Month: February 2012

WASHINGTON, DC, February 22, 2012. In a press release issued yesterday, authors affiliated with the Centers for Disease Control claim that the rate of outbreaks caused by unpasteurized milk and products made from it was 150 times greater than outbreaks linked to pasteurized milk.” The authors based this conclusion on an analysis of reports submitted to the CDC from 1993 to 2006.

Washington, DC ( November 17, 2011)—In a statement issued on November 1, concurrent with a raw milk freedom rally held outside FDA headquarters in Silver Spring, Maryland, the agency conceded that it "has never taken, nor does it intend to take, enforcement action against an individual who purchased and transported raw milk across state lines solely for his or her own personal consumption". This statement reverses FDA’s prior position in which the agency reserved the option of taking action against individual consumers crossing state lines with raw milk. Federal regulation 21 CFR § 1240.61 prohibits the introduction of raw milk for human consumption into interstate commerce.

A caravan of moms brought raw milk across state lines on November 1 and served it to rally participants in front of FDA headquarters.

“Unfortunately, FDA’s announcement allowing individuals to transport raw milk across state lines is filled with the same misinformation that the agency has spread in the past,” says Sally Fallon Morell, president of the Weston A. Price Foundation, an organization that sponsors A Campaign for Real Milk, aimed at universal access to clean raw milk. “FDA continues to insist that raw milk is dangerous, when even the agency’s own exaggerated list of outbreaks shows that raw milk is safer than other foods.”

“FDA lists outbreaks associated with raw cheese, produced in less than sanitary conditions, as ‘outbreaks caused by raw milk,’ thereby inflating the number of illnesses associated with raw milk,” says Fallon Morell. “The actual number of illnesses associated (but not necessarily proved) with raw milk is about forty-two per year, which makes raw milk a very safe food given the large number of raw milk consumers.  No deaths have been associated with raw milk during the past twelve years, but three people have died from tainted pasteurized milk.”

FDA insists that raw milk drinkers constitute less than 1 percent of the population. Yet a 2007 government survey found that about 3 percent of the population consumes raw milk, or about nine million people.  This number is likely to be higher today as raw milk consumption is growing rapidly. Even in the state of Maryland, where raw milk sales are illegal, over 3 percent of respondents stated that they drank raw milk.  “This milk is coming from Pennsylvania, where raw milk sales are legal,” says Pete Kennedy, president of the Farm-to-Consumer Legal Defense Fund, “to the great detriment of Maryland farmers.”  According to Kennedy, hundreds of thousands of dollars of farm sales each year flow from Maryland to Pennsylvania.

The Farm-to-Consumer Legal Defense Fund is currently representing citizens challenging the interstate ban on raw milk in an Iowa federal district court .

According to Fallon Morell, “FDA continues to insist that no science exists to substantiate the nutritional and health benefits of raw milk, yet we now have five European studies, published in peer reviewed journals, showing that raw milk provides powerful protection against asthma and allergies. And there is copious scientific research showing that pasteurization of milk denatures and diminishes the effectiveness of enzymes and vitamins in the milk.”

Moreover, raw milk is designed to build the immune system—the components that do this are denatured by the heat process of pasteurization.  FDA claims that the elderly, the immune-compromised, children and pregnant women especially should avoid raw milk. “These are the very people who need it the most,” says Fallon Morell.

 

When patients who received cortisone injections were re-examined at 6 and 12 months, the results were alarming. Overall, people who received cortisone shots had a much lower rate of full recovery than those who did nothing or who underwent physical therapy. They also had a 63 percent higher risk of relapse than people who adopted the time-honored wait-and-see approach. The evidence for cortisone as a treatment for other aching tendons, like sore shoulders and Achilles-tendon pain, was slight and conflicting, the review found. But in terms of tennis elbow,the shots seemed to actually be counterproductive. In other words, in some way, the cortisone shots impede full recovery, and compared with those who do nothing but rest,  those getting the shots are worse off. Those people receiving multiple injections may be at particularly high risk for continuing damage. In one study that the researchers reviewed, an average of four injections resulted in a 57 percent worse outcome when compared to one injection.

