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Magnesium

Peppermint Oil for Irritable Bowel Syndrome

 

https://www.amazon.com/Heathers-Tummy-Tamers-Peppermint-Capsules/dp/B0002UDK4Q?th=1

IBS

White Meat vs Dark Meat (Plus the skin)

by Cat Ebeling
co-author of the best-sellers: The Fat Burning Kitchen &The Top 101 Foods that Fight Aging

White meat chicken and turkey have been the darling of health and weight loss folks, and its been promoted as the ‘low fat/low calorie’ meat that was the perfect protein. White meat has about half the saturated fat of dark meat, and for this reason alone it has been falsely pushed as the healthier alternative because of outdated health beliefs by many gurus. While white meat is largely a protein delivery system–dark meat contains many more nutrients and its time to become a ‘leg man’—or woman!

White meat has had its day, and its time to go to the darker side, which has merits above and beyond white meat. According to the Department of Agriculture, an ounce of boneless, skinless turkey breast contains about 46 calories and 1 gram of fat, compared with roughly 50 calories and 2 grams of fat for an ounce of boneless, skinless thigh. And don’t forget the skin! Also, if you are eating free-range, organic turkeys and chickens, that fat is generally healthy fat—good for your skin, joints and immune system–and full of healthy omega 3 fats, as well, depending on what the turkeys or chickens ate.

So what makes white meat white, and dark meat dark?

Well it has to do with how much that particular muscle was used. Since chickens and turkeys, especially the free-range ones, use their legs to cruise around the farmyard, but generally don’t fly or use their wings much, their legs and thighs are dark. This is because of a compound in the blood that results from the movement of the muscles. The more movement, the darker the muscle. Dark meat contains myoglobin, similar to hemoglobin, that is a substance in poultry blood that allows for transport of oxygen—necessary for muscles that are being used. Muscles that are well-used, are also full of readily available iron, which is useful in our bodies as well, to help transport oxygen to all parts of the body as well.

Besides iron, dark meat contains more selenium, zinc, vitamins A and K, riboflavin, thiamine, and B6 and B12, as well as a supernutrient called taurine.  Taurine is a nutrient known be an anti-inflammatory nutrient, helps in blood pressure regulation, healthy nerve function, production of bile acid, (which breaks down fat), and other important functions. According to a new study by researchers at the New York University School of Medicine, taurine, significantly lowers the risk of heart disease, reducing mortality by as much as 80%, as well as protecting against diabetes and high blood pressure.

Many U.S. doctors recommend eating white or light meat instead of dark meat, because it is lower in saturated fat, but we now know that saturated fats are actually mostly healthy, and not the villain they were made out to be in the 80s and 90s fat-phobia period.

In fact, the NYU study demonstrates how dark meat ultimately packs a stronger nutritional punch. The study appears online in the European Journal of Nutrition. Taurine is such a powerful nutrient that it is considered a primary nutritional factor for longevity. Taurine also promotes insulin sensitivity, electrolyte balance, eyesight and hearing. Certain diets, especially vegetarian and vegan diets lack taurine and it has been found that diseases such as liver, kidney, heart disease, as well as diabetes and cancer, cause an even greater deficiency in taurine. Age is another factor that creates an extra need for taurine, as our bodies slow down the production of it as we age.

And new research is looking at the benefits of taurine for the human brain. Taurine, is one of the most important cognitive supplements, and can help to slow down age-related loss of memory and cognitive powers, as well as protecting against environmental toxins. High taurine levels are especially associated with eating dark meat chicken, oysters and clams.

Show me some skin!

Many people pay extra just to have “boneless, skinless” chicken or turkey meat, but its time to start eating the whole bird for maximum benefits!

There are a lot more edible parts to chicken or turkey than just the meat. When we strip away the skin, we are stripping away the healthy fats (provided it is organic and free range) and collagen, as well as other benefits. Chicken and turkey skin contain a large amount of monounsaturated fat, the same healthy fat you find in olive oil. Olive oil as you know, contains many healthy benefits for the whole body, as does the oleic acid in chicken and turkey skin. In fact, the majority of fat in chicken skin is actually heart-healthy unsaturated fats, according to Harvard School of Public Health. The U.S. Department of Agriculture (USDA) National Nutrient Database reports that 1 ounce of chicken skin contains about 3 grams of saturated fat, but provides 8 grams of unsaturated fat.  Although the amount of saturated fat is actually a useless fact, since we’ve already established that saturated fat is not bad for our health in any way.

