Posted By Administration,
Monday, February 14, 2011
Updated: Friday, April 18, 2014
New research shows a link between use of two pesticides, rotenone and paraquat, and Parkinson's disease. People who used either pesticide developed Parkinson’s disease approximately 2.5 times more often than non-users.
The study was a collaborative effort conducted by researchers at the National Institute of Environmental Health Sciences (NIEHS), which is part of the National Institutes of Health, and the Parkinson's Institute and Clinical Center in Sunnyvale, Calif.
"Rotenone directly inhibits the function of the mitochondria, the structure responsible for making energy in the cell," said Freya Kamel, Ph.D., a researcher in the intramural program at NIEHS and co-author of the paper appearing online in the journal Environmental Health Perspectives. "Paraquat increases production of certain oxygen derivatives that may harm cellular structures. People who used these pesticides or others with a similar mechanism of action were more likely to develop Parkinson's disease.
The authors studied 110 people with Parkinson’s disease and 358 matched controls from the Farming and Movement Evaluation (FAME) Study (http://www.niehs.nih.gov/research/atniehs/labs/epi/studies/fame/index.cfm) to investigate the relationship between Parkinson’s disease and exposure to pesticides or other agents that are toxic to nervous tissue. FAME is a case-control study that is part of the larger Agricultural Health Study (http://www.niehs.nih.gov/research/atniehs/labs/epi/studies/ahs/index.cfm), a study of farming and health in approximately 90,000 licensed pesticide applicators and their spouses. The investigators diagnosed Parkinson's disease by agreement of movement disorder specialists and assessed the lifelong use of pesticides using detailed interviews.
There are no home garden or residential uses for either paraquat or rotenone currently registered. Paraquat use has long been restricted to certified applicators, largely due to concerns based on studies of animal models of Parkinson's disease. Use of rotenone as a pesticide to kill invasive fish species is currently the only allowable use of this pesticide.
"These findings help us to understand the biologic changes underlying Parkinson’s disease. This may have important implications for the treatment and ultimately the prevention of Parkinson's disease," said Caroline Tanner, M.D., Ph.D., clinical research director of the Parkinson’s Institute and Clinical Center, and lead author of the article.
The NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit www.niehs.nih.gov. Subscribe to one or more of the NIEHS news lists (www.niehs.nih.gov/news/releases/newslist/index.cfm) to stay current on NIEHS news, press releases, grant opportunities, training, events, and publications.
The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visitwww.nih.gov.
Reference: Tanner CM, Kamel F, Ross GW, Hoppin JA, Goldman SM, Korell M, Marras C, Bhudhikanok GS, Kasten M, Chade AR, Comyns K, Richards MB, Meng C, Priestly B, Fernandez HH, Cambi F, Umbach DM, Blair A, Sandler DP, Langston JW. 2011. Rotenone, paraquat and Parkinson’s disease. Environ Health Perspect; doi:10.1289/ehp.1002839 [Online 26 January 2011].
Source: National Institutes of Health (NIH). February 11, 2011. NIH study finds two pesticides associated with Parkinson's Disease. http://www.nih.gov/news/health/feb2011/niehs-11.htm?
Posted By Administration,
Tuesday, February 8, 2011
Updated: Friday, April 18, 2014
The US Department of Agriculture last Friday gave farmers the go-ahead to resume planting Roundup Ready sugarbeets—claiming it’s the only way to avoid a nationwide shortage of sugar!
Hot on the heels of the deregulation of genetically engineered (GE) alfalfa, the USDA said it would once again allow the GE sugarbeet to be planted, contrary to the order of district court judge Jeffrey S. White, who said a full environmental impact statement (EIS) needed to be done first. As the Wall Street Journal points out, an EIS of the type ordered by the judge is usually thousands of pages long and takes years to conduct. That would have kept the genetically modified sugarbeets out of the hands of farmers at least through 2012.
This would allow farmers to begin planting GE sugarbeets this spring. But the environmental and organic seed groups that originally sued the USDA said Friday they would ask Judge White to block this latest move by the USDA.
Processors say there aren’t enough non-GE sugarbeet seeds around for farmers to plant this spring. A study conducted for the sugar industry predicted that US sugar production would plunge 20% if the judge’s ban stays in place, and it appears this study alarmed food companies enough that they were able the pressure USDA into acting now. (For more on sugar and sweeteners, see our article elsewhere in this issue.)
In this case, the sugarbeets are being “partially deregulated”: USDA is permitting farmers to plant genetically modified sugarbeets this year only if they adhere to rules designed to prevent the plant’s wind-blown pollen from reaching organic fields, where its biotechnology traits could spread—though if the rules themselves prove ineffective, organic sugarbeets will be contaminated.
That contamination is what is most worrisome. The Organic Consumers Association had this to say about the deregulation of alfalfa: “[It is] guaranteed to spread its mutant genes and seeds across the nation; guaranteed to contaminate the alfalfa fed to organic animals; guaranteed to lead to massive poisoning of farm workers and destruction of the essential soil food web by the toxic herbicide, Roundup; and guaranteed to produce Roundup-resistant superweeds….” Health advocates have the same concerns about sugarbeets.
If you haven’t already done so, please visit the Aliance for Natural Health's Action Alert page where you can write to President Obama, Congress, and the USDA, and tell them to reverse this terrible decision. Please contact them today!
Posted By Administration,
Friday, February 4, 2011
Updated: Friday, April 18, 2014
Tom D. Thacher, MD and Bart L. Clarke, MD
The past decade has seen renewed interest in the sunshine vitamin, vitamin D, because new data suggest that its benefits extend beyond healthy bones. Accompanying this renewed interest has been a proliferation of published studies related to the effects of vitamin D in many varying clinical conditions. This article discusses the definition of vitamin D insufficiency, identifies the sources of variation in vitamin D status, reviews the evidence for the clinical benefits of vitamin D, and recognizes indications for vitamin D testing.
Representative studies were selected to highlight some of the limitations of current knowledge related to vitamin D insufficiency and the clinical benefits of vitamin D. We selected studies with the strongest level of evidence for clinical decision making related to vitamin D and health outcomes from our personal libraries of the vitamin D literature and from a search of the PubMed database using the term vitamin D in combination with the following terms related to the potential nonskeletal benefits of vitamin D: mortality, cardiovascular, diabetes mellitus, cancer, multiple sclerosis, allergy, asthma, infection, depression, psychiatric, and pain. The level of evidence was assessed with the following hierarchy: meta-analyses of randomized controlled trials (RCTs), RCTs, nonrandomized intervention studies, meta-analyses of observational studies (cohort and case-control studies), and observational studies.
The road to the discovery of vitamin D began with recognition of the childhood bone disease of rickets. The first formal medical treatise on rickets was published by Francis Glisson in 1650, when it was identified as a new disease that was more frequent in the rich than in the poor. During the industrial revolution of the 1800s, the prevalence of rickets increased dramatically, ranging from 40% to 60% among children in crowded and polluted urban areas. In 1822, Sniadecki was the first to recognize and report the association of rickets with a lack of sunlight exposure. By the mid-1800s, cod liver oil had been established as an effective treatment for rickets. The work of Mellanby and McCollum led to the discovery of vitamin D as the agent in cod liver oil that had antirachitic properties. This discovery eventually led to the fortification of milk and other foods with vitamin D in the 1930s, and as a result rickets all but disappeared in North America and Europe.
VITAMIN D METABOLISM
The terminology related to the biochemistry of vitamin D can be confusing. Vitamin D has 2 forms and several metabolites. The 2 forms are vitamin D2 and vitamin D3, also calledergocalciferol and cholecalciferol, respectively. Vitamin D3 is produced in the skin in response to ultraviolet B radiation from sunlight or can be obtained from the diet (ie, animal sources such as deep sea fatty fish, egg yolks, or liver) or from supplements. Few foods naturally have substantial vitamin D content, and dietary vitamin D is obtained primarily through fortified foods or supplements. Vitamin D2, which is found in some plants in the diet and is produced commercially by irradiation of yeast, is used for fortification and supplementation. Both vitamin D2 and vitamin D3 can be used for supplementation.
Vitamin D metabolism. Ca = calcium; 1,25(OH)2D = 1,25-dihydroxyvitamin D; 25(OH)D = 25-hydroxyvitamin D; PTH = parathyroid hormone.
Both forms of vitamin D undergo identical metabolism (Figure). Some evidence indicates that vitamin D2 may be metabolized more rapidly than vitamin D3,but with regular daily intake they can be considered bioequivalent. Both forms of vitamin D are converted to 25-hydroxyvitamin [25(OH)D] in the liver, and the serum level of 25(OH) D is measured to determine the adequacy of vitamin D status. In the kidney, 25(OH)D is hydroxylated to 1,25-dihydroxyvitamin D [1,25(OH)2D], which is the only biologically active form of vitamin D. Acting principally on the duodenum, 1,25(OH)2D increases calcium absorption. It also acts on bone cells, both osteoblasts and osteoclasts, to mobilize calcium.
The characteristics of 1,25(OH)2D are those of a hormone, and consequently vitamin D is a prohormone rather than a true vitamin. The structure of 1,25(OH)2D is similar to that of other steroid hormones. As long as sunlight exposure is adequate, 1,25(OH)2D can be produced by the body without the requirement for ingestion in the diet. Like other hormones, 1,25(OH)2D circulates at picogram concentrations that are 1000 times less than those of the precursor 25(OH)D. Based on the need for increased calcium absorption, the synthesis of 1,25(OH)2D is tightly regulated and stimulated primarily by serum parathyroid hormone (PTH), as well as low serum calcium or phosphorus levels, and inhibited by circulating FGF23 produced by osteocytes. Although produced in the kidney, 1,25(OH)2D acts at a distance in the intestinal cell to increase calcium absorption or in the bone to stimulate differentiation and activation of osteoblasts and osteoclasts.
ASSESSING VITAMIN D STATUS
Determination of vitamin D status is not based on measurement of serum 1,25(OH)2D concentrations. Vitamin D status is assessed by measuring the prohormone 25(OH) D, which is an indicator of supply rather than function. The most stable and plentiful metabolite of vitamin D in human serum, 25(OH)D has a half-life of about 3 weeks, making it the most suitable indicator of vitamin D status. In the past, vitamin D deficiency was identified by the presence of bone disease, either rickets or osteomalacia. Bone disease caused by vitamin D deficiency is associated with serum 25(OH)D values below 10 ng/mL (to convert to nmol/L, multiply by 2.496). More recently, the term vitamin D insufficiency has been used to describe suboptimal levels of serum 25(OH)D that may be associated with other disease outcomes. Precisely defining vitamin D deficiency or insufficiency on the basis of 25(OH)D values is still a matter of much debate. A useful but rather simplistic classification of vitamin D status is shown in the Table. A cutoff value of 30 ng/mL is sometimes used for optimal vitamin status. On the basis of measured concentrations of 25(OH)D, many patients are given a diagnosis of vitamin D deficiency or insufficiency when most have no evidence of disease.
Classification of Vitamin D Status by 25(OH)D Concentrationa,b
As discussed in detail in recent reviews, investigators have considered various functional measures to assess the adequacy of vitamin D status. One functional definition of optimal vitamin D status is the 25(OH)D level that maximally suppresses PTH secretion, because the major stimulus for PTH secretion is a low level of serum ionized calcium. In adults, multiple cross-sectional examinations of the relationship between serum PTH and 25(OH)D levels demonstrate a plateau in suppression of PTH when the 25(OH)D level reaches approximately 30 ng/mL. This is the rationale for selecting 30 ng/mL as the cutoff value for defining optimal vitamin D status. However, this definition represents an average value at a population level but does not account for the wide variation in the 25(OH) D level that represents adequacy at an individual level. Many patients have very low 25(OH)D values without evidence of increased production of PTH, and conversely, 25(OH)D levels greater than 30 ng/mL do not guarantee PTH suppression. Another limitation of this definition is that, in children, an elevated PTH level does not indicate inadequate vitamin D status and has been associated with increased calcium absorption. In puberty, the PTH concentration increases, which may stimulate increased periosteal bone formation and increased bone accrual. In fact, preliminary evidence suggests that, with adequate calcium intake, a high-normal PTH level and low-normal 25(OH)D level may result in greater bone size and mass during puberty.
Another method used in some research studies for defining optimal vitamin D status is the 25(OH)D level at which there is no incremental increase in 1,25(OH)2D levels after administration of vitamin D, because the level of 1,25(OH)2D is adequate to meet demand. Similar to the findings related to PTH in adults, an incremental increase in the level of 1,25(OH)2D was observed after administration of vitamin D in children when values of 25(OH)D were less than 25 to 30 ng/mL. In situations of very low calcium intakes, some evidence suggests that the demand for 1,25(OH)2D may be greater.Thus, vitamin D requirements may vary based on customary calcium intake.
Another functional measure of vitamin D status is the 25(OH)D level that results in maximal intestinal calcium absorption. By combining the results of 3 studies in adults, Heaney concluded that optimal calcium absorption occurred at 25(OH)D levels of 32 ng/mL or greater. In contrast, another study found no association between 25(OH)D levels and calcium absorption in healthy women. Fractional calcium absorption was high (>50%) in Nigerian children with presumed dietary calcium deficiency rickets and low dietary calcium intakes despite low normal serum 25(OH)D concentrations. After vitamin D administration and a marked increase in 25(OH) D and 1,25(OH)2D concentrations, fractional calcium absorption did not increase any further. In these studies in children, fractional calcium absorption was not related to serum 1,25(OH)2D levels either before or after vitamin D administration. In a study of adults attending an osteoporosis clinic, concentrations of 1,25(OH)2D and intestinal calcium absorption did not appear to decline until 25(OH) D concentrations fell to 4 ng/mL or less, a level that is generally considered to be indicative of severe vitamin D deficiency.
More recently, the criterion for optimal vitamin D status has moved away from being defined as the 25(OH) D concentration needed to achieve skeletal health to that which demonstrates optimal benefits on nonskeletal health outcomes. The evidence related to these outcomes will be considered later in this review.
SOURCES OF VARIATION IN VITAMIN D STATUS
Factors known to influence 25(OH)D levels include race, vitamin D intake, sun exposure, adiposity, age, and physical activity. Even when all the factors known to influence 25(OH)D concentrations are taken into account, most of the individual variation of 25(OH)D values is difficult to explain. Consequently, it is difficult to assess the risk of clinical or biochemical consequences of vitamin D insufficiency in a patient on the basis of concentrations of 25(OH) D alone. The duration of vitamin D insufficiency, the responsiveness of the vitamin D receptor, dietary calcium intake, and individual calcium requirements likely modify the clinical consequences of vitamin D deficiency or insufficiency based on levels of 25(OH)D.
A single exposure to summer sun in a bathing suit for 20 minutes produces the equivalent of 15,000 to 20,000 IU of vitamin D3. In a study of Hawaiian surfers with sun exposure of at least 15 hours per week for the preceding 3 months, 25(OH)D levels ranged from 11 up to 71 ng/mL, demonstrating wide individual variation. Outdoor sun exposure and time spent outdoors are better predictors of serum 25(OH)D values than dietary vitamin D intake.
The 25(OH)D level achieved with the same oral dose of vitamin D varies widely by individual. The level of 25(OH)D that results in clinical consequences probably varies with calcium intake, race, age, body fat, and individual genetic factors, all of which may influence calcium homeostasis. Genetic variation represented by polymorphisms of certain genes in the vitamin D metabolic pathway explains some of the interindividual variability of 25(OH)D concentrations, particularly polymorphisms of the enzyme 7-dehydrocholesterol reductase in the skin, cytochrome P450 25-hydroxylase in the liver, and vitamin D–binding protein in the circulation. The functional effect of a particular level of 25(OH)D depends on the uptake of 25(OH)D by target cells and the efficiency of 1α-hydroxylation to produce 1,25(OH)2D.
MEASUREMENT OF 25(OH)D LEVELS
Some controversy exists regarding the best method for measuring 25(OH)D levels. Radioimmunoassay has been the most common method reported in the literature and was the method used in some of the large-scale population studies of vitamin D, such as the National Health and Nutrition Examination Survey (NHANES) and the Women's Health Initiative (WHI).
The accuracy of measurement varies widely between individual laboratories and between different assay methods. In one study, identical serum samples were provided to 6 different laboratories, and the chemiluminescent assay tended to return higher values for 25(OH)D. Competitive protein-binding assays are also known to generally yield higher 25(OH)D values. When serum samples were spiked with an additional 20 ng/mL of 25(OH)D, the increment in 25(OH)D level was less than 20 ng/mL in all the laboratories, except the one using high-performance liquid chromatography. Antibodies used in some radioimmunoassays do not detect both 25(OH)D2 and 25(OH)D3. The use of a standard cutoff value for adequate vitamin D status is problematic if applied to all laboratories and all methods. A single serum sample could be assessed as showing adequate vitamin D status in one laboratory and an insufficient level in another, with differences of up to 17 ng/mL.
More recently, large medical laboratories have begun using liquid chromatography–tandem mass spectrometry, which identifies the 25-hydroxylated forms of both vitamin D2and D3. The total 25(OH)D, which is the sum of 25(OH)D2 and 25(OH)D3, is used to evaluate vitamin D status. Since 2003, there has been more than a 15-fold increase in the volume of 25(OH)D measurements at Mayo Clinic in Rochester, MN (Singh R., personal communication), reflecting the increasing attention clinicians are giving to vitamin D status.
CLINICAL MANIFESTATIONS OF VITAMIN D DEFICIENCY
The classical manifestation of vitamin D deficiency is nutritional rickets, which results from inadequate mineralization of growing bone. Consequently, rickets is a disease of children. Far from being eradicated, nutritional rickets continues to occur throughout the world, with reports from at least 60 countries in the past 20 years. In a review of published cases of rickets in the United States, most occurred in children younger than 30 months. The vast majority of cases in the United States occurred in African American infants who were fed with breast milk rather than formula. Florid rickets manifests with leg deformities; enlargement of the growth plates of the wrists, ankles, and costochondral junctions; and rib cage deformities. Subtle symptoms that should raise the clinical suspicion of rickets in children include bone pain in the legs, delayed age of standing or walking, frequent falling, and delayed growth. Hypocalcemic seizures in the first year of life may be the initial manifestation of rickets.
Radiography of the long bones at the knees and the wrists is necessary to confirm the diagnosis of rickets. Radiography demonstrates impaired mineralization of the growth plates, evident by widening of the growth plate and fraying of the margin of the metaphyses. Biochemical features most consistently include hypophosphatemia and an elevated alkaline phosphatase level. As a result of vitamin D deficiency, serum concentrations of 25(OH)D are very low in patients with rickets, usually less than 5 ng/mL. However, concentrations of 25(OH)D may not be markedly reduced if rickets results from calcium deficiency or if the child has recently received vitamin D or sun exposure. In some tropical countries, where sun exposure is plentiful, calcium deficiency is more important than vitamin D deficiency as a cause of rickets. However, even in the United States, only 22% of children with nutritional rickets had deficient levels of 25(OH)D, indicating that calcium deficiency as a cause of rickets needs to be considered domestically as well.
Osteomalacia refers to the failure of organic osteoid formed by osteoblasts to become mineralized with calcium and phosphorus. Although histological osteomalacia is characteristic of rickets, the term osteomalacia is generally used to describe the bone disease caused by vitamin D deficiency in adults, who no longer have growing bones. The clinical manifestations of these 2 conditions are different.
Bone pain is a characteristic feature of osteomalacia, and it can be confused with arthritis or fibromyalgia. Bone pain due to osteomalacia primarily affects the bones between the joints, whereas arthritis usually causes predominantly joint pain, and fibromyalgia causes more diffuse muscle and soft tissue pain; however, it can be difficult to distinguish between these disorders. Proximal muscle weakness and gait instability are often present. Because the growth plates have closed in adults, the radiographic features differ from those typical of rickets. Radiography may reveal pseudofractures of the pelvis, femurs, metatarsals, or lateral margins of the scapulae. The biochemical features of osteomalacia are similar to those of rickets, with increased serum alkaline phosphatase and PTH values, and low calcium, phosphorus, and 25(OH)D values in most cases. A review of all the archived cases of bone biopsy–proven osteomalacia seen by the Bone Histomorphometry Laboratory at Mayo Clinic concluded that radiographic examination as well as serum calcium, phosphorus, and alkaline phosphatase assays are adequate screening tests in patients who have a clinical presentation suggestive of osteomalacia, but that 25(OH)D values may be normal.
In a cross-sectional study of iliac bone biopsy specimens obtained at autopsy, an excess accumulation of osteoid, which corresponds with histological osteomalacia, was found only in patients with 25(OH)D values less than 25 ng/mL. However, even patients with very low values of 25(OH)D did not consistently have evidence of osteomalacia.
POTENTIAL BENEFITS OF VITAMIN D
Apart from the deficiency diseases of rickets and osteomalacia, recent evidence suggests other skeletal and nonskeletal benefits of vitamin D. In evaluating the evidence, it is important to recognize the limitations inherent in the study design and methodology. Important issues that apply to vitamin D research include the following:
Was the study design observational, which can only demonstrate associations and is subject to confounding, or was it an RCT that generally balances unmeasured confounding variables?
How was the intake of vitamin D measured? Was the serum 25(OH)D value considered a proxy measure of vitamin D intake?
What outcome was measured to assess the benefit of vitamin D? Was it the achieved 25(OH)D level or a specific clinical outcome that matters to the patient? Was assessment of the outcome the primary aim of the study?
Is 25(OH)D the most appropriate biomarker of vitamin D status in all situations?
In the following section, representative studies of the available evidence related to the skeletal and nonskeletal effects of vitamin D are reviewed.
Bone Density. In addition to the treatment and prevention of vitamin D–deficiency rickets in children, vitamin D has been associated with other beneficial skeletal effects. A retrospective cohort study of pubertal girls demonstrated increased bone mineral density (BMD) of the femoral neck, but not of the spine or radius, among those who received supplemental vitamin D in infancy. Evidence of a positive association between BMD and serum 25(OH)D concentrations in adolescents is fair, but the evidence for a positive association in infants is inconsistent. Serum 25(OH)D concentration was related to hip BMD in community-dwelling women and men aged at least 20 years who participated in the US NHANES III survey. Higher calcium intake was significantly associated with higher BMD only for women with 25(OH)D values less than 20 ng/mL. One of the limitations of a cross-sectional study like the NHANES survey is that it can demonstrate only associations, not cause-and-effect relationships. Another confounding factor may be associated with low vitamin D intake and low bone density. For example, healthier people who exercise more outside in the sun may have greater bone density because of their exercise and higher 25(OH)D levels because of sun exposure. The WHI calcium and vitamin D supplementation trial showed that hip bone density was 1.06% higher in women receiving calcium and vitamin D supplementation vs placebo at 9 years, but that their lumbar spine and total body bone density did not differ significantly from those receiving placebo during this interval.
Fractures and Falls. On the basis of RCTs, the strongest evidence for the benefit of vitamin D relates to the prevention of fractures and falls. In a meta-analysis of 12 RCTs, a reduced nonvertebral fracture risk was demonstrated only for doses of vitamin D greater than 400 IU/d (relative risk [RR], 0.80; 95% confidence level [CI], 0.72-0.89). Similarly, a meta-analysis of 8 RCTs demonstrated that vitamin D reduced the risk of falls (RR, 0.78; 95% CI, 0.64-0.94), but only if the dose was 700 IU/d or greater and the 25(OH)D concentration was at least 25 ng/mL. The benefit of vitamin D could have been limited to those with unrecognized osteomalacia, which is associated with proximal muscle weakness and gait instability. These high-quality studies provide clear evidence that a minimum dose of 800 IU/d of vitamin D will reduce the risk of falls and fractures in older adults. However, a recent RCT of a 500,000 IU annual dose of vitamin D in women of advanced age increased the median 25(OH)D concentration from 20 ng/mL to 48 ng/mL one month later but resulted in an increased risk of falls and fractures in the group receiving this regimen.
Interest in the nonskeletal effects of vitamin D has been increasing since the discovery of vitamin D receptors and the 1α-hydroxylase enzyme in multiple tissues, including cells of the pancreas, immune system, macrophages, vascular endothelium, stomach, epidermis, colon, and placenta. In these tissues, 25(OH)D can be converted to 1,25(OH)2D locally, without altering serum 1,25(OH)2D concentrations. Through these paracrine effects, 1,25(OH)2D influences the expression of genes in local tissues. However, the evidence for the nonskeletal benefits of vitamin D is not as strong as the evidence for the skeletal effects.
Lower Mortality Rate. In a prospective observational study of adults older than 65 years participating in NHANES III, the risk of death was 45% lower in those with 25(OH)D values greater than 40 ng/mL compared with those with values less than 10 ng/mL (hazard ratio [HR], 0.55; 95% CI, 0.34-0.88). However, this may simply reflect the fact that people with underlying illness or immobility (who are more likely to die) tend to have lower 25(OH)D levels, in part as a result of having spent less time outdoors or of having less adequate nutrition. Because vitamin D is sequestered in adipose tissue, obesity is also associated with lower 25(OH)D levels. However, observational studies cannot prove whether low 25(OH)D status is the cause of greater mortality or just a marker of other underlying risk factors.
