In a Study scientists have discovered that Happiness born out of purposeful Life ,happiness born out of cherished and realized Goals showed very favorable gene-expression profiles in their immune cells.
Happiness and Genes.
In simpler terms, your Genes develop better qualitatively than the Genes that have been coded in people who had relatively high levels of hedonistic well-being ” the type of happiness’ that comes from consummation self-gratification .(hedonistic or eudaimonic well-being. Hedonic well-being is defined as happiness gained from seeking pleasure; eudaimonic well-being is that gained by having a deep sense of purpose and meaning in life.
Genes become better with the Happiness that comes from having a deep sense of purpose and meaning in life.
These people have better Antiviral properties,
It goes to prove the age-old wisdom that Happiness that comes out of pursuing Ideals and finding/attempt to finding of the meaning of Life is better for the Organism.
The happiness of higher order comes with contentment that is born of Maturity and the realization that there are things that we can not control and yet we should try to seek the Truth or the meaning of Life.
One may note that it is the attempt at the realization or the Goal increases and consequently changes the Genes for the better, not the actual realization of the Ideal!
So Hinduism’s assertion that though Human Beings are limited, they can attempt at Realization of the Reality and in the process would become Happy in the Philosophical Sense.
This is the purpose of Yoga as well.
Story:
Steven Cole, a professor of medicine at the University of California, Los Angeles has spent the last 10 years trying to figure out what makes the human genome tick. Specifically, how our genes respond to stress, misery, fear and various other forms of negative psychology.
But in his latest foray, Cole and his colleagues decided to look on the brighter side; they set out to see what biological implications happiness has on genes.
The researchers assessed and took blood samples from 80 healthy adults who were classified as having either hedonic or eudaimonic well-being. Hedonic well-being is defined as happiness gained from seeking pleasure; eudaimonic well-being is that gained by having a deep sense of purpose and meaning in life.
The team then mapped the different biological affects of both camps by using a gene-expression profile known as conserved transcriptional response to adversity (CTRA). The CTRA is a shift associated with an increase of inflammation and a decrease inantiviral activities with the genes, reports Medical News Today.
The study showed that people who had high levels of eudaimonic well-being showed favorable profiles with low levels of inflammatory gene expression and exhibited a strong expression of antiviral and antibody genes. For the pleasure seekers, the opposite was true; those with high levels of hedonic well-being showed an adverse gene-expression profile, giving high inflammation and low antiviral/antibody expression.
The differences in genes persisted even though both groups were happy and felt comparable amounts of well-being.”
Actress and activist Angelina Jolie’s recent decision to have a preventive double mastectomy highlights the difficult choices facing women who find out they have a high risk for breast cancer because of their genes.
Although relatively rare, mutations in the BRCA1 and BRCA2 genes raise the risk of breast cancer by as much as 80%, experts say. The mutations also raise the risk of ovarian cancer.
Jolie describes in a New York Times op-ed piece why she decided to go through with the surgery. At 37, the mother of six wants to stay healthy and active for her family — and to reassure them that she is doing everything possible to avoid the disease that took her mother’s life: cancer.
“I wanted to write this to tell other women that the decision to have a mastectomy was not easy,” Jolie writes. “But it is one that I am very happy I made. My chances of developing breast cancer have dropped from 87 percent to under 5 percent. I can tell my children that they don’t need to fear they will lose me to breast cancer.”….
Angelina Jolie.
I think most breast cancer experts would agree that the choice is really the patient’s to make, and I really want to emphasize, it is a choice.
Preventive mastectomy is one very excellent choice. But another choice women can consider when they know they carry a BRCA mutation is early detection. And that comes with more active screening.
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If a woman knows she has a BRCA mutation and does not want to have a mastectomy, a good alternative is to have a mammogram and a breast MRI every year.
You can do both at once or choose to alternate. [For my patients] I choose to alternate, doing one test every 6 months.
It’s not as effective because by definition you are picking up cancer as it develops. But it is effective at picking up cancer at a very early stage.
If a woman has a preventive double mastectomy, what are the benefits and risks?
In women at higher risk — those with BRCA mutations — preventive surgery can reduce the risk of breast cancer by 90%. If the [increased] risk is 80% as it is for many BRCA carriers, this can reduce the risk of breast cancer by 90%.
In other words, this can reduce the risk to that lower than the general population. The risks [of the mastectomy] are not that great. Most women having preventive mastectomies are younger patients, and many choose to get reconstruction. A lot of the risk has to do with the implants, like implant complications, or other risks [linked with surgery] such as infections or bleeding.
Who should consider BRCA testing?
