Understanding Our Adrenal System: Norepinephrine

Author:   Vanessa Bennington

Quelle:  http://breakingmuscle.com/health-medicine/understanding-our-adrenal-system-norepinephrine

 

There is a lot of talk about adrenal health lately, particularly adrenal fatigue.

Most of us get the gist of it. If you stress your body out too much, for too long your adrenals just up and quit on you. Most of us also understand that when our adrenals are not functioning properly our energy levels and moods suffer, as well as our mental and physical performance. But how many of us really understand the chemicals and hormones made by the adrenals?

I am going to explain these adrenal chemicals one by one, so we can all better understand the complex mechanisms of adrenal function and how to maintain or regain healthy adrenal function to maximize our athletic performance. The first chemical up is norepinephrine.

Norepinephrine, also referred to as noradrenaline, along with epinephrine is what most of us think of as the “fight-or-flight” hormones.

It’s technically a catecholamine, but it functions as a hormone and neurotransmitter and is produced by the adrenal gland, postganglionic neurons of the sympathetic nervous system, and part of the brain called the locus coerules. From the locus coerules, noradrenergic neurons branch out and form a system that enables norepinephrine to be delivered to different parts of the brain. In a similar fashion, the postganglionic neurons enable norepinephrine to be delivered directly to target organs and cells in the body. The adrenal glands dump norepinephrine directly into the blood. These mechanisms usually come into play when we are under stress.

That release of norepinephrine (as well as epinephrine) is what gets your blood pumping and heart pounding, giving you the shakes when you’re put in a stressful situation. It triggers the release of glucose into the blood stream  and increases blood pressure, heart rate, mental alertness, and respiratory rate. When released from the locus coerules, it has an anti-inflammatory effect on the brain. It also shunts blood away from the skin and to the heart, brain, muscles, and kidneys. (Ever wonder why you have to urinate constantly right before a super tough workout?)

In other words, norepinephrine gets you ready to respond physically to a perceived stressor. It is also used as a drug to maintain blood pressure and treat bradycardia (slow heartbeat), among other things.

Norepinephrine is synthesized by tyrosine, an amino acid, through a series of steps in the adrenal medulla and part of the sympathetic nervous system. L-tyrosine is converted to L-DOPA, L-DOPA to dopamine, and dopamine to norepinephrine. Norepinephrine is then stored in synaptic vesicles where it stays until something stimulates the release. Once released norepinephrine can bind with adrenergic receptor sites that enable it to carry out its actions (increasing heart rate, respirations, releasing glucose, etc.).

Norepinephrine’s effects are then terminated by either the degradation of norepinephrine or its reuptake. However, there are many substances that either cause norepinephrine to be released or inhibit that release. There are also substances that influence the termination of norepinephrine’s effect on the cell.

Since, we know that norepinephrine, in the right amounts and at the right time, is essential for optimal mental and physical health, it warrants a brief overview of some of the ways its production and actions may be altered. I won’t get into the specifics of disease processes and treatments.

Just be aware that depression, anxiety, blood pressure problems, heart rate issues, and many other illness can be attributed, at least partially, to the deregulation of norepinephrine production and function in the body. 

 We’ll address the specifics of disease processes and treatments related to adrenal function in another article in the future, but I want you to have a basic understanding of how norepinephrine production and function might be changed.

First we need tyrosine available to make dopamine and eventually norepinephrine. If we don’t have enough of the raw materials we can’t make the hormone.

Tyrosine is considered a conditionally essential amino acid. Most of the time, we do not need to actually ingest foods high in tyrosine. We can use phenylalanine, another amino acid that must be ingested, to make tyrosine.  

However, if the diet is lacking in phenylalanine then tyrosine is considered essential and we will need either supplementation or diet to be changed to include foods higher in phenylalanine and tyrosine. Foods high in phenylalanine include meat, fish, and some dairy like cottage cheese.

Foods high in tyrosine include meat and dairy as well as bananas and seaweed.

