The Health Benefits of Dark Chocolate

Ask most women and they'll tell you that a good dose of chocolate really takes the edge off. It's not a joke. Science confirms that eating dark chocolate helps relieve emotional stress and also lowers blood pressure.

A study published in the Journal of Proteome Research found that consuming 40 grams (about 1.4 ounces) of dark chocolate daily for a period of two weeks reduced levels of the stress hormone cortisol and catecholamines, the fight-or-flight hormones.

The authors also concluded that their study "provides strong evidence that a daily consumption of 40 g of dark chocolate during a period of 2 weeks is sufficient to modify the metabolism of ... healthy human subjects."

Other studies had already suggested that chocolate relieved stress but this study provided evidence of the biochemical mechanism at work in relieving stress.
Chocolate lowers heart attack and stroke risk

Another study, published in the European Heart Journal, followed almost 20,000 Germans for 10 years and found that those who ate the most chocolate (an average of 7.5 grams a day – or a little more than a quarter of an ounce) had lower blood pressure and a 39% lower risk of having a heart attack or stroke compared to those who ate the least amount of chocolate (1.7 grams a day).

The lead researcher, Dr. Brian Buijsse, a nutritional epidemiologist at the German Institute of Human Nutrition commented that "...if people in the group eating the least amount of chocolate...increased their chocolate intake by six grams a day, 85 fewer heart attacks and strokes per 10,000 people could be expected to occur over a period of about ten years."

The investigators had hypothesized that because chocolate appears to have a positive effect on blood pressure, chocolate consumption would lower the risk of strokes and heart attacks and that is, in fact, what the study found.

Since chocolate comes from the cacoa plant (don't forget, it's a vegetable!) it contains flavanols, a type of antioxidant. These antioxidants resist or repair damage caused by free radicals which are formed by normal bodily processes and exertion, or by environmental contaminants.

The researchers believe that these flavanols may explain why chocolate seems to be good for people's blood pressure and heart health.

But remember, the more cacoa is processed, the more flavanols are destroyed, so the best source of chocolate antioxidants comes from dark chocolate. Look for chocolate with a cacoa content of 70% or more.

An even better source of flavanols is raw cacoa. Available as beans, nibs or powder, raw cacao has the highest concentration of antioxidants of any food.
Chocolate's Many Health Benefits

Stress relief and blood pressure regulation can now be added to a long list of rationales we can cite to justify indulging our chocolate cravings. Other health benefits of chocolate include:

• Improved blood flow by reducing platelet activation

• Prevention of cholesterol oxidation

• Improved insulin resistance

• Protection against coronary artery disease

• Improved cardiovascular health

There are, of course, other sources of antioxidants and other foods that are effective to lower blood pressure and relieve stress, but this research gives all stressed out chocoholics something to celebrate.
Source: http://www.greenmedinfo.com/blog/dark-chocolate-relieves-stress-and-lowers-blood-pressure

Yet Another Breakthrough in Medical Marijuana for Treating a Major Disease

Image: wikimedia.org

Elizabeth Renter | Natural Society

Several studies have been conducted focusing on marijuana’s potential to treat and ease symptoms associated with multiple sclerosis –  a disease that affects the central nervous system, often causing daily pain and difficulty moving, speaking, and swallowing. A new study adds even more insight into how MS patients can use marijuana, finding that cannabinoids within the vilified healing plant can help treat multiple sclerosis-like diseases by preventing inflammation in the brain and spinal cord.

The study, published in the Journal of Neuroimmune Pharmacology, set out to see if the anti-inflammatory compounds in marijuana known as tetrahydrocannabinol (THC) and cannabidiol (CBD) could be used to treat the inflammation associated with MS.

“Our study looks at how compounds isolated from marijuana can be used to regulate inflammation to protect the nervous system and its functions,” explains Dr. Ewa Kozela. “Inflammation is part of the body’s natural immune response, but in cases like MS, it gets out of hand.”