Skin is almost pure collagen.Collagen as you may already know, is one of the most important nutrients you can add to your diet. So important, it’s probably worth writing a whole other blog on just how beneficial that stuff is. You can get plenty of collagen from the skin of chicken and turkey, bones, tendons, and ligaments. You know those crunchy parts on the ends of the legs? That’s cartilage, and it’s packs a whopping amount of collagen! So chew it up!

Our hunter-gatherer ancestors naturally ate a LOT more collagen compared to muscle meat than modern humans, since hunter-gatherers generally ate the entire animal instead of wasting the most nutrient dense organs, skins, and cartilage like modern humans do.

And don’t forget to take that chicken or turkey carcass, add water or broth and cook it slowly for 24 hours or more to create a delicious bone broth or soup base full of collagen and glucosamine. Collagen helps fight diseases like diabetes, improve your joints (drastically!), speed up healing time from athletic injuries, reduce wrinkling and sagging skin, and add strength and elasticity to hair and nails.We need collagen—it is essential!!

And lastly, don’t forget that deliciously decadent taste of freshly roasted crackly skin. That flavor and satisfaction go a long way towards making you feel full and satisfied.

What’s the takeaway? Stop buying those stripped-down boneless, skinless parts and eat the whole bird! Dark meat, skin, bones and cartilage. Just choose organic or pasture-raised if you can find it. Your body will thank you!

References

http://findyourbalancehealth.com/2015/04/6-reasons-why-chicken-skin-is-good-for-you/
http://www.lifeextension.com/search#q=taurine&sort=relevancy&f:hierarchicalcategory=[Magazines]
http://www.nytimes.com/2007/11/20/health/nutrition/20real.html
http://www.lifeextension.com/magazine/2013/6/the-forgotten-longevity-benefits-of-taurine/page-01
http://www.livescience.com/18848-dark-meat-heart-healthy.html

Making Sense of Your Cholesterol Levels and Assessing Your Heart Disease Risk

cholesterol levels infographic

Acid-Blocking Drugs Increase Heart Disease Risk

Put down the antacids! New study shows that acid blockers are detrimental to cardiovascular health.

Introduction

Proton-pump inhibitors (PPIs) are a group of drugs whose main action is blocking the secretion of gastric acid. They are dominant medical treatment of peptic ulcers, gastroesophageal reflux disease (GERD), and indigestion. Popular examples include Nexium, Prilosec, Protonix, Prevacid, and Aciphex. Use of these powerful antacids is associated with an increased risk for osteoporosisheart arrhythmias, intestinal infections, bacterial pneumonia, and multiple nutrient deficiencies. A new study from Stanford University adds another issue with these drugs – they double the risk of dying from a heart attack or stroke. Continue reading Acid-Blocking Drugs Increase Heart Disease Risk

Chickpeas offer 4 surprising health benefits

naturalhealth365.com/chickpeas-garbanzo-beans-1951.html

8/29/2016

(NaturalHealth365) Nutritionists and natural healers have long held chickpeas in high regard due to their undeniable merit as a superfood. These versatile little legumes not only boast a delicate, nutty flavor and a pleasing consistency, but they are also packed with high-quality plant protein, soluble and insoluble fiber, and beneficial polyunsaturated fatty acids.

However, recent studies have revealed that there is much more to chickpeas than their nutritive value.  Chickpeas, also known as garbanzo beans, Egyptian peas, ceci beans and chana, actually combat life-threatening diseases – on four different fronts.  As researchers come forward to credit chickpeas with life-extending effects, they are beginning to better understand the nuts and bolts of how these tasty little morsels work their magic. Continue reading Chickpeas offer 4 surprising health benefits

Specific change of histamine metabolism in acute magnesium-deficient young rats.

Drug Nutr Interact. 1987;5(2):89-96.

Specific change of histamine metabolism in acute magnesium-deficient young rats.