While at times its tempting to go for the quick fix, in this case it can actually result in a longer healing time. There are in fact over two dozen adverse health effects associated with steroid injections in the medical literature. Conservative treatment should always be first (Chiropractic, Physical Therapy, Nutritional Supplements), when that fails, then its time to explore the more invasive options. Unfortunately, in reality it’s usually the other way around – we see patients who have tried everything – pain meds, cortisone shots, surgery- before visiting us as a “last resort”. Hopefully more studies like this will begin to change that.

Introduction

The importance of vitamin D as an essential nutrient is well known, given its role in calcium and phosphate homeostasis. Over the past two decades, the influence of vitamin D on the immune system has become increasingly clear.[1] Recent work has elucidated that vitamin D harbors actions more akin to hormones and pro-hormones. The discovery of the vitamin D receptor (VDR) has stimulated more research into the nature of this vitamin which has, subsequently, been shown to be a steroid hormone. This steroid constitutes a component of a complex endocrine pathway termed the 'Vitamin D endocrine system'.[2] Investigators have found that vitamin D plays an integral role in the induction of cell differentiation, inhibition of cell growth, immunomodulation, and regulation of other hormonal systems.[3] This review seeks to highlight the recent research with respect to vitamin D and its role in chronic rhinitis and chronic rhinosinusitis (CRS).
Chronic Rhinitis and Chronic Rhinosinusitis Pathophysiology

The pathophysiology of CRS occurs, primarily, at the interface of the nasal mucosa with the external environment. The nasal mucosa is a highly specialized immunologic barrier that has evolved to process a constant load of foreign antigens with minimal collateral inflammation. Anatomically, the nasal mucosa consists of an epithelial layer of ciliated, pseudostratified, columnar cells. The cilia and tight junctions interconnecting the epithelial cells constitute a mechanical barrier to antigenic stimulation.[4]

Deep in the epithelium reside a variety of immune cells including lymphocytes and antigen-presenting cells (APCs), specifically dendritic cells and macrophages. These are key components of the acquired immune response.[4] The trigger for and modulation of the nasal acquired immune response has yet to be fully elucidated. Pattern-recognition receptors (PRRs), located in the cytoplasm and on the cell membrane, recognize antigens on microbial organisms. PRRs are also capable of detecting debris from necrotic cells, consequently triggering a process that culminates in the production of antimicrobial, antiviral, and antiproteinase products that facilitate pathogen clearance and help maintain the mechanical barrier.[4]

Vitamin D, as an immunomodulatory steroid hormone, directly affects dendritic cell, monocyte, macrophage, B cell, and T cell functions[5,6] (Fig. 1).|

    Figure 1.

Vitamin effects on the immune system: vitamins A and D take center stage. Systemic or locally produced vitamin D exerts its effects on several immune cell types, including macrophages, dendritic cells, T and B cells. Macrophages and dendritic cells constitutively express vitamin D receptor (VDR), whereas VDR expression in T cells is only upregulated following activation. Vitamin D also induces monocyte proliferation and the expression of interleukin-1 (IL-1) and cathelicidin, thereby contributing to innate immune responses to some bacteria. In T cells, vitamin D decreases the production of IL-2, IL-17, and interferon-γ (IFNγ) and attenuates the cytotoxic activity and proliferation of CD4+ and CD8+ T cells. Finally, vitamin D blocks B-cell proliferation, plasma-cell differentiation, and immunoglobulin production. Reproduced with permission from [1].

The VDR and vitamin D metabolizing enzymes are expressed by several cells of the immune system. For example, Th1 and Th2 cells are direct targets of the activated form of vitamin D, 1,25-dihydroxyvitamin D3, otherwise known as calcitriol. Indeed, activation of CD4+ T cells results in a five-fold increase in VDR expression, enabling calcitriol to regulate at least 102 identified genes.[7]