In contrast, a meta-analysis of 18 RCTs of vitamin D supplementation in postmenopausal women of advanced age, with dosages ranging from 300 to 2000 IU/d, reported a 7% lower risk of death in those receiving a vitamin D supplement (RR, 0.93; 95% CI, 0.87-0.99). This highlights the difference often found between RCTs and observational studies. The effect sizes found in observational studies are often attenuated or absent in RCTs.The situation with vitamin D is analogous to that of hormone replacement therapy (HRT) in postmenopausal women. The beneficial effects of HRT were demonstrated for multiple health outcomes in observational studies, but the WHI RCT in older postmenopausal women failed to confirm the beneficial effects of HRT on dementia and cardiovascular disease. In the observational trials, healthier women were more likely to use estrogen replacement and had fewer adverse health outcomes, indicating a “healthy user” bias. Only an RCT definitively demonstrated that the risks of first-time use of HRT outweighed the benefits in women older than 60 years.
Despite the slight reduction in mortality associated with vitamin D supplementation, the primary aim of the RCTs included in the meta-analysis was not to assess mortality. Not all trials of vitamin D reported mortality outcomes, so those trials could not be included in the meta-analysis. Trials that showed a mortality effect would be more likely to report this outcome, leading to a high likelihood of reporting bias that could render the slight mortality reduction statistically insignificant.
Lower Cardiovascular Mortality. The reduced mortality in the aforementioned observational study mirrored in large part the reduced cardiovascular mortality in those with 25(OH)D values greater than 40 ng/mL compared with those with values less than 10 ng/mL (HR, 0.42; 95% CI, 0.21-0.85). In another observational cohort study, patients who had angiography and 25(OH)D measurements were followed up for 8 years. Those from the highest 25(OH)D quartile (median, 28 ng/mL) had a lower mortality (HR, 0.45; 95% CI, 0.32-0.64) than those from the lowest quartile (median, 8 ng/mL). Although these observational studies do not demonstrate that low 25(OH)D values accelerate cardiovascular mortality, low 25(OH)D concentrations were associated with serum markers of inflammation that are indicators of cardiac risk.
Recently, concern has been expressed that vitamin D could potentially accelerate vascular disease. In a study of African Americans with type 2 diabetes mellitus, 25(OH)D levels correlated with increased calcified plaque in the aorta and carotids, but not in the coronary arteries.Vascular disease associated with chronic kidney disease, especially that associated with very low bone turnover, may also be accelerated with supplementation with standard doses of vitamin D. Furthermore, concern has been raised recently that other disorders characterized by vascular inflammation, such as diabetes mellitus, rheumatoid arthritis, or systemic lupus erythematosus, may not benefit from standard recommended doses of vitamin D supplementation.
Vitamin D may affect other cardiovascular and metabolic disease risks. In an observational study of adolescents in NHANES III, those with the lowest 25(OH)D values (<15 ng/mL) had more than a 2-fold greater odds of having an elevated blood pressure compared with the group of adolescents with higher 25(OH)D levels (>26 ng/mL) (odds ratio [OR], 2.4; 95% CI, 1.3-4.2).
The NHANES III data in adults indicated that those with 25(OH)D levels of less than 21 ng/mL had an increased risk of hypertension, diabetes, obesity, and high triglyceride levels—all metabolic manifestations associated with increased cardiovascular mortality. Although obesity is associated with lower serum 25(OH)D levels because of the sequestration of vitamin D in adipose tissue, it is likely not the consequence of low 25(OH)D levels. Additionally, the 25(OH)D level may be a marker of other factors associated with obesity, such as physical inactivity and reduced outdoor sun exposure.
Reduced Risk of Diabetes Mellitus. A meta-analysis of 5 observational studies of vitamin D supplementation in childhood reported a nearly 30% reduction in the risk of type 1 diabetes in children who had ever received vitamin D supplements (OR, 0.71; 95% CI, 0.60-0.84). Unfortunately, most studies had no information about vitamin D dosage or adherence. Because these were observational studies, and vitamin D was not randomly assigned to children, it is possible that characteristics of families who provided supplemental vitamin D to their children contributed to the decreased risk of type 1 diabetes in children receiving supplements.
Vitamin D receptors are present in pancreatic β cells, and vitamin D may augment insulin secretion and insulin sensitivity. Adolescents in NHANES III with serum 25(OH)D levels of less than 15 ng/mL were more likely to have elevated blood glucose levels than those with the highest 25(OH)D values (>26 ng/mL) (OR, 2.5; 95% CI, 1.0-6.4). The observational Nurses Health Study found that vitamin D supplementation and calcium supplementation were both associated with a reduction in risk of type 2 diabetes.Current data related to vitamin D and the risk of type 2 diabetes are limited by inadequate adjustment for confounding variables, post hoc analyses, and inability to identify the separate effects of calcium and vitamin D. Because milk is the major source of both vitamin D and calcium in the diet, it is difficult to identify the independent effects of dietary calcium and vitamin D on the basis of intake or 25(OH)D levels. Skim milk intake is also inversely associated with obesity, which could account for an association between the intake of dietary calcium and vitamin D and a reduced risk of type 2 diabetes.
Reduced Risk of Cancer. Vitamin D is known to promote cellular differentiation, inhibit cellular proliferation, and reduce the growth of certain tumors in laboratory animals. A meta-analysis of case-control studies of those with and without colon cancer found that, for each 20 ng/mL increase in serum 25(OH)D levels, the odds of colon cancer were reduced by more than 40% (OR, 0.57; 95% CI, 0.43-0.76). Other studies have shown that dietary calcium intake is also associated with reduced colon cancer risk and adenoma formation. Because milk intake is a major determinant of serum 25(OH)D levels, it is difficult to separate the effect of vitamin D from that of calcium intake.
In the case of colon cancer, one large RCT was performed to evaluate the effect of combined supplementation with calcium and vitamin D on the risk of colon cancer. In the WHI trial, supplementation with calcium and vitamin D had no significant effect on the risk of colorectal cancer during 8 years of follow-up. Several limitations of this study may have contributed to this lack of effect. Colorectal cancer is a long latency disease, and 8 years may not have been sufficient time to observe the effect of calcium and vitamin D. Another criticism is that the relatively low dose of 400 IU of vitamin D may have not been protective or sufficient to increase serum 25(OH)D levels adequately. Concentrations of 25(OH)D were measured at baseline but not during follow-up. Declining adherence over time would have further reduced the effective doses of calcium and vitamin D.
Breast cancer has also been associated with vitamin D insufficiency. A meta-analysis combining 7 observational studies reported a lower risk of breast cancer among women in the highest compared with the lowest quartile of 25(OH) D values (OR, 0.55; 95% CI, 0.38-0.80). As with colon cancer, calcium intake was also associated with a reduced risk of breast cancer. Because obesity is associated with an increased risk of breast cancer and low 25(OH)D levels, it is a confounding factor in the association between breast cancer risk and vitamin D.
As with colon cancer, the WHI RCT of a combined regimen of calcium and vitamin D showed no benefit of supplementation on the risk of breast cancer, again highlighting the different conclusions of observational studies and RCTs. The limitations of the breast cancer study are similar to those of the study focused on colon cancer. This study demonstrated the potential confounding effects of physical activity and obesity. Baseline 25(OH)D levels were greater among women with lower body mass index and more recreational physical activity. When controlling for body mass index and physical activity, serum 25(OH)D concentration was not associated with breast cancer risk.
In a meta-analysis of 11 observational studies, prostate cancer was not associated with serum 25(OH)D levels. The evidence regarding an association between pancreatic cancer and 25(OH)D levels is conflicting. A multinational cohort study found no protective association between greater 25(OH)D values and gastric, esophageal, endometrial, ovarian, kidney, non-Hodgkin lymphoma, and pancreatic cancers. Drake et al recently showed that event-free survival and overall survival were reduced in vitamin D–insufficient patients newly diagnosed as having diffuse large B-cell lymphoma and T-cell lymphoma during 34.8 months of follow-up.
To date, studies have not shown impressive effects of vitamin D treatment on malignancies.
Reduced Risk of Multiple Sclerosis. The incidence of multiple sclerosis increases with increasing latitude, corresponding with reduced ultraviolet B sun exposure and lower serum levels of 25(OH)D. A case-control study demonstrated that the odds of having multiple sclerosis were lower in the group with the highest 25(OH)D levels. However, the association was found only in white patients [OR, 0.59; 95% CI, 0.36-0.97 for a 20 ng/mL increase in 25(OH)D], not in African American patients. It is difficult to exclude the possibility that other confounding exposures associated with increasing latitude and greater indoor activity during winter months contribute to the risk of multiple sclerosis. Little evidence supports a therapeutic role for vitamin D in the treatment of multiple sclerosis.
Reduced Risk of Allergy and Asthma. Several lines of evidence demonstrate the effects of vitamin D on proinflammatory cytokines, regulatory T cells, and immune responses, with conflicting interpretation of the effects of vitamin D on allergic diseases. In a cross-sectional study of Costa Rican children, low 25(OH)D levels were associated with elevated IgE and eosinophil counts, as well as with increased asthma-related hospitalizations and use of anti-inflammatory medication. However, an association does not prove causation, and alternative explanations can account for this association. For example, children with more severe asthma may spend more time indoors and have less sun exposure.
Low maternal vitamin D intake in pregnancy has been associated with an increased likelihood of childhood wheezing at ages 3 and 5 years. In contrast, maternal 25(OH)D levels of greater than 30 ng/mL in pregnancy have been associated with childhood eczema at age 9 months and asthma at age 9 years. Vitamin D supplementation in infancy has been associated with increased atopy and allergic rhinitis in adulthood. Increasing 25(OH)D levels were associated with increasing risk of allergic rhinitis among adults in NHANES III. The conflicting data indicate the need for RCTs to demonstrate the effect of vitamin D on the prevention and control of allergic diseases.
Reduced Risk of Infection. Vitamin D is required for the expression of cathelicidin by macrophages, which is involved in bacterial killing. A meta-analysis of 7 observational studies noted a reduced risk of active tuberculosis in those with the highest vs the lowest values of 25(OH)D (OR, 0.68; 95% CI, 0.43-0.93). However, an RCT in a West African population with baseline mean 25(OH)D values of 31 ng/mL showed no effect of 100,000 IU of supplemental vitamin D given at the beginning and at 3 and 8 months of tuberculosis treatment on the rate of sputum conversion or resolution of markers of clinical severity. However, this dose of vitamin D may have been insufficient because the increase in 25(OH)D concentration during treatment did not differ between the supplement and placebo groups.
In observational data from NHANES III, persons with 25(OH)D values lower than 10 ng/mL were more likely to have had a recent upper respiratory tract infection than those with higher 25(OH)D values in all 4 seasons of the year. This association was even stronger in those with asthma or chronic obstructive pulmonary disease. Whether this association is explained by the fact that people who remain indoors are more likely to catch colds remains unclear.
A case-control study reported that mean 25(OH)D values were lower in children with bronchiolitis or pneumonia admitted to the pediatric intensive care unit than in healthy control children or in children with pneumonia admitted to the general pediatric ward.
Reduced Risk of Mental Illness. A cohort of Finnish children who received supplemental vitamin D in their first year of life had a lower risk of developing schizophrenia.However, the significance of this association is unclear because it was unrelated to adherence to vitamin D supplementation, was only evident in males, and was not found with any other mental illness.
To examine the effect of vitamin D on depression, overweight and obese patients were randomized to receive 20,000 or 40,000 IU of vitamin D or placebo weekly for 1 year. At baseline, those with 25(OH)D concentrations lower than 16 ng/mL had greater Beck Depression Inventory scores, indicating that they were more depressed, than those with higher 25(OH)D levels. The 2 groups receiving vitamin D supplementation had significant improvement in their scores, whereas the placebo group did not.
Less Musculoskeletal Pain. A small descriptive study reported that most patients (93%) with persistent musculoskeletal pain had 25(OH)D values of 20 ng/mL or less. In one RCT, patients with diffuse musculoskeletal pain or osteoarthritis and 25(OH)D values lower than 20 ng/mL were randomized to receive vitamin D or placebo for 3 months.Those given vitamin D had no improvement in their pain compared with baseline or compared with placebo-treated patients. In another double-blind RCT, primary care patients with 25(OH)D levels of 10 to 25 ng/mL were randomized to receive 50,000 IU of vitamin D or placebo weekly for 8 weeks. The treated group showed significantly greater improvement in fibromyalgia assessment scores than the placebo group. Patients with 25(OH)D values lower than 10 ng/mL were treated in an unblinded fashion with 50,000 IU of vitamin D weekly for 8 weeks but had no symptom improvement.
Reduced Risk of Renal Disease. In a subgroup analysis of the NHANES III data set, low 25(OH)D values were associated with a greater risk of kidney failure in African American but not in white participants. However, the opposite trend was observed in whites.
INDICATIONS FOR VITAMIN D TESTING
Measurement of serum 25(OH)D levels is indicated in select circumstances. If clinical symptoms of rickets in children or osteomalacia in adults are present, measurement of 25(OH)D levels will confirm vitamin D deficiency. Such testing would be appropriate in adults or children with bone pain, elevated serum alkaline phosphatase or PTH levels, and low serum calcium or phosphorus levels. Persons of advanced age, those with osteoporosis, or those at increased risk of falls or fractures may also benefit from measurement of 25(OH)D levels. However, one could argue that providing at-risk groups with routine supplementation of adequate doses of vitamin D may make testing for vitamin D insufficiency unnecessary. When to test and how to treat adults with vitamin D deficiency have recently been reviewed in this journal. No evidence shows benefit for screening 25(OH)D levels in the asymptomatic population.
Critically evaluating the evidence regarding the purported benefit of vitamin D on a multitude of health outcomes is difficult. The bulk of current data is based on observational, epidemiological studies, which are useful for generating hypotheses but not for proving causality. It is particularly difficult to tease out the effects of confounding variables that relate both to health outcomes and to vitamin D status, such as physical activity, milk intake, and adiposity. Few of the observational associations have been confirmed by RCTs, and many of the interventional studies of vitamin D also included calcium supplementation. Future clinical trials, including a National Institutes of Health–funded 5-year 20,000-participant prospective RCT comparing the effect of supplementation with 2000 IU/d of vitamin D3 or placebo, will help clarify the benefits and risks of vitamin D supplementation in many of the disorders discussed in this review.
On the basis of the current data, it seems prudent for persons older than 60 years to take a vitamin D supplement of 800 to 2000 IU/d to reduce the risk of falls and fractures. These recommendations are consistent with the recently released report of the Institute of Medicine, which recommended that healthy adults take 600 IU/d to maintain skeletal health and also concluded that information about the health benefits beyond bone health could not be considered reliable. Dark-skinned infants who are exclusively breast-fed are at greater risk of rickets and should receive 400 IU/d of supplemental vitamin D. Vitamin D supplementation in these ranges is likely to prevent bone loss, may improve bone density, may reduce fractures, and appears to reduce falls. Although vitamin D intoxication has been associated only with intakes of 50,000 to 1 million IU/d over the course of months or years, the potential risks of kidney stones, vascular disease, and fractures with high-dose vitamin D regimens are unclear. Until more data from RCTs are available, a healthy dose of skepticism should be maintained regarding the other health claims for vitamin D.
Harbour R, Miller J. A new system for grading recommendations in evidence based guidelines. BMJ. 2001;323(7308):334-336.
Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89(11):5387-5391.
Trang HM, Cole DE, Rubin LA, Pierratos A, Siu S, Vieth R. Evidence that vitamin D3 increases serum 25-hydroxyvitamin D more efficiently than does vitamin D2. Am J Clin Nutr. 1998;68(4):854-858.
Holick MF, Biancuzzo RM, Chen TC, et al. Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D. J Clin Endocrinol Metab. 2008;93(3):677-681.
Thacher TD, Obadofin MO, O'Brien KO, Abrams SA. The effect of vitamin D2 and vitamin D3 on intestinal calcium absorption in Nigerian children with rickets. J Clin Endocrinol Metab. 2009;94(9):3314-3321.
Plum LA, DeLuca HF. The functional metabolism and molecular biology of vitamin D action. In: Holick MF, ed. Vitamin D: Physiology, Molecular Biology, and Clinical Applications. 2nd ed. New York, NY: Humana Press; 2010:61-97.
Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-281.
Kennel KA, Drake MT, Hurley DL. Vitamin D deficiency in adults: when to test and how to treat. Mayo Clin Proc. 2010;85(8):752-757.
Prentice A, Goldberg GR, Schoenmakers I. Vitamin D across the lifecycle: physiology and biomarkers. Am J Clin Nutr. 2008;88(2):500S-506S.
Chapuy MC, Preziosi P, Maamer M, et al. Prevalence of vitamin D insufficiency in an adult normal population. Osteoporos Int. 1997;7(5):439-443.
Abrams SA, Griffin IJ, Hawthorne KM, Gunn SK, Gundberg CM, Carpenter TO. Relationships among vitamin D levels, parathyroid hormone, and calcium absorption in young adolescents. J Clin Endocrinol Metab. 2005;90(10):5576-5581.
Tylavsky FA, Ryder KM, Li R, et al. Preliminary findings: 25(OH)D levels and PTH are indicators of rapid bone accrual in pubertal children. J Am Coll Nutr.2007;26(5):462-470.
Peacock M, Selby PL, Francis RM, Brown WB, Hordon L. Vitamin D deficiency, insufficiency, sufficiency and intoxication: What do they mean? In: Norman AW,Schaefer K, Grigoleit H-G, Herrath DV, eds. Vitamin D: Chemical, Biochemical and Clinical Update. Berlin, Germany: Walter de Gruyter; 1985:569-570.
Thacher TD, Fischer PR, Isichei CO, Pettifor JM. Early response to vitamin D2 in children with calcium deficiency rickets. J Pediatr. 2006;149(6):840-844.
Docio S, Riancho JA, Perez A, Olmos JM, Amado JA, Gonzalez-Macias J.Seasonal deficiency of vitamin D in children: a potential target for osteoporosis-preventing strategies? J Bone Miner Res. 1998;13(4):544-548.
Steingrimsdottir L, Gunnarsson O, Indridason OS, Franzson L, Sigurdsson G. Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake. JAMA. 2005;294(18):2336-2341.
Thacher TD, Fischer PR, Obadofin MO, Levine MA, Singh RJ, Pettifor JM.Comparison of metabolism of vitamins D(2) and D(3) in children with nutritional rickets. J Bone Miner Res. 2010;25(9):1988-1995.
Heaney RP. Functional indices of vitamin D status and ramifications of vitamin D deficiency. Am J Clin Nutr. 2004;80(6 suppl):1706S-1709S.
Aloia JF, Chen DG, Yeh JK, Chen H. Serum vitamin D metabolites and intestinal calcium absorption efficiency in women. Am J Clin Nutr. 2010;92(4):835-840.
Graff M, Thacher TD, Fischer PR, et al. Calcium absorption in Nigerian children with rickets. Am J Clin Nutr. 2004;80(5):1415-1421.
Need AG, O'Loughlin PD, Morris HA, Coates PS, Horowitz M, Nordin BE.Vitamin D metabolites and calcium absorption in severe vitamin D deficiency. J Bone Miner Res. 2008;23(11):1859-1863.
Hollis BW, Wagner CL, Drezner MK, Binkley NC. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: an important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007;103(3-5):631-634.
Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr. 2003;77(1):204-210.
Aloia JF, Patel M, Dimaano R, et al. Vitamin D intake to attain a desired serum 25-hydroxyvitamin D concentration. Am J Clin Nutr. 2008;87(6):1952-1958.
Ahn J, Yu K, Stolzenberg-Solomon R, et al. Genome-wide association study of circulating vitamin D levels. Hum Mol Genet. 2010;19(13):2739-2745.
Binkley N, Krueger D, Cowgill CS, et al. Assay variation confounds the diagnosis of hypovitaminosis D: a call for standardization. J Clin Endocrinol Metab.2004;89(7):3152-3157.
Granado-Lorencio F, Mosteiro JS, Herrero-Barbudo C, Navarro ED,Blanco-Navarro I, Perez-Sacristan B. 25-OH-vitamin D assay variation and subject management in clinical practice. Clin Biochem. 2010;43(4-5):531-533.
Singh RJ. Quantitation of 25-OH-vitamin D (25OHD) using liquid tandem mass spectrometry (LC-MS-MS). Methods Mol Biol. 2010;603:509-517.
Thacher TD, Fischer PR, Strand MA, Pettifor JM. Nutritional rickets around the world: causes and future directions. Ann Trop Paediatr. 2006;26(1):1-16.
Weisberg P, Scanlon KS, Li R, Cogswell ME. Nutritional rickets among children in the United States: review of cases reported between 1986 and 2003. Am J Clin Nutr. 2004;80(6 suppl):1697S-1705S.
↵ Thacher TD, Fischer PR, Pettifor JM, Lawson JO, Manaster BJ, Reading JC.Radiographic scoring method for the assessment of the severity of nutritional rickets. J Trop Pediatr. 2000;46(3):132-139.
Fischer PR, Rahman A, Cimma JP, et al. Nutritional rickets without vitamin D deficiency in Bangladesh. J Trop Pediatr. 1999;45(5):291-293.
Thacher TD, Fischer PR, Pettifor JM, et al. A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children. N Engl J Med.1999;341(8):563-568.
DeLucia MC, Mitnick ME, Carpenter TO. Nutritional rickets with normal circulating 25-hydroxyvitamin D: a call for reexamining the role of dietary calcium intake in North American infants. J Clin Endocrinol Metab. 2003;88(8):3539-3545.
Bingham CT, Fitzpatrick LA. Noninvasive testing in the diagnosis of osteomalacia. Am J Med. 1993;95(5):519-523.
Priemel M, von Domarus C, Klatte TO, et al. Bone mineralization defects and vitamin D deficiency: histomorphometric analysis of iliac crest bone biopsies and circulating 25-hydroxyvitamin D in 675 patients. J Bone Miner Res.2010;25(2):305-312.
Wagner CL, Greer FR. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics. 2008;122(5):1142-1152.
Zamora SA, Rizzoli R, Belli DC, Slosman DO, Bonjour JP. Vitamin D supplementation during infancy is associated with higher bone mineral mass in prepubertal girls. J Clin Endocrinol Metab. 1999;84(12):4541-4544.
Cranney A, Horsley T, O'Donnell S, et al. Effectiveness and safety of vitamin D in relation to bone health. Evidence Report/Technology Assessment No 158. Published August 2007. AHRQ Publication No 07-E013. Rockville, MD: Agency for Healthcare Research and Quality.
Bischoff-Ferrari HA, Kiel DP, Dawson-Hughes B, et al. Dietary calcium and serum 25-hydroxyvitamin D status in relation to BMD among U.S. adults. J Bone Miner Res. 2009;24(5):935-942.
Jackson RD, LaCroix AZ, Gass M, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med. 2006;354(7):669-683.
Bischoff-Ferrari HA, Willett WC, Wong JB, et al. Prevention of nonvertebral fractures with oral vitamin D and dose dependency: a meta-analysis of randomized controlled trials. Arch Intern Med. 2009;169(6):551-561.
Bischoff-Ferrari HA, Dawson-Hughes B, Staehelin HB, et al. Fall prevention with supplemental and active forms of vitamin D: a meta-analysis of randomised controlled trials. BMJ. 2009;339:b3692.
Sanders KM, Stuart AL, Williamson EJ, et al. Annual high-dose oral vitamin D and falls and fractures in older women: a randomized controlled trial. JAMA.2010;303(18):1815-1822.
Ginde AA, Scragg R, Schwartz RS, Camargo CA Jr.. Prospective study of serum 25-hydroxyvitamin D level, cardiovascular disease mortality, and all-cause mortality in older U.S. adults. J Am Geriatr Soc. 2009;57(9):1595-1603.
Autier P, Gandini S. Vitamin D supplementation and total mortality: a meta-analysis of randomized controlled trials. Arch Intern Med. 2007;167(16):1730-1737.
Lawlor DA, Davey Smith G, Kundu D, Bruckdorfer KR, Ebrahim S. Those confounded vitamins: what can we learn from the differences between observational versus randomised trial evidence? Lancet. 2004;363(9422):1724-1727.
Grady D, Rubin SM, Petitti DB, et al. Hormone therapy to prevent disease and prolong life in postmenopausal women. Ann Intern Med. 1992;117(12):1016-1037.
Grodstein F, Manson JE, Stampfer MJ. Postmenopausal hormone use and secondary prevention of coronary events in the nurses' health study: a prospective, observational study. Ann Intern Med. 2001;135(1):1-8.
Kawas C, Resnick S, Morrison A, et al. A prospective study of estrogen replacement therapy and the risk of developing Alzheimer's disease: the Baltimore Longitudinal Study of Aging. Neurology. 1997;48(6):1517-1521.
Shumaker SA, Legault C, Rapp SR, et al. Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in postmenopausal women: the Women's Health Initiative Memory Study: a randomized controlled trial. JAMA.2003;289(20):2651-2662.
Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women's Health Initiative randomized controlled trial. JAMA. 2002;288(3):321-333.
Dobnig H, Pilz S, Scharnagl H, et al. Independent association of low serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels with all-cause and cardiovascular mortality. Arch Intern Med. 2008;168(12):1340-1349.
Freedman BI, Wagenknecht LE, Hairston KG, et al. Vitamin D, adiposity, and calcified atherosclerotic plaque in African-Americans. J Clin Endocrinol Metab.2010;95(3):1076-1083.