I mentioned above there are substances that can influence or inhibit the release of norepinephrine from the synaptic vesicle. These are called release modulators and can be broken down into inhibitory and stimulatory modulators. 

Substances like dopamine, acetylcholine, norepinephrine itself, epinephrine, 5-HT, adenosine, histamine, ATP, and enkaphalin cause the body to reduce the release of norepinephrine.

This might seem weird since some of these are stress hormones and why would norepinephrine itself decrease its on release.

To put it simply, once the body has enough of these hormones circulating, it will down regulate the release of more in order to maintain or return to homeostasis. Epinephrine (tricky devil, playing both sides) and angiotensin II both increase norepinephrine release.

There are also substances that can alter the way norepinephrine’s actions are terminated, either by changing how norepinephrine binds with receptors or how it is taken up and out of the system.

The results can either be an increase or decrease of its actions causing increased or decreased circulating norepinephrine or an increase or decrease in its ability to bind to receptors an initiate its effects.

Drugs like cocaine, amphetamines, and antidepressants alter the reuptake of norepinephrine. Alpha and beta blockers (also drugs) alter how norepinephrine binds with receptors.

So, there’s a lot that can go wrong when you look at all the things that can interfere with proper production and function of norepinephrine.

We know that we want our norepinephrine production to be on point. Not too much. Not too little.
Without that balance we develop problems involving our moods, energy levels (adrenal fatigue), blood pressure, and more. All of which can negatively affect your fitness, ability to reach your goals, and ability to enjoy your workouts.


Quelle:  http://breakingmuscle.com/health-medicine/understanding-our-adrenal-system-norepinephrine
 

JÖRG LINDER AKTIV-TRAINING - www.aktiv-training.de

Mauerbergstraße 110

76534 Baden-Baden

Tel.: 07223 / 8004699

Mobil: 0177 / 4977232

Mail: info@aktiv-training.de

Fax: 07223 / 8005271 

Mobility-Walking: http://mobility-walking.blogspot.com
Personal Fitness: www.personal-fitness-4u.de

Glutens and Lectins: A Dangerous Dietary Duo

Artikel von:  Carolyn Pierini

Quelle: http://www.cpmedical.net/articles/glutens-and-lectins-a-dangerous-dietary-duo

Healthcare practitioners and patients alike are familiar with the increasing incidence and widening spectrum of gluten-related disorders. Although celiac disease is the national icon of gluten sensitivity, “atypical” presentations of the disease are rapidly becoming more common, as is the concept of non-celiac gluten sensitivity.

Presently, gluten sensitivity or intolerance might best be defined as a state of heightened immunological responsiveness in genetically susceptible people. Gluten-related issues represent another star in a constellation of growing public health concerns plaguing the U.S. population.

Gluten Sensitivity on the Rise

On the surface, celiac disease offers an easy model of epigenetic interplay—genetic predisposition (as HLA-DQ 2 or HLA-DQ 8) meets dietary trigger as wheat gluten. In reality, gluten sensitivity is more complex and better understood through the influence of diet and environment on epigenetic factors responsible for amplifying or silencing multiple genes.

Celiac disease represents one of at least 200 medical conditions, involving nearly every organ of the body, which are now being linked to gluten sensitivity.¹ In people with celiac disease, however, the overall clinical picture is more severe and is accompanied by the concurrence of tissue transglutaminase autoantibodies.² Transglutaminase enzymes are comprised of a family of eight enzymes found throughout the body, including prostate, skin, lungs, testicles and elsewhere. Because gluten triggers reactivity of this enzyme, all of these tissues can be potentially affected.
Moreover, newly published research, sometimes inconsistent, is unveiling the health effects of not only gluten, but other components of wheat and non-wheat grains. The fact is, modern-day grain science is in its infancy with regard to its impact on human health.

Given this, you, as clinicians, should understand why grain—and, in particular, wheat-related gastrointestinal and related disorders—may be increasing in your patient population.

