Saturday, October 31, 2009

Are Commercial Genetic Tests Worth Taking? What are BRCA1 and BRCA2?


HealthProfessor.com

Experts cautious about validity, usefulness of some on the market.

Peter Orszag, the 40-year-old head of the White House Office of Management and Budget, is reported to drink so much tea, hot and iced, that he took a genetic test to see if his body could metabolize his voluminous intake of caffeine.

According to the results, his body is perfectly suited to the task, and Orszag can easily go about his busy day, according to published reports.

Like Orszag, droves of people are flocking to get genetic tests -- which are now marketed direct-to-consumer -- ranging from the $179 CaffeineGen to assess caffeine metabolism to those that claim to gauge risk for Alzheimer's disease. There's also a $79 HomeDNA Home Paternity Testing System that includes, for an additional $25, lab services for the "alleged" father and one child.

But whether or not the commercially available genetic tests currently entering the market actually provide any useful information is another question.

According to Dr. Muin J. Khoury, director of the Office of Public Health Genomics at the U.S. Centers for Disease Control and Prevention, some 1,800 to 2,000 genetic tests have been developed, most of which are relevant only to rare genetic conditions that don't affect too many people.

"A growing number of these tests are suggested to be used to target interventions [pharmacogenetics], and to do early detection or susceptibility testing," Khoury said.

Khoury participated in a recent conference hosted by the National Academy of Sciences in Washington, D.C., that looked at direct-to-consumer marketing of genetic tests. Among other things, panelists discussed how valid and useful these tests are. Probably some will prove useful, and some will not, the experts said.

"With very few exceptions, we still have some big gaps in evidence," said Dr. Marc S. Williams, director of clinical genetics at the American College of Medical Genetics and director of Intermountain Healthcare, Clinical Genetics Institute, in Salt Lake City. "Do we really know if this works or not?"

"We don't know what they do to help people or hurt them," Khoury added.

Some are tried and true, such as those to detect the BRCA 1 and 2 genes, which heighten a woman's risk for breast and ovarian cancer, or specific tests to figure the risk for Lynch syndrome, a hereditary form of colon cancer.

But take the example of several much-hyped genetic tests to help determine what type or what dose of antidepressant would be effective for different individuals.

"Researchers have found that even clinically available tests that are supposed to inform someone about specific doses or specific medications use virtually no evidence. We don't even know what to do with the results of tests in terms of dosing, etcetera," Williams said. "People are promoting this test to choose which SSRI [selective serotonin reuptake inhibitor] they should use and at what dose with almost no evidence. We'd love to be able to predict which drug to use, but the evidence just isn't there to support that."

And results could be alarming to some people, said Sandra Soo-Jin Lee, senior research scholar and medical anthropologist at the Stanford University Center for Biomedical Ethics, although one recent study reported that people who discovered they had a higher risk for Alzheimer's through a genetic test were not psychologically distressed by the results.

Perhaps they kept in mind that genes are only one factor that determine risk. The environment also has a lot to do with it.

For instance, "there is a fairly robust history of research around genetic variations a population might express in terms of how they take up those chemicals. So, in terms of caffeine metabolism, there may be some individuals that are fast metabolizers of caffeine so it goes through their system fairly quickly," Lee said.

"But there may also be other things about that person and that person's environment that affect how they metabolize caffeine. For now, we just don't know what's what in terms of tests and results," she added.

"Right now, the direct-to-consumer genetic testing companies are working in an unregulated space. It's sort of a no man's land," Lee said. "But I think there are some indications that we are moving in a direction of creating some hopeful policies. One of the first steps is making sure all the stakeholders come together and discuss what would be helpful in terms of regulation. That not only means health-care providers and patients, but companies themselves."



BRCA1 and BRCA2: Cancer Risk and Genetic Testing
Key Points www.cancer.gov

* BRCA1 and BRCA2 are human genes that belong to a class of genes known as tumor suppressors. Mutation of these genes has been linked to hereditary breast and ovarian cancer (see Question 1).
* A woman's risk of developing breast and/or ovarian cancer is greatly increased if she inherits a deleterious (harmful) BRCA1 or BRCA2 mutation. Men with these mutations also have an increased risk of breast cancer. Both men and women who have harmful BRCA1 or BRCA2 mutations may be at increased risk of other cancers (see Question 2).
* Genetic tests are available to check for BRCA1 and BRCA2 mutations. A blood sample is required for these tests, and genetic counseling is recommended before and after the tests (see Question 5).
* If a harmful BRCA1 or BRCA2 mutation is found, several options are available to help a person manage their cancer risk (see Question 11).
* Federal and state laws help ensure the privacy of a person’s genetic information and provide protection against discrimination in health insurance and employment practices (see Questions 14 and 15).
* Many research studies are being conducted to find newer and better ways of detecting, treating, and preventing cancer in BRCA1 and BRCA2 mutation carriers. Additional studies are focused on improving genetic counseling methods and outcomes. Our knowledge in these areas is evolving rapidly (see Question 18).

1. What are BRCA1 and BRCA2?

BRCA1 and BRCA2 are human genes that belong to a class of genes known as tumor suppressors.

In normal cells, BRCA1 and BRCA2 help ensure the stability of the cell’s genetic material (DNA) and help prevent uncontrolled cell growth. Mutation of these genes has been linked to the development of hereditary breast and ovarian cancer.
The names BRCA1 and BRCA2 stand for breast cancer susceptibility gene 1 and breast cancer susceptibility gene 2, respectively.

2. How do BRCA1 and BRCA2 gene mutations affect a person's risk of cancer?

Not all gene changes, or mutations, are deleterious (harmful). Some mutations may be beneficial, whereas others may have no obvious effect (neutral). Harmful mutations can increase a person’s risk of developing a disease, such as cancer.

A woman’s lifetime risk of developing breast and/or ovarian cancer is greatly increased if she inherits a harmful mutation in BRCA1 or BRCA2. Such a woman has an increased risk of developing breast and/or ovarian cancer at an early age (before menopause) and often has multiple, close family members who have been diagnosed with these diseases. Harmful BRCA1 mutations may also increase a woman’s risk of developing cervical, uterine, pancreatic, and colon cancer (1, 2). Harmful BRCA2 mutations may additionally increase the risk of pancreatic cancer, stomach cancer, gallbladder and bile duct cancer, and melanoma (3).

Men with harmful BRCA1 mutations also have an increased risk of breast cancer and, possibly, of pancreatic cancer, testicular cancer, and early-onset prostate cancer. However, male breast cancer, pancreatic cancer, and prostate cancer appear to be more strongly associated with BRCA2 gene mutations (2–4).

The likelihood that a breast and/or ovarian cancer is associated with a harmful mutation in BRCA1 or BRCA2 is highest in families with a history of multiple cases of breast cancer, cases of both breast and ovarian cancer, one or more family members with two primary cancers (original tumors that develop at different sites in the body), or an Ashkenazi (Eastern European) Jewish background (see Question 6). However, not every woman in such families carries a harmful BRCA1 or BRCA2 mutation, and not every cancer in such families is linked to a harmful mutation in one of these genes. Furthermore, not every woman who has a harmful BRCA1 or BRCA2 mutation will develop breast and/or ovarian cancer.

According to estimates of lifetime risk, about 12.0 percent of women (120 out of 1,000) in the general population will develop breast cancer sometime during their lives compared with about 60 percent of women (600 out of 1,000) who have inherited a harmful mutation in BRCA1 or BRCA2 (4, 5). In other words, a woman who has inherited a harmful mutation in BRCA1 or BRCA2 is about five times more likely to develop breast cancer than a woman who does not have such a mutation.

Lifetime risk estimates for ovarian cancer among women in the general population indicate that 1.4 percent (14 out of 1,000) will be diagnosed with ovarian cancer compared with 15 to 40 percent of women (150–400 out of 1,000) who have a harmful BRCA1 or BRCA2 mutation (4, 5).

It is important to note, however, that most research related to BRCA1 and BRCA2 has been done on large families with many individuals affected by cancer. Estimates of breast and ovarian cancer risk associated with BRCA1 and BRCA2 mutations have been calculated from studies of these families. Because family members share a proportion of their genes and, often, their environment, it is possible that the large number of cancer cases seen in these families may be due in part to other genetic or environmental factors. Therefore, risk estimates that are based on families with many affected members may not accurately reflect the levels of risk for BRCA1 and BRCA2 mutation carriers in the general population. In addition, no data are available from long-term studies of the general population comparing cancer risk in women who have harmful BRCA1 or BRCA2 mutations with women who do not have such mutations. Therefore, the percentages given above are estimates that may change as more data become available.
3. Do inherited mutations in other genes increase the risk of breast and/or ovarian tumors?

Yes. Mutations in several other genes, including TP53, PTEN, STK11/LKB1, CDH1, CHEK2, ATM, MLH1, and MSH2, have been associated with hereditary breast and/or ovarian tumors (4, 6, 7). However, the majority of hereditary breast cancers can be accounted for by inherited mutations in BRCA1 and BRCA2 (8). Overall, it has been estimated that inherited BRCA1 and BRCA2 mutations account for 5 to 10 percent of breast cancers and 10 to 15 percent of ovarian cancers among white women in the United States (6).
4. Are specific mutations in BRCA1 and BRCA2 more common in certain populations?

Yes. For example, three specific mutations, two in the BRCA1 gene and one in the BRCA2 gene, are the most common mutations found in these genes in the Ashkenazi Jewish population. In one study, 2.3 percent of participants (120 out of 5,318) carried one of these three mutations (9). This frequency is about five times higher than that found in the general population (10). It is not known whether the increased frequency of these mutations is responsible for the increased risk of breast cancer in Jewish populations compared with non-Jewish populations.