The women who should absolutely consider it are those who themselves have had a triple-negative breast cancer, the kind associated with BRCA mutations, at an early age, under 45, people who have had both ovarian and breast cancer in family members, and people who have breast cancer in the family and are of Ashkenazi Jewish descent.
What is involved in testing for BRCA mutations?
It is a simple blood test, or they can swab the inside of your cheek. The best way to get this test is to go for counseling from a genetic counselor. Have them talk to you about the possibility of testing positive. Women really need to be counseled about what this means, what the results mean, what their risk is, and then to make the decision about whether to get the test.
If you only get tested for the three most common mutations, results take about 2 weeks. The more comprehensive test, where they do gene sequencing, can take a month.
This along with the metal pressures being built up by the scams of Pedophile Priests and Gay Issues hastened his decision to abdicate as a Pope in Seven Centuries .
“One cannot fail to be moved by the 85-year-old leader’s recognition that he no longer possesses sufficient “strength of mind and body,” leaving him unable “to adequately fulfill the ministry entrusted to me.”
He made the announcement on February 11. He will leave his post on February 28. Shortly thereafter, a conclave of cardinals, the top leaders of the Church, will meet to select a new pope from among themselves.
Benedict XVI’s resignation is a witness to aging and human mortality.
Pope Benedict XVI.
No matter what our beliefs about religion, this simple but profound action gives us pause to reflect on how we can accept our own human limitations.
For the Huntington’s disease community, it also provides an opportunity to recall the ethical, social, and spiritual dimensions of our collective struggle.”
Huntington’s disease is caused by a genetic defect on chromosome 4. The defect causes a part of DNA, called a CAG repeat, to occur many more times than it is supposed to. Normally, this section of DNA is repeated 10 to 28 times. But in persons with Huntington’s disease, it is repeated 36 to 120 times.
As the gene is passed down through families, the number of repeats tend to get larger. The larger the number of repeats, the greater your chance of developing symptoms at an earlier age. Therefore, as the disease is passed along in families, symptoms develop at younger and younger ages.
There are two forms of Huntington’s disease.
The most common is adult-onset Huntington’s disease. Persons with this form usually develop symptoms in their mid 30s and 40s.
An early-onset form of Huntington’s disease accounts for a small number of cases and begins in childhood or adolescence.
If one of your parents has Huntington’s disease, you have a 50% chance of getting the gene for the disease. If you get the gene from your parents, you will develop the disease at some point in your life, and can pass it onto your children. If you do not get the gene from your parents, you cannot pass the gene onto your children.
Symptoms
Behavior changes may occur before movement problems, and can include:
Behavioral disturbances
Hallucinations
Irritability
Moodiness
Restlessness or fidgeting
Paranoia
Psychosis
Abnormal and unusual movements include:
Facial movements, including grimaces
Head turning to shift eye position
Quick, sudden, sometimes wild jerking movements of the arms, legs, face, and other body parts
There is no cure for Huntington’s disease, and there is no known way to stop the disease from getting worse. The goal of treatment is to slow down the symptoms and help the person function for as long and as comfortably as possible.
Medications vary depending on the symptoms.
Dopamine blockers may help reduce abnormal behaviors and movements.
Drugs such as amantadine and tetrabenazine are used to try to control extra movements.
There has been some evidence to suggest that co-enzyme Q10 may also help slow down the course of the disease, but it is not conclusive.
Depression and suicide are common among persons with Huntington’s disease. It is important for all those who care for a person with Huntington’s disease to monitor for symptoms and treat accordingly.
As the disease progresses, the person will need assistance and supervision, and may eventually need 24-hour care.
Cancer is such that any attempt to glean an insight into its treatment is often visited by tragedy.
However a step ahead.
English: Gross appearance of the cut surface of a pneumonectomy specimen containing a lung cancer, here a Squamous cell carcinoma (the whitish tumor near the bronchi). (Photo credit: Wikipedia)
But isn’t the price great?
Yet these tragedies can not be avoided.
Let’s Pray that the price paid is compensated by the Greatest Good.
Story:
In 2005, after she had spent more than a year going from specialist to specialist, a dermatologist figured it out. Mrs. McDaniel, then 62, had Sezary syndrome, a rare T cell lymphoma, in which white blood cells become cancerous and migrate to the skin. All her doctors could tell her was that the disease was incurable, that there was no standard treatment, and that on average patients at her stage die within a few years.
“Of course I was shocked,” Mrs. McDaniel said in an interview last September.
She wept that day as her husband drove her home. And she asked God to help her cope.
