ADD THESE FOODS TO YOUR PLATE
Extra virgin olive oil
The benefits: Olive oil isn’t only loaded with risk-reducing antioxidants and phytonutrients — including squalene which inhibits tumor growth — it also has a higher monounsaturated fat content than other oils. Monounsaturated fats don’t oxidize in the body. Oxidation, a process that produces chemicals called free radicals, increases cancer risk.
Extra virgin olive oil
Reap the rewards: Add at least two tablespoons of olive oil a day to your diet, perhaps even tossing vegetables in oil, which will make veggies tastier and encourage you to eat more. Use one tablespoon of extra virgin olive oil for every cup of veggies. Although it can be high in calories — about 120 calories per tablespoon– studies have found that the more extra virgin olive oil in your diet, the lower your risk.
Cruciferous vegetables
The benefits: Cruciferous veggies contain phytonutrients that stop the spread of cancer and halt cancer cells from forming. These phytonutrients also shift estrogen metabolism so your body produces a form of estrogen that doesn’t drive breast cancer.
Broccoli
Reap the rewards: Load your diet with broccoli, broccoli rabe, brussels sprouts, cabbage and kale. To get a bigger cancer-busting bang, cook them in oil, preferably extra virgin olive oil, which will help your body absorb more nutrients.
Dark green leafy vegetables
The benefits: Leafy veggies are loaded with folate, a B vitamin that strengthens your DNA. Low levels of folate have been linked to increased cancer risk.
Spinach
Reap the rewards: Choose spinach and kale, as the darker the leaves, the better.
Fatty fish
The benefits: Women who consumed fish oil supplements had a 32 percent lower risk of developing breast cancer after six years compared to non-users, according to a study from the journal Cancer Epidemiology, Biomarkers & Prevention. Fatty fish contains omega-3 fatty acids, which may decrease inflammation in the body. Researchers believe chronic inflammation may encourage breast cancer development.
Oily fish
Reap the rewards: Although women in the above study took supplements, researchers recommend getting omega-3s directly from fish. Chomp at least two 3.5-ounce servings of fatty fish like salmon, tuna and mackerel each week.
Tomatoes
The benefits: Tomatoes are packed with lycopene, a powerful antioxidant that not only gives tomatoes their redness but also protects against breast cancer by stopping cancer cell growth.
Lycopene is a powerful antioxidant
Reap the rewards: Your body absorbs lycopene best when tomatoes are cooked, concentrated or processed. Top sources include canned tomatoes, tomato sauces and tomato paste so you no longer have to feel guilty about indulging in pasta and pizza (as long as it’s veggie).
GO EASY ON THESE FOODS
Red meat
Why it’s bad: Grilling red meat creates compounds called heterocyclic amines (HCA), which drive cancers. Red meat also contains amino acids that stimulate the production of insulin and increase oxidation in the body, both of which boost cancer risk. In one study, women who ate well-done meat three times a week increased breast cancer risk by over 400 percent.
Red meat
Tame your tastebuds: You don’t have to give up your meat-eating ways and turn vegetarian, but do limit red meat consumption, eating no more than six ounces a month.
Grapefruit
Why it’s bad: Grapefruit may elevate levels of estrogen, which is associated with increased breast cancer risk. In a study from the British Journal of Cancer, women who ate a quarter grapefruit or more a day had a 30 percent increased risk of breast cancer.
Grapefruit
Tame your tastebuds: If you’re a grapefruit junkie, switch to other citrus fruits until more research is done, especially if you’ve had estrogen receptor-positive breast cancer.
Vegetable oils
Why they’re bad: Vegetable oils, including soybean, safflower, sunflower and corn, are high in polyunsaturated fats, which increase cancer-promoting oxidation in the body.
Vegetable oils
Tame your tastebuds: Replace vegetable oils with extra virgin olive oil or canola oil. Unfortunately, you should also eliminate mayonnaise (unless it’s made with olive or canola oil and contains no partially hydrogenated fats), margarine and foods that contain partially hydrogenated oil (i.e. peanut butter, cookies and muffins), as all of these foods contain vegetable oils. The upshot? You now have permission to eat butter again.