Reis JP, von Muhlen D, Miller ER III., Michos ED, Appel LJ. Vitamin D status and cardiometabolic risk factors in the United States adolescent population.Pediatrics. 2009;124(3):e371-e379.
Martins D, Wolf M, Pan D, et al. Prevalence of cardiovascular risk factors and the serum levels of 25-hydroxyvitamin D in the United States: data from the Third National Health and Nutrition Examination Survey. Arch Intern Med.2007;167(11):1159-1165.
Zipitis CS, Akobeng AK. Vitamin D supplementation in early childhood and risk of type 1 diabetes: a systematic review and meta-analysis. Arch Dis Child.2008;93(6):512-517.
Pittas AG, Dawson-Hughes B, Li T, et al. Vitamin D and calcium intake in relation to type 2 diabetes in women. Diabetes Care. 2006;29(3):650-656.
Pittas AG, Lau J, Hu FB, Dawson-Hughes B. The role of vitamin D and calcium in type 2 diabetes: a systematic review and meta-analysis. J Clin Endocrinol Metab.2007;92(6):2017-2029.
Yin L, Grandi N, Raum E, Haug U, Arndt V, Brenner H. Meta-analysis: longitudinal studies of serum vitamin D and colorectal cancer risk. Aliment Pharmacol Ther. 2009;30(2):113-125.
Jenab M, Bueno-de-Mesquita HB, Ferrari P, et al. Association between pre-diagnostic circulating vitamin D concentration and risk of colorectal cancer in European populations: a nested case-control study. BMJ. 2010;340:b5500.
Pufulete M. Intake of dairy products and risk of colorectal neoplasia. Nutr Res Rev. 2008;21(1):56-67.
Wactawski-Wende J, Kotchen JM, Anderson GL, et al. Calcium plus vitamin D supplementation and the risk of colorectal cancer. N Engl J Med.2006;354(7):684-696.
Chen P, Hu P, Xie D, Qin Y, Wang F, Wang H. Meta-analysis of vitamin D, calcium and the prevention of breast cancer. Breast Cancer Res Treat.2010;121(2):469-477.
Chlebowski RT, Johnson KC, Kooperberg C, et al. Calcium plus vitamin D supplementation and the risk of breast cancer. J Natl Cancer Inst.2008;100(22):1581-1591.
Gandini S, Boniol M, Haukka J, et al. Meta-analysis of observational studies of serum 25-hydroxyvitamin D levels and colorectal, breast and prostate cancer and colorectal adenoma [published online ahead of print July 21, 2010]. Int J Cancer.doi: 10.1002/ijc.25439.
Stolzenberg-Solomon RZ. Vitamin D and pancreatic cancer. Ann Epidemiol.2009;19(2):89-95.
Helzlsouer KJ, VDPP Steering Committee. Overview of the cohort consortium vitamin D pooling project of rarer cancers. Am J Epidemiol. 2010;172(1):4-9.
Drake MT, Maurer MJ, Link BK, et al. Vitamin D Insufficiency and Prognosis in Non-Hodgkin's Lymphoma. J Clin Oncol. 2010;28(27):4191-4198.
Krishnan AV, Trump DL, Johnson CS, Feldman D. The role of vitamin D in cancer prevention and treatment. Endocrinol Metab Clin North Am.2010;39(2):401-418.
Munger KL, Levin LI, Hollis BW, Howard NS, Ascherio A. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA.2006;296(23):2832-2838.
Ascherio A, Munger KL, Simon KC. Vitamin D and multiple sclerosis. Lancet Neurol. 2010;9(6):599-612.
Litonjua AA. Childhood asthma may be a consequence of vitamin D deficiency.Curr Opin Allergy Clin Immunol. 2009;9(3):202-207.
Wjst M, Dold S. Genes, factor X, and allergens: what causes allergic diseases?Allergy. 1999;54(7):757-759.
Brehm JM, Celedon JC, Soto-Quiros ME, et al. Serum vitamin D levels and markers of severity of childhood asthma in Costa Rica. Am J Respir Crit Care Med.2009;179(9):765-771.
Camargo CA Jr., Rifas-Shiman SL, Litonjua AA, et al. Maternal intake of vitamin D during pregnancy and risk of recurrent wheeze in children at 3 y of age. Am J Clin Nutr. 2007;85(3):788-795.
Devereux G, Litonjua AA, Turner SW, et al. Maternal vitamin D intake during pregnancy and early childhood wheezing. Am J Clin Nutr. 2007;85(3):853-859.
Gale CR, Robinson SM, Harvey NC, et al. Maternal vitamin D status during pregnancy and child outcomes. Eur J Clin Nutr. 2008;62(1):68-77.
Hypponen E, Sovio U, Wjst M, et al. Infant vitamin D supplementation and allergic conditions in adulthood: northern Finland birth cohort 1966. Ann N Y Acad Sci. 2004;1037:84-95.
Wjst M, Hypponen E. Vitamin D serum levels and allergic rhinitis. Allergy.2007;62(9):1085-1086.
Liu PT, Stenger S, Li H, et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science. 2006;311(5768):1770-1773.
Nnoaham KE, Clarke A. Low serum vitamin D levels and tuberculosis: a systematic review and meta-analysis. Int J Epidemiol. 2008;37(1):113-119.
Wejse C, Gomes VF, Rabna P, et al. Vitamin D as supplementary treatment for tuberculosis: a double-blind, randomized, placebo-controlled trial. Am J Respir Crit Care Med. 2009;179(9):843-850.
Ginde AA, Mansbach JM, Camargo CA Jr.. Association between serum 25-hydroxyvitamin D level and upper respiratory tract infection in the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2009;169(4):384-390.
McNally JD, Leis K, Matheson LA, Karuananyake C, Sankaran K,Rosenberg AM. Vitamin D deficiency in young children with severe acute lower respiratory infection. Pediatr Pulmonol. 2009;44(10):981-988.
McGrath J, Saari K, Hakko H, et al. Vitamin D supplementation during the first year of life and risk of schizophrenia: a Finnish birth cohort study. Schizophr Res.2004;67(2-3):237-245.
Jorde R, Sneve M, Figenschau Y, Svartberg J, Waterloo K. Effects of vitamin D supplementation on symptoms of depression in overweight and obese subjects: randomized double blind trial. J Intern Med. 2008;264(6):599-609.
Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc.2003;78(12):1463-1470.
Warner AE, Arnspiger SA. Diffuse musculoskeletal pain is not associated with low vitamin D levels or improved by treatment with vitamin D. J Clin Rheumatol.2008;14(1):12-16.
Arvold DS, Odean MJ, Dornfeld MP, et al. Correlation of symptoms with vitamin D deficiency and symptom response to cholecalciferol treatment: a randomized controlled trial. Endocr Pract. 2009;15(3):203-212.
Melamed ML, Astor B, Michos ED, Hostetter TH, Powe NR, Muntner P. 25-hydroxyvitamin D levels, race, and the progression of kidney disease. J Am Soc Nephrol. 2009;20(12):2631-2639.
Source: Mayo Clin Proc. 2011 Jan;86(1):50-60. Thacher TD, Clarke BL. Department of Family Medicine, Mayo Clinic, Rochester, MN 55905, USA. firstname.lastname@example.org. http://www.mayoclinicproceedings.com/content/86/1/50.long
More than 80,000 chemicals now in use have never been fully assessed for toxic impacts on human health and the environment. Many of these chemicals are linked to increased incidence of cancer. Watch this shocking and disturbing video by expert Linda Greer, the Director of the Health Program at NRDC, the Natural Resources Defense Council, one of the most effective environmental protection groups. She clearly states that there is a lack of government oversight by the, EPA, the U.S. Environmental Protection Agency, the very department that is supposed to be protecting us, but protects corporate interests instead, putting our lives and our children’s health and wellbeing at risk.
The chemical industry should have to demonstrate that a chemical isn’t dangerous before it’s used in everyday products. But the Toxic Substances Control Act (TSCA) has no such requirements. These regulations have not been updated since 1976. It’s time to require that all chemicals be tested for safety and grant the EPA the authority to protect the public from toxic chemicals. But chemicals are “innocent until proven guilty”. This means chemicals are in use that have no proven safety record. Watch the video
The Breast Cancer Fund has a comprehensive report on the link between environmental toxic chemicals and breast cancer. The President's Cancer Panel released a report in April 2010 detailing the link between cancer and toxic exposures including chemicals used in industry, in the military and in medicine. The report states that “the link between exposure and cancer is strong” and ”the risk of cancer increases with more exposure”. Children, the unborn fetus and pregnant women are at greatest risk.
If you wish to be informed about the chemicals in products that you use at home and work, visit the website of the Environmental Working Group. They also have another website devoted to the many unregulated toxic chemicals found in personal care products such as shampoos, lotions, toothpaste and cosmetics. Another educational site that shows you how to feed your family safe and healthy food and reduce your chemical exposures at home is Organic Authority.
Dr. Sanjay Gupta, MD, a medical doctor and medical journalist produced a television series "Toxic America" which reveals the most common chemicals that are linked to a multiplicity of health problems, including many cancers that are ubiquitous in our daily lives. This report brings to light the many chemicals that find their way into the womb and into newborns who are come into life on day one with high levels of toxic chemicals in their tiny and developing bodies and then nurse on toxin laden breast milk increasing their body burden of dangerous chemicals.
Probiotics, we hear all about them now, on TV, radio and print ads! It’s great, considering that just a few years ago, most people didn’t know what they were.
Probiotics, otherwise known as “good germs”, are part of the normal flora of our intestinal tract. They begin to inhabit our intestinal tract as soon as we’re born (by vaginal delivery, rather than caesarian delivery). They are nourished by eating healthy foods from infancy, starting by drinking mother’s milk (rather than cow’s milk or soy milk). As we age and are exposed to poor diet, antibiotics, chlorinated water, steroids and environmental pollutants (xenoestrogens), their numbers begin to decline. When their numbers decline, pathogenic yeast begin to overgrow (as well as bacteria), causing symptoms in both men and (more obviously in) women (such as vaginal discharge).
Known functions of probiotics include:
The manufacture of B vitamins (such as folic acid, biotin, B3 and B6).
The manufacture of the enzyme “lactase”.
Produce antibacterial substances.
Produce anti-carcinogenic compounds.
Help reduce high cholesterol levels.
Improve the efficiency of the digestive tract.
Help recycle hormones such as estrogen.
Protect against radiation.
Deactivate certain toxins, among many others.
The primary bacteria inhabiting the small intestine is Lactobacillus acidophilus while that of the colon is Bifidobacterium bifidum. It is essential that these organisms be replaced when taking antibiotics of any kind.
In today’s world, it’s a good idea to incorporate probiotics in a wellness program because of the antibiotics that we’re unknowingly exposed to (from food and perhaps, our water supply). There are different brands available. Some need to be refrigerated while others do not. They come in various forms such as powders, liquid, capsules or “pearls”. To find out which brands are better, check out a study done by Consumer Labs. In the study, they found out that claims made by some companies such as number of viable organisms in their product somehow vary from the actual live cells. Factors such as improper storage and handling as well as shelf life affect these numbers. Therefore, it’s always important to do your own research.
Complexity and the roots of depression have always been a major and complex health issue. Depression contains other health issues such as behavioral, psychological, social, cultural, religious and the spiritual aspects of ones life. Because of the complexity aspects of depression, it should always be treated with one and the “Whole Person” ideology in mind.
The depression epidemic has gotten worse since the September 11th tragedy and all that followed. The stress of the tragedy has put a lot of old wounds of mind back in the front seat, dominating the daily activity in every aspect of everyone’s life, not only in the United States, but also throughout the world.
Dr. Jane Mak, a Neuropsychologist and clinical psychologist has stated that many of her past patients including children, have been back for visits to seek resolution to their flared up old wounds.
Today, four out of every six Americans are having difficulty concentrating on their jobs. Three out of 4 patients take some form of supplements totally unsupervised. Many take the supplements with or without their physician’s knowledge and sometimes in combination with prescription drug/s, presenting safety issues.
Despite the various aches and pains, irritability, difficulty concentrating, fatigue, digestive problems, anxiety, guilt and much more, Depression is not a disease by medical evidence. Depression is not more than a “trapped inward feeling”, with no two people experiencing exactly the same symptoms.
Depression may have underlying factors such as Thyroid Disease, Cardiovascular or Endocrine System problems, deficiency and or imbalances of certain nutrients, digestion, food sensitivities, artificial lighting, inactivity, numerous toxic environment chemicals found in the household. Heavy metal poisoning, adrenal, ovarian or testical problems, immune deregulation, anemia, blood sugar fluctuations, prolonged physical illness and many more symptoms can cause Depression.
True “healing” cannot be achieved by simply “relieving” the pain and symptoms. Studies have shown that if the cause and effect relationship between depression and functional decline is not understood properly, depression can become a killer disease.
Contrary to today’s only approach of treatment, stopping the pain, we must hear the message (the symptom) and understand the message (the symptom) that the body is trying to tell us. The message is simple, something is wrong somewhere. I recommend we stop shooting the messenger (pain) and start being a good listener to our body’s warning signs. My simple message to you, do not self-treat!
I often see patients who have decided to self-prescribe medications or supplements for various problems, depression included. Not only do they mask the real problem, not listening to their body and its symptoms, they run the risk of having dangerous drug interactions. If you are currently on any medication or supplements, please take the time to read the following Drug/s Interaction Dangers. It could save your life.
“Add-on” interactions are the most common type and can be the most dangerous, even fatal. These occur between drugs that have similar effects, either depressant + depressant or stimulant + stimulant.
Depressants include: alcohol, antianxiety agents, tranquilizers, anticonvulsants, antihistamines, certain high blood pressure drugs, muscle relaxants, narcotics and the popular pain reliever propoxyphene (e.g., Darvon).
Stimulants include: antidepressants (MAO inhibitor type drugs and tricyclics family drugs), appetite suppressants, some asthma drugs, caffeine, nasal decongestants, methylphenidate (Ritalin) and pemoline (Cylert). You should always ask your doctor and/or pharmacist about these types of interactions before you take any medication.
Amine-containing foods + MAO inhibitors:
MAO inhibitors are used in some cases of clinical depression. This can be a life threatening combination that may result in a dangerous rise in blood pressure, with severe headache, fever, visual disturbances, and confusion, possibly followed by brain hemorrhage/stroke.
Caution: Avoid amine-containing foods, even for several weeks after stopping MAO-inhibitor type antidepressant drugs.
Both types of antidepressant drugs MAOIs and Tricyclics require close monitoring to determine proper dosage. The drugs must be taken for at least three weeks before mood improves. And the side effects associated with these two families (Gambini’s and Kapone’s) can be severe and debilitating.
Trycyclics can induce dry mouth, constipation, weight gain, blurred vision, heart attacks, stroke, high or low blood pressure, heart block, seizure, hallucinations, delusions, confusion, disorientation, in coordination, tingling, abnormal involuntary movements, anxiety, insomnia, nightmares, dizziness, ocular pressure, rashes, bone marrow depression, elevation or lowering of blood sugar, edema, hair loss and more.
MAOI’s can provoke the same side effects plus an increased risk of hypertension and hepatitis.
Medical aromatherapy or the use of essential oils for therapeutic purposes, is one of the oldest forms of medicine and cosmetics known to man. According to Egyptian hieroglyphics and Chinese medical manuscripts, physicians and priests were using essential oils thousands of years before Christ to heal the sick. What are essential oils anyway? Essential oils are the subtle, aromatic and volatile liquids extracted from the flowers, seeds, stems, leaves, bark and roots of herbs, shrubs and trees. The extraction process is done primarily through distillation. Some of the oils that have been used since Biblical times include frankincense, myrrh and cinnamon. Modern clinical research has been confirming the medicinal properties of these oils. For instance, frankincense has been found to have superior immune stimulating properties while cinnamon has blood sugar regulating properties.
Are all essential oils equal? Unfortunately, that’s not the case. For example, the majority of the rose oils come from Bulgaria. In order to keep up with demand from the perfume or cosmetic industry, they have to produce large volumes and in the process compromise quality by using solvent extraction instead of steam distillation.
Some of the modern applications of oils include eugenol (from clove), which is used in the dental industry and thymol (from thyme) which is used as an antiseptic. For one of the best sources of essential oils, check out www.cleanbodycare.com.
If you’re like millions of Americans who regularly tune into the news, you probably heard about the vitamin D report issued in November 2010 by the Institute of Medicine’s Food & Nutrition Board (FNB), a committee of 14 medical scientists appointed to assess current data of health outcomes associated with these two nutrients. The FNB report concluded that most North Americans get enough of this “sunshine vitamin” through their diets, and moreover that consuming extra vitamin D is unlikely to help protect the public from cancer, heart disease, diabetes, or other chronic diseases. Among the report’s other conclusions:
• Raise the recommended daily amount of vitamin D to 600 international units (IU), up from the 200 IU level that had been recommended in 1997. People over age 70 are advised to get 800 IU daily. Our response: Most experts agree that it is virtually impossible to significantly raise your vitamin D levels when supplementing at only 600 to 800 IU/day. Michael Holick, MD, PhD, director of the General Clinical Research Center at Boston University Medical Center and author of numerous scientific reports on vitamin D, has recommended that all adults supplement with 2000 IU daily. Holick himself takes 3000 IU per day and has many patients taking at least that much. Robert Heaney, a professor of medicine at Creighton University in Omaha who has long studied vitamin D’s health benefits, says people should consider taking up to 4,000 IUs a day.
• The risk of harm increases at daily vitamin D intake levels greater than 4000 IU. Our response: This would suggest that a daily intake of 10,000 IU/day would cause toxicity in humans; however, the FNB report provided no evidence to support this position, citing only one poorly conducted study indicating 20,000 IU/day may cause mild elevations in serum calcium but not clinical toxicity. Several leading vitamin D researchers have proposed that the new upper tolerable limit should be 10,000 IU, based on extensive observations of adults taking this dose or higher.
• Regarding the serum 25-hydroxyvitamin-D level—the primary indicator of vitamin D status—the FNB report deemed that a level of 20 ng/mL is sufficient for all persons. Our response: The most widely used benchmark for sufficiency has been 32 ng/mL, and many experts suggest that higher levels may be needed for specific health outcomes.
The FNB report made headlines across the country, and prompted many people to either cut back on their vitamin D dose or stop supplementing altogether. However, we see several serious limitations in the FNB’s approach and conclusions. First, the guidelines are based on the minimum amount of vitamin D needed to ensure bone health and do not address the amount that may affect other health outcomes, such as the prevention of cancer and heart disease, or improvement in muscle and joint health. Ostensibly, the FNB committee believed that evidence was insufficient to determine the role of vitamin D in the prevention of these other chronic diseases and health outcomes. However, many leading vitamin D authorities throughout the world would take issue with this perspective.
For example, a comprehensive evidence-based review, published in the November-December 2009 Journal of the American Board of Family Medicine, concluded that, “Low vitamin D levels are associated with increased overall and cardiovascular mortality, cancer incidence and mortality, and autoimmune diseases such as multiple sclerosis.” Even more recently, an international committee of 25 experts from various medical disciplines proposed clinical guidelines for vitamin D intake. Their focus was on the vitamin D needs of adult patients with or at risk for fractures, falls, cardiovascular or autoimmune diseases, and cancer. The expert panel reached strong agreement about the need for vitamin D supplementation in these specific groups of patients and the need for assessing their 25(OH)D serum levels “for optimal clinical care.” A target range of “at least 30 to 40 ng/mL” was recommended—about twice the level proposed by the FNB report. These recommendations were published in the September 2010 issue of Autoimmunity Reviews.
Against this backdrop, it’s also important to realize that the FNB’s guidelines have nothing to do with the requirements for optimal functioning and overall health. Physicians who carefully observe what happens with their individual patients are better able to discern the effects of different doses of vitamin D in the context of specific health situations. For someone with low blood levels of vitamin D, an initially high supplemental dose—on the order of 5000 to 10,000 IU per day—may result in better mood, increased muscle strength, relief of joint aches, and other clinical benefits. But one size does not fit all; the same dose of vitamin D is not appropriate for everyone. This is why individual testing and expert supervision are so important when trying to pinpoint the optimal dose for you personally.
The Sunshine Deficiency
Vitamin D has emerged in recent years as a nutrient with astounding potential for promoting human health.The vitamin’s most recognized function is the enhancement of calcium absorption and bone mineral metabolism. In 2007, the Dietary Supplement Education Alliance estimated that appropriate use of calcium with vitamin D by older adults for five years could lead to the elimination of approximately 776,000 hospitalizations and nursing stays linked to hip fractures, resulting in an annual savings of $16.1 billion. In other words, supplements such as calcium and vitamin D serve as a potent form of “biological insurance” that can help keep the human frame intact. As we explain in a moment, however, the benefits of improving your vitamin D status extend far beyond healthy bones.
Vitamin D is classified as a vitamin, but it’s really a hormone your body generates in response to sunlight. Fair-skinned people can generate 20,000 IU of vitamin D through 20-30 minutes of mid-day sun exposure; in contrast, dark-skinned individuals may require at least four times this level of exposure to attain the same output. (Note that these levels far surpass any amount obtainable through diet alone, which helps explain why the US recommended dietary allowance of vitamin D is set at a mere 200-400 IU for people aged 1-70 years.)
Your body’s production of vitamin D depends on the amount of skin surface exposed and the quality of sunlight. Direct-overhead sun exposure provides the strongest stimulus for the skin’s synthesis of vitamin D. In temperate regions, almost all of this “human photosynthesis” occurs in summertime, because the angle of sunlight largely determines the intensity of ultraviolet radiation, hence the rate of vitamin D production.
Given these facts, it comes as no surprise that most cases of vitamin D deficiency are due to a sunlight deficit, not a dietary one. If you were to totally avoid the sun and regularly took two standard multivitamins every day for several years, each containing 400 IU of vitamin D as your sole source of vitamin D, you would eventually become vitamin D deficient. (Remember, most people meet 90% of their vitamin D needs from very casual sun exposure, like the sunlight that strikes your face, arms and hands when stepping outside for a few minutes in the middle of the day.)
These days, due to fears of developing skin cancer, many people get too little sunshine. This results in a low or suboptimal blood level of 25-hydroxyvitamin D—the sole measure of one’s vitamin D status. If this level is low—say, below 50 nanomoles per liter (nmol/L) — research indicates that you may be more prone to developing a host of health problems. The classical disorder linked with vitamin D deficiency is known as osteomalacia, a painful softening of the bones. In children, the deficiency causes the shafts of leg bones to irreversibly bow or bend, resulting in the grotesque disfigurement known as rickets. Sunbathing or taking cod liver oil (which contains vitamin D) were eventually found to prevent rickets, which is now extremely rare, thanks mainly to the practice of fortifying dairy products with vitamin D.
But lack of vitamin D can also lead to various other health problems, including osteoporosis, osteopenia, heart disease, hypertension, diabetes, osteoarthritis, joint problems, muscle weakness, chronic muscle pain, fibromyalgia, multiple sclerosis, Type 1 diabetes, depression, mental illness and yes, many types of cancer as well. Let’s take a quick look at what science is telling us about the connections between vitamin D and these various disorders.
Osteoporosis and Osteopenia. When you’re lacking in vitamin D, you’re more prone to developing osteoporosis, osteopenia, and osteomalacia (as mentioned above), and your risk of experiencing a fracture increases. Achievement of optimal blood vitamin D levels is essential for boosting bone mineral density and maximizing bone strength, which is why elderly people with osteoporosis—particularly those being treated with bisphosphonates—are advised to boost their intake to at a range of 800 to 2000 IU, along with calcium. Again, however, if your vitamin D status is poor initially, it’s important to supplement at a higher dosage level in order to truly improve the blood levels of 25(OH)D. Daily supplementation at the right level—again, relative to the blood test result—is especially important for older adults because aging is linked with a reduced capacity to synthesize vitamin D in the skin upon sun exposure.
Cardiovascular Disease and High Blood Pressure. Vitamin D deficiency has been linked with a greater risk of cardiovascular disease and high blood pressure. For example, a meta-analysis of 18 studies found that the lower the serum vitamin D level, the higher the risk of high blood pressure, as reported in the 28 December 2010 Journal of Hypertension. In addition, we know that vitamin D can impact several key mechanisms involved in heart disease, such as inhibiting inflammation as well as vascular muscle proliferation and vascular calcification. To date, however, studies evaluating vitamin D supplementation have not consistently shown a benefit, possibly due to suboptimal levels of vitamin D (no studies have yet looked at doses higher than 2000 IU, even in deficient individuals) or a lack of consideration for other factors that impact cardiovascular health.
Cancer. People living in colder climates not only experience more bone thinning with age but also have higher rates of various cancers. These individuals tend to spend more time indoors, so they get less sun exposure. It’s also interesting to note that cancer mortality rates tend to be lowest in the summer, when vitamin D levels are highest. Laboratory studies indicate that high-dose vitamin D may help block the growth of cancers of the breast, colon, rectum, prostate, lung and head/neck region, as well as lymphoma, leukemia and multiple myeloma. Generally, the lower one’s overall sun exposure and vitamin D intake, the greater the risk of developing and dying from cancer. In a five-year clinical trial conducted out of Creighton University in Nebraska, women who regularly took 2000 IU of vitamin D3 showed a 77% reduction in overall cancer rates compared to women taking a placebo pill, as reported in the June 2007 issue of the American Journal of Clinical Nutrition. This 2000 IU level of vitamin D3 has also been shown to reduce PSA levels in men with prostate cancer.