Before cancer, she had had a vibrant life, hiking in the mountains, traveling the world, entertaining her wide network of friends. Her disease destroyed all of that. She could not even enjoy her luxuriant garden because sun on her inflamed skin was agony.
Although there is no standard treatment, for five years chemotherapy held her disease at bay. But in the summer of 2010, she got worse, much worse, with hundreds of tumorspopping up under her skin. Some grew as large as kiwi fruits and split open.
Her son, Dr. McDaniel, decided he would orchestrate the use of the most advanced techniques of gene sequencing and analysis to take on her cancer. Because of his job — he works for Illumina, a company that does DNA sequencing — Dr. McDaniel had read scientific reports and gone to medical conferences where he heard talks on whole genome sequencing. He noticed that the patients all seemed to have rare cancers.
“Every time I heard one of those stories, I thought, ‘That’s my mom,’ ” he said.
For now, there are not many drugs that can target specific gene mutations in cancer cells.
But the hope is that when more is known and more drugs are developed, doctors will treat cancer by blocking several major genes at once. With several escape routes barred, the cancer will not be able to break free of the drugs stopping its growth.
……..
He worked all night, found a paper by scientists who had deliberately fused those very genes and discovered that, yes, the genetically altered T cells had their growth signals reversed.
At 5:45 a.m. Dr. McDaniel sent an e-mail to his collaborators.
“I was so tired at that point that, believe it or not, I had forgotten about the drug,” he said.
He fell asleep and woke at 11 a.m., rushing back to his computer. The melanoma drug he had forgotten in his exhaustion should hit that target. And that could stop his mother’s cancer from growing. “My jaw was just hanging open,” Dr. McDaniel said. “The implications were so tantalizing that I didn’t dare believe them.”
A Remarkable Turnaround
Mrs. McDaniel had her first infusion on July 28, and the result seemed remarkable. Her oncologist, Dr. Gohmann, was overwhelmed. Her son, who had been terrified that he and the doctors might have made a terrible mistake, was overjoyed.
Mrs. McDaniel, who had not left her house for several months except to see her doctors, began going to movies and restaurants every day.
On Sept. 2, she and her husband went to the Heirloom Restaurant, in the middle of horse country, to celebrate their 50th wedding anniversary.
She had given away so many of her clothes when she thought she was dying that she puzzled over what to wear. She had a favorite blouse that was loosefitting and comfortable, but Mr. McDaniel recalled, “It was long gone.” She could not drink wine with the medicines she was taking, so she and her husband sipped iced tea in the quiet dining room.
“We reminisced, but also talked about the future as we hoped it would be,” Mr. McDaniel said.
But the reprieve lasted only weeks. By the end of September, the cancer was back.
Dr. McDaniel did not want to give up. Mrs. McDaniel’s tumor was sequenced again, looking for a new mutation, but there was nothing striking. As Dr. McDaniel sifted through the data, he called his parents every day. They began calling him the governor, hoping he would bring his mother another stay of execution.
The doctors considered a less appealing target, a mutated gene that T cells use to stop growing. Unpublished studies in mice suggested that a kidney cancer drug might stop the growth of T cells with this mutation.
By then, Mrs. McDaniel’s body was ravaged by the cancer and her treatments. She had entered hospice care, with a hospital bed in her home and a nurse and an assistant to help.
“We had this shaky evidence, based on the genome and on unpublished data,” Dr. McDaniel said.
But the drug’s side effects were mild, and her family and doctors decided she should try it.
“If we do nothing, she will be dead in one to six weeks,” Dr. McDaniel explained.
Mrs. McDaniel took the drug on Nov. 26. But she was so ill that she was unable to get out of bed, unable to drink from a straw. Her son Tim took his children to her bedroom one at a time so they could say goodbye.
“She wasn’t talking, but her eyes were open, and she acknowledged each one with a weak chuckle,” Dr. McDaniel said.
Three days later, she briefly rallied. Her husband held her hand.
“She said, ‘I love you,’ ” Mr. McDaniel said. “She then repeated it twice more. I kissed her forehead and told her that I loved her. Those were our last words to each other.”
The next morning, Nov. 30, Mr. McDaniel woke early and went to his wife’s room. Her breathing had become erratic. Worried, he stepped out and asked the hospice nurse to call the doctor. “In the seconds that I was absent, she died,” Mr. McDaniel said.
The team that tried to save her was heartbroken too, and was left with a long list of what-ifs. “If you really look at it, what did we buy her?” Dr. de Castro asked. Mrs. McDaniel was dying last January. Yet would she have survived as long even without the sequencing or the drugs? Did the team make a difference?
“I hope we did,” Dr. de Castro said, “but it’s hard to know.”.
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