Understanding Selected Vital Test Data - My Results

Understanding Selected Vital Test Data: my results from 4-1-2012 are in red
Omega-3 ALA
This is the total amount of ALA (alpha-linolenic acid) in your blood, as a percentage of all fatty acids. Certain plant foods contain this “short-chain” omega-3 fatty acid, less than 10 percent of which the body may convert into the “long-chain” omega-3 HUFA (EPA and DHA) it actually needs.

The average person eating the Standard American Diet will have an ALA score of less than 1%.
For optimal health, the ALA level in your blood should exceed 2%. 0.8

Omega-3 EPA
This is the total amount of EPA (eicosapentaenoic acid) in your blood, as a percentage of all fatty acids.

The average person eating the Standard American Diet will have an EPA score of less than 1%.
For optimal health, the EPA level in your blood should exceed 3%. 2.90

Omega-3 DPA
This is the total amount of DPA (docosapentaenoic acid) in your blood, as a percentage of all fatty acids. DPA is a lesser-known omega-3 fatty acid that is increasingly seen as important to health, in part because it can be converted to DHA by the body.

The average person eating a Standard American Diet will have a DPA score of less than 2%.
For optimal health, the DPA level in your blood should exceed 2%. 1.51

Omega-3 DHA
This is the total amount of DHA (docosahexaenoic acid) in your blood, as a percentage of all fatty acids.

The average person eating the Standard American Diet will have a DHA score of less than 3%.
For optimal health, the DHA level in your blood should exceed 5%. 5.51

Total Omega-6 Score
Omega-6 fatty acids are essential to health, but occur in extreme excess in the Standard American Diet. This is especially true of polyunsaturated linoleic acid (LA), which predominates in the most commonly used vegetable oils (corn, soy, safflower, sunflower, cottonseed) and the processed foods made with them. LA is converted in the body to an omega-6 HUFA called AA (arachidonic acid).

Omega-6 AA is the precursor to various hormone-like compounds called eicosanoids (eye-cos-ah-noyds), which strongly influence immune system processes. Having an excess of AA in your blood tends to produce a pro-inflammatory environment in the body.

The average person eating the Standard American Diet will have an AA score of about 13%.
For optimal health, the AA level in your blood should be less than 9%. 11.43

DGLA (dihomo-gamma-linolenic acid) is created when the body converts dietary omega-6 LA to omega-6 AA. People’s DGLA levels don’t generally reveal much about their heart health. Although other omega-6s generally promote and sustain inflammation, DGLA typically exerts inflammation-moderating effects.

Omega-6/Omega-3 Ratio
This result provides a general measure of where you stand in comparison to the U.S. average and to the optimal ratio (less than 5:1 omega-6s to omega-3s).

By itself, your Omega-6/Omega-3 Ratio has limited meaning because it does not reflect the amounts of these fatty acids in your blood. Having a “good” (low) ratio of omega-6s to omega-3s might provide a false sense of security if the amounts of both are too low. However, it’s good news if you have a low Omega-6/Omega-3 Ratio (less than 5:1) and your Total Omega-3 Score equals or exceeds the “optimal” level (more than 9%).

AA/EPA Ratio
This is the ratio of the omega-6 AA to the omega-3 EPA in your blood. AA is essential to human health and only becomes bad in excess.

For optimal health, you should have no more than five times as much AA as EPA; i.e., your ratio should not exceed 5:1. 3.85:1

Total Omega-3 Score
This reveals all of the omega-3 fatty acids in your blood, not just your omega-3 HUFA (EPA, DHA, and DPA). For example, if your omega-3 score is 5%, it means that 5% of all the fatty acids in your blood are omega-3s.

The Total Omega-3 Score is useful for monitoring your levels, but isn’t nearly as valuable an indicator of risk for coronary health disease as your Vital O-Mega Scores.

Optimally, your Total Omega-3 Score should be higher than 9%. 10.82

According to the results of several major epidemiological and clinical studies, this optimal score is linked to:

• 40% lower risk of all heart-related deaths (Dolecek TA 1992)
• 19-28% reduction in risk of sudden death from any cause (Albert CM et al. 2002)
• 50% reduction in the risk of sudden cardiac arrest (Siscovick DS et al. 1995)
• 10-30% drop in the risk of a stroke or second heart attack (Marchioli R et al. 2001)

People from regions where seafood is consumed in abundance – such as Japan and Greenland – often have total omega-3 scores greater than 15%.

Omega-3 Index
The Omega-3 Index measures the concentration of EPA and DHA as a percent of total fatty acids in red blood cell membranes. In recent years a significant body of research has been published showing the Omega-3 Index to be a good predictor of heart disease risk, and especially the risk of dying from a sudden heart attack, which contributes to over half of heart disease-related deaths.