One other key application concerns cancer treatment. Vitamin D has a synergistic effect against malignant disease when combined with several kinds of anti-cancer drugs, including the taxanes (Taxol and Taxotere), platinum compounds (e.g., cisplatin), dexamethasone, tamoxifen, and mitoxantrone. Soy isoflavones, too, seem to synergize with vitamin D in combating cancer. Finally, there’s good evidence that vitamin D can be very effective in slowing down the breakdown of bone and lessening bone pain in patients with advanced cancers.
Obesity and Metabolic Syndrome. Vitamin D is fat-soluble and therefore stored in fatty tissue. This explains why obese people have a greater capacity to store the vitamin; however, obese people have been shown to produce about half the vitamin D produced by people of a normal weight when exposed to the same amount of sunshine. Moreover, the vitamin D in those who are lean is more available for the body's metabolic needs than in those who are obese. In a 2007 report for Clinical Nutrition, about half of all morbidly obese individuals were found to be vitamin D deficient. Those with the lowest levels of vitamin D had the greatest risk for the so-called metabolic syndrome. (The latter condition includes the presence or more of the following factors: excess abdominal fat, elevated triglyceride levels, low HDL cholesterol, elevated blood pressure, and elevated fasting glucose and insulin levels.)
Autoimmune Diseases. Lack of vitamin D has been linked with multiple sclerosis, rheumatoid arthritis, type I diabetes, lupus, and Crohn’s disease. For example, babies deficient in vitamin D may have a greatly increased risk of developing type I diabetes by age 30 compared to those who are not deficient. Animal studies suggest that a vitamin D supplement will greatly impede the development of type I diabetes in susceptible individuals. A 2009 report in Arthritis Research & Therapy concluded that vitamin D deficiency is highly prevalent in patients with lupus and rheumatoid arthritis. However, whether supplementation can help patients with these disorders remains to be proven.
Colds and Flus. Sharply reduced levels of vitamin D, due to the low intensity of solar UV radiation, may have some connection to the increased occurrence of colds and the flu in winter. Scientists have found that people with low vitamin D levels are less capable of fighting off infections, and that supplementing with vitamin D boosts resistance to colds and the flu. In a randomized controlled trial conducted in Japan, researchers gave 1,200 IU/day of vitamin D3 for six months to Japanese 10 year-olds and compared them to children receiving a placebo. As reported in the May 2010 American Journal of Clinical Nutrition, there was a 42% reduction in the incidence of influenza A, along with an 83% reduction in asthma attacks in the vitamin D group compared to the placebo group. Had those researchers followed the new FNB recommendations and used 400 IU instead of 1,200 IU, it is unlikely that the children would have experienced any benefit at all.
The problems just mentioned are only the tip of the proverbial iceberg. Low levels of vitamin D also have been linked with mood disorders (e.g., depression), mental illness, autism, muscle weakness, periodontal disease, unexplained bone and muscle pain, infertility, preeclampsia, cystic fibrosis, psoriasis, and age-related cognitive decline. In some cases, clinical benefits have been seen following vitamin D supplementation—for example, reductions in depressive moods in adults, and improvements in muscle strength and function in children with autism.
How Much Is Needed?
These days, most of us just don’t get out in the sun as much as our ancestors did. We spend far more time indoors, and yet the sunshine that comes through glass windows will not stimulate vitamin D synthesis. Even if we did get outdoors on a regular basis, we’d then have to reckon with problems associated with getting too much sun—problems such as sunburn, premature aging of the skin, and a heightened risk of skin cancer, especially in fair-skinned people. Older individuals and obese people have more difficulty synthesizing vitamin D, so they would need to be out in the sun longer, thus further increasing the skin cancer risk.
Aside from sunshine, we can get additional vitamin D from foods like fatty fish and fortified milk. Unfortunately, most fortified dairy products contain synthetic vitamin D, which confers fewer biological benefits than vitamin D3. Moreover, relying on fatty fish may not be a suitable way to get your vitamin D, because you’d have to eat a large amount of fish every day. For many people, vitamin D-rich cod liver oil is a great source, one that has been used in northern regions for well over a century.
This brings us back to vitamin D supplements. Vitamin D in its natural form is called vitamin D3 or cholecalciferol. This form of vitamin D generally has more drawn-out effects and need not be taken daily; in contrast, synthetic forms such as calcitriol need to be taken daily for optimal effectiveness. Also whereas vitamin D is relatively cheap, calcitriol can be quite expensive – and your insurance company may or may not provide coverage.
So how much do we really need? Many of the leading vitamin D authorities say that, if you rarely if ever get any mid-day summertime sun exposure, most adults can benefit by supplementing in the range of 2,000 and 5,000 IU per day. A recent clinical trial by Dr. Reinhold Vieth confirmed that the 5000 IU amount was safe even for elderly people. For people who do get exposed to 15 or 20 minutes of mid-day sunshine in the spring, summer and fall, the recommended amount is about 2,000 IU per day. You can also take your week’s worth of vitamin D (say 15,000 to 20,000 IU) all on the same day, once a week. This makes it much easier to take the vitamin, but there are those individuals who may still have problems absorbing this much Vitamin D at one time, in which case daily dosing is still better.
The only caveat of taking higher doses of vitamin D is that some individuals may be prone to a condition known as hypercalcemia (excessive calcium in the blood). Symptoms of hypercalcemia include weakness, fatigue, somnolence, headache, anorexia, dry mouth, metallic taste, nausea, vomiting, cramps, diarrhea, muscle pain, bone pain and irritability. If you have cancer and certain other conditions, your physician should monitor you for hypercalcemia in order to safeguard against this problem. If you do happen to become hypercalcemic, your physician will have you discontinue the vitamin D and then check your blood calcium level daily until it has normalized, and then twice weekly on a lower dose of vitamin D.
John Cannell, MD, founding director of the Vitamin D Council, notes that thousands of individuals reading the Council’s newsletter routinely have taken 5,000 IU/day for up to eight years. “Not only have they reported no significant side effects, indeed, they have reported greatly improved health in multiple organ systems,” Dr. Cannell states. “My advice: especially for pregnant women, continue taking 5,000 IU/day until your 25(OH)D is between 50 ng/ml and 80 ng/ml—the vitamin D blood levels obtained by humans who live and work in the sun and the mid-point of the current reference ranges at all American laboratories.” The FNB recommendations are a major disappointment to Cannell and many other proponents of higher vitamin D intake. Given the low cost of vitamin D, as well as the large body of evidence for safety and benefit at intakes well above these recommendations, why not take a chance of achieving those benefits?
John C. Pittman, MD, is the Medical Director of the Carolina Center for Integrative Medicine in Raleigh, NC, and is certified by the American Board of Clinical Metal Toxicology. Mark N. Mead, MSc, serves as the Center’s Nutrition Educator and Integrative Medicine Research Consultant.
Are mercury, lead, and other toxic metals likely culprits in classic autism, ADHD, Asperger Syndrome, and other Autism Spectrum Disorders (ASDs)? Can yeast overgrowth and intestinal imbalances have a substantial impact on many ASDs? Do kids with ASDs often suffer from an inability to detoxify toxic compounds? Can these children benefit from therapies aimed at removing these toxic factors and correcting the underlying biological problems?
The answer to all these questions, based on our clinical experiences and training at the Autism Research Institute, is a resounding yes. But if this is the case, why is there so much disagreement among pediatricians and public health scientists? The reason: Much of the population-based research to date has focused on the more superficial aspects of ASDs, and in doing so has helped engender the misunderstanding that such toxic factors as mercury and fungal toxins are of little relevance to the child with autism.
Of Detox Defects and Vulnerable Brains
A recent study, published in a 2010 issue of Acta Neurobiologiae Experimentalis, found that individuals diagnosed with ASD had blood mercury levels that were approximately double those observed in non-ASD individuals. However, closer examination of the data revealed a threshold blood mercury level below which no autism was seen. Specifically, the total blood mercury level did not increase the odds of having autism until it was greater than 26 nmol/L (>5.2 μg/L). Individuals with a blood level higher than 26 nmol/L were three times more likely to be diagnosed with autism than individuals whose blood level was lower than 26 nmol/L.
These findings, which come from the Institute of Chronic Illnesses, Inc., in Silver Spring, Maryland, are consistent with multiple studies showing increased levels of mercury in the teeth and brains of children diagnosed with an ASD relative to non-ASD kids. Several studies also found increased mercury in the urine and fecal samples following chelation therapy, as well as associated urinary porphyrins among ASD individuals relative to the control groups. Moreover, a 2009 report in the Journal of Toxicology demonstrated a strong relationship between the severity of autism and the relative body burden of toxic metals.
Now, some scientists may reasonably argue that blood mercury levels are not consistently linked with ASDs, and they would be correct. However, blood mercury levels do not reflect chronic exposures or tissue levels—only acute exposures, for example, from industrial accidents, eating mercury-laden fish, or off-gassing from dental amalgams. The metals that accumulate from pre- and post-natal exposure are not reliably detected by a blood test, only by a combination of urinary porphyrins and urinary mercury following administration of metal-binding agents. Doctors who have studied heavy metal toxicology understand this.
Also seemingly paradoxical is the finding of lower hair levels of mercury in very young children with ASDs. This suggests that ASD kids are unable to excrete the mercury that has accumulated in their bodies. Indeed, we find that virtually all children with autism show measurable defects in their detoxifying capacity. These defects render the children unable to eliminate or neutralize many brain-toxic factors such as lead, mercury, and pesticides—and more prone to the brain-injuring effects of inflammation and oxidative stress. Many of these kids also have immune system imbalances that keep ther brains inflammed as well as rendering them even more susceptible to harmful bacteria and other microbes and their toxins.
The implications of this complex profile of susceptibility are profound. These children are like the proverbial “canaries in the coal mine”—far more vulnerable to the pollutants that other children’s bodies handle with ease. If you’re not taking into account the detoxification and immunologic problems commonly found in autistic children, then population-based comparisons of exposure levels have less relevance.
Deficiencies in key nutrients and metabolites that support detoxification pathways also are extremely common among children with ASDs. For example, many of these kids show low glutathione or its metabolites in their blood and urine. Since glutathione is the core detoxifying molecule in our cells, this deficiency greatly limits the child’s ability to process and eliminate mercury and other toxicants from the blood. Those children who are genetically less capable of detoxification, or whose detox mechanisms are overwhelmed with other toxins, are far more prone to toxic overload—and thus to the neurologic and behavioral problems linked with ASDs.
Developmental Delay or True Treatment Effect?
Another common criticism you will hear of doctors who are using this innovative approach is that autism is a condition of developmental delay, and that at least some of these children—possibly 5 to 19 percent—will go on to develop and function fairly well. Without conducting randomized controlled trials, these critics say, you never can know whether the development and improvement of symptoms would have occurred anyway with time, or whether the improvement could simply be attributed to behavioral and occupational therapy.
Going further, the critics contend that the single-person level of observation can be very deceiving, and that you can easily be fooled into believing that what you are observing is a real benefit versus something that might have happened by chance.
Here’s the main problem with this view, and perhaps the most profound myth-busting truth of all. You cannot be fooled by what you’re seeing when improvements occur on the integrative treatment program, and then those same improvements vanish if the child goes off the program. If your child quickly gets worse every time they go off their program, and then improves again every time they go back on, this is clearly due to the treatment. This is what separates clinical trials from case-by-case observations in the clinical setting, and it is incredibly important in the context of ASDs, since every case is so different and requires a high degree of individual tailoring based on testing results.
Let’s take the example of intestinal candidiasis, or yeast overgrowth. When children with ASDs are treated for an obvious yeast overgrowth, at some point they begin to show a dramatic improvement in their behavior—showing great eye contact, communicating well or even animatedly, becoming more peaceful and attentive. When they go off the anti-yeast treatment, their behavior can spin wildly out of control again.
Another example: Many children are sensitive to gluten. Take them off gluten-containing foods for three weeks, then reintroduce those foods and watch what happens. Very often there will be some improvement in behavior during the time off gluten, but if the child has an underlying intestinal infection or yeast overgrowth situation, that must be resolved first.
Our approach at the Carolina Center for Integrative Medicine addresses the problems that are common to virtually all children with ASDs, including detoxification weaknesses, toxic overload, nutritional deficiencies, and intestinal imbalances such as yeast overgrowth. Various nutrient deficiencies have been documented in children with ASDs, and targeted nutritional strategies are often very helpful and again make other strategies more effective. In addition, we help identify certain “trigger” foods, such as casein-containing dairy products, wheat and other gluten sources, sugar, chocolate, preservatives, and food colorings.
As implied in the mention of gluten and yeast (see above), proper sequencing of the treatments is part of the art of medicine when it comes to helping kids with ASDs. For example, the full benefits from heavy metal detoxification and hyperbaric therapy (pressurized oxygen) are only likely to occur when the GI tract problems are addressed first. Children undergoing this integrative approach may show rapid improvement in language and social skills, as well as better sleep, moods, and overall disposition.
The medical-scientific community is beginning to wake up to the power of this perspective. In November 2009, the American Academy of Pediatrics, Autism Speaks, and the North America Society for Pediatric Gastroenterology, Hepatology and Nutrition, hosted a symposium of researchers and physicians to address GI problems seen in children with ASDs. The symposium was intended to raise awareness among specialists about GI disorders in autism and to educate doctors about new treatment strategies for ASDs.
Overcoming Autism: A Success Story
When it comes to harnessing the power of this integrative approach, one of the keys to therapeutic success is catching ASDs at an early age, when there is still sufficient neuro-plasticity or brain plasticity. The term plasticity refers to the central nervous system’s ability to change neurons and neuronal pathways, and ultimately to re-organize entire neural networks. A good example of this early-life therapeutic advantage is the story Mike Simpson, now age 5, who was diagnosed in November 2006 with autism. At the time of his diagnosis, several physicians had told Mike’s parents, John and Suki Simpson, that no treatment options existed and that recovery was impossible.
Mike’s pediatrician referred the parents to the state’s behavioral intervention program. Although they found the program somewhat helpful, it clearly was only a start, and his behavior remained that of a child with classic autistic disorder. “At the time, Mike did not respond to his own name,” Suki Simpson recalls. “He was unable to sit in a chair or by a table, and he could not focus on any activity for any extended period of time.” Due to these limitations, it seemed unlikely that he could reasonably benefit from the behavioral program.
In his first year of life, Mike appeared to be deaf because he would not respond to his name, nor did he react to loud noises, such as the doorbell ringing or a car horn honking. Testing revealed that his hearing was fine. In fact, as the parents later learned, Mike was quite sensitive to sound—but was not responding because he was tuning the sound out due to the pain it caused. This phenomenon is fairly typical among children with autism.
One glance at Mike’s diet at the time might have provided some insight into his behavioral issues. From the moment he began eating solid foods, according to the Simpson parents, he seemed to constantly crave carbohydrate items such as crackers, pizza, chicken nuggets and Cheerios. His diet as a whole was quite limited, and he invariably shunned new foods. The parents began to wonder whether his diet might have something to do with the abnormal behaviors he was exhibiting.
“We began to speculate about how nutrition could be impacting Mike’s body and mind,” says John Simpson. “Perhaps his limited diet was giving him headaches, or perhaps he lacked the nutrition needed for normal brain function. Perhaps he was unable to sleep because his stomach was upset, or he was not eating well because the food did not taste good to him. These kinds of questions prompted us to begin looking into alternative approaches to autism.” As the parents looked further, they came to believe that a “leaky gut” and possibly other digestive problems, along with poor nutrition, could be fueling Mike’s abnormal behaviors.
When Mike turned age two in the spring of 2007, the parents placed him on a gluten-free, casein-free (GFCF) diet—a diet free of cow’s milk, wheat and most other grain products. “Immediately, we saw several of his behaviors improve,” Suki Simpson says. “Soon afterward, we added digestive enzymes as supplements to his diet six months later. This led to small but continual improvements in his focus and communication, including his very first ‘Mama.’ That was immensely exciting. We realized then that there had to be an underlying biological reason for his behavioral symptoms.”
In December 2007, after an Internet search of physicians listed in the Defeat Autism Now! (DAN!) directory, the parents sought my expertise and scheduled an office visit with me at the Raleigh-based Carolina Center for Integrative Medicine. (Much of the Carolina Center’s approach to autism is adapted from the DAN! program. To help decide which supplements and which parts of the program to emphasize, we recommend individualized, in-depth clinical and laboratory testing.)
After an extensive evaluation that included laboratory testing to look for signs or markers of hidden infection, I determined that Mike had an overgrowth of Candida yeast and bacteria in his intestines. The first treatment priority was to reduce the yeast levels in order to improve his digestive function health. In addition to pharmaceutical and herbal anti-fungals, Mike received specific supplements aimed at killing disease-causing organisms, as well as replacing those microbes with beneficial bacteria.
Our second effort was targeted towards vitamins and other nutrients his body lacked, and were intended to help him feel and function normally. At the same time, the parents also elected to have him start hyperbaric therapy, involving the use of pressurized oxygen to activate neurons in his brain. Children undergoing hyperbaric therapy often show rapid progression in language skills and the expansion of their vocabulary, as well as a range of behavioral improvements. Later in his treatment, Mike received an antiviral medication called Valtrex, which is thought to work as a brain anti-inflammatory agent. Recent research, all published in peer-review medical journals, has highlighted the benefits of this integrative medical approach. For some excellent summaries of this research, see the August and December 2002 issues of Alternative Medicine Review, as well as the February 2008 Journal of Alternative & Complementary Medicine.
The multi-pronged treatment—including anti-microbial therapy, physiological rehabilitation, and nutritional and behavioral interventions—led to rapid and dramatic improvements. Within four months, Mike not only knew his own name and made good eye contact, he also began speaking the name of everyone with whom he was coming into contact on a daily basis. He could speak in full sentences and quickly developed a huge vocabulary. He could count to 40, and his ability to recite the alphabet, identify letters, and put letters together was that of a first grader. To his parents’ delight, Mike became very sociable, talkative and interactive, singing songs and playing games like tag and Hide-and-Seek. He made friends easily at school, and it was very clear to his teachers that he had a keen ability to learn.
“If we had not seen it happen before our own eyes, we would not have believed it to be possible,” says Suki Simpson. “Recovery from autism is possible. In the beginning, teaching Mike was like driving down a dead end street. Today, we are cruising along a highway with interaction in both directions.” Suki adds that Mike has been thriving both socially and intellectually in a mainstream classroom at their local elementary school. “He has lots of friends,” she says. “And he talks with them and us all the time. We couldn’t be happier with his complete turnaround, and for that, we give credit to the Carolina Center’s approach.”
In short, there is now light at the end of the tunnel. At this writing, we have seen hundreds of children with ASDs go from having all types of aberrant behaviors to becoming playful, sociable, and communicative. Many of them have gone from extreme isolation to being mainstreamed in a normal school, performing just as well as their peers, sometimes even ending up at the top of their class. Yes, behavioral interventions such as speech therapy, occupational therapy, and Applied Behavior Analysis still have an integral role to play, but very often the results they achieve are limited. By addressing the underlying biological issues, autism and other ASDs can be greatly improved. And in some cases, as we saw with young Mike Simpson, autism and ASD symptoms may disappear altogether.
John C. Pittman, MD, is the Medical Director of the Carolina Center for Integrative Medicine in Raleigh, NC, and is certified by the American Board of Clinical Metal Toxicology. Mark N. Mead, MSc, serves as the Center’s Nutrition Educator and Integrative Medicine Research Consultant.
Rossignol DA. Novel and emerging treatments for autism spectrum disorders: a systematic review. Ann Clin Psychiatry. 2009;21(4):213-36.
Bradstreet JJ, Smith S, Baral M, Rossignol DA. Biomarker-guided interventions of clinically relevant conditions associated with autism spectrum disorders and attention deficit hyperactivity disorder. Altern Med Rev. 2010;15(1):15-32.
Landrigan PJ. What causes autism? Exploring the environmental contribution. Curr Opin Pediatr. 2010; 22(2):219-25.
Adams JB, Baral M, Geis E, Mitchell J, et al. The severity of autism is associated with toxic metal body burden and red blood cell glutathione levels. J Toxicol. 2009;2009:532640.
Adams JB, Baral M, Geis E, Mitchell J, et al. Safety and efficacy of oral DMSA therapy for children with autism spectrum disorders: Part A--medical results. BMC Clin Pharmacol. 2009;9:16.
O'Hara NH, Szakacs GM. The recovery of a child with autism spectrum disorder through biomedical interventions. Altern Ther Health Med. 2008;14(6):42-4.
Kidd PM. An approach to the nutritional management of autism. Altern Ther Health Med. 2003;9(5):22-31
Kidd PM. Autism, an extreme challenge to integrative medicine. Part 2: medical management. Altern Med Rev. 2002;7(6):472-99.
Kidd PM. Autism, an extreme challenge to integrative medicine. Part: 1: The knowledge base. Altern Med Rev. 2002;7(4):292-316.
Yes, carbs can indeed elevate cholesterol. This sentence is not a typo.
Assume that you have an unfavorable cholesterol profile (low HDL, high triglycerides and low LDL). The typical scenario is as follows: You have high cholesterol, you pursue a million dollar workup with your cardiologist, including a stress test, EKG, blood work, etc, and the ultimate recommendation is to follow the Dean Ornish Diet. This diet was based on a five year intervention study called the Lifestyle Heart Trial which followed 48 men with heart disease and told them to exercise, manage stress, stop smoking, get psychological help, and go on a high fiber, low fat and low calorie diet. Of the 48 men, 20 actually completed the study, where all the recommendations were adhered to.
The results showed that there was actually some reversal of heart disease! The bottom line that was extracted from this study was that a low fat diet helps to reverse heart disease. Seldom were the other factors addressed. Since then, most patients have been advised by their cardiologists and internists to stay on a diet of this nature.
Thereafter, many have tried to comply with the low fat diet and noticed that cholesterol was not dropping. Hmmm… Let’s look at the science to figure this out.
I am going to break this one down to the nitty gritty details, so beware.
How Carbs Actually Elevate Cholesterol
You are eating your whole grain toast or dairy item in the morning with fruits, pasta for lunch and a rice dish with a protein for dinner. Your desserts are always fresh or dried fruits. You are drinking juices with your meals. Once the digestive juices are appropriately secreted and the food is churned, the necessary nutrients are absorbed through the intestinal walls. Glucose (derived from carbs), amino acids (derived from proteins), and fatty acids ( derived from fats) are passed through a corridor (the portal vein) and enter the liver.
The pancreas is paying very close attention to the molecules passing through this corridor into the liver.
It gets quite excited when it sees glucose and quickly shows its affection by secreting insulin. Insulin does several things:
It stimulates the production of cholesterol. Many of you have heard of statin drugs. They work by inhibiting an enzyme called HMGcoA reductase. Insulin stimulates this enzyme! How can it be possible for your cholesterol to go down if the foods that you are eating stimulate the very enzyme that cholesterol reducing drugs are trying to decrease?
Insulin slows down an amino acid called carnitine. Carnitine is important because it functions to shepherd the fatty acids into the part of the cell where they will be converted into usable energy. Insulin can therefore harbor weight gain by not allowing the fatty acids to be converted into energy effectively, via the mechanism of carnitine.
Insulin causes cells in the liver, muscles and fat to take up glucose. In the liver, the glucose is stored as glycogen. Here is the interesting part… There is not that much glycogen in the liver, so whatever sugar the liver is unable to hold is spilled over to another processing system. The glucose is packaged neatly into triglycerides. Yes, the ones associated directly with cardiovascular disease. This was the bottom line, ladies and gents. VLDL (very low density lipoprotein ) is then stimulated by the liver and LDL, the bad cholesterol) is made. Whew!
When there is not much glucose in he body, as in the case in a lower-carb diet, there is no signal to release the insulin. Insulin is absent (or low), glucose is not taken up by the cells and triglycerides are not manufactured from the spillover of glucose. Therefore, the above process is not as robust. With low insulin levels, the body begins to use fat as an energy source since it does not have the glucose. Using fat as an energy source is one of the mechanisms of weight loss. Let’s pause for the “ahaa” moment.
So there it is, eat low carb and see the weight come off and cholesterol decrease. A common mistake is that patients eat BOTH low and high carb simultaneously. They also focus on meats that are not lean. They come into my office telling me about all the healthy proteins they have been eating. Only problem is that they are having tons of rice or pasta along with a small amount of fatty protein. Taking the above mechanism of action into consideration, this is truly counterintuitive,.
Please reread the mechanism several times. Once you understand it, you will be able to intelligently change your diet. Being informed is crucial.
Although diets rich in marine lipids and fish-oil supplements have staked a claim to heart disease prevention, controversy remains. A recent study examining the role of omega-3-enriched margarine as a functional food for secondary prevention of heart attacks yielded negative results;1 publication of the study spawned skeptical and even derisive headlines in the popular press: Omega-3 Fats Offer No Protection Against Heart Disease—Study and Low Doses of Omega-3s Don't Help with Heart Disease: Say it Ain't So, Fish Oil!.