This regulatory effect has a downstream impact on the levels of circulating chemokines and cytokines. Th1 cells secrete interferon gamma (IFNγ), interleukin (IL)-2, IL-12, and tumor necrosis factor alpha (TNFα), all of which augment the cell-mediated defense against intracellular pathogens. Th2 cells express IL-4, IL-5, and IL-13, which further propagate the Th2 response. These Th2-derived cytokines modulate the immune response against parasites and are also associated with the regulation of atopy and asthma.[8,9] Vitamin D exerts a strong suppressive effect on the expression of IL-2 and IFNγ in a VDR-regulated mechanism. The suppression of IL-2 production, in turn, inhibits T-cell proliferation – indeed, addition of exogenous IL-2 can rescue T-cells from the antiproliferative effects of vitamin D.[1] Evaluation of T-lymphocyte subpopulations demonstrates that vitamin D blocks the induction of Th1 cytokines, especially IFNγ, while simultaneously enhancing Th2 responses through the enhancement of IL-4 production.[8,9] Overall, vitamin D decreases cell-mediated immune responses. This suppressive effect on humoral immunity is facilitated through the effect of vitamin D3 on APC. In APCs, calcitriol inhibits the production of IL-12, a cytokine that normally enhances the Th1 response.[10••] In effect, vitamin D acts as a physiologic 'brake' on humoral immunity.

Similarly, the innate immune system can also be inhibited by vitamin D. Here, vitamin D has been shown to inhibit the differentiation, maturation, and immune-stimulating ability of dendritic cells by downregulating the expression of MHC class II molecules.[1] Dendritic cells have important functions in maintaining both protective immunity and self-tolerance. Immature dendritic cells promote T-cell tolerance, whereas mature dendritic cells activate naive T cells. Physiologic levels of vitamin D inhibit the maturation of dendritic cells and maintain an immature and tolerogenic phenotype with inhibition of activation markers such as MHC class II, CD40, CD80, and CD86 and upregulation of inhibitory molecules. Vitamin D concurrently suppresses IL-12 and enhances IL-10 production in these dendritic cells.[10••]

The net response is a decrease in Th1 responses and proliferation of T regulator cells which act as a further 'check' on the immune response. The immune response is skewed towards a Th2 response with a significant suppression of the Th1 response.[8,9] Thus, vitamin D may have a suppressive effect on inflammation at the level of the nasal mucosa, potentially influencing the development and propagation of CRS. Interestingly, vitamin D has also been shown to have a stimulatory effect on monocytes in vitro, suggesting a complex role in immune hemostasis rather than a purely suppressive effect on the immune system.[1] The extent of this physiologic balance has yet to be fully elucidated.

PRRs activate dendritic cells causing them to acquire chemokine receptors and to migrate to lymph nodes.[4]Similarly, various cytokines and microbial products induce a potent activating response on macrophages and these, in turn, produce both proinflammatory and anti-inflammatory mediators.[5] In the lymph nodes, the activated dendritic cells regulate the differentiation of naïve T cells towards a Th1 or Th2 phenotype.[5] This is largely based on the associated cytokine profile which is distinct between each type of T-helper response.[4] The drive towards either a Th1 or Th2 response is modulated by the type of triggering stimulus and by cues from the external environment.[5] In essence, APCs exert a profound regulating effect on the downstream inflammatory response of the sinonasal mucosa.
Vitamin D and Cathelicidin

Vitamin D also influences the immune response through the regulation of cathelicidin, which is the only antimicrobial peptide produced by humans.[11] Cathelicidin is produced by neutrophils, macrophages, and the cells lining the epithelial surfaces of the skin, respiratory tract, and gastrointestinal tract – the sites which are constantly exposed to potential pathogens[10••] (Fig. 2).

    Figure 2.

Vitamin D stimulates innate immunity and enhances antimicrobial activity via interaction with vitamin D receptor to upregulate the synthesis of the antimicrobial peptide cathelicidin. Reproduced with permission from [6].

Cathelicidin has a broad antimicrobial activity against Gram-positive and Gram-negative bacteria, as well as certain viruses and fungi. Vitamin D treatment upregulated cathelicidin mRNA in several cell lines and primary cultures including keratinocytes, neutrophils, and macrophages.[12] Vitamin D levels were also found to be significantly lower in patients in the intensive care unit with sepsis when compared with healthy controls. In these patients, serum vitamin D directly correlated with serum cathelicidin, suggesting that systemic levels of cathelicidin may be regulated by vitamin D status, and that this may be important in the control of infections such as in CRS.[13]

 
Vitamin D and Chronic Rhinosinusitis

There currently exists a paucity of literature specifically evaluating the role of vitamin D in the pathophysiology of CRS. Recently, Mulligan et al. [5] were able to demonstrate several interesting trends with respect to vitamin D and CRS. They were able to show that patients with CRS and allergic fungal rhinosinusitis demonstrate insufficient levels of vitamin D (<32 ng/ml) when compared with controls (Fig. 3).
 