These studies have shown that an Omega 3-Index of 8% or greater is desirable for its cardio-protective benefits, and a score below 4% is undesirable. 11.78

So all of this was achieved on diet alone, eating salmon 2-3 days per week on average. I have choesn to add Tuna Omega 3 (slightly low EPA and DHA) at 4 perles and wheat germ oil (to increase ALA) at 2 perles in an attempt to move all my values to optimal level. I plan to recheck in 3 months. I'll let you know.

Don

Taking vitamin D with the largest meal improves absorption

J Bone Miner Res. 2010 Apr;25(4):928-30.
Taking vitamin D with the largest meal improves absorption and results in higher serum levels of 25-hydroxyvitamin D.

Abstract
Many patients treated for vitamin D deficiency fail to achieve an adequate serum level of 25-hydroxyvitamin D [25(OH)D] despite high doses of ergo- or cholecalciferol. The objective of this study was to determine whether administration of vitamin D supplement with the largest meal of the day would improve absorption and increase serum levels of 25(OH)D. This was a prospective cohort study in an ambulatory tertiary-care referral center. Patients seen at the Cleveland Clinic Foundation Bone Clinic for the treatment of vitamin D deficiency who were not responding to treatment make up the study group. Subjects were instructed to take their usual vitamin D supplement with the largest meal of the day. The main outcome measure was the serum 259(OH)D level after 2 to 3 months. Seventeen patients were analyzed. The mean age (+/-SD) and sex (F/M) ratio were 64.5 +/- 11.0 years and 13 females and 4 males, respectively. The dose of 25(OH)D ranged from 1000 to 50,000 IU daily. The mean baseline serum 25(OH)D level (+/-SD) was 30.5 +/- 4.7 ng/mL (range 21.6 to 38.8 ng/mL). The mean serum 25(OH)D level after diet modification (+/-SD) was 47.2 +/- 10.9 ng/mL (range 34.7 to 74.0 ng/mL, p < .01). Overall, the average serum 25(OH)D level increased by 56.7% +/- 36.7%. A subgroup analysis based on the weekly dose of vitamin D was performed, and a similar trend was observed.

Thus it is concluded that taking vitamin D with the largest meal improves absorption and results in about a 50% increase in serum levels of 25(OH)D levels achieved. Similar increases were observed in a wide range of vitamin D doses taken for a variety of medical conditions.

Low Levels of Omega-3 Fatty Acids May Cause Memory Problems

A diet lacking in omega-3 fatty acids, nutrients commonly found in fish, may cause your brain to age faster and lose some of its memory and thinking abilities, according to a study published in the February 28, 2012, print issue of Neurology®, the medical journal of the American Academy of Neurology. Omega-3 fatty acids include the nutrients called docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA).
“People with lower blood levels of omega-3 fatty acids had lower brain volumes that were equivalent to about two years of structural brain aging,” said study author Zaldy S. Tan, MD, MPH, of the Easton Center for Alzheimer’s Disease Research and the Division of Geriatrics, University of California at Los Angeles.

For the study, 1,575 people with an average age of 67 and free of dementia underwent MRI brain scans. They were also given tests that measured mental function, body mass and the omega-3 fatty acid levels in their red blood cells.

The researchers found that people whose DHA levels were among the bottom 25 percent of the participants had lower brain volume compared to people who had higher DHA levels. Similarly, participants with levels of all omega-3 fatty acids in the bottom 25 percent also scored lower on tests of visual memory and executive function, such as problem solving and multi-tasking and abstract thinking.

Released: 2/21/2012 3:00 PM EST 
Source: American Academy of Neurology (AAN)

Home Test: The Vital Omega-3 and 6 HUFA Test™

The Vital Omega-3 and 6 HUFA Test™ measures the blood levels of these two families of essential nutrients, which strongly influence genetic “switches”, and hormone-like agents called prostaglandins.

• Easy, comfortable, at-home blood test
• Receive your results by email in about 3 weeks
• Reveals your key omega-3 and omega-6 blood levels
• Provides a heart-risk grade, based on your test results

Which omega-3 and omega-6 HUFA are included in your report?
The five most abundant highly unsaturated fatty acids (HUFA) in human blood – and the ones most significant to human health – are omega-3 EPA, DHA, and DPA* and omega-6 AA* and DPA**:

However, your Vital Omega-3 and 6 HUFA Test™ measures and reports the full spectrum of all nine omega-3 and omega-6 HUFA found in human blood.