Other ethnic and geographic populations around the world, such as the Norwegian, Dutch, and Icelandic peoples, also have higher frequencies of specific BRCA1 and BRCA2 mutations.

In addition, limited data indicate that the frequencies of specific BRCA1 and BRCA2 mutations may vary among individual racial and ethnic groups in the United States, including African Americans, Hispanics, Asian Americans, and non-Hispanic whites (11–13).

This information about genetic differences between racial and ethnic groups may help health care providers in selecting the most appropriate genetic test(s) (see Question 5).
5. Are genetic tests available to detect BRCA1 and BRCA2 mutations, and how are they performed?

Yes. Several methods are available to test for BRCA1 and BRCA2 mutations (14). Most of these methods look for changes in BRCA1 and BRCA2 DNA. At least one method looks for changes in the proteins produced by these genes. Frequently, a combination of methods is used.

A blood sample is needed for these tests. The blood is drawn in a laboratory, doctor's office, hospital, or clinic and then sent to a laboratory that specializes in the tests. It usually takes several weeks or longer to get the test results. Individuals who decide to get tested should check with their health care provider to find out when their test results might be available.

Genetic counseling is generally recommended before and after a genetic test. This counseling should be performed by a health care professional who is experienced in cancer genetics (see Question 17). Genetic counseling usually involves a risk assessment based on the individual’s personal and family medical history and discussions about the appropriateness of genetic testing, the specific test(s) that might be used and the technical accuracy of the test(s), the medical implications of a positive or a negative test result, the possibility that a test result might not be informative (an ambiguous result) (see below), the psychological risks and benefits of genetic test results, and the risk of passing a mutation to children.
6. How do people know if they should consider genetic testing for BRCA1 and BRCA2 mutations?

Currently, there are no standard criteria for recommending or referring someone for BRCA1 or BRCA2 mutation testing.

In a family with a history of breast and/or ovarian cancer, it may be most informative to first test a family member who has breast or ovarian cancer. If that person is found to have a harmful BRCA1 or BRCA2 mutation, then other family members can be tested to see if they also have the mutation.

Regardless, women who have a relative with a harmful BRCA1 or BRCA2 mutation and women who appear to be at increased risk of breast and/or ovarian cancer because of their family history should consider genetic counseling to learn more about their potential risks and about BRCA1 and BRCA2 genetic tests.

The likelihood of a harmful mutation in BRCA1 or BRCA2 is increased with certain familial patterns of cancer. These patterns include the following (15):
* For women who are not of Ashkenazi Jewish descent:
o two first-degree relatives (mother, daughter, or sister) diagnosed with breast cancer, one of whom was diagnosed at age 50 or younger;
o three or more first-degree or second-degree (grandmother or aunt) relatives diagnosed with breast cancer regardless of their age at diagnosis;
o a combination of first- and second-degree relatives diagnosed with breast cancer and ovarian cancer (one cancer type per person);
o a first-degree relative with cancer diagnosed in both breasts (bilateral breast cancer);
o a combination of two or more first- or second-degree relatives diagnosed with ovarian cancer regardless of age at diagnosis;
o a first- or second-degree relative diagnosed with both breast and ovarian cancer regardless of age at diagnosis; and
o breast cancer diagnosed in a male relative.

* For women of Ashkenazi Jewish descent:
o any first-degree relative diagnosed with breast or ovarian cancer; and
o two second-degree relatives on the same side of the family diagnosed with breast or ovarian cancer.

These family history patterns apply to about 2 percent of adult women in the general population. Women who have none of these family history patterns have a low probability of having a harmful BRCA1 or BRCA2 mutation.
7. How much does BRCA1 and BRCA2 mutation testing cost?

The cost for BRCA1 and BRCA2 mutation testing usually ranges from several hundred to several thousand dollars. Insurance policies vary with regard to whether or not the cost of testing is covered. People who are considering BRCA1 and BRCA2 mutation testing may want to find out about their insurance company’s policies regarding genetic tests.
8. What does a positive BRCA1 or BRCA2 test result mean?

A positive test result generally indicates that a person has inherited a known harmful mutation in BRCA1 or BRCA2 and, therefore, has an increased risk of developing certain cancers, as described above. However, a positive test result provides information only about a person’s risk of developing cancer. It cannot tell whether an individual will actually develop cancer or when. Not all women who inherit a harmful BRCA1 or BRCA2 mutation will develop breast or ovarian cancer.

A positive genetic test result may have important health and social implications for family members, including future generations. Unlike most other medical tests, genetic tests can reveal information not only about the person being tested but also about that person’s relatives. Both men and women who inherit harmful BRCA1 or BRCA2 mutations, whether they develop cancer themselves or not, may pass the mutations on to their sons and daughters. However, not all children of people who have a harmful mutation will inherit the mutation.
9. What does a negative BRCA1 or BRCA2 test result mean?

How a negative test result will be interpreted depends on whether or not someone in the tested person’s family is known to carry a harmful BRCA1 or BRCA2 mutation. If someone in the family has a known mutation, testing other family members for the same mutation can provide information about their cancer risk. If a person tests negative for a known mutation in his or her family, it is unlikely that they have an inherited susceptibility to cancer associated with BRCA1 or BRCA2. Such a test result is called a “true negative.” Having a true negative test result does not mean that a person will not develop cancer; it means that the person’s risk of cancer is probably the same as that of people in the general population.

In cases in which a family has a history of breast and/or ovarian cancer and no known mutation in BRCA1 or BRCA2 has been previously identified, a negative test result is not informative. It is not possible to tell whether an individual has a harmful BRCA1 or BRCA2 mutation that was not detected by testing (a “false negative”) or whether the result is a true negative. In addition, it is possible for people to have a mutation in a gene other than BRCA1 or BRCA2 that increases their cancer risk but is not detectable by the test(s) used.
10. What does an ambiguous BRCA1 or BRCA2 test result mean?

If genetic testing shows a change in BRCA1 or BRCA2 that has not been previously associated with cancer in other people, the person’s test result may be interpreted as “ambiguous” (uncertain). One study found that 10 percent of women who underwent BRCA1 and BRCA2 mutation testing had this type of ambiguous result (16).

Because everyone has genetic differences that are not associated with an increased risk of disease, it is sometimes not known whether a specific DNA change affects a person’s risk of developing cancer. As more research is conducted and more people are tested for BRCA1 or BRCA2 changes, scientists will learn more about these changes and cancer risk.
11. What are the options for a person who has a positive test result?

Several options are available for managing cancer risk in individuals who have a harmful BRCA1 or BRCA2 mutation. However, high-quality data on the effectiveness of these options are limited.
* Surveillance—Surveillance means cancer screening, or a way of detecting the disease early. Screening does not, however, change the risk of developing cancer. The goal is to find cancer early, when it may be most treatable.

Surveillance methods for breast cancer may include mammography and clinical breast exams. Studies are currently under way to test the effectiveness of other breast cancer screening methods, such as magnetic resonance imaging (MRI), in women with BRCA1 or BRCA2 mutations. With careful surveillance, many breast cancers will be diagnosed early enough to be successfully treated.

For ovarian cancer, surveillance methods may include transvaginal ultrasound, blood tests for CA–125 antigen, and clinical exams. Surveillance can sometimes find ovarian cancer at an early stage, but it is uncertain whether these methods can help reduce a woman's chance of dying from this disease.

* Prophylactic Surgery—This type of surgery involves removing as much of the "at-risk" tissue as possible in order to reduce the chance of developing cancer. Bilateral prophylactic mastectomy (removal of healthy breasts) and prophylactic salpingo-oophorectomy (removal of healthy fallopian tubes and ovaries) do not, however, offer a guarantee against developing cancer. Because not all at-risk tissue can be removed by these procedures, some women have developed breast cancer, ovarian cancer, or primary peritoneal carcinomatosis (a type of cancer similar to ovarian cancer) even after prophylactic surgery. In addition, some evidence suggests that the amount of protection salpingo-oophorectomy provides against the development of breast and ovarian cancer may differ between carriers of BRCA1 and BRCA2 mutations (17).

* Risk Avoidance—Certain behaviors have been associated with breast and ovarian cancer risk in the general population (see Question 16). Research results on the benefits of modifying individual behaviors to reduce the risk of developing cancer among BRCA1 or BRCA2 mutation carriers are limited.

* Chemoprevention—This approach involves the use of natural or synthetic substances to reduce the risk of developing cancer or to reduce the chance that cancer will come back. For example, the drug tamoxifen has been shown in numerous clinical studies to reduce the risk of developing breast cancer by about 50 percent in women who are at increased risk of this disease and to reduce the recurrence of breast cancer in women undergoing treatment for a previously diagnosed breast tumor. As a result, tamoxifen was approved by the U.S. Food and Drug Administration (FDA) as a breast cancer treatment and to reduce the risk of breast cancer development in premenopausal and postmenopausal women who are at increased risk of this disease. Few studies, however, have evaluated the effectiveness of tamoxifen in women with BRCA1 or BRCA2 mutations. Data from three studies suggest that tamoxifen may be able to help lower the risk of breast cancer in BRCA1 and BRCA2 mutation carriers (18–20). Two of these studies examined the effectiveness of tamoxifen in helping to reduce the development of cancer in the opposite breast of women undergoing treatment for an initial breast cancer (19, 20).

Another drug, raloxifene, was shown in a large clinical trial sponsored by the National Cancer Institute (NCI) to reduce the risk of developing invasive breast cancer in postmenopausal women at increased risk of this disease by about the same amount as tamoxifen. As a result, raloxifene was approved by the FDA for breast cancer risk reduction in postmenopausal women. Since tamoxifen and raloxifene inhibit the growth of breast cancer cells in similar ways, raloxifene may be able to help reduce breast cancer risk in postmenopausal BRCA1 and BRCA2 mutation carriers. However, this has not been studied directly.
12. What are some of the benefits of genetic testing for breast and ovarian cancer risk?