    Figure 3.

Chronic rhinosinusitis with nasal polyps (CRSwNP) and allergic fungal rhinosinusitis (AFRS) have insufficient levels of circulating 25-OH vitamin D3 (VD3). Compared with control and CRSwNP, AFRS and CRSwNP have significantly lower plasma VD3 levels. Reproduced with permission from [5].

Pinto et al. [14] explored the relationship of vitamin D levels in African American patients with CRS as compared to age and sex matched controls. This group found that vitamin D levels were significantly lower in the African American patients with CRS as compared with age and sex matched controls.

In the study by Mulligan and co-investigators,[5] an inverse relationship between vitamin D and the levels of various immune cells was established in CRS patients. In the subset of patients diagnosed with CRS with nasal polyposis or allergic fungal rhinosinusitis, lower levels of vitamin D correlated to elevated levels of dendritic cells as compared with controls. As discussed, dendritic cells play an important role in directing the differentiation of T-helper cells into Th1 or Th2 subtypes – without vitamin D, the inflammatory response is skewed towards a Th1 subtype promoting a chronic local inflammatory response. The investigators were also able to show that plasma levels of prostaglandin E2 and granulocyte monocyte-colony stimulating factor were upregulated in patients with CRS, and that these chemokine levels were inversely associated with serum vitamin D levels. Furthermore, an interesting correlation between serum levels of vitamin D and the severity of bone erosion on computed tomography scans was noted. Specifically, bone remodeling in patients with insufficient levels of serum vitamin D was significantly greater than in patients with adequate vitamin D levels. This is, perhaps, unsurprising given the well documented role of vitamin D in the regulation of calcium metabolism and bone homeostasis.

Although these results are extremely compelling, the Mulligan study suffers from a small sample size. Future work may extrapolate these data to a larger patient set, ideally through a prospective study, which would help clarify the role of vitamin D in the pathophysiology of CRS. Systemic vitamin D levels could, potentially, be added to the routine workup of patients suffering from CRS and these data could be used to help determine the disease severity and possibly even treatment. To this end, a recent Polish study[15] evaluated the role of vitamin D in the reduction of fibroblast proliferation in vitro from nasal polyps in patients with CRS. Tissue samples were subject to varying doses of calcitriol and a vitamin D analog, tacalcitol, with and without budesonide. A statistically significant decrease in fibroblast proliferation was noted with calcitriol and tacalcitol treatment. Furthermore, increasingly higher doses induced a greater suppressive effect on fibroblast proliferation. This study is a first step towards investigating the utility of topical vitamin D analogs for the treatment of CRS.

Conclusion

Early research suggests that vitamin D is involved in the pathophysiology of chronic rhinitis and CRS. However, this is an area that clearly requires further basic science and clinical research. Nonetheless, it is intriguing to consider the possibility that abnormal vitamin D blood levels – or even the local tissue concentration of vitamin D – could be a critical influencing factor in chronic rhinitis and CRS pathophysiology. The concept of the unified airway would suggest that similar associations from the asthma literature will be found with regards to allergic rhinitis, chronic rhinitis, and CRS. Randomized controlled trials are needed to further evaluate vitamin D and its relationship to allergic rhinitis, chronic rhinitis, and CRS. These findings may then direct researchers to pursue clinical trials aimed at evaluating vitamin D and its analogs as potential therapeutic interventions.