The following list shows the scientific names (e.g., docosahexaenoic acid) and alpha-numeric identifiers (e.g., 22:6w3) for all nine HUFA, as well as the acronyms (e.g., DHA) commonly used for the five major HUFA:

Omega-3 HUFA covered by your report
DHA (docosahexaenoic acid - 22:6w3) • EPA (eicosapentaenoic acid - 20:5w3) • DPA (docosapentaenoic acid - 22:5w3) • eicosatrienoic acid (20:3w3) • eicsoatetraenoic acid (20:4w3)

Omega-6 HUFA covered by your report
AA (arachidonic acid - 20:4w6) • di-homo-gamma linolenic acid (20:3w6) • adrenic acid (22:4w6) • DPA (docosapentaenoic acid - 22:5w6)

I'll post my results as soon as I get them as a sample to what the provide....more soon

Don

Omega-3 Fatty Acids and Heart Health

Omega-3 reduces risk of death from cardiovascular causes by between 30 to 50% following a myocardial infarction

 

Lancet. 1999 Aug 7;354(9177):447-55.

From October, 1993, to September, 1995, 11,324 patients surviving recent (< or = 3 months) myocardial infarction were randomly assigned supplements of n-3 PUFA (1 g daily, n=2836), vitamin E (300 mg daily, n=2830), both (n=2830), or none (control, n=2828) for 3.5 years.

The Italian GISSI study says taking just 850 mg of EPA DHA Omega-3 per day showed a dramatic reduction of sudden death.

This risk reduction isn’t from cholesterol reduction.

The risk reduction comes from:

• reduction in triglycerides
• reduction in inflammation
• providing antiarrhythmic properties
• improved endothelial function

Follow up Report

Omega-3 Fatty Acids and Heart Failure
Curr Atheroscler Rep. 2009 Nov;11(6):440-7.

Abstract
During the past three decades, the protective role of omega (n)-3 polyunsaturated fatty acids (PUFA), mainly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in patients with coronary heart disease has been widely reported. The Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-Heart Failure (GISSI-HF) study, a large-scale clinical trial, recently showed that n-3 PUFA (850-882 mg/d) reduced mortality and admission to the hospital for cardiovascular reasons in patients with chronic heart failure (HF) who were already receiving recommended therapies. The favorable effects of n-3 PUFA in GISSI-HF suggest that marine fish oils could confer protection in HF mainly through their antiarrhythmic action and in part by influencing the mechanisms related to HF progression. This article reviews recent clinical and experimental evidence on the effect of n-3 PUFA in coronary heart disease, with particular attention on HF and its pathophysiologic mechanisms.

Don

Low Levels of Omega-3 Fatty Acids May Cause Memory Problems

A diet lacking in omega-3 fatty acids, nutrients commonly found in fish, may cause your brain to age faster and lose some of its memory and thinking abilities, according to a study published in the February 28, 2012, print issue of Neurology®, the medical journal of the American Academy of Neurology. Omega-3 fatty acids include the nutrients called docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA).
"People with lower blood levels of omega-3 fatty acids had lower brain volumes that were equivalent to about two years of structural brain aging," said study author Zaldy S. Tan, MD, MPH, of the Easton Center for Alzheimer's Disease Research and the Division of Geriatrics, University of California at Los Angeles.

For the study, 1,575 people with an average age of 67 and free of dementia underwent MRI brain scans. They were also given tests that measured mental function, body mass and the omega-3 fatty acid levels in their red blood cells.

The researchers found that people whose DHA levels were among the bottom 25 percent of the participants had lower brain volume compared to people who had higher DHA levels. Similarly, participants with levels of all omega-3 fatty acids in the bottom 25 percent also scored lower on tests of visual memory and executive function, such as problem solving and multi-tasking and abstract thinking.

Mueller's new book, Extra Virginity: The Sublime and Scandalous World of Olive Oil

NPR - interview! You can listen to it here

Mueller's new book, Extra Virginity: The Sublime and Scandalous World of Olive Oil, chronicles how resellers have added lower-priced, lower-grade oils and artificial coloring to extra-virgin olive oil, before passing the new adulterated substance along the supply chain. (One olive oil producer told Mueller that 50 percent of the olive oil sold in the United States is, in some ways, adulterated.)

The term "extra-virgin olive oil" means the olive oil has been made from crushed olives and is not refined in any way by chemical solvents or high heat.

"The legal definition simply says it has to pass certain chemical tests, and in a sensory way it has to taste and smell vaguely of fresh olives, because it's a fruit, and have no faults," he tells Fresh Air's Terry Gross. "But many of the extra-virgin olive oils on our shelves today in America don't clear [the legal definition]."