Gluten Primer

The term “gluten” actually refers to a mixture of proteins found in many grains including wheat, spelt, rye and barley. Lectins, often included in this group, are technically not glutens, but are equally important proteins found in several food groups, including grains. Gluten literally means glue in Latin and is primarily composed of “storage” proteins called glutelins (glutenins) and prolamines (named for the high proline and glutamine content).

Gliadin is a type of prolamine and therefore a type of protein found in gluten. Gliadins constitute the majority of protein found in wheat and are thus far the most well-studied components of celiac disease.³ Different types of glutens and lectins can be found in grain.

Many people are also sensitive to glutens and lectins found in other non-wheat grain, particularly corn. Corn antibodies have been found in patients with celiac disease, Crohn’s disease and ulcerative colitis.⁴ Each seed or grain is composed of an outer bran layer, an endosperm that houses 90 percent of these prolamines, and the germ nucleus, which contains the developing plant embryo that will use the storage protein as a nitrogen source during germination.

The Wheat Has Changed

The rise of wheat sensitivity in general may reflect the convergence of many phenomena. The first point to consider is that modern commercial wheat bears little resemblance to the wheat that sustained our ancestors, which remained largely the same for 10,000 years... until recent years.
In the past few decades, agricultural science has and continues to use extensive hybridization, introgression and crossbreeding, making “synthetic” wheat plants that are more resistant to drought and pathogens. This has greatly increased dough properties but, more importantly, yield and profit.

Seeds are equipped with anti-nutrients such as lectin, gluten, phytates and enzymes to ensure protection from predation and resist digestion long enough to be spread across the land through excretion. Genetically selecting for anti-nutrients in an attempt to make the plant more resistant and less costly to grow appears to have added an increased threat to the gut immune system. New strains of wheat have undergone innumerable, drastic transformations in their genetic code yet, incredibly, no human or animal safety studies were performed to gauge their suitability for human or animal consumption.⁵

The hybridization process increases the quantity of genes for gluten proteins in modern wheat, including uniquely new gluten proteins not found in the parent plants. This process is likely contributing to gluten-related disease.^6-8 Perhaps it should not be surprising that there is a naturally protective immune response to ingesting more of something that is specifically designed to resist digestion.⁵ To quote one gluten researcher, “If we view celiac disease not as an unhealthy response to a healthy food but a healthy response to an unhealthy food, classical celiac symptoms like diarrhea may make more sense.”⁹

A Hidden Culprit

Also, beware of assuming that the primary causes of wheat intolerance are directly attributable to gluten alone. In previous articles, we’ve exposed wheat lectin for the serious problem it is. The wheat seed embryo contains a tiny lectin called wheat germ agglutinin (WGA). It is largely responsible for many pervasive ill-effects of wheat consumption. WGA is inflammatory and capable of inflicting direct damage to the majority of tissues in the body. It may help explain why degenerative conditions are associated with heavy wheat-consuming populations, even when wheat sensitivities appear uncommon.

By nature, lectins are resilient and resist degradation. Thus soaking, sprouting, cooking and fermenting were historically implemented in an effort to make grains such as wheat more digestible. Being a powerful insecticide for the germinating seed, WGA has not escaped the attention of biotech firms, which create genetically modified plants with built-in WGA pest control.

As with gluten, selective breeding for particular proteins has unfortunately led to proportionate increases in the WGA content of modern-day wheat. The list of WGA-induced disruptions to health is extensive and a reminder of how important the understanding of lectins is.
Eating wheat delivers WGA to the gastrointestinal tract, where it can cause mucosal injury and initiate inflammatory imbalance. WGA is small enough to gain even greater access systemically through a leaky gut. Anything that increases intestinal permeability, such as gluten or NSAIDs, increases the likelihood of systemic inflammatory imbalance created by WGA.