Using immune cells isolated from paralyzed mice, the researchers used THC or CBD to determine how these compounds affected the production of inflammatory markers, specifically one called interleukin 17 (IL-17). This inflammatory marker is strongly associated with MS and is harmful to nerve cells.

“The presence of CBD or THC restrains the immune cells from triggering the production of inflammatory molecules, and limits the molecules’ ability to reach and damage the brain and spinal cord,” wrote the researchers, finding the amount of IL-17 was far fewer in mice treated with the cannabis compounds.

This isn’t the first clue that marijuana could hold treatment options for inflammatory conditions. It’s already being used, legally or otherwise, by countless people for the treatment of pain and muscle stiffness associated with inflammation.

Read: 4 Natural Treatments for Multiple Sclerosis

Likewise, it isn’t the first study looking at the marijuana-MS connection. In 2011, a study found that CBD helps treat MS symptoms in mice by preventing immune cells from attacking nerve cells in the spinal cord. Another study coming to similar conclusions found that:

“The study met its primary objective to demonstrate the superiority of CE (cannabis extract) over placebo in the treatment of muscle stiffness in MS. This was supported by results for secondary efficacy variables. Adverse events in participants treated with CE were consistent with the known side effects of cannabinoids. No new safety concerns were observed”

Mice suffering from MS-symptoms were treated with CBD and went from being partially paralyzed and immobile to walking with a limp. These mice had less inflammation in their spinal cord than those untreated.

Research on CBD is particularly exciting because it offers the benefits of cannabis without the psychoactive effects. In other words, when isolated from other compounds in the plant, it won’t get you “high”. Add to this the fact that there are few, if any, known side effects of treating with CBD and this and other studies are extremely promising.

“When used wisely, cannabis has huge potential,” Dr Kozela says. “We’re just beginning to understand how it works.”

Source: naturalsociety.com
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The Evidence Against Aspirin And For Natural Alternatives

As far back as the 5^th century BC, the Greek physician Hippocrates wrote about the use of a bitter powder extracted from willow bark that reduced fevers and eased aches and pains.  Native Americans also used an infusion of willow bark for similar purposes. What was this remarkable "healing" principle within the bark that relieved disease?
Known as salicylic acid (from the Latin salix, willow tree), this pain-killing compound is widely distributed throughout plants, where it functions as a hormone.  The more vegetables and fruits you consume, the more likely you are to have a physiologically significant concentration of salicylic acid in your blood.  This is why, for instance, vegans and vegetarians generally have higher levels than most grain- and meat-based consumers. [1]
The chemical acetyl-salicylic acid, commonly known as aspirin, is a synthetic form of salicylic acid, a compound which is formed when salicin, a bitter compound naturally found within plants like white willow bark, is broken down within the human body. Salicylic acid can also be synthesized endogenously from benzoic acid, and its urinary metabolite, salicyluric acid, has been found to overlap levels in patients on low-dose aspirin regimens. Cell research indicates that salicylic acid compounds (known as salicyclates) actually compare surprisingly well to aspirin in reducing inflammatory activity.[2]
While salicylic acid is found naturally in plants as salicylates, acetyl-salicylic acid does not exist in nature, is not formed as byproduct of natural salicylate consumption,[3] and is produced only through industrial synthesis. For example, this is one method of synthesis:

Also, the chemical modification of natural salicylic acid with an acetyl group results in the acetylation of hemoglobin,[5] essentially chemically altering the natural structure-function of our red blood cells and subsequent hemodynamics. In essence, aspirin, a semi-synthetic compound, makes the blood tissue itself semi-synthetic.
This could be why aspirin has been linked to such a broad range of unintended adverse health effects, including but not limited to:

• Gastric Ulcer [6]
• Hearing Loss/Tinnitus[7] [8] [9] [10] [11] [12]
• Cerebral Bleeding [13]
• Influenza Mortality [14]
• Reye Syndrome
• Crohn's Disease[15]
• Helicobacter Pylori Infection[16]