Abstract

The effects of dietary magnesium (Mg) deficiency on histamine metabolism were studied. Young Wistar rats were fed a Mg-deficient diet (0.001% Mg diet) ad libitum for 8 days with control groups (0.07% Mg diet), food-restricted groups (0.21% Mg diet, but restricted to 5 g/rat/day), and refeeding groups (0.001% Mg diet for 6 days ad libitum, after that fed with a 0.21% Mg diet ad libitum for 2 days). Compared to the other groups, the plasma Mg level was markedly lower in the Mg-deficient group. A return from the lower Mg level to the controls took place after feeding them a 0.21% Mg diet for 2 days. Urinary histamine level increased rapidly after 4 days and reached a maximum on the eighth day of Mg deficiency. The high urinary histamine level in Mg-deficient rats decreased rapidly after feeding them a 0.21% Mg diet for 2 days. Histamine contents in some tissues increased on the eighth day of Mg deficiency. Other groups showed no significant change. The increased histamine content in Mg-deficient rats showed a tendency to return to control levels after feeding them a 0.21% Mg diet for 2 days. Histidine decarboxylase (HDC) activity in some tissues of Mg-deficient rats increased markedly. The increased HDC activity dropped nearly to control levels after feeding them a 0.21% Mg diet for 2 days. Diamine oxidase (DAO) activity in the duodenum was high in control rats. Duodenal DAO activity decreased gradually and reached half the value of controls on the eighth day of Mg deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID:
3111814
[PubMed – indexed for MEDLINE]

Inflammation, Not Acid, Cause of GERD, Study Suggests

Veronica Hackethal, MD

May 17, 2016

Gastroesophageal reflux disease (GERD) may be caused by an immune reaction, rather than direct chemical injury from stomach acids, according to results from a small, single-center study published online May 17 in JAMA.

“In this preliminary study of 12 patients with severe reflux esophagitis successfully treated with PPI therapy, stopping PPI medication was associated with T lymphocyte–predominant esophageal inflammation and basal cell and papillary hyperplasia without loss of surface cells,” write first author Kerry Dunbar, MD, PhD, from the Dallas Veterans Affairs Medical Center in Texas, and colleagues.

“If replicated, these findings suggest that the pathogenesis of reflux esophagitis may be cytokine-mediated rather than the result of chemical injury,” they add.

Since 1935, convention has held that GERD, which affects about 20% of Americans, results from irritation of the esophageal lining as a result of refluxed acid from the stomach. A recent study in rats, however, has suggested that GERD may not be a result of chemical injury but, rather, a result of an immune reaction. That prompted researchers to test this new hypothesis in humans.

The study included 12 patients (11 men; mean age, 57.6 years) seen at the Dallas Veterans Affairs Medical Center for severe reflux esophagitis successfully treated with PPIs. Participants were told to stop taking their PPIs and received evaluations at baseline, as well as 1 and 2 weeks after stopping medication. Assessments included 24-hour esophageal pH and impedance monitoring (an index of mucosal integrity) and esophagoscopy (which included high-resolution confocal laser endomicroscopy). Researchers biopsied noneroded areas of the esophagus, where immune activity was assumed to be lower than in eroded areas.

At baseline, almost all participants (11/12) had no visible evidence of esophagitis. By 2 weeks after stopping PPIs, all participants developed esophagitis, and five had severe esophagitis.

Within 2 weeks of stopping PPIs, all participants developed abnormalities characteristic of GERD: basal cell and papillary hyperplasia (P < .01), papillary elongation (P < .01), dilated intercellular spaces in the esophageal squamous cell epithelium (P <. 001), reduced mucosal impedance (P = .001), and increased distal esophageal acid exposure. Between baseline and 2 weeks, acid exposure increased by 16.2% (95% confidence interval, 4.4% – 26.5%; P = .005).

Biopsies showed significant increases in infiltration of intraepithelial lymphocytes 1 and 2 weeks after stopping PPIs, with predomination of T cells (week 1, P = .005; week 2, P = .002) and few or no neutrophils and eosinophils.