Are the results of this study (perhaps somewhat prematurely titled "The Alpha Omega Trial") definitive? How do clinicians reconcile these negative findings with the vast body of references that support the cardiovascular benefits of fish consumption and omega-3 supplementation? And most important, what are the implications for consumers and for potential advocacy by health-care professionals?
The current regulatory climate for fish-oil claims underscores this uncertainty. Lovaza (omega-3-acid ethyl esters), the only FDA-approved fish-oil supplement, is indicated only for its pharmacologic effect of lowering elevated triglycerides. FDA labeling specifically qualifies that "The effect of Lovaza on cardiovascular mortality and morbidity in patients with elevated triglyceride levels has not been determined."2
No comparable approval, either explicit or tacit, exists in the United States for the application of fish-oil supplements to primary or secondary prevention of cardiovascular disease (CVD). But a considerable proportion of the population consumes these supplements, and a high percentage of health-care providers embrace such recommendations—if not for their patients, then for themselves and their families.
While the exact proportions are not known, a recent investigation showed that 62% of U.S. doctors surveyed agreed that one of their roles as a health-care professional is to provide information to patients about appropriate dietary supplements.3 The most popular supplements among cardiologists were multivitamins, omega-3s/fish oil, and vitamin C.
Even regulatory language governing claims for cardioprotection via consumption of omega-3-rich foods remains highly circumscribed. In September 2004, the FDA announced permission for "qualified health claims on omega-3 fatty acids" to the effect that, "Supportive but not conclusive research shows that consumption of eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA] omega-3 fatty acids may reduce the risk of coronary heart disease."4
Compounding the controversy are international discrepancies vis a vis the prescription of fish-oil supplements. A front-page article in The New York Times pointed out that while 57% of family clinicians in Washington State acknowledged fish oil's potential benefits in preventing a second heart attack, only 17% identified themselves as frequent prescribers of fish oil.5
The situation in the United States stood in contrast with that in Europe where, according to Dr. Massimo Santini, chief of cardiology at Rome's San Filippo Neri hospital, a doctor's failure to prescribe fish oil to a heart patient "would be considered tantamount to malpractice."5
The article concluded that in the United States, "community doctors do not learn how to use [fish oil]," while insurers will not pay for cardiovascular prevention via fish-oil supplementation because it is not specifically approved by the FDA for that indication.5
In its scientific statement on fish consumption, fish oil, omega-3 fatty acids, and CVD, the American Heart Association (AHA) acknowledges that: "[Randomized controlled trials] have demonstrated that omega-3 fatty acid supplements can reduce cardiac events (e.g., death, nonfatal MI, nonfatal stroke) and decrease progression of atherosclerosis in coronary patients. However, additional studies are needed to confirm and further define the health benefits of omega-3 fatty acid supplements for both primary and secondary prevention."6
After some equivocation to the effect that dietary approaches to omega-3 supplementation are preferable, the AHA allows that certain individuals, whose dietary preferences preclude adequate intake from natural sources, "in consultation with their physician, could consider supplements for coronary heart disease [CHD] risk reduction."6
What lines of evidence support fish-oil supplementation for cardiovascular prevention? Early impetus came from epidemiologic studies. As early as 1944, Sinclair noted the decreased prevalence of CVD in Arctic Eskimos who subsisted largely on omega-3-rich fish and aquatic mammals.7 In the 1970s, Danish researchers noted improved cardiovascular profiles and lower MI mortality among Greenland Eskimos consuming a low-carbohydrate, fat-rich diet when compared with subjects consuming a Western diet on the Danish mainland.8
Three large randomized trials have documented the effects of omega-3 polyunsaturated fatty acid (PUFA) in primary and especially in secondary prevention of CHD.9 More than twenty years ago, the Diet and Reinfarction Trial demonstrated a 29% reduction in mortality—almost entirely attributable to decreased cardiovascular death—in subjects consuming high amounts of omega-3 from fish sources or supplements.10The reduction in cardiovascular events was particularly impressive in individuals consuming fish-oil capsules.
A subsequent prevention trial corroborated the benefits of fish-oil supplementation for secondary prevention in MI survivors, namely with one Lovaza capsule per day delivering 850 mg of EPA/DHA in a 1.2:1 ratio. Researchers demonstrated a 21% and a 30% reduction, respectively, in total death and cardiovascular death over the one-year duration of the study.11 These results were driven by an impressive 46% reduction in sudden cardiac death. Reductions in major clinical events continued to be demonstrated at 3.5-year follow-up.12
Additional evidence for the protective effects of omega-3 supplementation comes from the Japan EPA Lipid Intervention Study, published in 2007. In a mixed trial of primary and secondary prevention, 18,645 patients with hypercholesterolemia (70% women) were randomized to statin alone or statin and highly purified EPA 1,800 mg/day. At the end of the five-year study, those randomized to statin plus EPA had a 19% reduction in major cardiovascular events.13
How do clinicians reconcile these results with those of the Alpha Omega Trial, which demonstrated no secondary prevention benefits of supplementation with an omega-3-enriched margarine spread?
Researchers leading the Alpha Omega Trial assigned 4,837 MI survivors to one of four experimental groups. For 40 months, participants consumed either (1) placebo margarine, (2) margarine with a combined total of 400 mg of EPA/DHA, (3) margarine with 2 g of alpha-linolenic acid (ALA), a plant-derived precursor to EPA/DHA, or (4) a margarine containing a combination of EPA/DHA and ALA. State-of-the-art antihypertensive, antithrombotic, and lipid-modifying therapy was implemented in all four groups.
The results showed that neither the EPA/DHA nor the ALA (nor a combination of both) proved more beneficial than placebo. Does this constitute a repudiation of the omega-3 CVD prevention hypothesis?
Critics of the Alpha Omega Trial were quick to point out specific objections to its methodology. First, aggressive pharmacologic management may have masked some of the advantages conferred by fish oil. Additionally, it was thought that the results did not disqualify a putative benefit of omega-3-enriched margarines in primary prevention.
Some have claimed that the choice of a margarine-like spread as a delivery system might have compromised the efficacy of the active omega-3 component. The caloric load provided by daily consumption of 18.8 g of omega-6-rich vehicle and the attendant consumption of multiple slices of high glycemic index bread on which the margarine-like substance was spread, might have acted as confounders.
But most important, the low-dose of EPA/DHA (400 mg) employed in the trial is well below the threshold noted in some studies to influence cardiovascular outcome. The study might best be viewed as merely contravening the hoped-for cardio-protective role of a specific functional food—with inherent limitations to palatability attributable to fish oil's inability to being disguised in neutral vehicles. Therefore, it would be an overstatement to claim, as some have, that the Alpha Omega Trial is the death knell for omega-3 supplementation in CVD.
How then are omega-3 PUFAs thought to influence CVD progression and reduce mortality? Several pathways have been investigated.
Hypolipidemic. It is well established that omega-3s reduce lipid levels, and this is the basis for the approved indication for use of Lovaza in hypertriglyceridemia. It is generally acknowledged that doses >3-4 g/day are required. The mechanism of omega-3's triglyceride reduction relates to its favorable effects on reducing hepatic production and secretion of very-low-density lipoprotein (VLDL) and VLDL apo B particles, its favorable effects on plasma lipolytic activity through lipoprotein lipase-mediated clearance, and its ability to stimulate beta-oxidation of other fatty acids in the liver.14
Generally, omega-3s produce no significant improvements in LDL, except in patients with elevated triglycerides, in whom modest improvements in LDL and HDL are sometimes seen. Even when absolute LDL levels are not significantly impacted by fish-oil supplementation (or even when they increase, as has occasionally been reported), there is evidence that omega-3s may shift particle size to a more benign, "fluffier" LDL, thus favorably impacting the atherogenic profile.
Antithrombotic. Fish oils produce platelet inhibition and reduce fibrinogen. Although some experts contend that higher doses (>3-4 g/day) are required, others argue for a lower threshold. Epidemiologic evidence of fish oil's anti-clotting effects comes from several studies that link higher intake of fish oil to a reduction in ischemic strokes with coincident increased risk of hemorrhagic strokes. This leads to a net gain in protection, since ischemic strokes outnumber hemorrhagic strokes by 85% to 15%.
Antihypertensive. Fish oil is thought to exert an antihypertensive effect in several ways. It supports flow-mediated vasodilation, enhances vascular reactivity, and may balance autonomic tone by reducing adrenergic drive.
An analysis of randomized trials revealed that consumption of approximately 4.0 g/day of omega-3 fatty acid was associated with a significant 1.7- and 1.5-mm Hg reduction in systolic and diastolic BP, respectively; these reductions were more pronounced in older patients and in individuals with higher BP. Evidence suggests that lowering systolic BP by as little as 2 mm Hg can yield reductions of 4% in CAD mortality.15
Adiponectin. A hormone produced by fat cells, adiponectin plays a role in regulating lipids and glucose. Low levels of this hormone are associated with obesity, and higher levels have been shown to confer protection against heart disease. When administered to obese individuals, 1.8 g/day of EPA increased the level of adiponectin.16
Insulin regulator. To date, research in the area of insulin regulation has been inconclusive. While numerous studies support a role for EPA/DHA in attenuating insulin resistance, and omega-3 deficiency has been associated with the metabolic syndrome, the Agency for Healthcare Research and Quality reports, "Among 18 studies of type 2 diabetes or the metabolic syndrome, omega-3 fatty acids . . . had no effect on fasting blood sugar, or glycosylated hemoglobin, by meta-analysis. Omega-3 fatty acids had no effect on plasma insulin or insulin resistance in type 2 diabetics or patients with the metabolic syndrome, by qualitative analysis of four studies."17
Antiarrhythmic. The principle cause of sudden cardiac death (SCD) is sustained ventricular arrhythmia. Considerable evidence supports an antiarrhythmic role for omega 3s, probably via autonomic pathways. Studies show that EPA/DHA enhances sympatho-vagal tone, leading to slower heart rates and fewer arrhythmias, and in some studies, reduced incidence of SCD. Omega 3s have also been shown to favorably impact heart rate variability, a marker of autonomic adaptability.
Knowledge of fish oil's beneficial effects on arrhythmias recently prompted a trial of omega-3 supplementation in patients with implantable cardioverter defibrillators (ICDs). The results—which showed a higher incidence of ICD discharges in consumers of fish-oil supplements—and the consequent negative publicity have dampened enthusiasm over fish oil for this indication.
Some studies have shown impressive results for fish oil in prophylaxis of atrial fibrillation, particularly in patients at risk after coronary artery bypass grafting.18
Anti-inflammatory. Omega-3 fatty acids act as eicosanoid precursors to reduce inflammation. This may impact cardiovascular risk in several ways.
First, chronic inflammation is thought to play a critical role in endothelial damage that leads to compromised vascular reactivity and atherosclerotic changes. Additionally, inflammation promotes unstable plaque, a harbinger of thrombotic events.
Next, it is now commonly acknowledged that elevated high-sensitivity C-reactive protein (hs-CRP), a selective marker of intra-arterial inflammation, is a robust risk factor for CVD. Research on the potential for fish oil to lower this cardiospecific parameter has produced mixed results. One study found that atorvastatin (Lipitor), but not fish oil, reduced hs-CRP in obese, at-risk subjects.19 In other research, omega-3 supplements did not reduce hs-CRP in healthy subjects.20 Another set of findings showed that EPA/DHA reduced hs-CRP in patients on dialysis, a population known to be at higher risk for inflammation and CVD.21
Finally, fish oil has a less equivocal effect on other inflammatory mediators, specifically such cytokines as tumor necrosis factor-alpha, elevations of which are hallmarks of chronic congestive heart failure (CHF). Studies show improvement in cytokine levels in CHF patients taking EPA/DHA, with corresponding improvements in clinical outcomes.9
Prevention of restenosis. Accelerated restenosis following angioplasty or stenting is one of the thorniest problems in medicine, associated with numerous failed strategies. Because of fish oil's acknowledged antiatherosclerotic effects, it became a likely candidate for restenosis prevention. Early meta-analyses showed modest benefit and provided reason to be hopeful.22 Unfortunately, the Coronary Angioplasty Restenosis Trial demonstrated no reduction in restenosis rates with 5 g/day of Omacor, a precursor to Lovaza.23
Other benefits. Ancillary benefits of fish-oil supplementation are thought to be considerable. Therapeutic effects have been investigated, with various degrees of evidence, in such diverse conditions as bipolar disorder, depression, dementia, psychosis, certain cancers (including breast, colon, and prostate) cancer cachexia, rheumatoid arthritis, cystic fibrosis, inflammatory bowel disease, dysmenorrhea, IgA nephropathy, systemic lupus, asthma, chronic obstructive pulmonary disease, psoriasis, eczema, dry eye, macular degeneration, pre-eclampsia, and prevention of organ-transplant rejection.24
With regard to fish oil's role in secondary prevention of CVD, studies suggest potential amelioration of depression in heart attack survivors who take omega-3s. Depression is a known comorbidity following MI. It is also a negative prognostic, so, if proven, fish oil's antidepressant effects would be a valuable ancillary benefit.
A recent trial compared fish oil plus sertraline with sertraline alone in a group of post-MI patients. Mood improved in all the patients, but no difference was seen in depression scores between fish-oil-supplemented patients vs. controls.
"Whether higher doses of EPA, DHA, or sertraline, a longer duration of treatment, or the use of omega-3 as monotherapy can improve depression in patients with stable heart disease remains to be determined," the authors concluded.25
ADVERSE EFFECTS AND CONTRAINDICATIONS
The most commonly observed adverse effects of omega-3 PUFA supplementation are nausea, GI upset, and "fishy" burp. These problems can sometimes be ameliorated through the use of flavored, emulsified omega-3 formulations that are palatable even to children. Alternatively, enteric-coated forms of fish oil are designed to dissolve distal to the stomach, reducing the potential for oily reflux.
Because of fish oil's antiplatelet effects, concerns have been raised over the possibility that higher intakes will lead to an increase hemorrhagic complications. However, a comprehensive review concluded that no increased risk of clinically significant bleeding was noted with omega-3 PUFA doses of up to 7 g of combined DHA and EPA per day, even when coupled with antiplatelet therapy or warfarin.26 Results may vary in clinical practice, and such clotting disorders as Von Willebrand disease or thrombocytopenia may pose relative contraindications to high-dose fish-oil supplementation.
A recent study explored fish-oil supplements' synergy with aspirin and clopidogrel in post-stenosis patients. Resistance to platelet inhibition was overcome with no concomitant increase in adverse hemorrhagic events.27
To prevent excessive perioperative bleeding, patients undergoing elective surgery are typically advised to forgo fish-oil supplementation for several weeks, but some studies actually support a role for fish oil in improving surgical outcomes. Some researchers have credited fish oil with offering circulatory benefits, or alternatively with modulating immunity, perhaps by blunting the exaggerated cytokine response to surgery.28
Lately, concerns have been raised over fish oil's potential to down-regulate immunity in detrimental ways. One study observed that fish oil decreased resistance to influenza virus in a murine model,29 but the observation has not been extended to humans.
FISH-OIL SUPPLEMENTS ON THE MARKET
Fish-oil supplements come in a variety of forms. Cod-liver oil is the original article, but its disadvantages relative to omega-3 capsules include low ratio of EPA/DHA to overall calories, greater risk of mercury and PCB contamination, and potential for vitamin A and D toxicity with high levels of supplementation.
Most fish-oil capsules are free of significant mercury and PCB contamination, and industry standards for monitoring and disclosure are relatively stringent. Disparities exist, however, in the amount of active EPA and DHA delivered per capsule, and some ultra-discounted brands may be of dubious benefit due to the sheer number of capsules required to achieve clinically meaningful supplementation.
Manufacturers sometimes use the term "pharmaceutical grade" to imply greater potency or purity, but the claim is not regulated and almost meaningless. Also, controversy persists over relative advantages of two competing technologies for enhancing the EPA/DHA concentration: triglyceride substitution vs. ethyl esterification (used in Lovaza). Each camp claims superior bioavailability, but evidence remains inconclusive.
Finally, new formulation technology permits the offering of EPA/DHA in variable ratios designed to target specific clinical goals. EPA and DHA may have differing effects on desirable cardioprotective endpoints. The precise "optimal" ratio of EPA/DHA for heart disease prevention, if such a thing exists, has not yet been determined.
Uncertainty remains among health-care professionals as to the potential therapeutic application of fish-oil supplements in heart disease. A wide range of mechanistic, epidemiologic, and controlled-trial evidence substantiates a role for omega-3 fatty-acid supplementation in both primary and secondary cardiovascular prevention. An extensive margin of safety has been confirmed in most settings. More work remains to be done in studying the effects of fish oil in specific subpopulations and circumstances as well as in clarifying optimal dosage regimens and EPA/DHA ratios. Only then can specific guidelines for administration of omega-3 supplements coalesce into consistent and clear recommendations from health-care professionals.
Dr. Hoffman is founder and medical director of the Hoffman Center in New York City. The author has no relationships to disclose relating to the content of this article.
1. Kromhout D, Giltay EJ, Geleijnse JM; Alpha Omega Trial Group. n-3 fatty acids and cardiovascular events after myocardial infarction. N Engl J Med. 2010;363:2015-2026.
2. GlaxoSmithKline. Lovaza prescribing information. Available at us.gsk.com/products/assets/us_lovaza.pdf.
3. Natural Products Insider. Cardiologists recommend dietary supplements for a healthy heart. Available at multivu.prnewswire.com/mnr/lifesupplemented/36723/.
4. U.S. Food and Drug Administration. FDA announces qualified health claims for omega-3 fatty acids. Available at www.fda.gov/NewsEvents /Newsroom/PressAnnouncements/2004/ucm108351.htm#.
5. Rosenthal E. In Europe it's fish oil after heart attacks, but not in U.S. The New York Times. October 3, 2006: A1. Available at www.nytimes .com/2006/10/03/health/03fish.html.
6. Kris-Etherton PM, Harris WS, Appel LJ; American Heart Association. Nutrition Committee. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 2002;106:2747-2757. Available at circ .ahajournals.org/cgi/content/full/106/21/2747.
7. Sinclair HM. The diet of Canadian Indians and Eskimos. Proc Nutr Soc. 1953;12:69-82.
8. Dyerberg J, Bang HO, Hjorne N. Fatty acid composition of the plasma lipids in Greenland Eskimos. Am J Clin Nutr. 1975;28:958-966. Available at www.ajcn.org/cgi/reprint/28/9/958.pdf.
10. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet. 1989;2:757-761.
11. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico. Lancet. 1999;354:447-455.
12. Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002;105(16):1897-1903. Available at circ.ahajournals.org/cgi/content/full/105/16/1897.
13. Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis.Lancet. 2007;369:1090-1098.
14. Jacobson TA. Role of n-3 fatty acids in the treatment of hypertriglyceridemia and cardiovascular disease. Am J Clin Nutr. 2008;87:1981S-1990S. Available at www.ajcn.org/cgi/content/full/87/6/1981S.
15. Geleijnse JM, Giltay EJ, Grobbee DE, et al. Blood pressure response to fish oil supplementation: metaregression analysis of randomized trials. J Hypertens. 2002;20:1493-1499.
16. Itoh M, Suganami T, Satoh N, et al. Increased adiponectin secretion by highly purified eicosapentaenoic acid in rodent models of obesity and human obese subjects. Arterioscler Thromb Vasc Biol. 2007;27:1918-1925. Available at atvb.ahajournals.org/cgi/content/full/27/9/1918.
17. MacLean CH, Mojica WA, Morton SC, et al. Effects of omega-3 fatty acids on lipids and glycemic control in type II diabetes and the metabolic syndrome and on inflammatory bowel disease, rheumatoid arthritis, renal disease, systemic lupus erythematosus, and osteoporosis. Evid Rep Technol Assess (Summ). 2004;89:1-4. Available at www.ahrq.gov/downloads/pub/evidence/pdf/o3lipid/o3lipid.pdf.
18. Calò L, Bianconi L, Colivicchi F, et al. N-3 Fatty acids for the prevention of atrial fibrillation after coronary artery bypass surgery: a randomized, controlled trial. J Am Coll Cardiol. 2005;45:1723-1728.
19. Chan DC, Watts GF, Barrett PH, et al. Effect of atorvastatin and fish oil on plasma high-sensitivity C-reactive protein concentrations in individuals with visceral obesity. Clin Chem. 2002;48:877-883. Available at www.clinchem.org/cgi/content/full/48/6/877.
20. Geelen A, Brouwer IA, Schouten EG, et al. Intake of n-3 fatty acids from fish does not lower serum concentrations of C-reactive protein in healthy subjects. Eur J Clin Nutr. 2004;58:1440-1442. Available at www.nature.com/ejcn/journal/v58/n10/full/1601986a.html.
21. Saifullah A, Watkins BA, Saha C, et al. Oral fish oil supplementation raises blood omega-3 levels and lowers C-reactive protein in haemodialysis patients—a pilot study. Nephrol Dial Transplant. 2007;22):3561-3567. Available at ndt.oxfordjournals.org/content/22/12/3561.long.
22. O'Connor GT, Malenka DJ, Olmstead EM, et al. A meta-analysis of randomized trials of fish oil in prevention of restenosis following coronary angioplasty. Am J Prev Med. 1992;8:186-192.
23. Johansen O, Brekke M, Seljeflot I, et al. N-3 fatty acids do not prevent restenosis after coronary angioplasty: results from the CART study. Coronary Angioplasty Restenosis Trial. J Am Coll Cardiol.1999;33:1619-1626.
24. National Library of Medicine. Fish Oil. Available at www.nlm.nih.gov/medlineplus/druginfo/natural/993.html.
25. Carney RM, Freedland KE, Rubin EH, et al. Omega-3 augmentation of sertraline in treatment of depression in patients with coronary heart disease: a randomized controlled trial. JAMA. 2009;302:1651-1657. Available at jama.ama-assn.org/cgi/content/full/302/15/1651.
26. Harris WS. Expert opinion: omega-3 fatty acids and bleeding-cause for concern? Am J Cardiol.2007;99:44C-46C.
27. Gajos G, Rostoff P, Undas A, Piwowarska W. Effects of polyunsaturated omega-3 fatty acids on responsiveness to dual antiplatelet therapy in patients undergoing percutaneous coronary intervention: the OMEGA-PCI (OMEGA-3 fatty acids after PCI to modify responsiveness to dual antiplatelet therapy) study.J Am Coll Cardiol. 2010;55:1671-1678.
28. Tsekos E, Reuter C, Stehle P, Boeden G. Perioperative administration of parenteral fish oil supplements in a routine clinical setting improves patient outcome after major abdominal surgery. Clin Nutr.2004;23:325-330.
29. Schwerbrock NM, Karlsson EA, Shi Q, et al. Fish oil-fed mice have impaired resistance to influenza infection. J Nutr. 2009;139:1588-1594. Available at www.ncbi.nlm.nih.gov/pmc/articles/PMC2709305/.
All electronic documents accessed November 15, 2010.
The 2 running themes at the office this week seem to have been the stomach bug; which is making its way around Southern California, and Stress. My advice for the former is to wash your hands, and choose restaurants carefully when eating out.
Today’s discussion will be on the latter since Stress seems to be all around us, permeating some days more than others. It directly affects our health, (blood pressure being the quickest marker of it), our ability to restore and replenish (when it affects our sleep), and it robs us of being nourished through our daily interactions.
Below are 3 examples of how we must remain in the present, see the opportunity in adversity, and how nurturing ourselves through coping mechanisms can reduce our stress.
REMAIN IN THE PRESENT:
When we put ourselves on autopilot, motoring through life, day after day, the divine aspects of life lose their luster.
Our life becomes something we just do, instead of the wave of possibility that each new dawn can bring. One of my patients this week was mentioning how she initially came to the clinic. She had run into one of her friends at the car wash that she hadn’t seen in a while. They got to talking and she said to him, “there must be some reason why we were meant to meet.” He replied, “I bet your right, so let's just start talking and see where it leads.” They spoke about their lives, their challenges, their spouses, their health and so on. By the end of the conversation she heard how Naturopathic Medicine had helped him and confided that she too had been in search of a doctor or clinic that could help her get to the cause of her health issues as well, which in turn led her to my office. And so it goes….
The purpose of this example is not to say everyone needs a Naturopathic Doctor, it is to merely suggest that opportunities are within the people that we meet every day. When we are stressed we tend to withdraw and be focused on how we can just make it through the day. When this happens we tend to miss the “life-rafts” that get thrown our way.
Open yourself to the possibility within each interaction, sometimes the reason is revealed right away and sometimes it reveals itself over time, there are so many cross links within the divine plan.
OPPORTUNITY IN ADVERSITY:
Our life experiences change us and can spur us on in directions we never dreamed prior to their occurrence.
I don’t really know why but the end of one year and the beginning of another energetically seem to be filled with more births and deaths than usual. The ultimate cliché of when one life ends another begins, and so it is within the cycles of nature and time. I do know that when things are bad they never stay bad, and when things are good they never stay good, that is the organic nature of life; which can easily be seen within the real-estate market.
A patient of mine, who is a nurse, recently lost her mother to the complications of conventional medicine. (Not her cancer or her cardiovascular disease.) Through this experience, which left her disheartened with the conventional standards of care, she has changed her focus from dermatology to a career in alternative cancer therapies.
It is in this waking up that there is a shaking up, and a passion is invoked that was before dormant.