Extra-virgin olive oil wasn't created until stainless steel milling techniques were introduced in the 1960s and '70s. The technology allowed people to make much more refined olive oil.

"In the past, the technology that had been used had been used really by the Romans," says Mueller. "You grounded the olives with stone mills [and] you crushed them with presses."

The introduction of stainless steel milling techniques has allowed manufacturers to make more complex and flavorful extra-virgin olive oils, he says. But the process is also incredibly expensive — it costs a lot to properly store and mill extra-virgin olive oil. Mueller says that's why some people blend extra-virgin olive oil with lower-grade, lower-priced products.

"Naturally the honest people are getting terribly undercut," he says. "There's a huge unfair advantage in favor of the bad stuff. At the same time, consumers are being defrauded of the health and culinary benefits of great olive oil."

Bad or rancid olive oil loses the antioxidant and anti-inflammatory properties of olive oil, says Mueller. "What [good olive oil] gets you from a health perspective is a cocktail of 200+ highly beneficial ingredients that explain why olive oil has been the heart of the Mediterranean diet," he says. "Bad olives have free radicals and impurities, and then you've lost that wonderful cocktail ... that you get from fresh fruit, from real extra-virgin olive oil."

Your Olive oil may not be as virgin as you think it is.

The next time you reach for a bottle of extra-virgin olive oil, beware. A new study from the University of California- Davis claims more than two-thirds of random samples of imported so-called extra-virgin olive oil don't make the grade.

The Olive Oil Chemistry Lab overlooks many of the 2,000 olive trees on the Davis campus.

"It's like we have our own CSI: Olive Oil lab here," says chemist Charles Shoemaker, who manages the lab's forensics.

To be extra-virgin, olive oil can't be rancid or doctored with lesser oils. Shoemaker wasn't all that surprised that many of the 14 major brands failed certain tests.

"It's become a very sophisticated practice, the adulteration of olive oil throughout the world," Shoemaker says. He says the lab can prove defects, degradation and dilution in olive oil beyond what human taste buds can figure out. The lab testing zeroes in on specific flaws.

"We do spectroscopic studies looking for oxidation," he says. That means the oil's old or spoiled. Shoemaker also tests fatty acids "to make sure the oil is all from olives and not from soybean, sunflower or other types of oil."

The UC-Davis Olive Oil Report


No molecule can hide. Shoemaker revs up a small vacuum that removes solvents and isolates chlorophyll, which is always in oil made from green olives, but never in lesser-grade seed oil. As it sucks a sample, he's patient.

"It takes about 25 minutes per sample to do just this one step," he says.

The UC-Davis study was funded in part by the California Olive Oil Council. Oils were tested by some methods not yet recognized by international standards. For that reason, Bob Bauer of the North American Olive Oil Association, which represents importers, disputes the Davis study.

"It's irresponsible to create the misperception that they've done based on unrecognized tests," he says. "These results directly contradict our 20 years of more extensive sampling than what those results show."

There's never been a legal definition in the U.S. for any grade of olive oil, but mounting concern over truth-in-olive-oil-labeling has drawn in the USDA, and new American regulations will conform to international standards. Starting in October, olive oil from every olive oil-producing country, including America, will be subject to random sampling off retail shelve.

Diseases and Environmental Toxins Suspected to Cause Them

Here is a link to a table of Diseases and Environmental Toxins Suspected to Cause Them.

Don

The Inadvertent and Continuous Exposure of Fetuses to Environmentally Active Chemicals

There is a third type of exposure that needs to be addressed: the inadvertent and continuous exposure of fetuses to environmentally active chemicals, such as dioxins and BPA.                 

Dioxins

Depending on the context (time of exposure, organ, presence or absence of estrogens) dioxins have either estrogenic or antiestrogenic effects. Despite cross-talk between the aryl hydrocarbon and ERs (139), the mechanisms underlying these opposite effects have yet to be elucidated. Rats exposed prenatally (gestational d 15) to TCDD and challenged with the chemical carcinogen DMBA at 50 d of age showed increased tumor incidence, increased number of tumors per animal, and shorter latency period than rats exposed prenatally to vehicle and to DMBA at 50 d of age. These TCDD-exposed animals had increased numbers of terminal end buds at puberty (140). Because these structures are believed to be the site where mammary cancer arises, these results were interpreted as evidence that TCDD increased the propensity to cancer by altering mammary gland morphogenesis. Interestingly, Fenton (31) showed that prenatal exposure to TCDD results in impaired development of terminal end buds that remain in the gland for prolonged periods, whereas in the normal animals terminal end buds are transient structures that regress when ductal development is completed.