We have a section on our database dedicated to indexing the under-reported, unintended adverse effects of aspirin, related to 50 diseases which can be viewed here: Aspirin Side Effects. We also have a section which indexes research on natural compounds studied to prevent, reduce or reverse Aspirin-Induced Toxicity.
According to US EPA statistics, up to 500 thousand pounds of the chemical was produced in the United States in 1998 alone.[17]  Millions the world over take it for pain relief, including your typical headache, but also for the prevention of heart attacks and stroke.
Taking a "baby aspirin," i.e. an 81 mg dose, is considered safer -- which it is relative to a 325 mg "adult dose" – but is known to cause widespread and significant gastroduodenal damage.  A study published in 2009 in the journal Currrent Medical Research & Opinion titled, "Gastroduodenal toxicity of low-dose acetylsalicylic acid: a comparison with non-steroidal anti-inflammatory drugs," found the following:

Data suggest that ASA causes significant gastroduodenal damage even at the low doses used for cardiovascular protection. These effects (both systemic and possibly local) may be pharmacodynamically distinct from the gastroduodenal toxicity seen with NSAIDs.[18]

Another 2009 study found that 80% of healthy individuals who uses short-term (14 days), low-dose aspirin experienced small intestinal toxicity, including small bowel mucosal breaks and mucosal inflammation. [19]  Also, there are reports of esophageal mucosal lesions induced by low-dose aspirin and other antiplatelet medications mimicking esophageal malignancy.[20]
Data suggest that ASA [aspirin]causes significant gastroduodenal damage even at the low doses used for cardiovascular protection. These effects (both systemic and possibly local) may be pharmacodynamically distinct from the gastroduodenal toxicity seen with NSAIDs.[21]
Hemorrhagic side effects, in fact, are one of the greatest challenges facing those who use aspirin for prevention.  By taking a drug which prevents clotting, aspirin can work too well, resulting in bleeding disorders or events, some of which may be life-threatening, even lethal.
So, given the serious, unintended adverse health effects of aspirin therapy, what are some evidence-based natural alternatives?

Researched aspirin alternatives include:

• Pycnogenol: A human study published in 1999 in the journal Thrombotic Research found that pycnogenol was superior (i.e. effective at a lower dosage) to aspirin at inhibiting smoking-induced clotting, without the significant (and potentially life-threatening) increase in bleeding time associated with aspirin use.[22] The abstract is well worth reading in its entirety:

The effects of a bioflavonoid mixture, Pycnogenol, were assessed on platelet function in humans. Cigarette smoking increased heart rate and blood pressure. These increases were not influenced by oral consumption of Pycnogenol or Aspirin just before smoking. However, increased platelet reactivity yielding aggregation 2 hours after smoking was prevented by 500 mg Aspirin or 100 mg Pycnogenol in 22 German heavy smokers. In a group of 16 American smokers, blood pressure increased after smoking. It was unchanged after intake of 500 mg Aspirin or 125 mg Pycnogenol. In another group of 19 American smokers, increased platelet aggregation was more significantly reduced by 200 than either 150 mg or 100 mg Pycnogenol supplementation. This study showed that a single, high dose, 200 mg Pycnogenol, remained effective for over 6 days against smoking-induced platelet aggregation. Smoking increased platelet aggregation that was prevented after administration of 500 mg Aspirin and 125 mg Pycnogenol.

Pycnogenol also has about as many "side benefits" as aspirin has side effects. You can view them on our pycnogenol research page.