Although currently under-appreciated, WGA will eventually get its share of the spotlight. In fact, some studies propose that WGA may contribute in the pathogenesis of celiac disease. For example, one of the hallmarks of celiac disease (crypt hyperplasia) appears to be due to WGA’s ability to mimic the growth-promoting effects of epidermal growth factor.¹⁰ While serological antibody testing for WGA is currently not performed, in one test study, antibodies to WGA were demonstrated in the serum of celiac patients.¹¹

Our Love for Grains is Harming Us

A second point to consider is the sheer volume of ingested grain. In 2007, researchers in the United States, Italy and Great Britain hypothesized that the incidence of celiac disease was on the rise worldwide because wheat had become so prevalent in the Western diet that humans are actually overdosing on it.

It is true. Modern-day wheat is found in nearly everything we consume: cereal and flour-containing items, food and drink additives, grain-derived alcoholic beverages and even medications and cosmetics. This is exemplified by a 2005 study, which revealed that an unprecedented epidemic of symptomatic celiac disease in Sweden was at least half explained by an increase in infant exposure to comparatively large amounts of gluten as a result of national dietary recommendations and infant food content.¹²

Foundationally, microbial interactions in the gastrointestinal tract provide the cues for the development of regulated pro- and anti-inflammatory signals that promotes immunological tolerance.¹³ Doctors report that it is not uncommon to see patients with a conglomeration of gastrointestinal symptoms due to exposure to gluten and lectin of wheat and other grains.
The gliadin protein of gluten in all forms of wheat is capable of increasing intestinal permeability by triggering the release of zonulin, a protein that disassembles tight junctions between intestinal cells.¹⁴ Small intestine bacterial overgrowth (SIBO),¹⁵ gastroesophageal reflux disease¹⁶ and intestinal Candidiasis^17-18 are all associated with gluten intolerance. Additionally, a 2009 research review in the Journal of Gastroenterology suggests that patients with irritable bowel syndrome (IBS) be genetically tested for gluten sensitivity, as symptom resolution was observed with wheat elimination.

The health consequences of consuming wheat extend beyond the immune system, making diagnosis complicated for physicians. For example, wheat exorphins exhibit addictive effects on the brain and nervous system, and wheat’s high glucose-insulin effects contribute to cardiovascular disorders, diabesity, hormone imbalance and acne.^19-20 Complete removal of wheat or other grains is often necessary to deconstruct the clinical picture.

Gluten-Free Foods—Not Always the Perfect Answer

It is helpful to caution patients using “gluten-free” alternatives to replace the wheat proteins. In addition to being a source of insulin-provoking carbohydrate, alternatives such as sorghum, millet, corn, barley, oats or other grains and starches contain their own gluten/lectin proteins, which may cause problems in gluten-sensitive people.^21-23

The majority of the population is not aware that their present health and weight problems have anything to do with environmental factors, and certainly not the iconic “healthy” whole grains. After all, Americans are encouraged by government and private groups, advertising and elements of the healthcare community to eat them at every sitting.

There is a looming public perception that if you don’t have celiac disease, you don’t have a wheat problem. However, the belief that modern grain is a healthy food is just not sufficiently supported by facts. Grain education to change deeply held convictions about food will be a formidable challenge, but a worthy one.