There can be benefits to genetic testing, whether a person receives a positive or a negative result. The potential benefits of a negative result include a sense of relief and the possibility that special preventive checkups, tests, or surgeries may not be needed. A positive test result can bring relief from uncertainty and allow people to make informed decisions about their future, including taking steps to reduce their cancer risk. In addition, many people who have a positive test result may be able to participate in medical research that could, in the long run, help reduce deaths from breast cancer.
13. What are some of the risks of genetic testing for breast and ovarian cancer risk?

The direct medical risks, or harms, of genetic testing are very small, but test results may have an effect on a person’s emotions, social relationships, finances, and medical choices.

People who receive a positive test result may feel anxious, depressed, or angry. They may choose to undergo preventive measures, such as prophylactic surgery, that have serious long-term implications and whose effectiveness is uncertain.

People who receive a negative test result may experience “survivor guilt,” caused by the knowledge that they likely do not have an increased risk of developing a disease that affects one or more loved ones.

Because genetic testing can reveal information about more than one family member, the emotions caused by test results can create tension within families. Test results can also affect personal choices, such as marriage and childbearing. Issues surrounding the privacy and confidentiality of genetic test results are additional potential risks (see below).
14. What can happen when genetic test results are placed in medical records?

Clinical test results are normally included in a person’s medical records. Consequently, individuals considering genetic testing must understand that their results might not be kept private.

Because a person’s genetic information is considered health information, it is covered by the Privacy Rule of the Health Information Portability and Accountability Act (HIPAA) of 1996 (21). The Privacy Rule requires that health care providers and others protect the privacy of health information, sets boundaries on the use and release of health records, and empowers individuals to control certain uses and disclosures of their health-related information. Many states also have laws to protect the privacy and limit the release of genetic and other health information.

In 2008, the Genetic Information Nondiscrimination Act (GINA) became Federal law (see Question 15). GINA prohibits discrimination based on genetic information in relation to health insurance and employment, but the law does not cover life insurance, disability insurance, and long-term care insurance. When applying for these types of insurance, people may be asked to sign forms that give an insurance company permission to access their medical records. The insurance company may take genetic test results into account when making decisions about coverage.

Some physicians keep genetic test results out of medical records. However, even if such results are not included in a person’s medical records, information about a person’s genetic profile can sometimes be gathered from that person’s family medical history.
15. What is genetic discrimination, and are there laws to protect people from this type of discrimination?

Genetic discrimination occurs when people are treated differently by insurance companies or employers because they have a gene mutation that increases their risk of a disease, such as cancer. However, in 2008, GINA was enacted to protect U.S. citizens against discrimination based on their genetic information in relation to health insurance and employment (22, 23). The parts of the law relating to health insurers will take effect between May 2009 and May 2010, and those relating to employers will take effect by November 2009. The law does not cover life insurance, disability insurance, and long-term care insurance. In addition, the law does not cover members of the military.

Some of the protections under GINA with regard to health insurance include the following:
* Premiums or contributions to a group health plan cannot be increased based on the genetic information of an individual(s) enrolled in the plan.

* Insurers cannot require an individual or family member to undergo a genetic test before enrollment in a group health plan.

* Insurers cannot request, require, or purchase genetic information about an individual before the person’s enrollment in a group health plan or in connection with that person’s enrollment in the plan.

* Health insurers cannot use genetic information as the only basis upon which to claim a pre-existing condition is present and, therefore, to deny coverage.

Some of the protections under GINA with regard to employment include the following:
* Employers cannot refuse to hire and cannot fire individuals based on their genetic information.

* Employers cannot discriminate against employees with regard to salary, terms and conditions of employment, privileges, and opportunities for the future because of their genetic information.

* Employers cannot request, require, or purchase genetic information about an employee except under specific circumstances.

* Employers cannot disclose an employee's genetic information except under specific circumstances.

Before GINA was passed, many states enacted laws against genetic discrimination. The amount of protection provided by these laws varies widely from state to state. GINA sets a minimum standard of protection that must be met by all states. It does not weaken the protections provided by any state law.
16. In general, what factors increase or decrease the chance of developing breast cancer and/or ovarian cancer?

The following factors have been associated with increased or decreased risk of developing breast and/or ovarian cancer in the general population. It is not yet known exactly how these factors influence risk in people with BRCA1 or BRCA2 mutations. In addition, a significant portion of hereditary breast cancers are not associated with BRCA1 or BRCA2 mutations (8).
* Age—The risks of breast and ovarian cancer increase with age. Most breast and ovarian cancers occur in women over the age of 50. Women with harmful BRCA1 or BRCA2 mutations often develop breast or ovarian cancer before age 50.

* Family History—Women who have a first-degree relative (mother, sister, or daughter) or other close relative with breast and/or ovarian cancer may be at increased risk of developing these cancers. In addition, women with relatives who have had colon cancer may be at increased risk of developing ovarian cancer.

* Medical History—Women who have already had breast cancer are at increased risk of developing breast cancer again, or of developing ovarian cancer.

* Hormonal Influences—Estrogen is a hormone that is naturally produced by the body and stimulates the normal growth of breast tissue. It is thought that excess estrogen may contribute to breast cancer risk because of its natural role in stimulating breast cell growth. Women who had their first menstrual period before the age of 12 or experienced menopause after age 55 have a slightly increased risk of breast cancer, as do women who had their first child after age 30. Each of these factors increases the amount of time a woman’s body is exposed to estrogen. Removal of a woman’s ovaries, which are the main source of estrogen production, reduces the risk of breast cancer. Breast-feeding also reduces breast cancer risk and is thought to exert its effects through hormonal mechanisms (24).

* Birth Control Pills (Oral Contraceptives)—Most studies have shown a slight increase or no change in risk of breast cancer among women taking birth control pills (24). In contrast, numerous studies have shown that taking birth control pills decreases a woman’s risk of developing ovarian cancer (25). This protective benefit appears to increase with the duration of oral contraceptive use and persists up to 25 years after discontinuing use. It also appears that the use of birth control pills lowers the risk of ovarian cancer in women who carry harmful BRCA1 or BRCA2 mutations (26).

* Hormone Replacement Therapy—Doctors may prescribe hormone replacement therapy (HRT) to reduce the discomfort of certain symptoms of menopause, such as hot flashes. However, the results of the Women’s Health Initiative (WHI), a large clinical study conducted by the National Heart, Lung, and Blood Institute, part of the National Institutes of Health (NIH), showed that HRT with the hormones estrogen and progestin is associated with harmful side effects, including an increased risk of breast cancer and increased risks of heart attack, blood clots, and stroke. The WHI also showed that HRT with estrogen alone was associated with increased risks of blood clots and stroke, but the effect on breast cancer risk was uncertain (27). In addition, the WHI showed an increase in ovarian cancer risk among women who received estrogen and progestin HRT, but this finding was not statistically significant (28). Because of these potential harmful side effects, the FDA has recommended that HRT be used only at the lowest doses for the shortest period of time needed to achieve treatment goals.

No data have been reported to date regarding the effects of HRT on breast cancer risk among women carrying harmful BRCA1 or BRCA2 mutations, and only limited data are available regarding HRT use and ovarian cancer risk among such women. In one study, HRT use did not appear to affect ovarian cancer risk among women with BRCA1 or BRCA2 mutations (29).

When considering HRT use, both the potential harms and benefits of this type of treatment should be discussed carefully by a woman and her health care provider.

* Obesity—Substantial evidence indicates that obesity is associated with an increased risk of breast cancer, especially among postmenopausal women who have not used HRT (24). Evidence also suggests that obesity is associated with increased mortality (death) from ovarian cancer (30).

* Physical Activity—Numerous studies have examined the relationship between physical activity and breast cancer risk, and most of these studies have shown that physical activity, especially strenuous physical activity, is associated with reduced risk. This decrease in risk appears to be more pronounced in premenopausal women and women with lower-than-normal body weight (24).

* Alcohol—There is substantial evidence that alcohol consumption is associated with increased breast cancer risk. However, it is uncertain whether reducing alcohol consumption would decrease breast cancer risk (24).

* Dietary Fat—Although early studies suggested a possible association between a high-fat diet and increased breast cancer risk, more recent studies have been inconclusive. In the WHI, a low-fat diet did not help reduce breast cancer risk (31).

17. Where can people get more information about genetic testing for cancer risk?

A person who is considering genetic testing should speak with a professional trained in genetics before deciding whether to be tested. These professionals may include doctors, genetic counselors, and other health care workers trained in genetics (such as nurses, psychologists, or social workers). For help finding a health care professional trained in genetics, please visit NCI’s Cancer Genetics Services Directory at http://www.cancer.gov/search/geneticsservices on the Internet. Alternatively, please contact NCI’s Cancer Information Service (CIS) (see below for contact information). The CIS can provide more information about genetic testing and help in finding a health care professional trained in genetics.
18. What research is currently being done to help individuals with harmful BRCA1 or BRCA2 mutations?

Research studies are being conducted to find newer and better ways of detecting, treating, and preventing cancer in BRCA1 and BRCA2 mutation carriers. Additional studies are focused on improving genetic counseling methods and outcomes. Our knowledge in these areas is evolving rapidly.

Information about active clinical trials (research studies with people) for individuals with BRCA1 or BRCA2 mutations is available on NCI’s Web site. The following links will initiate searches of NCI’s clinical trials database and retrieve lists of trials open to individuals with BRCA1 or BRCA2 mutations.
* BRCA1 mutation carriers
* BRCA2 mutation carriers

In addition, NCI’s CIS can provide information about clinical trials and help with clinical trial searches (see below for contact information).