And so it is with our economy, more small business startups are beginning each day, as people no longer wait for their fate to be at the mercy of someone or something else. The creativity that is erupting from individuals and entrepreneurs can be seen across the Internet, YouTube, blogs, Facebook, digital marketing accounts, and smart phone applications. Many more people have found their voice and are using it to expand on their passion.
When things are going good it’s easier to be healthy and eat right. The challenge is to still make good food & life choices under stress.
Change is never easy and it’s hard to get up off of a couch that was really comfortable, the current stressors of today are upending that couch for many. It is affecting our health. The answer is not to look back to what was, the answer is to ask for the way to reveal itself, and develop healthy coping mechanisms in the interim.
Make your coping mechanisms a priority. Healthy coping mechanisms include anything that is supportive and nurturing to your mind, body, and spirit. (Some of you can rationalize that ice cream is nurturing. Frozen, fat, dairy, and sugar is in no way, shape or form nurturing.)
My last patient of the week, had been losing weight and really doing great on her food plan that she had been working on for about 2 months. She showed up completely frazzled, angry and hopeless at my office Friday afternoon regarding stress at work. When I took her blood pressure it was elevated, and she was giving herself hot flashes. She confided that she had not had any ice cream during the 2 months that we had been working together and that the incredible stress of the previous week sent her literally head first into the freezer. Although she knew that after eating ice cream she felt terrible, she couldn’t resist the urge to eat it right then and there. Negative coping mechanisms can be extremely deleterious to our health if we aren’t careful. Self-defeating choices include sweet treats, alcohol, smoking, soda, and impulsive behaviors.
This situation in particular is a classic case of emotional eating. Most of us do it to one extent or another, for some it’s mashed potatoes, chocolate, ice cream, or pastries, the list is endless. All sugar and carbohydrates boost our serotonin, which is a temporary antidepressant and makes us feel immediately better. Remember the nothing-good lasts, so then we crash, often feeling worse then before we ate it. She and I explored the situation, and discussed where she could work on directing her energy, we then discussed alternative coping mechanisms that included exercise, talking with friends or her spouse, walking on the beach, and others.
Stress, mental, physical, and emotional is all around us. Our stressors are actually becoming greater as the digital age continues to develop. This is because we now have within second’s access to events happening around the world, and to literally feel the impact of them. Now something happening in Asia can directly affect our bank account, and devastation in Haiti, can keep many of us awake at night for hours and be on our minds for days. Our nervous systems are busy integrating thousands of millibits of information per minute coming in from our computers, telephones, Internet, radio, and iPods. Now more than ever in order to be balanced and in good health, we must develop healthy coping mechanisms, see the opportunity in adversity, and stop to smell the flowers, watch a shooting star and embrace the beauty of each moment.
Menopause has been grabbing all the headlines lately, but half the world faces a comparable syndrome that is more insidious and less predictable. This disease entity is andropause.
Unlike menopause which usually occurs at a predictable time, men's testosterone levels decline at different ages and different rates, sometimes slowly, and sometimes precipitously. Testosterone production by the testes reaches adult levels by age 17 (300-1000 ng/dL). The testosterone level remains constant until the fifth decade at which point it declines at a rate of 1.2 percent per year. But in some men, testosterone can drop prematurely and precipitously.
In the Baltimore Longitudinal Study of Aging (2001), it was demonstrated that free testosterone decreased at a constant rate with age and this decline was not related to other causes. Another study demonstrated that poor health may accelerate the natural age-associated decline in testosterone concentrations. One interesting finding is that studies that measured testosterone in the morning were more likely to show a decline in testosterone when compared to studies that measured testosterone in the afternoon. The logic behind this is that older men have little variation in their levels of testosterone throughout the day, unlike young men, who have peaks in their testosterone levels in the morning and troughs in the evenings.
As one ages, there is an increase in fat cells, which in turn causes an elevation in an enzyme called aromatase. This enzyme transforms testosterone to estrogen in the body. Secondarily, estrogen can indirectly cause an increase in a protein called sex-hormone-binding-globulin (SHBG), which binds to free testosterone and prevents its action. This protein will ultimately cause a decrease in testosterone.
At this point you should be asking "Does this apply to me or to my spouse/partner?"
There are theories that demonstrate that a decline in testosterone can cause a decline in mental function. In a study published in the Journal Of Clinical Endocrinological Metabolism in 2002, 407 men were studied ages 50-91 and subsequently demonstrated that those classified as having a low testosterone had lower scores on memory and visuo-spacial performance. The results of several pilot studies have tied low testosterone levels to Alzheimer's disease, in which there is a build-up of a toxic peptide called beta-amyloid. These studies showed that the toxic effects of this peptide are reduced by testosterone. Interestingly, testosterone levels were lower in Alzheimer's patients as compared to controls. It is unknown if these low levels cause or are caused by Alzheimer's disease. According to Dr. Jonathan Wright (co-author of Maximize Your Vitality and Potency), low testosterone levels are associated with moodiness, feeling weak, passivity, and reduced interest in one's surroundings.
In addition to having an effect on cognitive function, studies have shown correlations between a declining testosterone level and a decline in sexual function as measured by frequency of orgasm or intercourse or by sexual satisfaction (Journal of Clinical Endoclinology 1983). Studies also show that muscle mass, muscle strength and bone mineral density decline with age.
The first step in diagnosing andropause starts with a thorough evaluation at your physician's office. First, your doctor will obtain a complete medical history from you and perform a series of blood tests to see if you have testosterone deficiency and what may be causing it. Before starting any treatment, however, it is imperative to rule out underlying prostate cancer, just as we would rule out breast cancer in a woman contemplating estrogen therapy. The following are some examples of causes of low testosterone and approaches to them.
First, as discussed, in obese patients, there is excess aromatase enzyme activity causing the testosterone to convert to estradiol causing estrogen overload and testosterone deficiency. Poor liver function is another entity that causes excess estrogen because the liver then cannot detoxify the small amounts of estrogen that even men have. In this case, total testosterone levels would be normal and estrogen levels would be high as much of the testosterone is being changed into estradiol, and the free or usable testosterone levels would be low. This often occurs with excess alcohol consumption.
If you fall into the above category, you should maintain an appropriately high level of aromatase inhibitors in your diet. The recommendation is zinc 80mg daily. A supplement call chrysin, a flavonoid, together with piperine for enhance absorption into the bloodstream, functions as a mild aromatase inhibitor as well. There is a more potent aromatase- inhibiting drug called Arimidex (anastrozole), which can only be prescribed by your doctor. Arimidex is prescribed to estrogen receptor positive breast cancer patients to prevent hormones in the body from aromatizing into estrogen. It has not yet been FDA approved for other indications.
A diet that does not adversely affect liver function should be adhered to. This will of course include an alcohol-free diet, since even small amounts of alcohol are shown to augment estrogen in both men and women. Special attention should be paid to medications affecting the liver and should be reviewed with your doctor in detail. As estrogen excess may be a problem in the setting of liver dysfunction, a substance called indole-3-carbinol (or diindole methane or DIM)) found in special supplements or cruciferous vegetables can help to neutralize the excess estrogen. Most importantly, it is essential that you lose weight as it is the excess aromatase enzyme that is produced by the fat cells that convert the testosterone into the estrogen.
Second, an excess of sex-hormone-binding-globulin can bind much of the free- testosterone and therefore inactivates it. In this case, one will have low free testosterone, normal or even high total testosterone and normal estradiol levels. In addition to following the protocol that inhibits aromatase activity, take saw palmetto which can block the estrogen receptor sites in the prostate cells and therefore reduce the effects of excess estrogen. Saw palmetto also blocks the conversion of testosterone into a hormone, DHT, which has been directly linked to the development of prostate disease.
Methanolic extract of nettle can also inhibit SHBG. It binds to SHBG and therefore blocks its testosterone binding effects, thus allowing more testosterone to be in its natural free state. This root has also been used for benign prostatic hyperplasia. It inhibits the binding of dihydrotestosterone ( DHT), a prostate growth stimulator, to the prostate.
A third cause of low testosterone is failure of the pituitary gland to produce a hormone called leutenizing hormone (LH). One of the functions of LH is to stimulate testosterone production by the testes. In this case, the levels of total testosterone would be low as there is a problem with production.
Fourth, if the testes themselves lose their ability to produce testosetrone, there would be an elevated LH, which would act as a stimulant to produce testosterone. Total testosterone would be low. Patients like these are candidates for testosterone replacement.
Lastly, DHEA, a precursor hormone to testosterone and estrogen, may be low and worsen the consequences of borderline testosterone. The solution here is to supplement DHEA under a doctor's supervision.
Physicians have prescribed testosterone administered via creams, tablets, patches, lozenges and injections. Such preparations can lead to normalization of testosterone and improvements in muscle strength, libido, mood and bone density. They may also be associated with side effects, so care must be taken to use the right form of replacement and dosage. There is no "one size fits all" approach.
After initiating testosterone, during the first few months, some men may note effects seen in normal puberty, such as acne and gynecomastia. In men over the age of 50, worsening of prostate symptoms may occur, although sometimes they improve. If, however, the testosterone is not taken in excess and used to maintain a normal serum testosterone, there is no reason to believe that these men are more likely to develop these conditions than men who produce their own natural testosterone. Nevertheless, a PSA and a digital rectal exam and close monitoring of hormone levels must be adhered to.
Besides looking at the mirror, another objective way of telling how fast a person is aging is through telomere testing. Before anything else, what are telomeres? Telomeres are sections of DNA at the end of each chromosome that serves as a cap to your genetic material. Every time a cell replicates, its telomere will become shorter. Shorter telomeres imply a shorter life span for the cell.
What effect does telomere length have on my health and wellness? Age adjusted telomere length is the best method to date to assess biological age using structural analysis of chromosomal change in the telomere. Serial evaluation of telomere length is an indicator of how rapidly one ages relative to a normal population. Therapies directed at slowing the loss of telomere length may slow aging and age-related diseases.
Does diet have any effect on telomere length and repair? An inflammatory diet, or one that increases oxidative stress will shorten telomeres faster. This would include refined carbohydrates, fast foods, processed foods, sodas, artificial sweeteners, trans fats and saturated fats. A diet with a large amount and variety of antioxidants that improve oxidative defense and reduces oxidative stress will slow telomere shortening. Consumption of 10 servings of fresh and relatively uncooked fruits and vegetables, mixed fiber, monounsaturated fats, omega-3 fatty acids, cold water fish and high quality vegetable proteins can prevent premature shortening. In addition, caloric restriction is advised combined with an exercise program. Fasting for 12 hours each night at least 4 days per week may also be protective.
What lifestyle modifications are likely to be helpful? One should achieve ideal body weight and body composition with low body fat (less than 22% for women and less than 16% for men). Decreasing visceral fat is very important. Regular aerobic and resistance exercise for at least one hour per day, sleeping for at least 8 hours per night, stress reduction, discontinuation of all tobacco products and bioidentical hormone therapy may decrease the rate of telomere loss.
How do you measure telomere length? The Patient Telomere Score is calculated based on white blood cells (T-lymphocytes). This is the average compared to telomere length on lymphocytes from a sample of the American population in the same age range. The higher the telomere score, the “younger” the cells. A Telomere Score that is above the average line is desirable.
What can I do to reduce my rate of telomere loss? Shorter telomeres have been associated with metabolic abnormalities, obesity, and several degenerative diseases including cancer, dementia, and cardiovascular disease. In vitro studies have shown that telomeres are highly susceptible to oxidative stress, which will shorten telomere length and enhance cellular aging. Minimizing associated risk factors that are linked to shortened telomere activity is recommended and include:
Reduce oxidative stress
Correct micronutrient deficiencies, especially vitamin D
A new research review reported in the November 17 issue of the Journal of the American Medical Association (JAMA. 2010;304:2161-2169) revealed that there is little consensus among doctors on how to diagnose and treat ear infections in children.
Acute Otitis Media (a highly prevalent type of ear infection) is the most common condition for which antibiotics are prescribed for US children. However, there is NO data available on the long term effects of antibiotic therapy in children! Further, there is a popular vaccine used, called PCV7, and the research shows that while it somewhat reduces the prevalence of one type of bacteria, Streptococcus pneumoniae,it INCREASES the prevalence of a major Flu virus, Haemophilus influenzae.
Two of the most common causes of childhood ear infections that we diagnose and treat at our medical practice are food allergies and low levels of nutrients that are essential for healthy immune function. A blood test done and interpreted correctly will reveal immediate and delayed food allergies and nutrient deficiencies related to immune function. If you or your child have a history of long term antibiotic use, it also becomes critical to supplement with a high quality probiotic, at one to two capsules per day.
In conversation with a wise woman in the desert last week, we contemplated the value of common sense in the practice of medicine. It makes sense that diet and nutrition play an important role in how well a child’s immune system will function. If you start there, the need for antibiotic therapy diminishes.
Posted By Administration,
Friday, December 3, 2010
Updated: Friday, April 18, 2014
Abstract: This paper analyzes the statistical correlation of urinary serotonin and dopamine data in subjects not suffering from monoamine-secreting tumors such as pheochromocytoma or carcinoid syndrome. Peer-reviewed literature and statistical analyses were searched and mono-amine (serotonin and dopamine) assays defined in order to facilitate their proper interpretation. Many research findings in the literature are novel. Baseline assays completed with no monoamine precursors differ from baseline assays performed on a different day in the same subject. There is currently no scientific basis, value, or predictability in obtaining baseline monoamine assays. Urinary assays performed while taking precursors can demonstrate a lack of correlation or unexpected correlations such as inverse relationships. The only valid model for interpretation of urinary monoamine assays is the “three-phase model” which leads to predictability between monoamine assays and precursor administration in varied amounts.
Purpose: This paper reviews the basic science of urinary monoamine assays. Results of statistical analysis correlating baseline and nonbaseline assays are reported and provide valid methods for interpretation of urinary serotonin and dopamine results.
Patients and methods: Key scientific claims promoting the validity of the urinary neurotransmitter testing (UNT) model applications are discussed. Many of these claims were not supported by the scientific literature. Matched-pairs t-tests were performed on several groupings. Results of all statistical tests were compared with peer-reviewed literature.
Results: The statistical analysis failed to support the UNT model. Peer-reviewed literature search failed to verify scientific clams made in support of applications of the UNT model in many cases.
Introduction Three applications have evolved with regard to urinary monoamine assays. The first is one of the older applications used in medicine. This is the use of monoamine assays for screening and diagnosing tumors that secrete serotonin or dopamine (herein referred to as the “tumor model”), such as pheochromocytoma (a catecholamine-secreting tumor) and carcinoid syndrome (a serotonin-secreting tumor). The validity of this type of monoamine testing application is well established in the scientific literature.
The second application is the use of monoamine assays for renal organic cation transporter functional status determination (ie, the OCT model). Even though this model is relatively new, having been developed in 2003, this approach and the urinary serotonin and urinary dopamine applications developed according to this model are supported by the scientific literature, having been discussed and documented in several articles since February 2009.
The basis for the OCT model requires two or more serial urinary serotonin and dopamine (ie, monoamine) assays while taking varied amino acid precursor daily dosing amounts. The results are then compared in order to determine the change in urinary serotonin and dopamine levels in response to changes in dosing. A urinary serotonin or dopamine value less than 80 or 475 µg of monoamine per g of creatinine, respectively, indicates a Phase II response. A urinary serotonin or dopamine value greater than 80 or 475 µg of monoamine per g of creatinine, respectively, is interpreted as being in Phase I or Phase III. Differentiation of Phase I from Phase III is as follows. If a direct correlation is found between amino acid dosing and urinary assay response, it is referred to as a Phase III response. An inverse correlation is referred to as a Phase I response. Unexpected results with matched-pairs t-test analysis revealed no significant difference when comparing baseline monoamine assays with assays performed while taking supplemental amino acid precursors in the same subject.
Peer-reviewed scientific publications discussing urinary serotonin and urinary dopamine phase analysis according to the OCT model were first published in 2009 and 2010. These publications outlined the mechanics of the three-phase model in connection with urinary serotonin and urinary dopamine under a novel renal transporter model. This transporter model potentially describes the etiology of the three-phase response of monoamine assays during the administration of varied amino acid precursor daily dosing values.
The third approach defining applications for the use of monoamine assays is the urinary neurotransmitter testing (UNT) model. This paper discusses the UNT model in depth because it is the only model of the three that lacks valid scientific literature discussing the model or supporting the monoamine assay applications that are being promoted.
The goal of this writing is to assess monoamine assay applications statistically and define the validity of monoamine assays in the absence or presence of supplemental amino acid precursors. The premise of the UNT model is that baseline monoamine assays correlate with and are a good predictor of the peripheral and central nervous system neurotransmitter functional status. The basic assumption for this assertion is that serotonin and dopamine cross the blood–brain barrier and are then filtered at the glomerulus and enter the urine without further interaction with the kidneys. This argument is used on the basis of the UNT model to justify the conclusion that monoamine assays, in the presence and absence of serotonin and dopamine amino acid precursors, correlate with central nervous system and peripheral neurotransmitter functional status. It also asserts that baseline testing is the best approach to determine the neurotransmitter functional status of the central and peripheral nervous systems.
Other conclusions made in support of utilizing monoamine assays under the urinary neurotransmitter testing model are as follows:
Administration of amino acid precursors directly impacts urinary monoamine levels; therefore, the results of mono-amine assays merely need to be interpreted as being either high or low values
Baseline testing of urinary monoamines prior to starting supplemental amino acid precursors is required in order to define the amino acid precursor starting dose needed in treatment
Baseline monoamine assays in the absence of supplemental amino acid precursors are required to diagnose and define the serotonin and dopamine imbalance in the central and peripheral nervous systems
Baseline monoamine assays can serve as a reference point to gauge treatment effectiveness after amino acid precursors are started
Baseline monoamine assays can be used to reduce the risk of side effects when amino acid precursor treatment is started.
Materials and methods Statistical analysis was performed for each analyzed grouping considered. The statistical analysis involved the matched-pairs t-test. After initiation of supplemental amino acid precursor administration or a change in daily dosing levels was maintained constant, a minimum period of seven days without missing one or more doses was required for data to be considered valid. This time period allows the amino acid precursors and the urinary monoamines to achieve equilibrium in order to ensure that valid urinary serotonin and urinary dopamine test results are obtained. A P value #0.05 was considered statistically significant. JMP software (SAS Institute, Cary, NC) was used to perform the statistical analysis.
Processing, management, and assay of the urine samples collected for this study were as follows. Urine samples were collected six hours prior to bedtime, with 4 pm being the most frequent collection time point. The samples were stabilized in 6 N HCl to preserve urinary dopamine and urinary serotonin. The urine samples were collected after a minimum of one week, during which time the patient was taking a specific daily dose of amino acid precursors of serotonin and dopamine. Samples were shipped to DBS Laboratories. Urinary dopamine and serotonin were assayed utilizing commercially available radio immuno assay kits (3 CAT RIA IB88501 and IB89527; Immuno Biological Laboratories, Inc., Minneapolis, MN). The DBS laboratory is accredited as a high complexity laboratory by Clinical Laboratory Improvement Amendments to perform these assays.
Results Two approaches to analyze the validity of the UNT modelwere undertaken. The first approach was a literature search intended to test claims made in support of applications for monoamine assays under the UNT model. After an exhaustive search, no in depth valid peer-reviewed studies were found documenting the UNT model. In most cases, the claims justifying use of urinary serotonin and urinary dopamine assays according to the UNT model were contrary to the identified scientific literature. The second approach was the statistical analysis of baseline monoamine assays in the presence or absence of supplemental amino acid precursors in order to assess the UNT model critically.
Five significant divergences from the UNT model from the existing scientific literature were identified. Specifically, divergences were noted from the established science, ie, serotonin and dopamine do not cross the blood–brain barrier and peripheral serotonin and dopamine are filtered at the glomerulus and then enter the proximal tubules. They are then actively transported into the proximal convoluted renal tubule cells where they are essentially completely metabolized. Due to the high efficiency of this metabolic process, significant amounts of serotonin and dopamine filtered at the glomerulus do not reach the urine in patients not suffering from a tumor secreting serotonin or dopamine. From a practical standpoint, urinary serotonin and urinary dopamine represent serotonin and dopamine that have not previously been in the central or peripheral nervous system. The literature notes that urinary serotonin and urinary dopamine are monoamines that are newly synthesized from serotonin and dopamine amino acid precursors by the kidneys in the proximal convoluted renal tubule cells. These newly synthesized serotonin and dopamine molecules are then either transported out of the proximal convoluted renal tubule cells across the basolateral membrane and then into the peripheral system via the renal vein or across the apical membrane and then into the urine. It is noted that there are many other renal interactions that exist between synthesis of serotonin and dopamine transported across the basolateral membrane and the apical membrane prior to arriving at the final destination of the renal vein or urine, respectively. These interactions appear small in comparison with the effects of the basolateral monoamine transporter and the apical monoamine transporter under the three-phase model. There is also no correlation between urinary serotonin and dopamine levels and the serotonin or dopamine levels within the central and peripheral nervous systems. The renal interaction of urinary serotonin, urinary dopamine, and their amino acid precursors is counter intuitive. It is expected that when serotonin and/or dopamine amino acid precursors are administered, levels of the associated urinary serotonin or urinary dopamine will increase or decrease with increases or decreases in the amino acid precursor daily dosing levels, ie, a direct relationship. The literature reveals that this is not the predominant response. Outcomes are not intuitive because the process is complex, and there is no simple, dominant, direct relationship between serotonin and dopamine amino acid dosing and monoamine assays. Instead, a complex interaction is found, giving rise to the three-phase model, as we have previously proposed. Furthermore, there is no significant statistical difference between baseline monoamine levels in the urine and those resulting from administration of monoamine precursors. Given that support for this is not found in the literature, the following statistical analysis is put forth. The data for the following analysis was obtained from the DBS Laboratories monoamine assay database. The database was assembled according to the criteria discussed in the Materials and methods section.
By definition, the laboratory baseline reference range for a given assay is calculated by taking all baseline data generated for that assay, then defining the group of values that are within two SDs from the mean. This grouping size represents approximately 95% of the initial group data generated. In the following reports of statistical analysis, when use of the reference range values is referred to, the following values were used. A laboratory promoting the UNT model has defined the urinary serotonin reference range as 150–300 µg of serotonin per g of creatinine. The same laboratory defined the urinary dopamine reference range as 150–300 µg of dopamine per g of creatinine.
Urinary serotonin at baseline versuswhile taking 5-hydroxytryptophan Matched-pairs groupings were queried from the database as follows. Two urinary serotonin samples from the same subject were obtained, one sample while taking no supplemental amino acid precursors and the other sample while taking 5-hydroxytryptophan (5-HTP), and these were match-paired together. A group of these matched-pairs samples were then defined for analysis, revealing a group of n = 167. The serotonin reference range values as reported above were used to query the baseline urinary matched-pairs serotonin group of n = 167 further, revealing a group of n = 103. The grouptaking 5-HTP was then queried from the group of n = 103 using the parameter 5-HTP, 301 mg per day, to give a final matched-pairs group of n = 78 for analysis.
The final matched-pairs group was then analyzed using at-test, and a P value of 0.0809 was found, indicating lack of a significant statistical difference between baseline urinary serotonin levels and serotonin levels when taking less than 301 mg of 5-HTP per day.
Urinary dopamine at baseline versus while taking levodopa Matched-pairs groups were queried from the database as follows. Two samples from each subject, one sample taking no supplemental amino acid precursors and the other sample taking levodopa, were paired together. This revealed a group of n = 617. The baseline assay portion of the entire matched-pairs group was queried with the dopamine reference range values reported earlier, to give a population size of n = 230. The group taking levodopa was then queried to find only subjects taking less than 361 mg of levodopa per day, leading to a final population size of n = 166. This matched-pairs group was then analyzed using a matched-pairs t-test, and a P value of 0.0742 was found, indicating no significant statistical difference between baseline dopamine assays and dopamine assays performed while taking less then 361 mg of levodopa per day.
Baseline serotonin assays from different days in the same subject Data were analyzed in the following manner, with the following numbers reported in µg of serotonin per g of creatinine. From a matched-pairs group of n = 146, the mean (SD) for both baseline serotonin urinary assay groups was determined. For Group 1, the mean serotonin value was found to be 239.0 (±2282.8). For Group 2 (baseline testing performed on a different day after the first assay) the mean serotonin value was found to be 273.2 (±8214.51). All data greater than the value found in calculating the sum of two SDs plus the mean were removed from consideration, revealing a group of n = 134. The matched-pairs grouping was then analyzed using the matched-pairs t-test. The baseline urinary serotonin assay grouping analysis revealed a P value of 0.0080. These findings indicate that baseline urinary levels do differ in a statistically significant manner when baseline assays are performed on different days for the same subject and are not uniform or reproducible from day to day.
Baseline dopamine assays from different days in the same subject Data were analyzed in the following manner, with numbers reported in µg of dopamine per g of creatinine. Froma matched-pairs group of n = 146, the mean SD for both baseline serotonin urinary assay groups was determined. For Group 1, the mean dopamine value was found to be 144.0(±286.9). For Group 2 (baseline testing performed on a different day after the first assay), the mean dopamine value was found to be 198.6 (±484.8). All data greater than the value found in calculating the sum of two SD plus the mean were removed from consideration, revealing a group of n = 138.The matched-pairs grouping was then analyzed using the matched-pairs t-test. The baseline urinary serotonin assay grouping analysis revealed a P value of 0.0049. These findings indicate that baseline urinary dopamine levels do differ in a statistically significant manner when baseline assays are performed on different days in the same subject, and are not uniform or reproducible from day to day.
