I had to chuckle when I saw today's edition of the Huffington Post showing that black cumin "MAY" treat pancreatic cancer and then quoting a study done at Thomas Jefferson University by Dr. Hwyda A. Arafat, MD, PhD, associate professor, departments of surgery and pathology, anatomy and cell biology. This study was done in 2007 and it is just now intriguing them. Is this not a give me a break moment.
There have been literally hundreds of papers written on the positive results done in this study and how miraculous this wonderful little black seed is. It was literally able to reduce the pancreatic tumors when no other medical treatment has been successful.
This little black seed has been used for thousands of years for everything from headaches to asthma and it is just now intriguing the Huffington Post? Excuse my ignorance but it should of intrigued the Huffington Post in 2007. As I pause for a moment to smile at the article, I again noticed that the author offered no hint of how to treat the cancers, only that it "May" help.
What is the point of reporting that a potential miracle herb has been created and then never give the way to treat the cancer. Black cumin is also called Nigella Sativa and kalonji. You can get it in several ways and finding a good source is pretty easy. Here are some links:
Black Cumin oil and seeds
The proper way to treat cancer is with a teaspoon of oil mixed with raw honey or juice 3 times a day. In addition the remedy calls for eating 4 cloves of garlic once a day.
It should be noted that in order for black cumin to work, you need to take it regularly, not just when you are sick. For further information on these wonderful seeds read here.
So if we smile a little today about the Huffington Post just now discovering the healing benefits of black cumin, let us all reflect as to the correct place to look for health news. That place is right here with Barbi Trejo's world.
Wednesday, June 30, 2010
Friday, June 11, 2010
New Potential Cause of Alzheimer's Disease
THURSDAY, June 10 (HealthDay News) -- Researchers have discovered that the mutation of a gene associated with early onset Alzheimer's may block a key recycling process necessary for brain cell survival -- a finding that points the way to possible treatment for the disease.
When it's working properly, this gene -- called presenilin 1 (PS1) -- performs a crucial house-cleaning service by helping brain cells digest unwanted, damaged and potentially toxic proteins. But in its mutated form, the gene fails to help cells recycle these potential toxins, suggesting an explanation for the damage to the brain characteristic of Alzheimer's disease.
"We believe we have identified the principal mechanism by which mutations of PS1 cause the most common genetic form of Alzheimer's disease," study co-author Dr. Ralph A. Nixon, professor in the departments of psychiatry and cell biology as well as director of NYU's Center of Excellence on Brain Aging and the Silberstein Alzheimer's Institute, said in a university news release.
"Presently, no effective treatment exists to either slow or prevent the progression of Alzheimer's disease," added Nixon, also director of the Center for Dementia Research at the Nathan S. Kline Institute for Psychiatric Research in New York City. "This discovery has the potential of identifying such a treatment."
Mutations of the PS1 gene have previously been thought to increase production of the toxic beta amyloid protein that appears to collect in the brains of Alzheimer's patients. In turn, scientists have theorized that by preventing amyloid deposits from accumulating, they might be able to slow or prevent Alzheimer's progression.
However, the current investigation into PS1 behavior side-steps this potential scenario -- without questioning its validity -- by focusing on the possibility that abnormal PS1 function may cause cell death unconnected to beta amyloid buildup. PS1 mutations and other factors could, therefore, promote Alzheimer's in entirely different ways, the team said.
"There is an urgent need now to see Alzheimer's disease as [caused by multiple factors] and approach the treatment from that perspective," said Nixon, who added that the current finding opens up a new target for Alzheimer's interventions down the road. Focusing on how to restore brain cells' normal recycling system is a promising therapeutic approach, he said, since its disruption appears to promote Alzheimer's.
Nixon and his colleagues report their findings in the June 10th online issue of the journal Cell.
When it's working properly, this gene -- called presenilin 1 (PS1) -- performs a crucial house-cleaning service by helping brain cells digest unwanted, damaged and potentially toxic proteins. But in its mutated form, the gene fails to help cells recycle these potential toxins, suggesting an explanation for the damage to the brain characteristic of Alzheimer's disease.
"We believe we have identified the principal mechanism by which mutations of PS1 cause the most common genetic form of Alzheimer's disease," study co-author Dr. Ralph A. Nixon, professor in the departments of psychiatry and cell biology as well as director of NYU's Center of Excellence on Brain Aging and the Silberstein Alzheimer's Institute, said in a university news release.
"Presently, no effective treatment exists to either slow or prevent the progression of Alzheimer's disease," added Nixon, also director of the Center for Dementia Research at the Nathan S. Kline Institute for Psychiatric Research in New York City. "This discovery has the potential of identifying such a treatment."
Mutations of the PS1 gene have previously been thought to increase production of the toxic beta amyloid protein that appears to collect in the brains of Alzheimer's patients. In turn, scientists have theorized that by preventing amyloid deposits from accumulating, they might be able to slow or prevent Alzheimer's progression.
However, the current investigation into PS1 behavior side-steps this potential scenario -- without questioning its validity -- by focusing on the possibility that abnormal PS1 function may cause cell death unconnected to beta amyloid buildup. PS1 mutations and other factors could, therefore, promote Alzheimer's in entirely different ways, the team said.
"There is an urgent need now to see Alzheimer's disease as [caused by multiple factors] and approach the treatment from that perspective," said Nixon, who added that the current finding opens up a new target for Alzheimer's interventions down the road. Focusing on how to restore brain cells' normal recycling system is a promising therapeutic approach, he said, since its disruption appears to promote Alzheimer's.
Nixon and his colleagues report their findings in the June 10th online issue of the journal Cell.
Tuesday, June 1, 2010
Green tea for your belly
Green tea for your bellyBelly fat is not just unbecoming, it is dangerous to your long term, health and well being. When excessive fat is stored inside your abdominal cavity it has devastating metabolic consequences.
This intra abdominal adipose tissue continually dumps fatty acids into the bloodstream poisoning your muscles so they become unresponsive to the normal action of insulin.
That means your insulin, sugar, cholesterol, and blood pressure levels go up, predisposing you to high blood pressure diabetes heart disease and even some forms of cancer.
Finding a way selectively burn this toxic belly fat has been the holy grail of scientists and dieters alike, but to has proved to be an elusive goal.
Evolving evidence points to green tea and its components like theanine and catechins as at least part of the answer to this problem.
You will need to drink about three to four cups of either caffeinated or decaffeinated green tea per day to see the full benefits including weight loss, increased metabolism and a shrinking waistline.
Green tea for your belly
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