Selected References

1. Kadouri L, Hubert A, Rotenberg Y, et al. Cancer risks in carriers of the BRCA1/2 Ashkenazi founder mutations. Journal of Medical Genetics 2007; 44(7):467–471.

2. Thompson D, Easton DF, the Breast Cancer Linkage Consortium. Cancer incidence in BRCA1 mutation carriers. Journal of the National Cancer Institute 2002; 94(18):1358–1365.

3. The Breast Cancer Linkage Consortium. Cancer risks in BRCA2 mutation carriers. Journal of the National Cancer Institute 1999; 91(15):1310–1316.

4. PDQ® Cancer Information Summary. National Cancer Institute; Bethesda, MD. Genetics of Breast and Ovarian Cancer (PDQ®) - Health Professional. Date last modified 04/24/2009. Available at: http://www.cancer.gov/cancertopics/pdq/genetics/breast-and-ovarian/healthprofessional. Accessed 05/15/2009.

5. National Cancer Institute. SEER Cancer Statistics Review, 1975–2005. Retrieved April 20, 2009, from: http://seer.cancer.gov/csr/1975_2005/index.html.

6. Campeau PM, Foulkes WD, Tischkowitz MD. Hereditary breast cancer: New genetic developments, new therapeutic avenues. Human Genetics 2008; 124(1):31–42.

7. Walsh T, Casadei S, Coats KH, et al. Spectrum of mutations in BRCA1, BRCA2, CHEK2, and TP53 in families at high risk of breast cancer. Journal of the American Medical Association 2006; 295(12):1379–1388.

8. Lynch HT, Silva E, Snyder C, Lynch JF. Hereditary breast cancer: Part I. Diagnosing hereditary breast cancer syndromes. The Breast Journal 2008; 14(1):3–13.

9. Struewing JP, Hartge P, Wacholder S, et al. The risk of cancer associated with specific mutations of BRCA1 and BRCA2 among Ashkenazi Jews. New England Journal of Medicine 1997; 336(20):1401–1408.

10. Warner E, Foulkes W, Goodwin P, et al. Prevalence and penetrance of BRCA1 and BRCA2 gene mutations in unselected Ashkenazi Jewish women with breast cancer. Journal of the National Cancer Institute 1999; 91(14):1241–1247.

11. John EM, Miron A, Gong G, et al. Prevalence of pathogenic BRCA1 mutation carriers in 5 U.S. racial/ethnic groups. Journal of the American Medical Association 2007; 298(24):2869–2876.

12. Vogel KJ, Atchley DP, Erlichman J, et al. BRCA1 and BRCA2 genetic testing in Hispanic patients: Mutation prevalence and evaluation of the BRCAPRO risk assessment model. Journal of Clinical Oncology 2007; 25(29):4635–4641.

13. Malone KE, Daling JR, Doody DR, et al. Prevalence and predictors of BRCA1 and BRCA2 mutations in a population-based study of breast cancer in white and black American women ages 35 to 64 years. Cancer Research 2006; 66(16):8297–8308.

14. Palma M, Ristori E, Ricevuto E, Giannini G, Gulino A. BRCA1 and BRCA2: The genetic testing and the current management options for mutation carriers. Critical Reviews in Oncology/Hematology 2006; 57(1):1–23.

15. U.S. Preventive Services Task Force. Genetic risk assessment and BRCA mutation testing for breast and ovarian cancer susceptibility. Retrieved April 20, 2009, from: http://www.ahrq.gov/clinic/uspstf05/brcagen/brcagenrs.htm.

16. Peshkin BN, DeMarco TA, Brogan BM, Lerman C, Isaacs C. BRCA1/2 testing: Complex themes in result interpretation. Journal of Clinical Oncology 2001; 19(9):2555–2565.

17. Kauff ND, Domchek SM, Friebel TM, et al. Risk-reducing salpingo-oophorectomy for the prevention of BRCA1- and BRCA2-associated breast and gynecologic cancer: A multicenter, prospective study. Journal of Clinical Oncology 2008; 26(8):1331–1337.

18. King MC, Wieand S, Hale K, et al. Tamoxifen and breast cancer incidence among women with inherited mutations in BRCA1 and BRCA2: National Surgical Adjuvant Breast and Bowel Project (NSABP–P1) Breast Cancer Prevention Trial. Journal of the American Medical Association 2001; 286(18):2251–2256.

19. Narod SA, Brunet JS, Ghadirian P, et al. Tamoxifen and risk of contralateral breast cancer in BRCA1 and BRCA2 mutation carriers: A case-control study. Lancet 2000; 356(9245):1876–1881.

20. Gronwald J, Tung N, Foulkes WD, et al. Tamoxifen and contralateral breast cancer in BRCA1 and BRCA2 carriers: An update. International Journal of Cancer 2006; 118(9):2281–2284.

21. U.S. Department of Health and Human Services. HIPAA Frequent Questions: About the Privacy Rule FAQs. Retrieved April 20, 2009, from: http://www.hhs.gov/hipaafaq/about/354.html.

22. H.R. 493. The Genetic Information Nondiscrimination Act of 2008. Retrieved April 20, 2009, from:
http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=110_cong_bills&docid=f:h493enr.txt.pdf.

23. The National Human Genome Research Institute. GINA: The Genetic Information Nondiscrimination Act of 2008: Information for Researchers and Health Care Professionals. Retrieved April 30, 2009, from: http://www.genome.gov/Pages/PolicyEthics/GeneticDiscrimination/GINAInfoDoc.pdf.

24. PDQ® Cancer Information Summary. National Cancer Institute; Bethesda, MD. Breast Cancer Prevention (PDQ®) - Health Professional. Date last modified 04/30/2009. Available at: http://www.cancer.gov/cancertopics/pdq/prevention/breast/healthprofessional. Accessed 05/15/2009.

25. PDQ® Cancer Information Summary. National Cancer Institute; Bethesda, MD. Ovarian Cancer Prevention (PDQ®) - Health Professional. Date last modified 04/03/2008. Available at: http://www.cancer.gov/cancertopics/pdq/prevention/ovarian/healthprofessional. Accessed 05/15/2009.

26. Whittemore AS, Balise RR, Pharoah PDP, et al. Oral contraceptive use and ovarian cancer risk among carriers of BRCA1 or BRCA2 mutations. British Journal of Cancer 2004; 91(11):1911–1915.

27. National Heart, Lung, and Blood Institute. Women’s Health Initiative. Retrieved April 20, 2009, from: http://www.nhlbi.nih.gov/whi.

28. Anderson GL, Judd HL, Kaunitz AM, et al. Effects of estrogen plus progestin on gynecologic cancers and associated diagnostic procedures: The Women's Health Initiative randomized trial. Journal of the American Medical Association 2003; 290(13):1739–1748.

29. Kotsopoulos J, Lubinski J, Neuhausen SL, et al. Hormone replacement therapy and the risk of ovarian cancer in BRCA1 and BRCA2 mutation carriers. Gynecologic Oncology 2006; 100(1):83–88.

30. Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. New England Journal of Medicine 2003; 348(17):1625–1638.

31. Prentice RL, Caan B, Chlebowski RT, et al. Low-fat dietary pattern and risk of invasive breast cancer: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association 2006; 295(6):629–642.

VH1 Celebrity Fit Club The Fat Smash Diet


 Dr. Smith’s diet has been featured on VH1’s number-one rated show, Celebrity Fit Club, where Hollywood celebrities follow his customized diet plan and compete to lose weight. Now, with The Fat Smash Diet, everyone will have access to the revolutionary eating plan that leads to lifestyle changes and permanent weight loss forever.

The Fat Smash Diet is not a gimmick or short-term fix. It is a four-phase diet that starts out with a natural detox phase to clean impurities out of the system. Once this nine-day phase is completed, the next three phases encourage the addition of everyday foods that promote significant weight loss. In just thirty days, most dieters will complete all four phases and be on their way to a thinner lifetime of good health. Best of all, there is no calorie counting, and Dr. Smith guarantees there never will be. As an added bonus, there are over fifty easy-to-cook, tasty recipes that make it easier to stick with Dr. Smith’s plan. The Fat Smash Diet is unlike any other program on the market. In fact, it’s the LAST DIET YOU’LL EVER NEED!

From the Back Cover

NO MORE COUNTING CALORIES!
NO MORE WASTING TIME!
NO MORE UNREALISTIC DIETS!
BUST THROUGH THE PLATEAU!
THE NEW YOU BEGINS NOW!

Millions of people have wasted time and money trying fad diets that simply won't work and in some cases even put their health at risk. But that doesn't mean you can't shed unwanted pounds. Finally, here is a scientifically based diet that will not only help you lose weight, but will improve your overall health and help prevent serious medical conditions such as diabetes, health disease, stroke, and osteoarthritis. There's no counting calories because it's already done for you.

The Fat Smash Plan Includes:
--A four phase diet that's easy to follow
--Simple, tasty, inexpensive, fast-to-cook recipes
--An eating strategy to stop the hunger pangs

This 90-day program offers you the opportunity to select the foods you like and physical activities you enjoy. The NEW YOU starts TODAY!

THE DIET PLAN USED ON VH1'S CELEBRITY FIT CLUB
www.fatsmashdiet.com

Amazon Reviews:

1. Let me give you my stats. I am beginning this diet at 5'5, 250 pounds and I'm a 25 year old, male. I have been going to the gym and weight lifting for 1 year and have already lost 100 pounds prior to this. I got stuck and needed a change. I am going to update this review as I go along this diet. So keep on checking as time goes on...