• Policosanol: Already well-known for its ability to modulate blood cholesterol levels as effectively as statins, but without their notorious side effects, this sugar cane wax extract has been found to be as effective as aspirin at inhibiting clotting, but at a lower, safer dose.[23]

There are actually a broad range of natural compounds, including foods and spices, with demonstrable platelet-inhibiting activity. You will find a list of them on our natural platelet inhibitor pharmacological actions page. Another highly relevant section on our website is the Thrombosis Research page.
Ultimately, however, cardiovascular disease and heart attacks, for instance, are not caused by a lack of aspirin. To explore further the research related to preventing and treating heart disease naturally, visit our Health Guide: Heart Health.

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RESOURCES

[1] C J Blacklock, J R Lawrence, D Wiles, E A Malcolm, I H Gibson, C J Kelly, J R Paterson. Salicylic acid in the serum of subjects not taking aspirin. Comparison of salicylic acid concentrations in the serum of vegetarians, non-vegetarians, and patients taking low dose aspirin. J Clin Pathol. 2001 Jul ;54(7):553-5. PMID: 11429429

[2] Pharmacokinetics of aspirin and salicylate in relation to inhibition of arachidonate cyclooxygenase and antiinflammatory activity. Proc Natl Acad Sci U S A. 1987 Mar ;84(5):1417-20. PMID: 3103135

[3] P L Janssen, M B Katan, W A van Staveren, P C Hollman, D P Venema. Acetylsalicylate and salicylates in foods. Cancer Lett. 1997 Mar 19 ;114(1-2):163-4. PMID: 9103279

[4] [Ullmann's Encyclopedia of Industrial Chemistry. 6th ed.Vol 1: Federal Republic of Germany: Wiley-VCH Verlag GmbH & Co. 2003 to Present, p. V31 725 (2003)]

[5] K R Bridges, G J Schmidt, M Jensen, A Cerami, H F Bunn. The acetylation of hemoglobin by aspirin. In vitro and in vivo. J Clin Invest. 1975 Jul;56(1):201-7. PMID: 237937

[6] Gastroduodenal toxicity of low-dose acetylsalicylic acid: a comparison with non-steroidal anti-inflammatory drugs. Curr Med Res Opin. 2009 Nov;25(11):2785-93. PMID: 19788350

[7] Analgesic use and the risk of hearing loss in men. Am J Med. 2010 Mar;123(3):231-7. PMID: 20193831

[8] Hearing loss in a woman on aspirin: the silent pharmacokinetic parameter. Ther Drug Monit. 2009 Feb;31(1):1-2. PMID: 19155962

[9] Too much of a good thing: long-term treatment with salicylate strengthens outer hair cell function but impairs auditory neural activity. Hear Res. 2010 Jun 14;265(1-2):63-9. Epub 2010 Mar 6. PMID: 20214971

[10] Long-term administration of salicylate enhances prestin expression in rat cochlea. Int J Audiol. 2009 Jan;48(1):18-23. PMID: 19173110

[11] Behavioral assessment and identification of a molecular marker in a salicylate-induced tinnitus in rats. Neuroscience. 2010 Feb 17;165(4):1323-32. Epub 2009 Dec 1. PMID: 19958810

[12] Salicylate-induced degeneration of cochlea spiral ganglion neurons-apoptosis signaling. Neuroscience. 2010 Jun 16;168(1):288-99. Epub 2010 Mar 15. PMID: 20298761

[13] Predictors of mortality in trauma patients with intracranial hemorrhage on preinjury aspirin or clopidogrel. J Trauma. 2008 Oct;65(4):785-8. PMID: 18849791

[14]  The effect on mortality of antipyretics in the treatment of influenza infection: systematic review and meta-analysis. J R Soc Med. 2010 Oct;103(10):403-11. PMID: 20929891

[15] Aspirin in the aetiology of Crohn's disease and ulcerative colitis: a European  prospective cohort study. Aliment Pharmacol Ther. 2011 Sep ;34(6):649-55. Epub 2011 Jul 26. PMID: 21790683

[16] Helicobacter pylori infection in bleeding peptic ulcer patients after non-steroidal antiinflammatory drug consumption. World J Gastroenterol. 2011 Oct 28 ;17(40):4509-16. PMID: 22110282