BPA, a ubiquitous xenoestrogen

The ubiquitous use of BPA provides great potential for exposure of both the developing fetus, indirectly through maternal exposure, and the neonate, directly through ingestion of tinned food, infant formula, or maternal milk (11). Indeed, BPA has been measured in maternal and fetal plasma and placental tissue at birth in humans (141). A recently published study conducted by the Centers for Disease Control, the first using a reference human population, showed that 92.6% of over 2500 Americans had BPA in their urine (142). Measured urine concentrations were significantly higher in children and adolescents compared with adults. BPA has also been measured in the milk of lactating mothers. These data indicate that the developing human fetus and neonate are readily exposed to this chemical.

In rodents, BPA has been shown to readily cross the placenta (143, 144) and bind α-fetoprotein (the estrogen-binding protein that prevents maternal estrogen from entering the circulation of the fetus) with negligible affinity relative to estradiol; this results in enhanced bioavailability during neonatal development. BPA is present in the mouse fetus and amniotic fluid during maternal exposure in higher concentrations than that of maternal blood.

The U.S. EPA has established the safe daily intake of BPA to be 50 μg/kg body weight/d based on the assumption that the main source of exposure is oral through food ingestion. However, recent publications suggest that food is not the only relevant source of exposure and that the half-life of BPA in humans is longer than expected (6). Numerous publications addressing fetal exposures to BPA have used parenteral administration. This practice was based on one hand on the fact that the fetus is exposed to BPA through the internal milieu of the mother, and on the other hand that parenteral administration via an osmotic minipump allows for a precise and constant level of exposure. Using this route of administration, exposure of a pregnant mouse dam to 25 and 250 ng BPA/kg body weight/d (namely, 2000 and 200 times lower than the safe dose) for 14 d beginning on d 8 gestation has been shown to impact certain aspects of development in their female offspring. When examined on gestational d 18, fetuses of mothers exposed to the higher dose of BPA exhibited altered growth parameters of the mammary gland anlagen. Changes in the appearance of the mammary epithelium were observed, such as decreased cell size and delayed lumen formation, as well as increased ductal area. In the stroma, BPA exposure promoted advanced maturation of the fat pad and altered localization of fibrous collagen (128). Because maturation of the fat pad is the driving event for ductal growth and branching, it is likely that the increased ductal area in BPA-exposed animals is due to the accelerated formation of their fat pads. By postnatal d 10, in the offspring born to mothers exposed to either dose of BPA, the percentage of proliferating epithelial cells was significantly decreased relative to those not exposed. At 30 d of age, the area and number of terminal end buds relative to the gland ductal area increased, whereas cell death in these structures decreased in BPA-exposed offspring compared with controls. It is likely that the reduced cell death in the terminal end buds of BPA-exposed females may be the cause of the observed ductal growth delay because cell death is essential for both the hollowing and the outward growth of the subtending duct. Collectively, these effects observed at puberty may be attributed to an increased sensitivity to estradiol that has been observed in the BPA-exposed animals (145). Because of the new epidemiological data cited above and the effects found in the low-dose animal studies using parenteral exposure, the EPA recommendations need to be reevaluated.

In animals exposed perinatally to BPA, there was also a significant increase of ductal epithelial cells that were positive for progesterone receptor at puberty. These positive cells were localized in clusters, suggesting future branching points. Indeed, lateral branching was significantly enhanced at 4 months of age in offspring born to mothers exposed to 25 ng BPA/kg body weight/d (145). These results are compatible with the notion that increased sensitivity to estrogens drives the induction of progesterone receptors in epithelial cells, leading to an increase in lateral branching. By 6 months of age, perinatally exposed virgin mice exhibit mammary glands that resemble those of a pregnant mouse, as reflected by a significant increase in the percentage of ducts, terminal ends, terminal ducts, and alveolar buds (146). Additionally, intraductal hyperplasias, which are considered preneoplastic lesions, were observed starting at 3 months of age (147).