I rated this book 4 stars because I believe that the jist of this diet is quite healthy and effective. However, the book is poorly written. I am a graduate student so it only took me 30min to read the book. The theory behind his diet is simple. He doesn't go into a whole lot of depth explaining it. This can be both positive and negative. It's simple to understand but if you are like me, you may want to more know of the "why?" behind it.

Also, the lists are a little confusing. If you stick with what "you are not supposed to eat" you will be fine. Even that list can be a little confusing because it's not all encompassing. You will notice the phase two list has foods that you are now allowed to eat that you weren't allowed to before. But those aren't listed on what you can't eat during phase one (corn for example). With that said, it's my educated guess that you don't have to follow the plan religiously. What i mean is, as long as you eat on a schedule (outlined in the book), do the excersize (also well outlined in the book)and do not eat the "bad" foods (or types of foods) listed during each phase you will lose weight.

As for the diet itself. The detox is simply 9 (I'm doing 10) days of the diet. It's simply meant to wean you off cafine and refined carbs/sugars and cleanse your system. It is hard to do and takes some commitment. You will be lethargic and you will crave bread, meat and sugar. This is all part of detoxing your system. I will write more about this as I am completing it.

In phase 2 you add some lean meat, seafood, eggs, cereal and drink options. There are portions listed and you should stick to them as close as possible. The excersize is very important. He is asking at this point, that you do about 35 min of cardio 5 days a week. This shouldn't be that hard. You can go to the gym, take a walk, walk the dog, walk around the mall, ride a bike, go to the zoo etc. As long as you are getting 35 min in.

In phase 3 you add some more foods including wheat bread/pasta and small desserts. The excersize is now up to 45 min of cardio 5 times a day.

In phase 4, he lists some recommended portions of fast foods, pizza, ham etc. The goal is to get 1hr of cardio 5 days a week and lift 2 days a week. In my opinion if you did 45 min of weights and 20 min of cardio 2 days a week then the hour 3 days a week you'd be fine. He's not suggesting you power lift. Just tone up because you are going to be losing a lot of weight.

Another important element to this diet is to surround yourself with supportive people. He says this in the beginning of the book. You are working on changing life-long eating habits and it is not going to be easy. But having folks who support you is very important.

My Journey...

So far I've been on the detox phase for 6 days. The first few days were really hard. I felt like I was starving and was very tired. Now it's getting better. I'm hungry 30-40% of the time. For most of my life I have been a meat and potatoes sort of guy. So tofu and vegis etc. didn't sound great. But I'm actually doing well with it. I actually ate tofu and liked it. Not to mention all the good fruits. I weighed myself and I've lost 9 pounds in 6 days. This is kind of fast but not for a detox period. My body is getting rid of a lot of junk. Technically, I don't think you are supposed to be eating vegi burgers but i did have one and it had a trace amount of seeds (which you aren't supposed to have). I also drank a smoothy made with soy milk one day. Compared to waht I was eating, this isn't so bad. I will post my weight at the end of this phase and keep updating.

Edit 1. I ended up doing the 9 days of detox as the book recommends. I weighed in at 240.4, That's almost 10 pounds lost! I will say that I felt quite lethargic during this time and my muscles felt sore. So far I am 2 days into phase 2. My muscles are feeling better overal but have started cramping occassionally. However, my energy level is much higher and I feel good about the diet. I look forward to weighing in at the end of this phase. I will keep you up to date...three weeks from now will be the end of phase 2 and i will be into phase 3.

2. First my profile. 39 years old, 5'9", starting weight of 192 pounds. About 30 pounds over my weight of 15 years ago. I was drinking 2-4 cups of coffee per day, at least 3 Mochas per week, and several glasses of beer or wine each night at dinner. I also developed high blood pressure in the last 18 months. All this and I am very athletic - running half marathons in addition to being a pretty serious recreational cyclist.

So I came to the realization I had to make a change. The Fat Smash book sounded like a great plan AND IT IS.

I just finished phase I and it was not that bad minus the headaches from I guess alchohol and caffiene withdrawal. After 9 days I lost 9 pounds. I was urinating a lot, which means a lot of that was water weight, but I don't care. I feel a TON better both physically and mentally.

I did not miss meat that much and after a couple of days did not miss the coffee or booze.

So I started Phase II yesterday (It lasts 3 weeks) and I'll stop back and update my progress after each phase.

I do still see a bag of potatoe chips and I'm craving them, but I'm sticking to this thing as best I can. One thing I really like about the philosophy of the book is he says you will most likely have days where you get off track. He just says go back to the phase one plan for a few days until you lose any weight you gained back when off track, and then start back into the phase you were on. Very realistic. Don't beat yourself up and screw it all up, just get back on the horse and keep riding.

Regarding the book. As many other reviewers stated, it isn't the greatest written book. None of the WHY am I doing this is covered and the suggested eating plans can be confusing. Maybe that is the idea. He doesn't give you an exact roadmap, but a roadmap that gets you 90% of the way there and you figure out the rest because you are smart and dedicated to the diet.

Example: No nuts are allowed in phase I, it is clearly written. But then in Phase II they are gone from the "Don't" list, but he doesn't add them to the "OK" list. So I take it that they are OK now and I had a handful for a pre-dinner snack last night.

I am rarely hungry as eating every three hours is actually pretty fun. Instead of an hour lunch at work, I take two 30 minute breaks, one arond 11:00, another around 2:30.

- Morning meals mainly are yogurt with frozen fruit, or oatmeal with frozen fruit.
- Mid-morning and afternoon meals I have primarily gone with all fruit on one, and then rice/beans on the next.
- Dinners - I am getting as creative as possible. Use the internet and check out vegan websites for recipes. I found a lot of good stuff. With meat and sweet potatoes comeing back into the menu for phase II, it'll be easier to cook for family.

At $10, I easily recommend the book. If you are feeling mentally weak at any given time, picking it up and re-reading some sections or looking ahead to when you can have certain foods again is reinforcing. I also look at is this way. If I lose 20 pounds and keep it off, I paid 50 cents per pound. A pretty good deal.

This diet works. So many reviews are saying it is all fruits and veggies. IT IS NOT. Beans, Brown Rice, Milk, Yogurt, Eggs, Nuts, Meat (after 9 days). I have not been hungry once since starting it.

Update on Progress:
- Starting Weight = 191 pounds
- Phase I, 9 days = lost 9 pounds (182 pounds)
- After two weeks = lost 13 pounds (178 pounds)
- After three weeks = lost 15 pounds (176 pounds - I guess this is when it starts to get more difficult. Just two pounds the past week. It is discussed in the book and what to do to jumpstart it. But honestly, 2 pounds a week is healthy so I won't change anything just yet. 15 pounds in three weeks is amazing).

3. I just finished Phase 1 and I am in love with this program! I went on this plan not just to lose some extra baggage, but also to become much healthier. I am a true believer in the mind, body, soul connection and that everything has to be inline in order to utilize your optimum self. I do have to mention that living off only fruits, veggies, tofu, and legumes is not hard for me, since I was a vegetarian for a few years back in college. The hardest part for me was not being able to eat any cheese, wine or sushi; I did crave blue cheese olives and sushi from time to time. But, it was well worth it, because not only have I lost a total of 9lbs in 9 days, my skin looks more radiant, my energy levels are way higher, I am sleeping better, and not to mention my clothes are getting much bigger on me. I don't view this as a diet at all. I also want to mention that I did drink coffee everyday with a little splenda and Horizon creamer and I did not get in 2 1/2 hours of working out the first week. I am going to move into Phase II today, which allows me to eat small portions of meat, fish, and cheeses again. I honestly could go on not eating meat, so I may stick to Phase I for awhile with occasional helpings of chicken and fish.

A few tips for people to help with this plan:
1. Middle Eastern food is a life saver. I ate a lot of Hummus with carrots and celery, Tabouli, Lentil Salad, Garbanzo Bean Salad, and Lentil Soup. I am spoiled with literally 7 Middle Eastern restaurants within a 5 mile radius of my house and two gourmet markets that carry several brands of this type of cuisine and also make their own versions fresh at the store. Important, read the labels. I noticed some brands of Hummus add a lot of extra junk into their recipes, steer clear of these.
2. If you have any Sushi restaurants/Japanese grocery stores by you, good picks are Miso Soup (I get the instant packs which are also sold at World Market) and Seaweed Salad.
3. If you have Trader Joe's and Whole Foods nearby, these are great places to find all sorts of frozen and fresh veggie dishes.
4. Sticking to eating 4-5 meals will make this plan easier than you can imagine. I was never hungry. I have a crazy work schedule and my job entails of meetings scattered at different locations in my area so I always bring a snack with me so I stick to the eating every 3 hours or so.
5. I grilled an assortment of veggies every couple days. My favorite is portabella mushrooms, eggplant, zucchini, yellow zucchini, red, orange, and yellow peppers. I tossed these veggies with either fat free Italian dressing or balsamic vinegar, garlic powder, sea salt and ground pepper.
6. For extra protein,in a blender, mix 1 scoop of Whey powder, fresh or frozen fruit, skim milk, and ice. This makes a very tasty shake. I prefer vanilla whey that doesn't have any added sugar.
7. Drink lots of water
8. Get creative with your dishes and utilize fresh herbs and spices.

How Much is Too Much Salt

How Much Sodium Is Too Much?