[17] Toxnet.nlm.nih.gov, Hazardous Substances Data Base: Aspirin

[18] Neville D Yeomans, Christopher J Hawkey, Wayne Brailsford, Jørgen Naesdal. Gastroduodenal toxicity of low-dose acetylsalicylic acid: a comparison with non-steroidal anti-inflammatory drugs. Curr Med Res Opin. 2009 Nov;25(11):2785-93. PMID: 19788350

[19] Incidence of small bowel injury induced by low-dose aspirin: a crossover study using capsule endoscopy in healthy volunteers. Digestion. 2009;79(1):44-51. Epub 2009 Feb 26. PMID: 19246922

[20] Esophageal mucosal lesion with low-dose aspirin and prasugrel mimics malignancy: a case report. World J Gastroenterol. 2011 Sep 21 ;17(35):4048-51. PMID: 22046096

[21] Gastroduodenal toxicity of low-dose acetylsalicylic acid: a comparison with non-steroidal anti-inflammatory drugs. Curr Med Res Opin. 2009 Nov;25(11):2785-93. PMID: 19788350

[22] M Pütter, K H Grotemeyer, G Würthwein, M Araghi-Niknam, R R Watson, S Hosseini, P Rohdewald. Inhibition of smoking-induced platelet aggregation by aspirin and pycnogenol. Thromb Res. 1999 Aug 15;95(4):155-61. PMID: 10498385

[23] M L Arruzazabala, S Valdés, R Más, D Carbajal, L Fernández. Comparative study of policosanol, aspirin and the combination therapy policosanol-aspirin on platelet aggregation in healthy volunteers. Pharmacol Res. 1997 Oct;36(4):293-7. PMID: 9425618

 Source: http://www.greenmedinfo.com/blog/aspirin-dangers-and-natural-evidence-based-alternatives

Herbicide and Pesticide Exposure Linked to Parkinson's Disease

A recent study from UCLA has confirmed that exposure to the herbicide Paraquat is linked with a heightened risk of Parkinson's disease. This combines with other research that has found other chemicals used on our foods and landscapes significantly increase the risk of Parkinson's.
The researchers, from UCLA's Fielding School of Public Health, studied 357 Parkinson's disease cases along with 754 control subjects - adults from Central California. The researchers determined increased exposure to the herbicide Paraquat through geographic mapping linking their home locations to agricultural use of the chemical on farms. Those living closer to farms that sprayed the herbicide were found to have a 36% increased risk of Parkinson's.

However, those who experienced a head injury combined with increased Paraquat exposure tripled their chances of having Parkinson's disease.

Researchers from Mexico's Unidad de Medicina Familiar also studied cases of Parkinson's together with exposure to the herbicide Paraquat among Mexican workers. They also found a positive association between exposure to this chemical and Parkinson's disease.
Paraquat is N,N′-dimethyl-4,4′-bipyridinium dichloride.

Learn safe detoxification methods.

A study published last year from the Louvain Center for Toxicology and Applied Pharmacology of Brussels' Catholic University of Louvain concluded that pesticide exposure was also significantly linked to Parkinson's. Here the researchers analyzed and calculated the data from twelve peer-reviewed clinical studies that investigated Parkinson's disease together with pesticide exposure. They collected research conducted between 1985 and 2011.

The meta-analysis found that all twelve studies individually and collectively established a link between pesticide exposure and Parkinson's disease.

After calculating meta-data ratios and relative risk, the researchers found that Parkinson's disease incidence as diagnosed by a neurologist was more than two-and-a-half times for those exposed to more pesticides compared to those less exposed. Other risk calculations showed the increased incidence of Parkinson's disease to range from nearly double to 28% - which was the average of all cases studied.

But when the research focused upon farm workers involved in the growing of bananas, pineapples or sugarcane, the incidence of Parkinson's disease more than doubled that of lower-exposure individuals.