To explore the links between prenatal BPA exposure and mammary gland neoplasia, a rat model was chosen because it closely resembles the human disease regarding estrogen dependency and histopathology. BPA was administered to pregnant dams at doses of 2.5, 25, 250, and 1000 μg/kg body weight/d. Fetal exposure to BPA, from gestational d 9 to postnatal d 1, resulted in the development of carcinomas in situ in the mammary glands of 33% of the rats exposed to 250 μg/kg body weight/d, whereas none of the unexposed animals developed neoplasias (148). These cancers were only observed after the animals had reached young adult age. Fetal exposure to BPA significantly increased the number of precancerous lesions (intraductal proliferation) by three to four times, an effect also observed in puberty and during adult life. The lesions observed in the BPA-exposed animals were highly proliferative and contained abundant ER-positive cells, suggesting that the proliferative activity in these lesions may be estrogen mediated. Comparable preneoplastic lesions were found in a study using a different rat strain (149). Additionally, this study found stromal alterations such as desmoplasia and mast cell invasion; these features are often observed during neoplastic development. Moreover, when challenged with a subcarcinogenic dose of nitrosomethylurea, only the BPA-exposed animals developed palpable tumors (carcinomas). The period of vulnerability of the mammary gland to BPA does not cease at the neonatal stage. BPA exposure during lactation followed to exposure to the carcinogen DMBA resulted in mammary tumor multiplicity and reduced tumor latency compared with control animals (exposed solely to DMBA) (150). These results indicate that perinatal exposure to environmentally relevant doses of BPA results in persistent alterations in mammary gland morphogenesis, development of precancerous lesions, and carcinoma in situ. Moreover, the altered growth parameters noted in the developing mammary gland on embryonic d 18 suggest that the fetal gland is a direct target of BPA, and that these alterations cause the mammary gland phenotypes observed in perinatally exposed mice at puberty and adulthood.

In summary, exposure to estrogens throughout a woman’s life, including the period of intrauterine development, is a risk factor for the development of breast cancer. The increased incidence of breast cancer noted during the last 50 yr may have been caused, in part, by exposure of women to estrogen-mimicking chemicals that have been released into the environment from industrial and commercial sources. Epidemiological studies suggest that exposure to xenoestrogens such as DES during fetal development, to DDT around puberty, and to a mixture of xenoestrogens around menopause increases this risk. Animal studies show that exposure in utero to the xenoestrogen BPA increases this risk. Moreover, these animal studies suggest that estrogens act as morphogens and that excessive perinatal exposure results in structural and functional alterations that are further exacerbated by exposure to ovarian steroids at puberty and beyond. These altered structures include preneoplastic lesions, such as intraductal hyperplasias, and carcinomas in situ. Additionally, these mammary glands are more vulnerable than their normal counterparts to carcinogenic stimuli. Exposures to other endocrine disruptors that are not estrogenic, such as dioxins, were reported to increase breast cancer incidence in humans and to alter mammary gland development in animal models. Collectively, these data support the notion that endocrine disruptors alter mammary gland morphogenesis and that the resulting dysgenic gland becomes more prone to neoplastic development.

Source: http://edrv.endojournals.org/content/30/4/293.full

Don

Endocrine Disruptors - What are they?

The group of molecules identified as endocrine disruptors is highly heterogeneous and includes synthetic chemicals used as industrial solvents/lubricants and their byproducts [polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), dioxins], plastics [bisphenol A (BPA)], plasticizers (phthalates), pesticides [methoxychlor, chlorpyrifos, dichlorodiphenyltrichloroethane (DDT)], fungicides (vinclozolin), and pharmaceutical agents [diethylstilbestrol (DES)].                 

Natural chemicals found in human and animal food (e.g., phytoestrogens, including genistein and coumestrol) can also act as endocrine disruptors. These substances, whereas generally thought to have relatively low binding affinity to ERs, are widely consumed and are components of infant formula (1, 2). A recent study reported that urinary concentrations of the phytoestrogens genistein and daidzein were about 500-fold higher in infants fed soy formula compared with those fed cow’s milk formula (3). Therefore, the potential for endocrine disruption by phytoestrogens needs to be considered.

It is difficult to predict whether a compound may or may not exert endocrine-disrupting actions. Nevertheless, in very broad terms, EDCs such as dioxins, PCBs, PBBs, and pesticides often contain halogen group substitutions by chlorine and bromine. They often have a phenolic moiety that is thought to mimic natural steroid hormones and enable EDCs to interact with steroid hormone receptors as analogs or antagonists. Even heavy metals and metalloids may have estrogenic activity, suggesting that these compounds are EDCs as well as more generalized toxicants. Several classes of EDCs act as antiandrogens and as thyroid hormone receptor agonists or antagonists, and more recently, androgenic EDCs have been identified.

Exposure occurs through drinking contaminated water, breathing contaminated air, ingesting food, or contacting contaminated soil.

Source: http://edrv.endojournals.org/content/30/4/293.full

Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement

If this doesn't one thinking about what's going in their body or the need to do a purification program yearly read again!