David L. Katz, MD
Photo: Mackenzie Stroh
Q: I'm 50 years old, and I love salt. My blood pressure is normal. I eat a very healthy diet with lots of fruit and veggies. Do I really need to watch my sodium intake?
— Shannon Dolph, Portland, Oregon

A: Given all the warnings about sodium raising blood pressure, you might think the link between the two is crystal clear. Actually, it's still a bit out of focus. One reason for the lack of clarity is that salt sends some people's blood pressure soaring while others seem able to tolerate heaps of it, no harm done. This inconsistent response has led to the notion of salt sensitivity, a trait generally thought to occur in at least 10 percent of the population. So far there's no easy way to test for salt sensitivity—or its absence (though researchers seem to be narrowing in on a "salt gene"). And since several studies suggest that most people benefit to varying degrees from minding their sodium intake, public health officials keep things simple by recommending that everyone cut back on salt. Besides, high blood pressure isn't the only concern: Even when blood pressure remains normal, high-sodium diets have been linked to heart disease (the theory is that excess sodium can directly damage the arteries and heart). And high-salt diets may rob your bones of calcium, potentially weakening bones and leading to osteoporosis.

But you may not need to worry if you eat a healthy diet and prepare most of your own meals: Five percent of the sodium in the average American's diet is added during cooking, 6 percent comes from the shaker on the table, another 12 percent occurs naturally in food, and the remaining 77 percent comes courtesy of processed, prepackaged foods. Cook your meals using fresh, whole ingredients and you'll get only a quarter of the 4,000 milligrams of sodium the typical American consumes in a day. That would put you well under the recommended daily limit of 2,300 milligrams.

One last note: Sodium can turn up in surprising places. That big, healthy-looking bran muffin on the coffee-shop counter can pack nearly 800 milligrams. Some breakfast cereals deliver up to 600 milligrams a bowl. Highly processed, sweetened foods may conceal a great deal of sodium and not taste salty at all.

Q. I use a lot of sea salt when I cook. Is it possible I could be falling short on iodine? —Ann Marshall, Greenville, South Carolina

A. It's unlikely, though recent research suggests that iodine deficiency isn't as rare as it once was. Adults need 150 micrograms a day, which we used to get easily from our diet. But in recent years, some of our main sources—restaurant and processed food—are less likely to contain iodized salt. We also get iodine from fish, shellfish, strawberries, yogurt, cow's milk, and eggs. Kelp contains the most, so sushi eaters get plenty. But it isn't wise to eat fish every day, and you need a constant supply of iodine because your body can't make or store it. The amounts in dairy vary, so keeping iodized salt on the table and using it occasionally in cooking can help prevent shortfalls.

A deficiency leaves your body unable to synthesize thyroid hormones. The gland will compensate by straining to produce more hormones, possibly leading to fatigue, depression, weight gain, and eventually a goiter—an enlarged, overworked thyroid.

While most American adults get enough, pregnant and breastfeeding women, infants, and children could be low, and they need it the most: Iodine is crucial for brain development. (Concerned mothers should check that their prenatal and postnatal vitamins deliver at least 150 micrograms a day.) If you are worried about your iodine intake or your thyroid, ask your doctor to check your level of TSH—thyroid-stimulating hormone. If it's normal, you'll know that your thyroid is happy with your iodine intake. If your TSH level is abnormal, you doctor will help you figure out why and whether the solution lies in your saltshaker.

Thursday, October 29, 2009

How Men Select Women


eioba.com
Youth

You have the most marvelous youth, and youth is the one thing worth having.…Someday when you are old and wrinkled and ugly, when thought has seared your forehead with its lines and passion branded your lips with its hideous fires, you will feel it. You will feel it terribly. Now, wherever you go you charm the world. Will it always be so? You have a wonderfully beautiful face, Mr. Gray.…And beauty is a form of genius-is higher, indeed, than genius, as it needs no explanation. It is one of the great facts of the world, like sunlight or springtime or the reflection in dark waters of that silver shell we call the Moon. It cannot be questioned. It has its divine right of sovereignty. It makes princes of those who have it. You smile-ah, when you have lost it you won't smile. People say sometimes that beauty is only superficial. That may be so, but at least it is not so superficial as thought is. To me, beauty is the wonder of wonders. It is only shallow people who do not judge by appearances. The true mystery of the world is the visible, not the invisible.
— Oscar Wilde, The Picture of Dorian Gray (1890)

Women with high reproductive value attract men. 19-year-old women are likely to produce the greatest number of children—twice as many as 30-year-old women.

Teenage boys, on average, prefer girls a year older. Men in their middle twenties usually prefer women a year or two younger. Thirtysomething men prefer women 5 to 10 years younger. Many men in their 40s and 50s prefer women 10 to 20 years younger.

Women of all ages up to about 45 prefer, on average, a man a few years older.

These statistical findings are mostly medians, however, and not necessarily the mode. In reality, age preferences vary widely from individual to individual, and sometimes from one stage of life to the next.

Neoteny

Neoteny is the retention of juvenile characteristics into adulthood.

In other primates, e.g., chimpanzees and gorillas, both male and female adults have tough skin, coarse body hair, Adam's apples, and deep voices. Humans, however, have characteristics of neoteny. Some of them appear in men, but most appear in women.


Adult women, for example, usually have higher voices like children. Men and women agree that attractive women have the large eyes and lips and small noses and chins of children. Attractive women's faces have the proportions of 11-to-14-year-old children.

Women further neoteny by using cosmetics, shaving their legs, and wearing children's clothing, e.g., Mary Jane shoes.

However, attraction of men toward pre-pubescent girls has no reproductive value. Mature women have features that distinguish them from pre-pubescent girls, yet are different from men. These secondary sexual characteristics include prominent breasts, clearly defined waists, and full hips. They reflect sexual maturity and fertility, offsetting the pre-pubescence that neotenous chracteristics could otherwise suggest.

Children's long dependency on their fathers is associated with neoteny. Fatherless children—a million years ago or today—were less likely to learn adult skills, inherit social status, and reproduce. Women who appeared young and remained strong were able to keep a man for twenty years, instead of losing him to a younger woman. A young-looking widow could find a second husband, whereas an older-looking counterpart of the same chronological age might not. Some statistical extrapolations suggest that someone is more likely to stay with one partner, the longer the partner continues to appear young. A hypothesis has been given to suggest that children with mothers who retain youthful characteristics were more likely to have both parents throughout their childhood, and grow up to reproduce and have descendants. Parents with neotenous characteristics would pass them on to their offspring. E.g., a mother who has certain features that cause her to look younger than other women her age is likely to have daughters having that appearance as well.


Beauty

Beauty standards are universal across cultures. People around the world have 91-94% agreement about the facial attractiveness of Asian, Hispanic, black, and white women. Even native people unexposed to mass media agree with the rest of the world.

Infants gaze longer and show more pleasure when looking at pictures of attractive male and female faces. One-year-olds play longer with facially attractive dolls than with unattractive dolls.

Beauty standards are cues to a woman's health: clear, smooth skin; full, lustrous hair; full lips; bright eyes; and symmetrical features.

Composite faces, made by combining many photographs on a computer, are more attractive than any individual face. Beauty is "average" looks, not unusual or "striking" features.

Men, in general, don't judge women as being fat or thin. Rather, men tend to consider women with a 70% waist-to-hip ratio to be beautiful. E.g., a woman with a 21-inch waist and 30-inch hips, a woman with a 24-inch waist and 35-inch hips, and a woman with a 28-inch waist and 40-inch hips are equally attractive. The 70% or higher waist-to-hip ratio, and the Golden ratio (62% waist-height-to-total-height ratio) indicate health and fertility.


Cultural Beauty Standards

Some beauty preferences vary between cultures, e.g., light or dark skin.

When a society experiences rapid change, it values youth and new, iconoclastic ideas. The 1920s and 1960s preferred thin, flat-chested, youthful women.

Conservative societies—e.g., the Victorian era, or the 1950s—value old ideas, and full-figured, mature women. Large metropolitan cities such as New York value very thin women; in contrast, small, rural towns prefer full-figured, fertile adult women.

American women chose thinner-than-average women as the most beautiful. American men prefer average-size women. Fashion models are thinner than porn stars.

Use cultural beauty standards to your advantage. Unlike your ancestors, you can move to a different city or even country. Select a culture where you're beautiful.


Media Effects on Beauty Standards

Our grandparents saw relatively few people. They saw even fewer beautiful people. In contrast, today we turn on a television and see nothing but attractive people made up to look their best, with the bad shots discarded. (Finally, a reason to praise Fox's "reality" television shows!)

Since the 1930s—the beginning of mass media—men have increased the importance of "good looks" in a wife by 40%. Women have increased the importance of a good-looking husband almost 80%. Women in 1996 valued "good looks" in husbands more than men in 1939 valued "good looks" in wives.

Photos of beautiful women made men rate their wives as less attractive, and feel less committed to their marriages, compared to men who looked at photos of "average" women.

Learn the game, then bend the rules. Before submitting a personal ad, have a "makeover" photo studio make you look like a glamorous model. When you marry, get rid of your television.

The media also affect men. Performers such as Jerry Seinfeld raise expectations of men's entertainment skills. As media images make women feel inadequately attractive, media entertainers make men feel inadequately entertaining. These men give up and say that they can't dance, sing, or tell jokes. The positive side is less competition for men who try to entertain women. Older men have an advantage here over younger men. Many young women have never had a man make them laugh, lead them on the dance floor, or play Chopin for an audience of one.


Beautiful Young Women Don't Have It Easy

For beautiful young women, the problem is sorting the wheat from the chaff. Finding a quality mate is no easier for them than for anyone else. They spend as much effort rejecting the wrong men as others spend finding men.

(Another problem is that a woman's power over men vanishes when a younger, more beautiful woman walks into the room.)

In the animal world, females initiate 80% of matings (see Flirting). Males who initiate mating are the males that no female will approach. Men who approach women pick young, beautiful women. Q.E.D., beautiful young women meet more than their share of losers.

Dating advice books tell men to ignore a woman to attract her attention. It's not that women like to be ignored. Rather, women know that if a man pays too much attention to a woman, he's a loser. (The converse isn't true—men's egos are attracted to women who pay attention to them.)