Resources
1. http://theglutensyndrome.net/primer.pdf.
2. Sapone A, et al. BMC Medicine. 2011;9:23.
3. www.glutenfreesociety.org.
4. Davidson IW, et al. Clin Exp Immunol. 1979 Jan;35(1):147-8.
5. Davis W. Wheat Belly. New York: Rodale. 2011 pg 14-30.
6. Song X, et al. Theor Appl Genet. 2009;118(2):213-25.
7. Gao X, et al. Planta. 2010;23(2):245-50.
8. Van den Broeck HC, et al. Theor Appl Genet. 2010;121(8):1527-39.
9. http://www.greenmedinfo.com/page/dark-side-wheat-new-perspectives-celiac-disease-wheat-intolerance-sayer-ji.
10. http://www.glutenfreesociety.org/gluten-free-society-blog/wheat-germ-agglutinin-wga/.
11. Sollid LM, et al. Clin. Exp. Immunol. 1986;63(1):95-100.
12. Ivarsson A, et al. Best Pract Res Clin Gastroenterol. 2005;19(3):425-40.
13. Vitetta L, et al. Inflammopharmacology. 2012 Mar 18.[Epub ahead of print].
14. Drago S, et al. Scand J Gastroenterol. 2006;41:408-19.
15. Rubio-Tapia A, et al. J Clin Gastroenterol. 2009;43(2):157-61.
16. Levine A, et al. Scand J Gastroenterol.2009;44(12):1424-8.
17. Nieuwenhuizen WF, et al. Lancet. 2003;361(9375):2152-4.
18. Staab JF, et al. Science. 1999;283(5407):1535-8.
19. Rudman SM, et al. J Invest Dermatol. 1997;109(6):770-7.
20. Cordain L, et al. Arch Dermatol. 2002;138:1584-90.
21. Kristjansson G, et al. Gut. 2005;54:769-74.
22. Sandhu JS, et al. Gut. 1983;24:825-30.
23. Troncone R, et al. J Pediatr Gastroenterol Nutr. 1987;6(3):346-50.
 
Quelle: http://www.cpmedical.net/articles/glutens-and-lectins-a-dangerous-dietary-duo

JÖRG LINDER AKTIV-TRAINING - www.aktiv-training.de

Mauerbergstraße 110

76534 Baden-Baden

Tel.: 07223 / 8004699

Mobil: 0177 / 4977232

Mail: info@aktiv-training.de

Fax: 07223 / 8005271 

Mobility-Walking: http://mobility-walking.blogspot.com
Personal Fitness: www.personal-fitness-4u.de

Eggs distinctly modulate plasma carotenoid and lipoprotein

in adult men following a carbohydrate-restricted diet

 

Untersuchung von: MUTUNGI et al

 

 

Abstract

We previously reported that carbohydrate restriction (CR) (10-15% en) during a weight loss intervention lowered plasma triglycerides (TG) by 45% in male subjects (P<.001). However, those subjects with a higher intake of cholesterol provided by eggs (640 mg additional cholesterol, EGG group) had higher concentrations of high-density lipoprotein (HDL) cholesterol (P<.0001) than the individuals consuming lower amounts (0 mg of additional cholesterol, SUB group). The objectives of the present study were to evaluate whether CR and egg intake (1) modulate circulating carotenoids and (2) affect the concentrations of plasma apolipoproteins (apo), lipoprotein size and subfraction distribution.

CR decreased the number of large and medium very low-density lipoprotein cholesterol subclasses (P<.001), while small low-density lipoprotein (LDL) were reduced (P<.001). In agreement with these observations, a decrease in apo B (P<.01) was observed. In addition, CR resulted in a 133% increase in apo C-II and a 65% decrease in apo C-III (P<.0001).

Although an increase of the larger LDL subclass was observed for all subjects, the EGG group had a greater increase (P<.05). The EGG group also presented a higher number of large HDL particles (P<.01) compared to the SUB group. Regarding carotenoids, CR resulted in no changes in dietary or plasma alpha- or beta-carotene and beta-cryptoxanthin, while there was a significant reduction in both dietary and plasma lycopene (P<.001).

In contrast, dietary lutein and zeaxanthin were increased during the intervention (P<.05). However, only those subjects from the EGG group presented higher concentrations of these two carotenoids in plasma, which were correlated with the higher concentrations of large LDL observed in the EGG group.

These results indicate that CR favorably alters VLDL metabolism and apolipoprotein concentrations, while the components of the egg yolk favor the formation of larger LDL and HDL leading to an increase in plasma lutein and zeaxanthin.

Copyright 2010 Elsevier Inc. All rights reserved.

Quelle / Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/19369056


Kurz gesagt: Eier sind sehr gesund und nährstoffreich und erhöhen das sog. "gute Cholesterin" (HDL).

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Mauerbergstraße 110

76534 Baden-Baden

Tel.: 07223 / 8004699

Mobil: 0177 / 4977232

Mail: info@aktiv-training.de

Fax: 07223 / 8005271 

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