Discussion The focus of this research is the applications of urinary serotonin and dopamine assays, whereby three distinctly different application models of monoamine assays are being promoted. The basis of the tumor model is screening for a monoamine-secreting tumor. This methodology is well founded. The OCT model is a relatively new application of monoamine assays, but its validity is supported by the literature. The third application model for monoamine assays, the urinary neurotransmitter testing model, has no indepth, valid, peer-reviewed scientific literature to support its use. The UNT model distinguishes itself from the two other approaches by requiring use of baseline urinary monoamine assays, and advocates a direct relationship between urinary serotonin and urinary dopamine when the serotonin and dopamine amino acid precursor daily dosing levels are varied. The following is a consolidation of the findings and scientific concepts discussed in this paper with the claims and approach for use of monoamine assay applications under the UNT model.
Significant challenges to the urinary neurotransmitter testing model include the widely recognized finding that serotonin and dopamine do not cross the blood–brain barrier. In support of applications for urinary serotonin and urinary dopamine assays, the UNT model claims that serotonin and dopamine do cross the blood–brain barrier. This assertion is widely known to be untrue.
No significant amount of serotonin and dopamine filtered at the glomerulus reaches the urine. Serotonin and dopamine found in the urine are newly synthesized in the kidneys, and their levels are a function of the interaction between the basolateral monoamine transporters and the apical monoamine transporters of the proximal convoluted renal tubulecells. The UNT model claims that serotonin and dopamine are merely filtered at the glomerulus, and then enter the urine without further renal interactions. This assertion is not supported by review of the relevant science.
Urinary serotonin and urinary dopamine found in the urine have no correlation with brain or peripheral serotonin and dopamine levels. Significant levels of urinary serotonin and urinary dopamine molecules assayed in the urine have never been shown in the brain or peripheral nervous system. The UNT model, based on assertions that serotonin and dopamine cross the blood–brain barrier and are then simply filtered at the glomerulus and enter the urine, claims that urinary monoamine assays represent the functional neurotransmitter status of the central nervous system, peripheral nervous system, and urine. This assertion again is not supported by the relevant science.
There is no consistent direct relationship between serotonin and dopamine amino acid precursor daily dosing levels and the amount of serotonin and dopamine that appears in the urine on monoamine assays. The peer-reviewed literature notes that there is no relationship between administration of the serotonin precursor, 5-HTP, in varied doses and subsequent urinary serotonin levels. The literature also notes that there is a correlation between administration of L-tyrosine and urinary dopamine levels, but this is an inverse relationship, and not the direct relationship predicted by the UNT model. The UNT model advocates that there is a dominant direct correlation between amino acid doses and urinary serotonin and urinary dopamine found on assay. This leads to the assertion under the UNT model that simply determining whether the urinary serotonin and urinary dopamine levels found on assay are high or low is the focal point of proper monoamine assay interpretation. This assertion is not supported on review of the science involved.
Statistical analysis of baseline monoamine assays reveals that these assays do not predict the response to precursor therapy. They differ significantly with subsequent baseline assays undertaken on different days from the same subject, and no significant difference exists with assays performed when amino acid precursors are taken. These findings are contrary to the assertions of the UNT model.
The UNT model claims that baseline monoamine assays obtained prior to ingestion of supplemental amino acid precursors can identify neurotransmitter imbalance in the central nervous system, peripheral nervous system, and urine. Due to the statistical difference in baseline monoamine assays in the same subject from day to day, an unlimited number of different neurotransmitter imbalances might theoretically be diagnosed with serial assays performed on many different days from the same subject. There is a statistical difference between baseline urinary serotonin and urinary dopamine assays in subjects not harboring a monoamine-secreting tumor. The assertion that baseline monoamine assays can diagnose central nervous system, peripheral nervous system, and urinary neurotransmitter dysfunction is not supported on review of the scientific literature.
The UNT model also claims that baseline assays of urinary serotonin and urinary dopamine are required prior to starting serotonin and/or dopamine amino acid precursors to assist in selecting the optimal daily serotonin and dopamine amino acid precursor doses. Using any laboratory criteria to diagnose serotonin and dopamine imbalance prior to selecting the starting point of amino acid dosing gives results that differ statistically from day to day and are not reproducible. The assertion on the part of the UNT model that baseline monoamine assays are needed to determine a starting point for serotonin and dopamine amino acid precursor treatment is not supported.
The UNT model claims that baseline assays are required to minimize side effects when treatment with amino acid precursors is started. The results of baseline assays obtained from the same subject on different days vary statistically,and are not reproducible relative to the first baseline assay obtained. The ability to minimize side effects claimed on the basis of the UNT model is not supported by the reported science.
The UNT model incorrectly asserts that baseline monoamine assays can serve as a reference point during treatment to gauge effectiveness of treatment when serotonin and dopamine amino acid precursors are started. As noted already,there is a significant statistical difference between values found with baseline monoamine assays and baseline assays performed on a different day in the same subject, leading to a host of different reference points being generated when baseline assays are obtained on multiple days. The baseline assays cannot be used as a reference point to measure treatment progress or indicate results of treatment.
The only valid correlation that exists between monoamine assays performed with and without administration of amino acid precursors in subjects not suffering from a monoamine-secreting tumor is the three-phase model described in the literature. When the three-phase model is applied correctly to urinary serotonin and urinary dopamine assay results, it leads to a predictable course of outcomes with urinary serotonin and urinary dopamine assay interpretation. Thethree-phase model is based on the interaction between thenewly synthesized serotonin and dopamine by the kidneys with the basolateral monoamine (serotonin and dopamine) transporters and the apical monoamine (serotonin and dopamine) transporters of the proximal convoluted renal tubule cells of the kidneys, leading to the serotonin and dopamine that is found in the urine on assay.
Conclusion The application and interpretation of baseline monoamine assays according to the urinary neurotransmitter testing model is not a valid approach because there is a significant statistical difference between baseline monoamine assays and monoamine assays obtained on a different day from the same subject and no significant statistical difference insubsequent monoamine assays performed while taking amino acid precursors. The UNT model has no ability to diagnose central or peripheral nervous system serotonin and dopamine imbalance using baseline monoamine assays in subjects not suffering from monoamine-secreting tumors. Urinary serotonin and urinary dopamine assays are not assays of serotonin and dopamine that have been in the central nervous system. Serotonin and dopamine do not cross the blood–brainbarrier. Significant amounts of urinary serotonin and urinary dopamine found on assay have not been in the brain or in the peripheral system. Urinary serotonin and urinary dopamine are filtered at the glomerulus and are then metabolized in the kidneys, with no significant amounts of serotonin or dopamine filtered at the glomerulus being found in the urine. Levels of urinary serotonin and urinary dopamine found on assay are newly synthesized in the kidneys, and are a function of the interaction between the basolateral monoamine transporters and apical monoamine transporters of the proximal convoluted renal tubule cells.
A simple direct relationship between the daily dosinglevels of amino acid precursors and monoamine assays does not exist in most cases. Due to complex renal physiologic interactions between serotonin and dopamine newly synthesized by the kidneys, a complex relationship is observed that is defined by the three-phase model described in the already published peer-reviewed literature.
The goal of this paper is to spark interest, research, awareness, and scrutiny of the topics discussed. A laboratory assay is only valid if properly interpreted. Correct interpretation of monoamine assays while taking amino acid precursors is complex, and not a direct linear relationship as predicted by the UNT model.
Disclosure TU and MH are director and owner of DBS Laboratories, Duluth, Minnesota respectively. AS and GT have no conflicts of interest to report in this work.
References 1. Oates JA, Sjoerdsma A. A unique syndrome associated with secretion of 5-hydroxytryptophan by metastatic gastric carcinoids. Am J Med.1962;32:333–342.
2. Szakacs JE, Cannon AL. Noreprinephrine myocarditis. Am J Clin Pathol.1958;30:425–434.
3. Hinz M. Depression. In: Kohlstadt I, editor. Food and Nutrients in Disease Management. CRC Press; 2009.
4. Trachte G, Uncini T, Hinz M. Both stimulatory and inhibitory effects of dietary 5-hydroxytryptophan and tyrosine are found on urinary excretion of serotonin and dopamine in a large human population. NeuropsychiatrDis Treat. 2009;5:227–235.
5. Hinz M, Stein A, Uncini T. The dual gate lumen model of renal monoamine transport. Neuropsychiatr Dis Treat. 2010;6:387–392.
7. Watkins R. Validity of urinary neurotransmitter testing with clinical applications of CSM (Communication System Management) model. Asheville, NC: Sanesco International; 2009. Available at: http://www.neurolaboratory.net/lab/neurolab%20pdf%20files/2009%20Urinary%20NT%20White%20Paper.pdf. Accessed 2010 Aug 4.
8. Theirl S. Clinical relevance of neurotransmitter testing. The Original Internist. Dec 2009. Available at: http://www.clintpublication.com/documents/Dec_OI_2009.pdf. Accessed 2010 Aug 4.
9. Sanesco. Neurolab baseline sample repor t. Available at: http://sanesco.net/images/files/resourcelibrary/baseline_sample_report.pdf Accessed 2010 Jul 2.
12. Carley C, Radulovacki M. Role of peripheral serotonin in the regulation of central sleep apneas in rats. Chest. 1999;115:1397–1401.
13. Volkow N, Fowler JS, Gatley J, et al. PET evaluation of the dopamine system of the human brain. J Nucl Med. 1996;37:1242–1256.
14. Wang Y, Berndt T, Gross T, Peterson M, So M, Know F. Effect ofinhibition of MAO and COMT on intrarenal dopamine and serotonin and on renal function. Am J Physiol Regul Integr Comp Physiol.2001;280:R248–R254.
15. Vieira-Coelho MA, Soares-Da-Silva P. Apical and basal uptake of L-dopa and L-5-HTP and their corresponding amines, dopamine and 5-H, in OK cells. Am J Physiol. 1997;272(5 Pt 2):F632–F639.
16. Pyle AC, Argyropoulos SV, Nutt DJ. The role of serotonin in panic: Evidence from tryptophan depletion studies. Acta Neuropsychiatr.2004;16:79–84.
17. Verde G, Oppizzi G, Colussi G, et al. Effect of dopamine infusion on plasma levels of growth hormone in normal subjects and in agromegalic patients. Clin Endocrinol (Oxf). 1976;5:419–423.
18. Gozzi A, Ceolin L, Schwarz A, et al. A multimodality investigation of cerebral hemodynamics and autoregulation in pharmacological MRI. Magn Reson Imaging. 2007;25:826–833.
19. Ziegler MG, Aung M, Kennedy B. Sources of human urinary epinephrine. Kidney Int. 1997;51:324–327.
This article was published in the following Dove Press journal: Open Access Journal of Urology 6 October 2010. Authored by: Marty Hinz, Clinical Research, Neuro Research Clinics, Inc., Cape Coral, FL, USA; Alvin Stein, Stein Orthopedic Associates, Plantation, FL, USA; George Trachte, Department of Physiology and Pharmacology, University of Minnesota Medical School, Mn, USA; Thomas Uncini, DBS Labs, Duluth, MI, USA.
Ebola, AIDS, MRSA, Vancomycin-resistant Pseudomonas, chloroquine-resistant Plasmodium (cause of Malaria). These are just a few of the super bugs that we could all possibly encounter in our world that’s rapidly getting smaller every day due to air travel. In recent times when sea travel was the main mode of transportation, people who were still asymptomatic would usually show signs and symptoms before they arrive at their destination. In today’s world of faster air travel, people infected may not show signs and symptoms until they arrive somewhere. This can cause the rapid spread/transmission of communicable diseases. This is especially true in a stressed-out, nutritionally-deficient, and unhealthy population.
What is the traditional answer to this issue? I think that we all know the answer to that. Suffice it to say, this reactionary approach (the race to find cures) doesn’t work well because these bugs are smarter than we think. By the time so-called cures are available, they’ve already mutated to a form that’s resistant to the “cure”. That’s one of the reasons why we have MRSA and Vancomycin-resistant Pesudomonas, among many others.
There is no one to blame for this scenario. Health care practitioners (by indiscriminate use) and patients (by insisting that they be given a medication) alike are responsible for the proliferation of super bugs.
What then can we do about it? I would say that we adopt what the traditional Chinese medicine practitioners did in earlier times. A doctor at the time would only get paid or compensated when their clients are healthy. If their clients get sick, the doctors don’t get paid. It does make a lot of sense to do this. This preventive approach would save billions of dollars in health care.
What are the things we can do to fortify our immune system? Let’s start with the basics before we even discuss specifics. Having a healthy diet, adequate water intake, enough exposure to sunlight and the earth’s electromagnetic energy, rest, exercise, good relationships and stress reduction all go a long way in building our immune defenses.
There are ways to strengthen the immune system with the use of dietary supplements. Here are just a few examples;
mixed carotenoids (natural vitamin A)- good for the mucous membranes (respiratory and intestinal tract protection)
vitamin C complex (natural vitamin C with bioflavonoids)- traditionally used to boost the immune system against infections and tumors but also good for formation of collagen, along with L-lysine and L-proline
vitamin D3- studies show that it could protect against the flu (low levels of exposure to sunlight during the winter months make one vulnerable to the flu) and against certain forms of cancer
selenium- one of the co-factors in the formation of glutathione, which is abundant in the spleen and lymphocytes, both involved in immune system health
zinc- has antimicrobial properties and also good for prostate health in men
manganese- helps in the production of SOD, one of the antioxidants endogenously produced in our bodies
probiotics- an essential nutrient especially if one has taken antibiotics in the past, helps prevent bacterial and fungal overgrowth in the intestine
clove- has the highest ORAC (antioxidant levels) level among all natural substances, has antimicrobial properties as well
thyme- its constituent thymol has antifungal properties
lemon- has d-limonene which has anti-carcinogenic properties, has anti-viral properties as well (along with other citrus oils)
cinnamon- has antibacterial properties, also regulates blood sugar
rosemary- antimicrobial and anti-inflammatory
chlorella and spirulina- immune stimulants
raspberries- rich in ellagic acid, which has anti-carcinogenic properties
apricots- rich in vitamin B 17, also has anti-carcinogenic properties
wolfberries- stimulates release of HGH from the pituitary
broccoli and other cruciferous vegetables- lowers xenoestrogens, cleanses liver
Posted By Administration,
Wednesday, December 1, 2010
Updated: Friday, April 18, 2014
Detox diets certainly have a loyal fan base — from best-selling books to celebrity endorsements, the popularity of these programs that promise to flush poisons from your body, boost your immune system, and purge excess fat can make you start to wonder if extreme measures are essential just to keep healthy. The answer, in short, is no. Your body can take care of toxins very well on its own. Conversely, extreme programs — such as the Master Cleanse — can undermine your health.
“Fasting detox programs are extreme, ineffective in the long run, and, in some cases, dangerous,” says Marnie Doubek, M.D., of Summit–Springfield Family Practice. “These programs are high in salt and low in nutrients. People following these plans are at risk of developing dehydration, electrolyte imbalances, muscle breakdown, malnutrition, and fatigue.”
Most health care practitioners recommend more natural methods that help create the best environment for your body to detox itself. Here are four ways that don’t come with warning labels:
A well-rounded diet and good digestive habits are essential to maintaining a healthy liver and kidneys, which are the body’s toxin-processing facilities. “Unfortunately, the average person’s eating dramatically hinders her ability to detox on her own; the standard American diet does not supply even a minimal amount of nutrients to our bodies,” says Joel Fuhrman, M.D., a family physician based in Flemington and the author of Eat for Health. “Most people need to detox first by eating right,” says Fuhrman, who advocates for a fiber-rich, near-vegan diet.
Also, take steps to keep your liver and kidneys healthy. Alcohol can harm these organs, so drink moderately. Take medicines wisely: Your liver and kidneys can be damaged if you take too much, take the wrong type, or mix certain medicines. It’s also important to adopt good digestive habits, such as chewing slowly. “If you’re a rapid eater, try putting your fork down between bites,” suggests Samantha Mark, a registered dietitian in Montville. She notes that juicing your own fruits and vegetables can be an excellent way to get vital nutrients you need, but check with your doctor first to make sure your diet will include enough fiber, iron, and protein.
Drink Water Throughout the Day
“Staying hydrated will take good care of the liver and kidneys,” says Mark. The standard benchmark of drinking 8 ounces of water 8 times a day is still solid, she says, but suggests you also check your urine color: If it’s dark, you’re not hydrated enough.
Target Fat Cells
“Studies over the past two years have found that fat cells not only store certain toxins, but also produce hormones that have estrogen-like properties,” says Deborah Neiman, M.D., of Step Ahead Weight Loss Center in Bedminster. Reducing your body fat will help you get rid of fat-soluble toxins and harmful estrogens. “When you lose weight, the toxic estrogens that are stored in the excess fat are released,” explains Scott Greenberg, M.D., at the Magaziner Center for Wellness in Cherry Hill. “This type of detox is particularly valuable because it reduces your risk of breast cancer from toxic estrogenic exposures.”
Reduce Your Exposure to Chemicals
Limit direct contact with toxins from cleaning and aerosol products, and insecticides. Also, watch your exposure to toxic heavy metals, such as mercury. “A high level of heavy metals in the body can have a negative impact on your endocrine system, which includes your thyroid function and hormonal function,” says Greenberg. Mercury enters your body through consumption of fish (the fish with the highest mercury content are shark, swordfish, and king mackerel), some vaccinations, and through the environment (mercury is emitted to the air and water system by industrial practices). While you can’t control the environmental exposure, you can inquire about mercury’s presence in vaccinations and select fish that contains less mercury, such as cod, any shellfish other than lobster, and canned chunk light tuna.
If you’re interested in testing your body’s mercury levels, Greenberg advises skipping a blood test — mercury remains in the blood for only a short time before entering the organs — or hair test, which he says are “inordinately inaccurate.” Instead, he suggests asking for a urine test using chelating agents, which bind onto and then draw the heavy metals out your body through your kidneys. (Greenberg notes that most holistic doctors will administer these tests.)
To keep your mercury levels low, Mark recommends eating foods that contain chelating agents — such as crushed, raw garlic; cilantro; vitamin C (in citrus fruits); or vitamin E (in wheat germ oil, almonds, and sunflower seeds) — which will naturally help your body rid itself of toxins. Drinking enough water and consuming fiber-rich foods (such as edamame) can go a long way to helping your body cleanse itself.
Source: New Jersey Life Health Beauty Magazine. Verbanas, Patti.
HCG (human chorionic gonadotropin) is the hormone that medical doctors test for in order to determine if a woman is pregnant. Measuring HCG is the success of companies such as EPT who conveniently created the urine pregnancy tests found in every drug store in the world. HCG is present in both men and women, but becomes detectable in pregnant women. During pregnancy, HCG almost completely controls metabolic functions. In non-pregnant persons, research suggests HCG increases metabolism in a similar way.
Although HCG is associated with pregnancy, both men and women that are looking to get their weight under control can safely use it. Let's take a closer look at what its job actually is. Nature created HCG as a way to ensure healthy full term pregnancies. One of the roles of HCG in pregnancy is to increase metabolism by allowing the fat that the pregnant woman has stored to be accessible to her during famine. In other words the fat stores can be broken down by the HCG and used as food for her and the baby should the food supply run out while she is pregnant. This ensures a healthy full term pregnancy.
In a non-pregnant person we can recreate this metabolic situation by administering HCG and putting the patient on a low calorie diet. When we do this, the fat that the patient wants to lose becomes the primary food source as it is broken down and used as energy. In essence, we are forcing the body to burn its own fat stores. Thousands of calories in stored fat are released and are used by the body or expelled.
HCG WHAT'S THE DIFFERENCE?
How HCG is different than other diet programs is that it is short term, the results are up front, participants eat real food, muscle mass is maintained, and it burns cellulite (toxic fat).What people lose with HCG isn't simply weight, but fat, a particular kind of fat. We generally think of fat as just "fat," but in fact there are three distinct kinds of fat. Two of which we need, and one we don't. If a person has tried dieting, perhaps diet after diet, and found that the weight comes back, it's because diets can't rid us of the one kind of fat that most needs to be eliminated. Of the three kinds of fat, structural fat is essential because it cushions our organs. Then there's the kind of fat that gives us a reserve of energy, fueling the body between meals. But a third kind of fat-the unsightly fat that ruins our appearance-is totally unhealthy. This unwanted fat is not only unhealthy, it just happens to be almost impossible to lose. It can be mobilized only in times of starvation and pregnancy. In women, this unhealthy fat tends to accumulate around the middle and thighs. In men, it's around the belly and chest. In both cases, it's extremely difficult to get rid of. The usual approaches to weight loss just don't budge it. The genius of Dr. Simeons, the doctor who discovered the role of HCG in weight loss, was to recognize that HCG triggers the body to burn this type of fat. The HCG program consists of a low calorie diet in combination with HCG hormone treatments. During the 30 days you regularly inject a small amount of HCG into your body. Be aware that the HCG itself does not cause weight loss, it just modifies your eating behavior, and mobilizes stored fat. This will make it possible to maintain the diet.
HCG allows you to rapidly lose a specific amount of weight in a 30-day period. You can safely and effectively lose up to 10% of your body weight on this program, and some can achieve 30 pounds of weight loss in 30 days. A very specific diet must be followed for the 4 weeks along with injections of HCG, a hormone that women produce during pregnancy. This program dramatically shifts your metabolism towards burning your own fat and allows you to create energy from the fat that you are melting away. HCG assists in controlling all cravings when you are on this low calorie diet. Vitamin injections are given to assist with energy and promote fat burning. HCG is completely safe for men and women. Following the 4 weeks of injections, you are then transitioned to a stabilization food plan for 3 weeks where your weight loss is stabilized. During stabilization all whole foods are re-introduced with the exception of sugar and starch. Stabilization is then followed by a maintenance food plan, which will allow you to maintain the weight you have lost while eating a healthy, whole food diet. Unlike other weight loss programs all of your weight is lost in the first month of this program. This means that your results are immediate.
CAVEAT FROM FDA:Since 1975, the FDA has required labeling and advertising of HCG to state: HCG has not been demonstrated to be effective adjunctive therapy in the treatment of obesity. There is no substantial evidence that it increases weight loss beyond that resulting from caloric restriction, that it causes a more attractive or “normal” distribution of fat, or that it decreases the hunger and discomfort associated with calorie-restricted diets.
HOW IS HCG USED IN MEDICAL CONDITIONS?
When HCG is prescribed in a medial scenario, it is either as a fertility medication (can be for both men and women), or to assist in restoring testosterone production in men.
ARE THERE SIDE EFFECTS?
The high levels of HCG that are produced during pregnancy have no negative effects on the pregnant woman’s body. In fact, doctors have used HCG for many years in order to help women experiencing hormonal issues or fertility problems. There are literally no major side effects. Small conditions such as low blood pressure and low blood sugar can be easily off set with proper medical supervision.
After supervising and coaching hundreds of patients through HCG here are a few of the trends I have noticed:
*Some patients feel euphoric, and can easily follow the program without much effort.
*Other patients are tired and feel the need to go to bed early each night. Otherwise they would cheat by eating to maintain energy.
*There is a window of the correct HCG dosage, some people need a little bit more than others. This can make a big difference in a person’s ability to stick with the diet.
*When using HCG it can up-regulate thyroid function in patients who are hypothyroid. This is something that needs to be addressed when a person completes the program.
*Cellulite is literally melted; it is nothing short of miraculous.
*Patients are elated at their success, and are more motivated to make good food choices to maintain their success.
*It is imperative that coaching on proper eating be done with each patient. A roadmap of healthy food choices & how to eat is the only guarantee of permanent weight loss.
*If a person is an emotional eater, that condition will not be corrected. Emotional eaters must be willing to explore the way they use food as a coping mechanism and consider healthier coping mechanisms to put in its place, including but not limited to therapy.
*Patients do not look gaunt or shriveled; weight loss is evenly distributed throughout the entire body.
*Weight loss is between ½ pound and 1 pound per day.
*The results of HCG are amazing and this can be a great option for patients who need to lose 25 pounds or get a jump start on their weight loss goals.
Sometimes I am asked – is Polycystic Ovarian Syndrome (PCOS) caused by eating too much sugar, unhealthy fat and our sedentary lifestyle? Interestingly, the disease of PCOS does not appear to increase in areas of the world where obesity is more prevalent. This indicates that this disease is not caused primarily by obesity. There are many ancient medical records describing women with PCOS conditions (including prolonged menstrual cycles, infertility, acne, abdominal fat, and hirsutism). A recent article in Fertility and Sterility proposes that PCOS is actually an ancient genetic condition that has persisted over thousands of years in women. But why would PCOS persist in our gene pool when it leads to infertility or decreased reproduction in women?