If women are too attractive, men stay in their cerebral cortexes. They'll date beautiful women to feel envy from their male friends. They have no reason to shift into their limbic brains and emotionally connect. When men are jerks and women are shallow, they're stuck in their cerebral cortexes.

Putting effort into clothes and make-up will get you more dates, but impair men's vision of your inner beauty, and attract the "wrong" kind of men (those who don't look deeper than the level of physical appearance). The ideal is to look nice, but don't overdo it. If you're getting many dates but aren't meeting quality men, work on improving yourself, not your wardrobe.

Encourage self-selection of potential mates. Tell suitors that you can't go out on a date, but they're welcome to join you volunteering, e.g., with Habitat For Humanity. The few men who show up to work are the ones worth dating.


Dress Against Your Stereotype

Stereotypically, unattractive women dress badly. They think that if they don't put effort into their appearance, men will think they have interesting minds. These women may read Dostoevsky but they look boring and stupid.

Or unattractive women dress well, but wear styles older than their age. E.g., you look like your grandmother buys your clothes. That's bad when you're 20, and really bad when you're 50.

Stereotypically, attractive women dress well. They spend time and effort on their clothes, hair, and make-up. These women may be shallow (e.g., reading nothing more challenging than Cosmopolitan) but they look sophisticated and intelligent.

And attractive women dress younger than their ages. Attractive 50-year-old women think it's fun to dress in teenagers' platform boots for Halloween.

If you were born with "unattractive genes", put more effort into your appearance. Dress younger than your age.

If you were born with "cover girl genes", leave the four-inch stilettos in your closet. Wear Converse sneakers and read The Brothers Karamazov at the coffee shop.


Education and Employment

Education, employment, and relationships are problematic for women. On the one hand, school and work are the most common places where couples meet (see Where Couples Met). Women who go to college and choose a professional career are more likely to meet men (especially if they choose traditionally male fields, e.g., science). And men prefer to marry women with good educations and good jobs.

On the other hand, career women sometimes must sacrifice relationships. E.g., a job may require moving to a new city. Women who choose professional careers postpone marriage until they're out of college and have started their careers—by which time they find that many of their male classmates and co-workers are married.

Conversely, women whose primary goal is to be a mother are least likely to meet men. Such women forego higher education and professional careers. E.g., a woman who loves children may seek employment in childcare—where she works with other women.


Emotional Connection

Emotional connection makes women want sex. Emotional connection makes men want long-term relationships.

Emotional connection makes men and women switch gender roles (see Becoming a Couple). Individuals who use masculine sexuality (usually, but not always, men) want to have sex with many partners. Individuals who use feminine sexuality (usually, but not always, women) want long-term committed relationships. Emotional connection makes women switch to masculine sexuality, and makes men switch to feminine sexuality.

A man using masculine sexuality shows off his social status, physique, and money to attract women's attention. But that's all stereotyped gender roles can do (attract attention). Once he has a woman's attention, she'll look for relationship skills, entertainment skills (e.g., a sense of humor), and, above all, the emotional connection of "chemistry."

A woman using feminine sexuality shows off her youth and beauty to attract men's attention. But that's all her stereotyped gender role can do. If they don't emotionally connect, he'll date her only as long as he thinks he might get to have sex.


Be Seen in Different Venues

Make your suitor feel emotionally connected by letting him see you in a variety of situations.

E.g., volunteer with a non-profit organization, take a continuing education class, and participate in a new sport. When a man approaches you in one venue, invite him to do the other activities with you. If you met him in a business computers night class, suggest that he join you volunteering with Habitat For Humanity on Saturday, or at a rock climbing class on Sunday.

He'll see you using a variety of emotions. You may be confident and professional in the business computers class, caring and nurturing with the non-profit organization, and scared—then triumphant—climbing a cliff.

Wednesday, October 28, 2009

Is it time to remove meat from our diet?


Ilustration



wwwtimesonline.co.uk
Going low-carbon at the table to save the planet need not be so very painful. The climate change guru Lord Stern of Brentford called yesterday for Times readers to turn vegetarian to slow global warming. But most authorities — including the head of the United Nations climate change programme — agree that we could make a good start merely by dropping meat one day a week. This is what the citizens of the Belgian city of Ghent have been doing, voluntarily, all this year, without noticeable ill effects. The British eat 50 per cent more meat than they did 40 years ago; roast beef and two veg is part of our culture but tinkering with the portion control will not kill off John Bull. And it would certainly make us healthier.

There are other more radical ideas for diehard carnivores. Time to Eat the Dog is the title of a new book by two New Zealand environmentalists (there are several recipes from Korea available, should you choose to follow this path). The eco-pawprint of a large dog is the same as that of a 4.6-litre SUV driving 10,000km, according to the authors, who are both scientists at Victoria University of Wellington. They state that an average dog eats 164kg of meat and 95kg of cereals every year, which means that it takes 0.84 hectares (a football pitch) of arable land and tens of thousands of litres of water to give the dog his Pedigree Chum.

This illustrates how fantastically inefficient — and selfish — meat-eating is, whether by dog or Man. It takes roughly 10kg of vegetable matter or cereals to produce 1kg of beef, which means that the resources for one meat-eater’s dinner might feed five times as many people, or more. If Americans cut their meat consumption by just 5 per cent, the savings in grain and soya would feed, it is said, 25 million people every day.

The maths is plain. The planet cannot afford to go on feeding the carnivores any more. We are running out of the necessary resources more surely than we are running out of crude oil. And that is true even before you take the possible effects of climate change into account. There will be 9.2 billion people on Earth in 40 years’ time — enough to demand the resources of two planets, not one. Food production, according to the United Nations Food and Agriculture Organisation, will have to double to feed them because, as nations develop, their richer citizens demand more meat. Meat consumption in China is twice what it was a decade ago, although at about 50g per head a year it is still much less than in richer nations. In Britain we eat 74kg per person, while Americans consume 123kg each. In India they eat about 5kg per year, in most of Africa even less.

Meat is a rich person’s habit, and it is damagingly indulgent to a degree that would impress Jeremy Clarkson. According to United Nations statistics, livestock farming generates more greenhouse gases than the emissions of the world’s cars, trains, planes and boats put together. Then there is the destruction of rainforest to grow soya to feed beef, and the further impact of the processing, refrigeration, transport and finally the cooking of meat. It adds up to more than half of all the CO2 derived from food production that the world emits — and that is a third of the total carbon emissions.

Not soaking the kidney beans yet? Try this: the extraordinary rise in modern times of a whole range of health problems, from bowel, colon and other cancers to heart disease, is blamed on the rise in the proportion of meat in our diets. These are largely illnesses of the rich world — and although Britons are relatively controlled carnivores, we still eat 50 per cent more protein than doctors recommend.
The only problem with Lord Stern’s proposal, it seems to me, is over methane and nitrous oxide. These greenhouse gases are far more harmful to the atmosphere than carbon dioxide, and the 1.3 billion flatulent cows that we currently keep on the planet produce an awful lot of them. But if we start eating all the vegetables, won’t we begin to — how can this be put delicately? — start to emit more gas ourselves? Hot air and green views do tend to go together.
The solution is compromise eating: a new dietary regime that I am going to call quasitarian. It’s a bit thrifty, a bit retro: a throwback to how our not-so-ancient ancestors ate. It is the way that a lot of people in healthy places of the tropical world prepare their food. In Thai and other South-East Asian cuisines, protein embellishes a dish rather than dominating it: some dried fish or pork is used to add flavour to the rice, rather than being the main event. Meat serves as spice and salt: it makes the carbs and vegetables more pleasurable.

If you believe the old household management books, the British family of 50 years ago would cook a large roast on Sunday. But they wouldn’t eat it all. On Monday and Tuesday there would be slices of the cold joint for supper. On Wednesday Mrs Beeton would make a “ragout” from the remaining scraps. Come Thursday, the bones went into the stock pot for a soup. On Friday our forebears ate fish. To live a little more like this would not, I think, be a sacrifice: indeed, the diet is a lot more interesting than a grilled beefburger or a chicken breast every night.

By planning better and throwing away less, most of us could quite easily cut our meat-buying by 10 per cent without even noticing it. Bear in mind that British households chuck out 30 per cent of the edible food that they purchase, according to the government waste agency, WRAP. The chicken that goes into domestic rubbish bins every year comes to the equivalent of 33 million birds.

Food manufacturing throws away as much or more. This year I watched a British butcher and an Italian one each cut up a 75kg pig: the Briton chucked out some 15kg of the animal as not commercially usable; the Italian only six. He made some great sausages.

Quasitarianism will be so much fun that you’ll soon pity the carnivores. And the vegetarians. It’s hardly difficult, and you will have a green glow of righteousness to light the way. You are still allowed 90g of farmed meat — a decent-sized sausage — a day, according to the calculations in a recent article of the medical journal The Lancet (currently we consume an average 205g).

We’ll allow you to bend the rules a bit if the meat that you buy is organic and local, both of which are major factors in cutting emissions. You may eat wild animals: pheasant and venison will suit at this time of year. Milk and cheese are not too much of a problem, as dairy cows live far longer lives than animals bred for meat and the growing of grass to feed them absorbs carbon.

And what of the dog? When you have eaten it, you can get a goldfish. Their annual carbon fin-print is no more than that of a couple of mobile phones.