Fibroids
Fibroids are small, noncancerous growths on the uterus. In some cases, they can cause pain, excessive bleeding and even infertility. A surgical procedure to remove the uterus called a hysterectomy is a guaranteed way to get rid of fibroids. Although the cause of fibroids is unknown, fibroid growth is linked to estrogen, according to Medline Plus. Drugs can block or suppress estrogen in order to treat fibroids. Gonadotropin releasing hormone medication can shrink fibroids by 30 to 90 percent by causing the ovaries to stop making estrogen, according to "The New York Times." Fibroids often shrink when women go through menopause, which is a time when they make less estrogen. Eating foods that reduce estrogen levels may therefore also shrink fibroids.

Fiber
The most important thing you can do to combat fibroids with your diet is to eat a high-fiber diet of vegetable-based foods. Aim for at least 20 to 30 grams of fiber daily, according to the authors of "What Your Doctor May Not Tell You About Premenopause." Apples, whole grains, oatmeal, nuts and seeds are all good sources of fiber. Eating a high-fiber diet helps significantly decrease your circulating estrogen levels. Too much estrogen causes your uterus to grow excessively, which sometimes causes fibroids. Less estrogen because of diet may cause your fibroids to shrink as your estrogen levels lower, just as fibroids shrink during menopause or when taking estrogen-lowering medications.

Phytoestrogens
Eating a vegetable-based diet is important because plant foods contain substances called phytoestrogens, or plant estrogens. These substances bind themselves to the same cell receptors as estrogen. This blocks estrogen's ability to affect your cells. Without the excess estrogen causing your uterus to grow, it can shrink along with your fibroids. Foods with high amounts of phytoestrogens include soy products, nuts, seeds and ground flaxseeds. Dr. Michael T. Murray, author of more than 30 books and a member of the Board of Regents of Bastyr University in Washington, recommends eating one to two tablespoons of ground flaxseeds every day.

Foods to avoid
Avoiding certain foods may also help lower estrogen levels. Dr. Murray suggests avoiding sugar, caffeine and saturated fat. The authors of "What Your Doctor May Not Tell You About Premenopause" also suggest that women with fibroids cut back on coffee, dairy products and non-organic meats to avoid contact with hormone drugs and pesticides.

Membrane Complex

The most cutting-edge research suggests that Alzheimer's may stem from an inability of the brain to process glucose, leading to cell death. But the brain has another source of fuel: ketones, produced by the body from mid-chain triglycerides like those found in coconut oil. In fat, the most promising experimental Alzheimer's drugs being tested today is nothing more than medium-chain triglycerides derived from coconut and palm kernel oil.

Coconut oil also turns out to be an extraordinary cooking oil because it resists smoking, even at high temperatures. Try cooking in coconut oil instead of olive oil (or cheaper vegetable oils) and you'll notice a clear difference. Finally, coconut oil is also a fantastic food storage item as long as you can keep it cool. It's a dense source of healthy calories that's usable as both food and medicine. In fact, it can be used as the base for many salves, pastes or even herbal suppositories.

The antioxidants in parsley are able to combat oxidative stress in vivo
The British Journal of Nutrition published a medical study to measure the antioxidant capabilities of parsley (Petroselinum crispum). Fourteen people ate a restricted diet for two weeks which was high in parsley, but low in other foods containing flavones and other natural sources of antioxidants. Urinary excretion of the flavone apigenin was measured before and during the ingestion of parsley. Apigenin levels were noticeably higher when parsley was added to the diet. The researchers noted that when the subjects were on the restricted diet, their oxidative stress markers rose. However, when the people added parsley during the second week of study, the parsley was able to reverse these numbers somewhat.

Parsley is a scientifically proven diuretic
In 2002, the Journal of Ethnopharmacology published a study confirming the diuretic effects of parsley, as claimed for years in folk medicine literature. Rats were given parsley seed tea to drink. Over a twenty-four hour period, the rats had a marked increase in urinary volume. The scientists believed that parsley works as a diuretic due to a mechanism in the herb which blocks the re-absorption of sodium and potassium. This causes more water to flow via osmosis, and hence, a greater urinary volume.