Review: Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement (2009)

Abstract
There is growing interest in the possible health threat posed by endocrine-disrupting chemicals (EDCs), which are substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction. In this first Scientific Statement of The Endocrine Society, we present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology. Results from animal models, human clinical observations, and epidemiological studies converge to implicate EDCs as a significant concern to public health. The mechanisms of EDCs involve divergent pathways including (but not limited to) estrogenic, antiandrogenic, thyroid, peroxisome proliferator-activated receptor γ, retinoid, and actions through other nuclear receptors; steroidogenic enzymes; neurotransmitter receptors and systems; and many other pathways that are highly conserved in wildlife and humans, and which can be modeled in laboratory in vitro and in vivo models. Furthermore, EDCs represent a broad class of molecules such as organochlorinated pesticides and industrial chemicals, plastics and plasticizers, fuels, and many other chemicals that are present in the environment or are in widespread use. We make a number of recommendations to increase understanding of effects of EDCs, including enhancing increased basic and clinical research, invoking the precautionary principle, and advocating involvement of individual and scientific society stakeholders in communicating and implementing changes in public policy and awareness.

Outline of what is covered in the position statement:

I. General Introduction to Endocrine Disruption

• A. Important issues in endocrine disruption
• B. The role of endocrinologists in discerning effects of EDCs

II. Overview of Endocrine Disruption and Reproductive Health from a Clinical Perspective                                            

• A. Clinical aspects of endocrine disruption in humans
• B. Clinical dimorphism of EDCs on male and female reproduction
• C. Experimental and clinical evidence of EDCs and potential mechanisms

III. Clinical and Translational Impacts of EDCs on Female Reproduction                                            

• A. Introduction to female reproductive development and function
• B. Polycystic ovarian syndrome (PCOS)
• C. Premature ovarian failure, decreased ovarian reserve, aneuploidy, and granulosa steroidogenesis
• D. Reproductive tract anomalies
• E. Uterine leiomyomas
• F. Endometriosis

IV. Endocrine Disruptors, Mammary Gland Development, and Breast Cancer                                            

• A. Windows of vulnerability to carcinogenic agents and “natural” risk factors
• B. Theories of carcinogenesis
• C. Susceptibility of the breast during puberty and adulthood
• D. Susceptibility of the mammary gland during the perinatal period
• E. Perinatal exposure to environmentally relevant levels of endocrine disruptors

V. Male Reproductive and Developmental Health: The Human Evidence                                            

• A. Introduction to male reproductive health
• B. Male reproductive function and development
• C. Semen quality: temporal trends and EDC exposure
• D. Male urogenital tract malformations
• E. Testicular germ cell cancer
• F. Conclusions

VI. Prostate Cancer                                            

• A. Introduction to prostate cancer
• B. Evidence and mechanisms for EDC effects on the prostate

VII. Neuroendocrine Targets of EDCs                                            

• A. Endocrine disruption of reproductive neuroendocrine systems
• B. Hypothalamic-pituitary-adrenal (HPA) effects of EDCs
• C. Thyroid, metabolism, and growth
• D. Hormonal targets of neuroendocrine disruption

VIII. Thyroid Disruption                                            

• A. Introduction to thyroid systems
• B. Environmental chemicals impacting thyroid function
• C. Environmental chemicals impacting thyroid hormone transport, metabolism, and clearance
• D. Environmental chemicals impacting the thyroid hormone receptor

IX. Environmental Chemicals, Obesity, and Metabolism                                            

• A. Introduction to EDCs and the obesity epidemic
• B. Environmental estrogens and obesity
• C. Peroxisome proliferator-activated receptor (PPAR) γ and organotins
• D. Phytoestrogens
• E. Endocrine disruptors, diabetes, and glucose homeostasis
• F. Endocrine disruptors and cardiovascular systems
• G. Estrogenic EDCs and cardioprotection
• H. Advanced glycation end-products (AGEs)
• I. Conclusions

Don

Commercial vs Whole Food Vitamin

Multivitamins

There has never been a single study, out of all that have been done, that shows the American public comes remotely close to consuming the minimum requirements for vitamins and minerals in their daily diet.  Disease prevention and health enhancement in the United States appear to be possible only through supplementation.

Studies due indicate levels of malnutrition.  Doctors have reported to me from the University of California Medical Center their disbelief at finding scurvy (Vitamin-C deficiency disease) in their patients.  Meanwhile, agricultural departments, such as at the University of Texas, are finding the nutritional levels of food are lower than ever historically, with a steady significant decline from the early 1900s up to the present.