“[E]sophageal basal cell and papillary hyperplasia developed in areas without surface erosions. If the traditional notion were true, that acute GERD is caused by refluxed acid directly inflicting lethal, chemical injury to surface epithelial cells, then basal cell and papillary hyperplasia would have been expected only in areas with surface erosions, and the infiltrating inflammatory cells would have been granulocytes primarily,” the authors write. They note that further studies are needed to confirm these results.

In a linked editorial, Peter Kahrilas, MD, from Northwestern Feinberg School of Medicine, Chicago, Illinois, notes that the “provocative findings from this investigation are in the details”: the earliest pathology occurred deep in the epithelium, not at the mucosal surface, and repair mechanisms started before the death of surface cells previously thought to provoke these changes.

“[A]lthough the inciting pathophysiology is unquestionably the reflux of gastric and duodenal secretions into the esophagus, this evidence suggests that the effect of that reflux is the initiation of cytokine-triggered inflammation rather than the long held belief of a direct chemical effect of acid, pepsin, and bile on the esophageal epithelium,” he wrote.

He notes that the participants in this study — men with high-grade erosive GERD and hiatal hernias — probably represent between 1% and 5% of all patients with GERD, so the findings may not apply to all patients with GERD. However, shifting the focus away from the “burning” effect of stomach acid toward an immune reaction may help explain subtypes of GERD that have been recently recognized.

The findings may also have implications for therapy, he notes. Although PPIs will probably remain the backbone of treatment, new therapies that target the inflammatory cascade may help treat patients with more severe or refractory GERD.

“Based on these findings, perhaps the mantra for treating refractory GERD should be ‘divide and conquer,’ according to the clinical findings and this new information about the disease process,” he concluded, “This is a heterogeneous patient group, and the therapeutic puzzle will only be solved piece by piece. Dunbar et al may have just placed a very important piece.”

The study was supported by a grant from the US Department of Veterans Affairs, the National Institutes of Health, and the American Gastroenterological Association. One or more authors reports consulting for one or more of the following: Interpace Diagnostics, Ironwood Pharmaceuticals, and Takeda Pharmaceuticals. The editorial was supported by a grant from the Public Health Service. Dr Kahrilas has disclosed no relevant financial relationships.

JAMA. 2016;315:2104-2112. Article abstractEditorial extract

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Cite this article: Inflammation, Not Acid, Cause of GERD, Study Suggests. Medscape. May 17, 2016.

Higher Vitamin D Levels Reduce Cancer Death Rates up to 52%

The Journal of Clinical Endocrinology & Metabolism published a meticulous analysis of past trials showing that patients with colorectal cancer, breast cancer, and lymphoma experienced a significantly reduced risk of mortality with higher serum vitamin D levels at diagnosis compared to those with low levels.*

Researchers selected 25 studies involving 17,332 cases of cancer for their meta-analysis.

Compared to lowest quartile, those with vitamin D levels in the top 25% range at the time of diagnosis had far better survival outcomes. For each of the following cancers, the risk of dying decreased by:

  • 37% for breast cancer patients
  • 45% for colorectal cancer patients
  • 52% for lymphoma patients

“By reviewing studies that collectively examined vitamin D levels in 17,332 cancer patients, our analysis demonstrated that vitamin D levels are linked to better outcomes in several types of cancer,” stated Dr. Hui Wang, MD, PhD, Professor of the Institute for Nutritional Sciences at the Shanghai Institutes for Biological Sciences at the Chinese Academy of Sciences in Shanghai. “The results suggest vitamin D may influence the prognosis for people with breast cancer, colorectal cancer, and lymphoma, in particular.”

Researchers found the strongest links between vitamin D levels and survival in breast cancer, lymphoma, and colorectal cancer. There was less evidence of a connection in people with lung cancer, gastric cancer, prostate cancer, leukemia, melanoma, or Merkel cell carcinoma.

Editor’s Note: Meta-analysis shows 4% reduction in death for all causes for every 4 ng/mL increase in circulating 25-OH vitamin D levels within the range the researchers examined. Serum vitamin D levels in those who don’t supplement are often below 13 ng/mL. By increasing vitamin D intake to 10,000 to 15,000 IU a day, optimal serum levels of 50 to 80 ng/mL can be achieved.

Reference
* JCEM . 2014 Apr 29.