The researchers concluded:

The present study provides some support for the hypothesis that occupational exposure to pesticides increases the risk of Parkinson's disease.

Since this review study came out, other studies have investigated some of the worst pesticides, and the mechanisms by which they produce Parkinson's disease.

A study from Korea's Yonsei University studied the broad spectrum pesticide Rotenone – and how it damages nerve cells and pathways. The researchers found that Rotenone induces cell death in a process called with G2/M cell cycle arrest. G2/M cell cycle arrest blocks the process of mitosis that enables cells and their DNA to replicate – and more importantly among nerve cells - repair any DNA damage. Thus the insecticide basically blocks the ability of the nerve cell to repair itself – lending to the cells eventually dying off or mutating.


Meanwhile, researchers from UCLA's David Geffen School of Medicine found that the fungicide Benomyl will block multiple cell processes. One of these blocks the production of aldehyde dehydrogenase (ALDH). This increases the dopamine metabolite 3,4-dihydroxyphenylacetaldehyde, which produces degeneration among neurons associated with the production of dopamine. One of the central dopamine-producing centers exists in the brain – the substantia nigra located within the midbrain.

When the nerve cells located in this region die off or become otherwise deranged, they stop producing dopamine and other neurotransmitters that help control coordination and movement throughout the body. A lack of these neurotransmitters will produce the shakiness and eventual loss of coordination characteristic amongst progressed Parkinson's patients.
Is eating non-organic food worth risking the health of not only our children and family? Is it worth risking the health of farm workers who are exposed to these toxic chemicals every day? And what about spraying pesticides and herbicides around the house?

Written by Case Adams, Naturopath

References

• Ryu HW, Oh WK, Jang IS, Park J. Amurensin G induces autophagy and attenuates cellular toxicities in a rotenone model of Parkinson's disease. Biochem Biophys Res Commun. 2013 Mar 29;433(1):121-6.
• Mostafalou S, Abdollahi M. Pesticides and human chronic diseases: evidences, mechanisms, and perspectives. Toxicol Appl Pharmacol. 2013 Apr 15;268(2):157-77.
• León-Verastegui AG. Parkinson's disease due to laboral exposition to paraquat. Rev Med Inst Mex Seguro Soc. 2012 Nov-Dec;50(6):665-72.
• Fitzmaurice AG, Rhodes SL, Lulla A, Murphy NP, Lam HA, O'Donnell KC, Barnhill L, Casida JE, Cockburn M, Sagasti A, Stahl MC, Maidment NT, Ritz B, Bronstein JM. Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease. Proc Natl Acad Sci U S A. 2013 Jan 8;110(2):636-41.
• Pan-Montojo F, Schwarz M, Winkler C, Arnhold M, O'Sullivan GA, Pal A, Said J, Marsico G, Verbavatz JM, Rodrigo-Angulo M, Gille G, Funk RH, Reichmann H. Environmental toxins trigger PD-like progression via increased alpha-synuclein release from enteric neurons in mice. Sci Rep. 2012;2:898.
• Lee PC, Bordelon Y, Bronstein J, Ritz B. Traumatic brain injury, paraquat exposure, and their relationship to Parkinson disease. Neurology. 2012 Nov 13;79(20):2061-6.
• Van Maele-Fabry G, Hoet P, Vilain F, Lison D. Occupational exposure to pesticides and Parkinson's disease: a systematic review and meta-analysis of cohort studies. Environ Int. 2012 Oct 1;46:30-43.
• Lundius EG, Stroth N, Vukojević V, Terenius L, Svenningsson P. Functional GPR37 trafficking protects against toxicity induced by 6-OHDA, MPP+ or rotenone in a catecholaminergic cell line. J Neurochem. 2013 Feb;124(3):410-7.

 Source: http://www.greenmedinfo.com/blog/herbicide-and-pesticide-exposure-linked-parkinsons-disease-0