Better Health Through Better Nutrition

The most recent in-depth study on multiple nutrients recognizes how difficult it is to generalize. (See Block G, Jensen CD, Nordus EP, Dalvi TB, Wong LG, McManus JF and Hudes ML, "Usage Patterns, Health and Nutritional Status of Long-term Multiple Dietary Supplement Users," a cross-sectional study that was published in the October 24, 2007 issue of Nutritional Journal.)   The study nevertheless could make some statistical statements based upon the 278 long-term users of multiple dietary supplements, 176 users of a single multivitamin/multimineral supplement, and 602 nonusers of supplements whom the scientists studied.

At least half of the subjects in the multiple dietary-supplements group consumed a multivitamin/mineral, B-complex, Vitamin C, carotenoids, Vitamin E, calcium with Vitamin D, omega-3 fatty acids, flavonoids, lecithin, alfalfa, Coenzyme Q10 with resveratrol, glucosamine, and an herbal immune supplement.

The majority of women in this group also consumed gamma linolenic acid and a probiotic supplement.  The majority of men additionally consumed zinc, garlic, saw palmetto, and a protein supplement.

Overall, the study showed that the use of multiple dietary supplements led to better health.  As the researchers themselves said, individuals who consume a number of nutritional supplements were found to have better biomarkers of health than those who do not consume any supplements or who only consumed a multivitamin/mineral.

Among other benefits, multiple-supplement users also had lower levels of C-reactive protein and triglycerides and higher levels of HDL (the so-called "good") cholesterol.  Other findings in the multiple supplements group included lower risks of elevated blood pressure, diabetes (73% less compared to nonusers), and coronary heart disease (52% less compared to nonusers).  Subjects consuming multiple dietary supplements also reported having "good or excellent" health status 74 percent more often than non-supplement users.

Other corollary findings included the discovery of various nutrient deficiencies in both the non-supplement users and the multivitamin/mineral users, especially with low levels of Vitamin C.  Far from being a danger to health as the mass media would have us believe, using multiple nutritional supplements confers various health benefits that merit further study, not blind condemnation.
Source: http://vitaminsinamerica.com/2009/03/

Selecting a Multivitamin

Additives and Quality

Often overlooked by consumers who see generic vitamin names on multivitamin labels and rarely look beyond, additives and quality are nevertheless of paramount importance.  And it is here where the two types of multivitamins have important differences.

Just consider one of the top-selling multiples in the marketplace, which happens to be a drug-store multiple supplement for seniors.  It is highly endorsed by both MDs and pharmacists.  First, let's look at its excipients (the extra chemicals needed to make the tablet, complete the filling of the capsule, or added for some other unknowable reason):

Polyethylene Glycol, Polyvinyl Alcohol, Pregelatinized Corn Starch, Sodium Benzoate, Sucrose, Talc, Maltodextrin, Calcium Stearate, Sodium Aluminosilicate, Sunflower Oil, Colloidal Silicon Dioxide, Corn Starch, Crospovidone, FD&C Blue No. 2 Aluminum Lake, FD&C Red No. 40 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake, Gelatin, Hydrogenated Palm Oil, Hypromellose, and Modified Food Starch.

Let's now look at a health-food based multivitamin and see the difference.

Catalyn by Standard Process

Proprietary Blend: 766 mg
Defatted wheat (germ), carrot (root), calcium lactate, nutritional yeast, bovine adrenal, bovine liver, magnesium citrate, bovine spleen, ovine spleen, bovine kidney, dried pea (vine) juice, dried alfalfa (whole plant) juice, mushroom, oat flour, soybean lecithin, and rice (bran).

Other Ingredients:
Honey, glycerin, arabic gum, ascorbic acid, calcium stearate, cholecalciferol, pyridoxine hydrochloride, starch, sucrose (beets), vitamin A palmitate, cocarboxylase, and riboflavin.

What Makes Catalyn Unique

Product Attributes: Whole food multivitamin.The nutrients in Catalyn are processed to remain intact, complete nutritional compounds. Contains important vitamins, minerals, enzymes, and trace minerals in combination with their naturally occurring synergistic cofactors. Combines vital nutrients from a wide variety of plant sources to introduce a unique diversity of complete vitamin and mineral complexes (Phytonutrients).

Phytonutrients (Phytochemicals):
Phytonutrients are the important nutrients found in plants that are necessary to maintain a healthy body. They may serve as antioxidants; support a healthy immune response; and support cell-to-cell communication. There are many phytonutrients that have been identified, while their possible functions/actions have yet to be discovered. Some of the best known phytochemicals are the carotenoids, like alpha- and beta-carotene and lycopene. At Standard Process, our multivitamins are packed with health-promoting phytonutrients, which ensure maximum efficacy.

Don