries. More specifically, the bacteria – along with the inflammation they precipitated – were found in plaques, those thickened areas that cause “hardening” of the arteries and that eventually occlude the vital conduits that carry blood and oxygen to the heart muscle.

It was an interesting finding, one which led some researchers to suggest that coronary artery disease – like peptic ulcer disease (another heretical notion, at first) – might be an infectious illness. However, statin drugs were rapidly becoming de rigueur for “informed” physicians, so much of the conjecture connecting infectious organisms with coronary artery disease fell quickly by the wayside.

Aggressively marketed as both prevention and cure for all vascular ills, statins grew in popularity – not coincidentally becoming a major source of revenue for pharmaceutical firms – and they are now part of the “standard of care” for dealing with any condition that is even remotely associated with cardiovascular disease: hypercholesterolemia, hypertension, diabetes, evil spirits…some experts now recommend that even our children should be taking these drugs.

Alas, there is a tiny, irritating fly in the ointment. Despite the “take-statins-for-everything” message that is continuously smeared across American television screens and that is slathered liberally over the pages of medical journals, it is actually inflammation – the perennial companion of a vigilant immune system – that is the perpetrator of cardiovascular disease. Study after study has implicated inflammation in the genesis of atherosclerosis and its nasty outcomes. Indeed, not long ago, high-sensitivity C-reactive protein, an indicator of vascular inflammation, was added to the array of blood tests that physicians can use to determine a person’s risk for coronary artery disease and heart attack.

This is not to say that aberrant lipid levels don’t play some role in heart attacks and strokes; they clearly do. However, our reliance on these markers – and our reflexive attempt to “normalize the numbers” at all costs – has been less than universally effective for preventing heart attacks…which was the hope of statin advocates when these medications first became vogue.

Research continues to reinforce the role of inflammation, a direct result of immunologic reactivity, in this all-too-common disease.

One might wonder when some research dollars will be spent on identifying the immunologic factors that lead to heart attacks and strokes. What trigger or triggers, for example, stimulate the macrophages in our arterial walls to ingest packets of low-density lipoproteins (LDLs), transform into foam cells, and release cytokines that encourage other immune cells to damage the linings of our vessels? In fact, are low-density lipoproteins really one of the root causes of cardiovascular disease, as statin proponents tell us, or are they merely another marker for an as yet unidentified inflammatory process?

These questions (and so many others) should interest responsible scientists, for a clearer understanding of the basic mechanisms behind coronary artery disease might lead to cheaper, safer preventive measures that would save a lot of lives and a lot of healthcare dollars.

In the case of coronary artery disease, we seem to have stepped once more to the verge of issues that were initially examined by curious people nearly two decades ago, but that were buried beneath avalanches of misinformation proffered by the moneymakers. Our pursuit of real answers is too often thwarted by profiteers.

To date, no one has thoroughly explored the association between immunity, inflammation and cardiovascular disease. Such an effort would apparently be unseemly, as it might just threaten the economic machine that is the statin market. I could be mistaken about that, though: I recently read an article attesting to a statin drug’s ability to lower the levels of inflammatory markers in people at risk for heart disease. So it won’t be long before statins are marketed as top-notch anti-inflammatories, too.

Thus, as long as we keep peddling statins to physicians and an unsuspecting public – promoting the drugs as panacea – we may not need real answers to all of those nagging questions.

After all, once dogma gets rolling, it has a lot of inertia.  

    

 

As we enter the height of cold and flu season, lots of folks are casting about for alternative treatments for the aches, fevers, coughs, and sniffles that accompany these viral illnesses. Probably just as many people are looking for ways to prevent those bugs from ever getting a foothold in the first place.

Purveyors of herbal remedies and other supplements, being keenly aware of the opportunity for profit, will market almost anything as a cold “preventive” or “treatment” (even though neither of these words can be legally used in the promotion of non-FDA-approved products).

A lot of studies attest to the immune-boosting or immunoprotective properties of various herbs, vitamins, minerals, and foods…just as there are studies showing no benefit whatsoever from these same preparations. Therefore, consumers must be willing to do a bit of their own research before deciding what works best for them.

Probiotics May Help to Prevent Colds and Reduce Their Severity

Probiotics are bacteria that normally inhabit the human gastrointestinal tract and the GI tracts of many other animals. These microorganisms constitute a large, heterogeneous group that has been extensively investigated as potential treatments for any number of problems, including diarrhea, constipation, celiac disease, irritable bowel syndrome, and allergic dermatitis.

More recently, probiotics have garnered attention for their potential utility in treating or preventing viral upper respiratory infections in children and adults. While the results of well-controlled trials have been mixed, the data to support the use of probiotics during seasons of peak viral activity are compelling.

The reason that probiotics improve our response to viral illness is, on the surface, fairly straightforward: these organisms stimulate immune cells (T lymphocytes, B cells, etc.) and evoke the production of protective antibodies, cytokines, and other factors in the very mucous membranes where viruses gain entrance to the human body. Over the millennia, we have developed a symbiotic relationship with those bacteria that have proven the most useful to us as individuals and as a species.

Modern diets, the widespread use of antibiotics, and exposure to all sorts of environmental toxins have, over the years, created an imbalance between our gastrointestinal tracts and the outside world. This may be one reason for the increasing incidence of celiac disease and other autoimmune conditions.

Notably, many of the studies suggesting a beneficial effect from probiotics have been conducted in the United States. Hence, detractors of foreign medical research (I’m not one of them, by the way; in fact, I believe that American-conducted research is suspect on the basis of its funding sources) won’t have much room to criticize emerging data on the basis of “inferior study design.”

Rather than enumerate the individual trials and discuss their results in detail, I’ll summarize what seems to be the consensus among researchers who found probiotics useful for reducing the incidence, symptom severity, and duration of colds and influenza-like illnesses:

  • Probiotics should contain a combination of several species, such as Lactobacillus acidophilus, L. rhamnosus, L. casei, L. plantarum, L. reuteri, Bifidobacterium bifidum, B. longum, B. lactis, Propionibacterium freudenreichii, Bacillus coagulens, etc.
  • Several million to several billion live organisms are needed on a daily basis for at least three to six months to confer the best protection.
  • Probiotics that are consumed along with prebiotics, such as fructooligosaccharides (FOS) or galactooligosaccharides (GOS) confer better protection than probiotics that are consumed without prebiotics (prebiotics provide a quick source of nutrition for probiotic bacteria).

There are a multitude of probiotic preparations on the market. People wishing to add probiotics to their daily routine should ensure the quality of their chosen preparation, and refrigeration is recommended for all preparations, despite claims of “room temperature stability.”

By the way, for people who don’t want to add yet another capsule to that handful of supplements they choke down each morning, live-culture yogurt and kefir are reasonable alternatives.

Let’s grow some good bugs for a change, shall we?     

        

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