Herbalists use parsley for kidneys, joint problems, nerves, and more
Dr. John R. Christopher, one of the greatest master herbalists of the twentieth century, used parsley in a variety of ways. He used the herb not only for all kidney and bladder issues, but also for jaundice and sexually-transmitted diseases. Dr. Christopher used parsley for water retention (edema), and suggested parsley root tea for stiff fingers and other joint issues. He said gallstones could be removed by drinking a pint of fresh parsley tea every day. The herb is also calming to the nerves and adrenal glands. Dr. Christopher recommended at least two quarts of strong parsley tea per day for these issues, or even up to a cup of tea every hour. To make fresh parsley tea, add a large handful of parsley to a pint of boiling water. Cover, steep, and drink the tea throughout the day.

According to Dr. Christopher, fresh parsley juice is a very potent healer. Parsley juice is an effective blood tonic, but it should be diluted with some other kind of fresh, organic juice, such as carrot juice. No more than an ounce or two of parsley juice should be taken at any one time.

According to the report, some labs voluntarily employ rigorous safety and security measures, including the Galveston National Laboratory in Texas, which is a highly-protected complex with at least eight levels of secured entry, closed-circuit video monitoring, and negative air flow and dedicated exhaust systems to prevent the accidental release of deadly pathogens. But many other such labs do not have this same tight level of a security, as federal law does not regulate the safety protocols used by private research labs.

"Galveston's strict security underlines a little-known fact about hundreds of labs working with bacteria and viruses that could make the 1918-19 Spanish flue epidemic — when as many as 40 million people died — seem like a summer cold," says the report. "Many of the precautions it takes are not required by law."

Will the militarized H5N1 avian flu strain be 'accidentally' released from an unsecured BSL facility?
The report conveniently comes just a few months after it was first announced that scientists in Europe had deliberately created a weaponized H5N1 avian bird flu strain capable of spreading between humans (http://www.naturalnews.com/034228_bioterrorism_flu_strain.html). And since that announcement, there has been a lot of chatter about whether or not the results of this creation should be published in scientific journals, and what the likelihood is that this vicious strain will someday get released into the wild where it could kill off populations around the world at pandemic levels.

The stage is being set, in other words, for the "accidental" release of one of these pathogens at some point in the future, upon which there will be a host of scapegoats to blame. And since all this private research being conducted on deadly viral and bacterial strains at private BSL-3 and BSL-4 labs around the world is apparently not much of a security concern to the federal government, it appears that it is only a matter of time before something catastrophic occurs.

There are also few specifics on the types of research that must be conducted in BSL-4 labs versus BSL-3 labs, which means that the deadly new H5N1 mutant strain can technically be conducted at either, even though BSL-3 labs are intended for less-serious bacterial and viral strains. This is highly concerning because, according to a 2009 Government Accountability Office (GAO) report, there were 400 accidents at BSL-3 labs just in the U.S. alone that year.

The decision comes not even five months after the Board voted to keep fluoridation intact, when mixed opinions on the matter prevented efforts to cut the city's budget in a practical way, as well as cease the forced medication of Bolivar's 10,000-or-so residents in the process.

"Instead of washing your mouth out with fluoride, how about brushing your teeth?" suggested Mayor Best at the recent meeting, pointing out all that drinking fluoride is far different from getting a topical fluoride treatment, which is how the chemical supposedly helps prevent tooth decay. "It's a topical treatment. It's not the ingestion of fluoride that works."

According to reports, four of the city's aldermen voted to discontinue fluoridation, three voted to keep it, and one abstained. Mayor Best later convinced the abstainer, however, to vote to keep fluoridation so that he could cast the tie-breaking vote. Either way, fluoridation is now a thing of the past in Bolivar, a relic of bad science that continues to poison millions across the country who still live in fluoridated towns and cities.

Commenting on suggestions made by some back in September that the Board should uphold fluoridation just because some health officials still believe it to be beneficial, Alderman Arleen Ferguson took a stand for critical thinking rather than blind adherence to tradition by suggesting to attendees at the meeting that fluoridation is more of a religious dogma than it is sound science. Alderman Ferguson, of course, voted to stop fluoridating Bolivar's water supply.

"I trust myself and what I read and I trust my ability to discern the different medical things that I have read," said Ferguson. "I think what [dentists are] presenting is what they have known and what they have had … and I know things do change. I do trust their ability … but I do trust myself and what I read and what I know as a person" (http://bolivarmonews.com).