Ancient Hunter-Gatherer communities and women with PCOS
There are several reasons why PCOS variants may have persisted in women over thousands of years. In ancient hunter gatherer communities those who had metabolisms which conserved energy and stored fat had definite survival benefits. Women with PCOS do carry these metabolic advantages. They tend to be metabolic energy conservers – something which is of great advantage in times of low food supply. Because women with PCOS generally had fewer children due to reduced fertility rates, they often had the survival advantage of caring for only one young child at a time and had greater resources for themselves and their families. Childbirth related complications were a common cause of death, so women with PCOS were also at a survival advantage due to decreased maternal mortality. In ancient cultures, there was less food supply, more physical activity and therefore less obesity, so women with PCOS generally had a lower BMI (Body Mass Index) compared to modern women. At times when food was in short supply, women with PCOS would tend to have more normal BMIs (leading to more normal levels of fertility). At these same times, women without PCOS would have lower BMIs and may have been more prone to have subfertility themselves.
Generally, fertility is lower amongst women with PCOS at all BMI levels. In times when BMIs are on average lower in the population, women with PCOS will have more normal reproductive rates. This illustrates the importance of achieving a healthy BMI for women with PCOS and that the condition actually is one of subfertility rather than infertility.
Another point to consider is that PCOS genes are also carried through males, who also carry these metabolic survival advantages and do not experience subfertility. PCOS genetic variants include greater lean muscle mass and bone density and these males could pass on these beneficial genes to their offspring. This explains how this genetic type could persist through thousands of years even though it is related to subfertility.
How this translates to modern women
In general, BMI levels tend to be increased with the modern western diet and lifestyle, so the effects on reproduction of PCOS are amplified compared to those in ancient times. Women with this condition must pay extra attention to achieving a healthy BMI. Although having a high BMI does not cause PCOS, it will definitely cause lower fertility levels. For those women who have a high level of insulin resistance (which is aggravated by the western diet), extra attention must be paid to working with insulin balance in the body. This can be done very effectively with the right diet and supplements.
Integrative medicine assessments
PCOS variants should be screened for in all women seeking fertility treatment who have a long cycle, acne, hirsutism, or abdominal fat accumulation (even in slimmer women). Many traditional assessments can miss mild cases of this condition or “leanings” towards the condition. Restoring pituitary and metabolic function in these women can effectively restore fertility and often heavy medical intervention is not required.
The following tests should be completed :
1) glucose to insulin ration and oral glucose tolerance testing
3) day 3 LH to FSH ratio
4) full early am androgen panel – (androstenedione, free testosterone, DHEA-S, 17-OH Progesterone)
5) am cortisol or diurnal cortisol
6) transvaginal pelvic ultrasound to check for cystic ovaries
In a women who has an elevated LH to FSH ratio we can assume much of the PCOS is related to hypothalamic pituitary dysfunctions. With a normal LH to FSH ratio other metabolic disorders are often more prevalent and contributing factors should be identified. Androgen balance is of great importance, and elevated levels should be identified. It is also important to note that PCOS variants can be closely mimicked or aggravated by adrenal conditions so assessment of the adrenal function including diurnal cortisol, and DHEA-S testing is very important.
Treatment very much depends on the individual characteristics of each woman’s condition. There are many different PCOS variants as this is a syndrome involving reduced frequency of ovulation and is not a discrete disease with one cause. A patient does not have to have all of the diagnostic criteria of PCOS to have her fertility affected by a milder variant of this disease. Each patient will require different treatment based on her lab values, metabolic characteristics, body type, severity of disease and level of inflammation.
Hunter-Gatherer diets and PCOS
Returning the patient to a healthy BMI is much more important for fertility than in women without PCOS. Thus, healthy diets with attention to glycemic index are of great effectiveness. I always counsel patients with PCOS extensively on nutrition and diet as this is an area of special need for them even if they are a “lean” type. A hunter-gatherer diet is often the best type of diet for PCOS. This diet is high in healthy proteins such as lean meats, seafood, fruits and berries, vegetables, and nuts and low in grains. Most especially of course, the diet should be low in sugar since hunter gatherer cultures had very low sugar intake overall.
A simple one day hunter-gatherer diet for PCOS variants:
Breakfast: Omelette made with onions and spinach.
Snack : Ambrosia (pear, avocado and 1/2 unripe banana – blend in blender until smooth and creamy) *Did you know unripe bananas have a glycemic index of 50 whereas a ripe banana has a glycemic index of 82?
Lunch: Tilapia fillet drizzled with olive oil, with brocolli or salad (dressing of fresh lemon, olive oil and fresh herbs)
Snack: Sliced baby cucumber with fresh lemon squeezed on top. 3 tbsp almonds and 1 cup of fresh blueberries
Dinner: Grilled chicken breast with pesto and baby bok choy
This diet would be varied with respect to quantity and calories for differing weight loss or maintenance requirements.
I use supplement therapy as a mainstay along with diet in the treatment of PCOS and have found the combination works wonderfully to restore cycle regularity. Supplements are aimed at restoring normal hypothalamic-pituitary function, increasing antioxidant status, improving insulin resistance, and minimizing excess androgen levels if required. Supplement protocols will vary widely with different “types” and lab results found in different PCOS variants.
Carmina E, Guastella E, Longo RA, Rini GB, Lobo RA. Correlates of increased lean muscle mass in women with polycystic ovary syndrome. Eur J Endocrinol 2009;161:583–9.
Di Carlo C, Shoham Z, MacDougall J, Patel A, Hall ML, Jacobs HS. Polycystic ovaries as a relative protective factor for bone mineral loss in young women with amenorrhea. Fertil Steril 1992;57: 314–9.
Good C, Tulchinsky M, Mauger D, Demers LM, Legro RS. Bone mineral density and body composition in lean women with polycystic ovary syndrome. Fertil Steril 1999;72:21–5.
Ricardo Azziz, Daniel A. Dumesic, Mark O. Goodarzi. Polycystic ovary syndrome: an ancient disorder? Fertility and Sterility – 27 October 2010
To WW, Wong MW. A comparison of bone mineral density in oligomenorrhoeic adolescents with polycystic ovaries and normal ovaries. Gynecol Endocrinol 2005;20:237–42.
The latest form of environmental pollution -- and one that industry, government and wireless consumers don't like to acknowledge -- may be the most devastating threat to health yet: electromagnetic fields (EMFs). A few years ago, I was so concerned that I took a certification course in the detection and harmful effects of EMFs. What it taught me, above all, was how much the scientific community is learning daily, and how little we in the medical profession knew. This area was both frightening and daunting in its scope. I'm grateful that following Devra Davis's Disconnect: The Truth About Cell Phone Radiation we now have Zappedto educate the public on this serious issue.
The UK's BioInitiative Report of July 2007 (updated in 2009) describes hundreds of studies that link EMF exposure to Alzheimer's disease, ALS (Lou Gehrig's disease), brain fog, cardiovascular disease, miscarriage, infertility, insomnia, learning impairment, as well as anxiety and depression. Wireless technologies -- like cell and cordless phones -- produce microwaves that increase the permeability of the blood-brain barrier, leading to changes in brain chemistry. Even low-level EMFs can cause brain cells to leak.
That's not all: Although actual tissue heating does not occur, EMFs also cause breaks in DNA, speed up cell division, disrupting the orderly process of chromosome matching and detaching, and activate stress protein or heat shock proteins. And as Anne Louise Gittleman writes in Zapped:
Most disturbing of all, the Swedish National Institute for Working Life found that people using cell phones for 2,000 hours -- a total most of us could easily rack up over the years -- had a 240 percent increased risk for malignant brain tumors on the side of the head where they usually held their phone.
So, what do we do to avoid these dangers? I'm relieved that Gittleman, my friend and colleague and author of over 30 bestselling books, has tackled this topic. We'll learn that most of us don't need to give up all the digital and electronic gadgets that make life so much easier. To protect ourselves, we first need to recognize the risks and then make smart choices in how we use all the available technological wonders.
Why Are EMFs So Dangerous?
What most people don't realize is the human body is naturally electrified. From the organic computer that is your brain, which sends out sensory messages like hunger and pain, to the energy that pumps your heart and makes your muscles contract, electricity powers your body. This innate electromagnetism within you is so critical to your daily functioning that modern medicine uses it in diagnostic testing (including electrocardiograms and MRIs) and, increasingly, to heal.
The "body electric" is an exquisitely tuned and sensitive creation, but unfortunately, human beings (and animals) respond favorably to only a very small range of electromagnetic frequencies. And there's a big difference between the body's natural electricity and the man-made electromagnetic frequencies that surround us 24/7 today. According to New York Times reporter B. Blake Levitt in Public Health SOS:
Most living things are fantastically sensitive to vanishingly small EMF exposures. Living cells interpret such exposures as part of our normal cellular activities (think heartbeats, brainwaves, cell division itself, etc.) The problem is, man-made electromagnetic exposures aren't "normal." They are artifacts, with unusual intensities, signaling characteristics, pulsing patterns, and wave forms. And they can misdirect cells in myriad ways.
Some of this radiation -- extremely low frequency (ELF) radiation in power lines, the radio frequency (RF)/microwave range where all things wireless live, intermediate frequencies ("dirty electricity" or freaky frequencies linked to sick building syndrome), and the highest frequencies (gamma and X-rays) -- is more damaging than natural frequencies to which humans (and animals) have adapted over millennia. Today, most Americans are constantly exposed to artificial frequencies, given the rapidly escalating pace of microwave and wireless expansion.
The bottom line is that electropollution -- from cell towers, computers, cordless and mobile phones, PDAs, Wi-Fi, even the electrical appliances and wiring in our homes, offices and public buildings -- continuously disturbs the sympathetic nervous system. This, in turn, elevates the body's fight-and-flight response, raising levels of the stress hormone cortisol. Fluctuations in cortisol lead to a wide range of health concerns ranging from belly fat and thinning skin to accelerated aging, blood sugar imbalance, cardiovascular problems, erratic sleep patterns and mood disturbances. Dr. Stephen Sinatra elaborates on this issue in his new book, Earthing.
Your body responds to EMFs as though they were public enemy number-one, triggering what two-time Nobel Prize nominee Robert Becker, M.D., in his 1998 book The Body Electric, called "subliminal stress." While intellectually you don't recognize this kind of stealth stress the way you would overwork or being stuck in traffic when you're late for an important appointment, your body's internal antennae pick up on it in several ways, according to the late scientist, Dr. W. R. Adey, from Loma Linda University:
The flow of blood and oxygen shuts down to all except major organs like the brain and heart.
Any systems -- including digestion and immunity -- that aren't necessary for fight or flight response are put on hold.
Blood pressure and heart rate as well as blood sugar levels increase to prepare your body for danger.
Recent research by Magda Havas, Ph.D., associate professor of Environmental and Resource Studies at Trent University in Canada, shows that dirty electricity -- EMFs in electrical wiring -- can raise blood sugar levels in diabetics and people at risk for diabetes. "Exposure to electromagnetic pollution in its various forms may account for higher plasma glucose levels and contribute to the misdiagnosis of diabetes," she writes. Dr. Havas' website is a goldmine of information on the entire topic of EMF pollution, as is Dr. Mercola's EMF site!
There are "canaries in the coal mine" -- hypersensitive individuals who are severely weakened by EMFs, and find themselves marginalized by the medical profession and society in general. Some must live in areas far from cell towers, Wi-Fi and the like. On a cellular level, these individuals have measurable damage to the mitochondria, the energy factories in each cell, and require reparative nutrients, for starters. I recently heard from a concerned family member of a man who had been exposed over time to a cell tower beaming through his office window. Quite ill, he was nonetheless unwilling to move his office location as I suggested, and I didn't hear from them again. Ignoring the messenger, however, doesn't solve the problem.
Zap-Proof Your Children
Today, an estimated 31 millions kids are on their cell phones close to four hours a day. Mobile phone companies are even marketing phones to preschoolers. Gittleman writes:
The trouble is, kids absorb 50 percent more electropollution than adults. One study finds that a cell phone call lasting only two minutes can cause brain hyperactivity that lasts up to an hour in children. Because their skulls are smaller and thinner than adults, EMFs penetrate much deeper into children's brains. Kids' brains are also more conductive due to their higher water and ion concentration.
The Toronto Board of Health recommends that children under eight use cell phones only for emergencies and that teens limit calls to under 10 minutes. If your kids have cell phones, encourage them to use the same smart tips you do.
Smart Use of Technology
The good news is most of us don't have to give up our smartphones if we use them wisely. Here are some of the many tips Gittleman highlights in Zapped:
Text, don't talk, whenever possible.
Use speaker mode to keep your phone as far away from your head as possible.
Go offline -- turn off your cell phone when you're not using it and shut off your wireless router at night. (You'll be amazed how much more soundly you'll sleep.)
Get your phone out of the your pocket; men who carry their mobile there have lower sperm counts than those who don't carry a cell phone.
Avoid tight spaces (buses, elevators, trains, and subways) where your phone has to work harder to get a signal out through metal.
Buy low, choosing a phone with a low SAR (specific absorption rate) number.
Replace your cordless phones with corded land line phones.
Don't cradle your laptop--putting it on your lap exposes your reproductive organs to EMFs.
Most important of all, restrict cell and cordless phone use during pregnancy. Heavy phone use then has been linked to increased risk of miscarriage and birth defects. And a 2008 survey of more than 13,000 children found that those whose mothers used a cell phone during pregnancy were more likely to have behavior problems like hyperactivity and trouble controlling their emotions.
Don't rely on the many stick-on devices available for your cell phone or computer that claim to protect you. Most are sold via network marketing, and I have yet to see the level of scientific proof that could convince me. You'll likely see comments to this blog, advertising them. Caveat emptor!
Even if you go back to wired technologies at home, Wi-Fi is expanding rapidly into schools and other public buildings. If the telecommunications industry has its way, we will all be bathed in a sea of artificial radiation from nonstop EMF exposure.
Due to their lobbying efforts, Section 704 of the Telecommunications Act of 1996 makes state and local governments powerless to prohibit cell towers and wireless antennas based on "environmental (i.e., human) health concerns." Write your congressmen and senators to change this legislation and to require the FCC to reduce exposure guidelines for EMFs.
Don't wait for the government to protect you, though. Get your copy of Zapped and take action!
Posted By Administration,
Wednesday, October 13, 2010
Updated: Friday, April 18, 2014
by Gina Nick, NMD, PhD
A study of 600 nursing facility residents has found that those with adequate zinc levels were about fifty percent less likely to develop pneumonia than those with low body concentrations of zinc. Also, those with sufficient levels of zinc received fewer prescriptions for antibiotics, had shorter durations of pneumonia and had lower mortality rates.
The researchers suggested that zinc supplementation for zinc-deficient elderly persons may result in a lower incidence of pneumonia and that further study is required to determine whether zinc supplements may be an effective and low-cost intervention to reduce pneumonia deaths among vulnerable populations who already have low zinc intakes. (An earlier analysis of the same data had shown that those who consumed 200 international units (IU) of vitamin E were less likely to get upper respiratory infections, such as colds.) The study was released August 10, 2010 and will be published in a future issue of the American Journal of Clinical Nutrition. In the meantime, it can be read online at by subscribers to the journal or those who pay the article access fee.
The evidence is mounting that proper nutrient levels keep us well. In general licensed Naturopathic Medical Doctors will not, however, advise that everyone run out and buy a high potency vitamin and mineral supplement. We are all unique, and what we have discovered at our office is that one person may have toxic levels of zinc in their body, while another may have a deficiency. That is why we are strong proponents for testing to discover what your unique nutrient, amino acid and fatty acid needs are. Armed with objective information on your body, we can then create a plan for you of what supplements to take, in what form, how often, and what dietary and lifestyle changes you can make to keep you healthy, well and safe!
Posted By Administration,
Thursday, October 7, 2010
Updated: Friday, April 18, 2014
by Stacey Kupperman, ND
We are in the midst of a paradigm shift. Our understanding of health and medicine is broadening, and both practitioners and patients are embracing a holistic, integrated approach. Patients are becoming more informed via the internet, word of mouth, and diligent research that there is something significantly missing from medicine in the current standard of care in the American healthcare system. What they are finding, and flocking to, is a group of physicians that have likewise embraced this broadened approach to medicine. Some of these practitioners adopted a more holistic approach after realizing that there was something missing from their medical training, and sought out like-minded individuals and organizations such as ACAM to further their education in this new model of healthcare. Other practitioners discovered their passion before entering medical school, and pursued the study of naturopathic medicine.
So thisbegets the questions, What is Naturopathic Medicine, and where does Naturopathic Medicine fit in the paradigm shift?
What is Naturopathic Medicine?
Naturopathic doctors (ND) are specialists in integrative medicine, combining extensive education and training in both natural and conventional allopathic medicine, emphasizing the use of the safest, least invasive methods to treat disease by restoring health. The education entails a 4-year graduate level program, national board examinations in basic and clinical sciences, and curriculum including basic sciences, clinical sciences, diagnostic techniques and tests, pharmacology, minor surgery, and range of naturopathic therapies including botanical medicine, nutrition and nutritional biochemistry, physical medicine, homeopathy, eastern and Chinese medicine and mind/body medicine.
Integral to naturopathic medicine is a unifying philosophical approach to health summed up in The Principals of Naturopathic Medicine, which recognizes the body’s innate wisdom and healing capacity (Vis Medicatrix Naturae) and the physician’s role to treat disease by restoring the body to its natural and balanced state (Tolle Causum). Treatment programs integrate multiple modalities, which may include nutrition and lifestyle modification, homeopathy, botanical medicine, nutraceuticals, IV nutrient therapy, and when warranted, pharmaceutical intervention. Naturopathic Doctors begin with the least invasive therapies and proceed to higher levels of intervention only as necessary. This approach is outlined in what is called “The Therapeutic Order.”
The Principals Of Naturopathic Medicine:
First Do No Harm, Primum Non Nocere – this principal is at the basis of any medical professional. Naturopathic physicians follow a therapeutic order which emphasizes the use of least force necessary to restore health, using the least toxic and minimally invasive interventions and only proceeding to more toxic and invasive interventions when necessary
The Healing Power of Nature,Vis Medicatrix Naturae – First described by Hippocrates as the healing power of nature. It is a person’s vital force within that allows an individual to overcome disease. Naturopathic Medicine recognizes an inherent ordered and intelligent self-healing process in each person. Naturopathic physicians act to identify and remove obstacles to healing and recovery, and to facilitate and augment this inherent self-healing process.
Identify and Treat the Cause, Tolle Causam – The Naturopathic physician seeks to identify and remove the underlying causes of illness rather than to merely eliminate or suppress symptoms the patient is experiencing.
Doctor As Teacher, Docere – Naturopathic physicians educate their patients and encourage self-responsibility for health. They also recognize and employ the therapeutic potential of the doctor/patient relationship.
Treat the Whole Person – Naturopathic physicians treat each patient by taking into account an individual’s physical, mental, emotional, genetic, environmental, social, spiritual, and other factors that contribute to one’s health.
Prevention – Naturopathic physicians emphasize the prevention of disease-assessing factors, heredity, and susceptibility to disease, and work towards making the appropriate decisions in partnership with their patients to prevent illness.
Naturopathic Therapeutic Order
Establish the conditions for health
Identify and remove disturbing factors
Institute a more healthful regimen
Stimulate the healing power of nature (vis medicatrix naturae): the self-healing processes, through low force methods such as constitutional hydrotherapy, homeopathy, acupuncture
Address weakened or damaged systems or organs (via botanical medicine, homeopathy, orthomolecular nutrients, glandulars, homeopathy, and other minimally invasive, safe, natural therapies)
Strengthen the immune system
Normalize inflammatory function
Optimize metabolic function
Balance regulatory systems
Harmonize life force
Correct structural integrity
use specific natural substances, modalities, or interventions
use specific pharmacologic or synthetic substances
Suppress or surgically remove pathology
As Gandhi said, we must “be the change you wish to see in the world.” Naturopathic Doctors practice the change they want to see in medicine. Despite the fact that it has not gained universal acceptance within the United States healthcare system, Naturopathic Doctors have taken a ‘leap of faith’, knowing that integrative medicine is the best medicine and will eventually gain not only parity, but prominence. Naturopathy extends beyond just integrating multiple therapies and modalities in treatment. It incorporates an integrative approach to all aspects of health and wellness. Starting from day one of a naturopath’s medical education and continuing throughout practice, every body system, function, disease, and treatment is viewed from a holistic perspective. It is very likely that almost every integrative medical practitioner shares at least some philosophical tenants with naturopathy, regardless of whether it is called “naturopathic” or “holistic” or “alternative”. It is also likely that many integrative practitioners differ on some philosophies, treatments and approaches. Having an underlying shared philosophical approach combined with different styles, opinions, ideas and discoveries fuel evolution, progress and change. As such, the philosophy and practice of Naturopathic Medicine is a part of the evolving consciousness and paradigm shift towards a more holistic and integrative approach to healthcare that will soon become the new standard for conventional medicine.
Posted By Administration,
Tuesday, October 5, 2010
Updated: Friday, April 18, 2014
Study done by William P. Work, MD
Patient: J.P., a 60 year old female, born on May 26, 1950, had 17 treatments as of March 26, 2010.
Diagnosed with Myasthenia Gravis (MG) after initial testing in her 40s for Multiple Sclerosis (MS).
Muscle weakness over whole body increasing with use
Drooping eyelid on right side
Sagging face on right side
Lack of facial expression on right side
Weakness of the hand muscles
Extreme tiredness in daytime
Sleep disturbance at night
J.P. experienced severe muscle weakness, drooping of right eyelid, sagging of right side of face and urgency incontinence. She didn't sleep well at night, but was sleepy during the day requiring frequent naps lasting more than one hour at a time. She was lethargic and had problems with balance, falling frequently.
ONDAMED treatments were started on January 18, 2010 at Ultimate Living Medical Clinic in Fresno, California. She received three treatments before I began seeing her on February 3, 2010. By her fifth treatment with ONDAMED, she started resting better. By March, she reported sleeping six hours a night undisturbed. The muscle tone of her face has greatly improved. (See comparison pictures.)
On March 10, I used the Program 160 on Janice. Immediately following the treatment, I gave her the treated bottle of water as usual only I forgot to open it for her. I usually opened the bottles because she had no hand strength to do so herself. J.P. took the bottle and without thinking, she opened the bottle. On a whim, she tried to walk one foot in front of the other, like a drunk-test, and was amazed she could do so for a few steps without stumbling or losing her balance.
On March 15, I began a 10-treatment protocol for her to address her main complaint - MG. J.P. started feeling more energetic and had to hold herself back from overdoing it. By the sixth treatment of the protocol, she reported not napping during the day at all, able to walk the drunk-test for seven steps without falling or losing her balance, and she had a bright, cheery attitude.
By treatment eight, she was sleeping six hours a night, undisturbed with no daytime napping. Her balance had improved to where she could walk the drunk-test for 20 feet without faltering and J.P. could stand on her tiptoes.
Treatment nine, March 26, 2010, J.P. complained of muscle soreness in her right arm and shoulder, and in her buttocks. The day before she played catch with her kids, something that she hasn't done for years. Her soreness came from running after the ball and pitching balls back - all without falling.
Treatment ten, March 29, 2010. J.P. said she thinks all the extra activity has caught up with her. She was feeling like she needed a nap today. She was having some trouble with motor function of her legs. I finished the first round of specialized treatments for her. Next treatment will be on Wednesday this week.
We started a second intense protocol session with J.P., altering the treatment programs to just four programs each day. The programs used were 47, 48, 160 and 170 alternating to 47, 112, 160, 100 every other day.
Treatment one, March 30, 2010. Motor function returned to her legs after last week's treatment.
Treatment two, March 31, 2010. She slept soundly the night before; said she didn't even hear her husband snoring nor his morning alarm. That is not usual for her.
Treatment five, April 5, 2010. J.P. reported sleeping very well, 1 a.m. to 9 a.m.
Treatment seven, April 8, 2010. J.P. said she was having some breathing/asthma issues the night before so I added programs 102 and 113. She was able to take deep breaths after the treatment.
Treatment eight, April 9, 2010. I added program 113 to the scheduled protocol for today.
Treatment ten, April 13, 2010. This is the last treatment in second course of MG protocol.
Patient left for vacation the week of April 19, 2010.
May 3, 2010. J.P. took a week-long vacation in Laughlin, Nevada. I saw her for treatment Monday, May 3. She had a good time on vacation, not experiencing any setback with the MG. She said it took her two days to recuperate, but that was characterized by sleep and in bed for two days. The third day, she said she was full of energy and ready for almost anything.
Her treatment was over a week after she returned. She had a treatment Friday, April 15, before she left for vacation on the week of April 19. J.P. went 15 days until her next treatment without any perceived loss of the previously attained results. Treatments are resuming at the frequency of three times weekly.
Current programs used are 47, 52, 113, and 160.
June 9, 2010 - The patient recently had a bad case of asthmatic bronchitis. She has asthma and deals with chronic bronchitis frequently. She related that she ended up in the hospital this last time. The doctors were concerned that the condition was heart related. After diagnostic procedure, it was determined she has COPD and a slightly enlarged heart. She was previously diagnosed by her cardiologist with arrhythmia that requires medication.
She went to see her cardiologist June 8 because of the enlarged heart finding. He determined the slight enlargement was due to her severe coughing spells. He was impressed though with his findings concerning the arrhythmia. Apparently, the condition is improving to where the medication needs adjusting. He is now aware of the use of Ondamed on the patient and accepts that it is affecting the condition of her heart.
The American College for Advancement in Medicine (ACAM) is a not-for-profit organization dedicated to educating physicians and other health care professionals on the safe and effective application of integrative medicine.