Monday, October 26, 2009

Anti-Gravity Treadmill, almost like exercising on Mars



Anti-Gravity Treadmill, almost like exercising on Mars

Want to get some exercise done in microgravity? Unless you travel to the International Space Station, exercise in a pool, or mount up on the pricey AlterG Anti-Gravity Treadmill, that was an impossibility until now. Expanding beyond the market of the super-rich and cash-awash pro sports teams, now AlterG will sell an anti-gravity treadmill for the merely rich, offering the $24,500 AlterG M300 for sale next month.
What the heck does it do? It creates air pressure strong enough to hold up a 400-pound behemoth. Using differential air pressure around your lower body to lift you up, it lets you move around in 20%-G or any variation between that and normal gravity. This is great for athletes recovering from leg injuries, old folks who can barely walk and need the exercise, and those of us who want to brag about running 500 miles this morning. Best of all, you can get a tremendous exercise benefit and weight loss without the stress on joints, bones, ligaments, and feet.
The exorbitantly expensive version is already used by half of the NBA teams, many NFL teams and 22 well-heeled collegiate athletic programs. You might not be able to buy one of these lower-cost M300-series models yourself, but look for the magnificent machines soon at a fancy rehab clinic or gym near you.



Anti-Gravity Treadmill, almost like exercising on Mars


Via AlterG  dvice.com

Bio-Identical Hormone Therapy has Staggering Health Benefits



Dr. Mark E. Richards with Ageless Impressions Plastic Surgery Institute is a nationally recognized plastic surgeon, and has been certified in both general surgery and plastic surgery. Every day at his plastic surgery in Washington, DC, he sees people who want to improve their appearance in some way to hopefully, look and feel better than ever about themselves. Aesthetics and appearances are part of his daily professional life – and now he wants to provide patients with the other half of what they are missing. “Cosmetic surgery can improve the way we look… bio-identical hormone therapy can improve our physical quality of life and feelings of youth.”

While bio-identical hormones have been known and available since the 1930’s, medical treatment with time release pellets has only been available in the United States since approximately 1990. Dr. Mark E. Richards, a Washington, DC plastic surgeon, is on a mission to educate his medical brethren and the general public about the magnitude of age-related ailments that can be reduced with time-release pellet bio-identical hormone therapy. As a plastic surgeon in the forefront of his profession, Richards is looking to improve a person’s quality of life in addition to their outside appearance.

Dr. Richards wants to help people overcome traditional physical and psychological ailments that occur with age, and believes the answer lies in bio-identical hormone therapy. As people get older, they are prone to: decreased bone density and muscle mass; increased body fat, blood sugars, and cholesterol; lack of energy; decreased libido; type-2 diabetes; and many other ailments. Many also begin to suffer from anxiety, symptoms of depression, and sleep disturbances. Dr. Mark Richards' research into these topics led him to discover that a large part of these common afflictions that occur as we get older are likely due to a decrease in the levels of our natural hormones – particularly testosterone and/or estradiol. “There’s been a search for anti-aging treatments for millennia. The answer lies within us. Many maladies are clearly linked to depletions in our hormone levels. Supplemental hormones can restore energy, health, and reduce the risks of developing some of these debilitating conditions.”

In fact, Dr. Richards says, increasing hormone levels could possibly eliminate 70-to-80% of osteoporosis, which leads to hip replacement, back pain, and other conditions. While decreasing hormone levels are often thought of as a “female” problem responsible for sleep disturbances, hot flashes, and fatigue, Dr. Richards states that osteoporosis rates are climbing in men along with complaints of lack of energy, depression, and erectile dysfunction. All these problems may significantly improve with increased hormone levels. Many conditions can be alleviated in people who start to exhibit symptoms and signs of the aging process once they hit their 40’s or 50’s, and sometimes even earlier. Dr. Richards says bio-identical hormones help in diminishing a host of problems, not only physical and psychological, but even financial. “As a result of preventing age-related health conditions, you could conceivably cause a dramatic cut in the cost of Medicare, and at the same time increase the percentage of seniors who are productive and contributing to our economy instead of draining away health care dollars for preventable diseases.”

Bio-identical hormones are hormones of the exact same chemical structures as those found in the human body. They are traditionally derived from an ingredient found in soy beans and yams. Dr. Richards says non-bio-identical hormones – those that have a different molecular structure than hormones produced by humans - are responsible for the known health risks and side effects when “hormones” are used in humans. Bio-identical hormones are just that: identical. “There has never been a single study showing bio-identical hormones are harmful when used in reasonable dosages.”

The treatments are administered to patients several times a year by inserting tiny, time-release pellets into the fat under the skin. Over a period of months, a steady stream of hormones is released into the bloodstream. Dr. Richards says this ultimately leads to the re-establishment of hormones’ protective benefits after our original levels have decreased, and can reduce the occurrence of the common diseases of aging, leading to a better long-term quality of life.

Even though Europe has been leading the way on this type of therapy for years, why isn’t bio-identical hormone therapy more popular in the U.S.? Dr. Richards says there are three main reasons: “Lack of appropriate physician education about bio-identical hormones (currently, hormone education is often funded by pharmaceutical companies with competing non-identical products); the prohibition on patenting human hormone molecules which explains the lack of widespread commercialization and distribution; and the inexplicable lack of attention being given to well done scientific studies suggesting the enormous health benefits of this cost effective therapy.”

Dr. Richards says he’s seen patients start to feel better after only a few weeks with the hormone pellets. The response so far has been enormously positive. “Both male and female patients have just been ecstatic. They tell me their moods and energy levels have been dramatically increased and that they feel refreshed when they wake up. Cholesterol and blood sugar levels have dropped. Women, particularly those near or after menopause, have called up giggling, saying they feel great.”

Dr. Richards says treatment with bio-identical hormone therapy needs much more serious attention, as the potential benefits both for individuals and society are too big to ignore. In addition to the relief of the above mentioned symptoms, he says there is credible evidence that these hormone supplements are prophylactic in the prevention of such illnesses as breast cancer and heart disease. “I feel that it’s a huge error that we’re not routinely testing hormone levels in people as soon as they display symptoms attributed to “aging”. Many costly and debilitating conditions can be prevented with bio-identical hormone therapy. We need to establish national prospective studies on this treatment, perhaps in conjunction with the National Institutes of Health’s Division on Aging.”

Sunday, October 25, 2009

NOW Grilled Chicken Gives You CANCER....What's Next? | Lawsuit Filed Against McDonalds, Burger King and Friendly's Restaurants


Lawsuit by Cancer Project seeks class action status

By Jon Hood

October 24, 2009
Mindful of the nation's concern with its collective waistline, fast food restaurants have in recent years sought to entice a more health-conscious group of customers through their front doors. Along with salads and fruit parfaits, almost every fast-food menu contains that staple of relatively healthful eating: grilled chicken.

Alas, grilled bird might pose a menacing risk of its own, according to a lawsuit filed in Hartford, Connecticut on Wednesday. The class action complaint, brought by the nonprofit Cancer Project on behalf of two Connecticut residents, alleges that McDonald's, Burger King, and Friendly's knowingly sold grilled chicken containing "substantial levels" of PhIP, a known carcinogen.

Daniel Kinburn, a Cancer Project lawyer, says that "Dozens of studies show even relatively small amounts of PhIP can increase the risk of various forms of cancer." McDonald's, Burger King, and Friendly's disagree; spokespeople for all three companies say that there is no evidence that small amounts of PhIP pose any appreciable risk.

The Cancer Project, based in Washington, D.C., focuses on preventing cancer and extending longevity in cancer survivors by promoting healthy lifestyles.

The complaint alleges not only that the defendants knew the chicken contained PhIP, but that they actively concealed this fact to prevent chicken sales from plummeting. The companies "concealed the presence of a known carcinogen in their grilled-chicken products to retain profits that would be lost, in whole or in part, as a result of properly informed consumers choosing other food products."

Maybe, but it's unclear which foods properly informed consumers would choose, at least if they still had to eat fast food. Even without considering the meteoric calorie levels and fat content of most fast food products, lately it seems that certain doom lurks around every greasy corner. Last month, a Chicago man sued Denny's, accusing the diner chain of hiding the fact that some of its foods contain sodium levels four times the recommended daily dosage. (Never mind that Denny's posts all nutrition information, including sodium content, right on its Web site.)

In July, the Cancer Project filed a suit in New Jersey demanding that hot dogs carry warnings similar to those found on cigarette packages. That suit cited clinical findings that two ounces of processed meat -- the amount in a typical hot dog -- increases the risk of colorectal cancer by a full 21 percent. The Cancer Project wants hot dogs labeled with a warning that "consuming hot dogs and other processed meats increases the risk of cancer."

The Cancer Project may end up seeking a similar remedy in this case. Kinburn said that, rather than preventing the sale of grilled chicken, his organization thinks the product "should be sold with a warning, like a chainsaw." Burger King already settled a similar suit in California, agreeing to post warnings in all restaurants in that state.

With all this talk of cancer, perhaps consumers should stick with a Big Mac? Maybe, but remember that the number one cause of death in America is heart disease, exacerbated by poor diet and inactivity. A recent study found that annual medical expenditures related to obesity have doubled in less than a decade, and might be as high as $147 billion every year.

And ground beef poses its own, uniquely terrifying risks: hamburger meat remains susceptible to E. Coli infection, which can be fatal. A recent New York Times expose detailed the struggle of a young dance instructor paralyzed by infected beef, and suggested that food inspection processes aren't much better than they were when The Jungle was published over 100 years ago.

So while statements like, "Even a grilled-chicken salad increases the risk of developing some cancers," -- offered by Cancer Group President Neal Barnard -- might be true (or they might not), the same can be said of a lot of things. It's very hard to live a normal life when you're constantly calculating the odds that today's lunch will land you in your deathbed. Consumers' best bet is to examine their diet as a whole, and consistently make the healthiest choices available to them.

Besides, we've heard that excessive worrying can lead to hypertension, which in turn can cause heart disease. So don't lose too much sleep over that grilled chicken sandwich.