Sweets
Why they’re bad: Women who reported consuming the most sweets, including desserts, sweetened beverages and added sugars, had a 27 percent greater risk of breast cancer than women who consumed less, according to the journal Cancer Causes and Control. A diet high in refined carbohydrates like those found in sweets is associated with higher levels of blood glucose, forcing the body to release insulin. That insulin encourages cancer cells to grow and could result in higher levels of estrogen, which may promote the development of breast cancer.
Sweets
Tame your tastebuds: Keep that sweet tooth in check. Although you don’t have to go cold turkey, view sweets as an occasional treat, not a daily indulgence.
Processed meats
Why it’s bad: Researchers suspect that compounds used as preservatives in processed meat like deli meats, bacon, ham and hot dogs morph into cancer-causing compounds in the body.
Processed meats
Tame your tastebuds: Cut all processed meat from your diet. If you must indulge, do so only during special occasions.
- Similar posts
- Cooked breakfast cuts fertility in men (16.5%)
- Foods for Your Heart (14.2%)
- More superfoods (12.3%)
- A to Z of food terms (10.3%)
- Health benefits of Olive Oil (6.4%)
The Daily Mirror today hails grapefruit as a “fruity ‘cure’ for diabetes”. The newspaper suggests that the chemical naringenin found in the fruit “can do the same job as two drugs used to treat type-2 diabetes”.
Surprisingly, the research in question only looked at the effects of naringenin on human and rat liver cells in the laboratory. This very preliminary research has certainly not identified a “cure” for diabetes. It only concentrated on how the chemical affected the fat metabolism of cells rather than processes directly related to diabetes. Until clinical trials are carried out in humans, it is not possible to say whether naringenin might be an effective medical treatment or whether it carries side effects.
Grapefruit is known to interact with enzymes in the body that break down many drugs. This can mean that consuming too much grapefruit can interfere with people’s drug treatment and cause harmful effects. Diabetics or other individuals taking medications should not attempt to replace or supplement their prescribed medication with grapefruit, as some news reports might suggest.
Where did the story come from?
The study was carried out by researchers from Shriners Hospitals in Boston and other research centres in the US, Israel and France. The study was funded by the US National Institute of Diabetes and Digestive and Kidney Diseases, the European Research Council and the Harvard Clinical Nutrition Research Centre. It was published in PLoS One, the peer-reviewed open-access journal of the Public Library of Science.
This study was covered by the Daily Mirror, Daily Mail and Daily Express. All of these newspapers claim that grapefruit can “fight” or “cure” diabetes, and that it has the same benefits as two diabetes drugs. These claims wildly over-extrapolate the findings of this preliminary laboratory research. None of the newspaper reports clarify that this was only laboratory research on isolated cells or that any potential benefits or side effects of naringenin will remain unclear until there are human studies.
What kind of research was this?
This was laboratory research looking at how a chemical called naringenin, found in grapefruit, affects liver cells under laboratory conditions.
The researchers were interested in doing this as studies have suggested that naringenin can reduce the level of one type of cholesterol (LDL) in humans and other animals. This study aimed to work out the chemical mechanism by which naringenin might have this effect. This type of study is appropriate for answering this type of question. However, it would not be appropriate to tell us what the effects of naringenin on the body as a whole would be.
What did the research involve?
Naringenin has anti-inflammatory properties and induces a chemical reaction called beta oxidation. The researchers say that these properties suggest it could be acting in a similar way to drugs such as fibrates and glitazones, which are used to treat people with high levels of fats in the blood and to treat type 2 diabetes respectively. Both increase the activity of proteins called PPAR alpha and PPAR gamma in cells.
Previous studies suggested that naringenin reduces the activity of an enzyme called HMGR, which is involved in cholesterol metabolism. HMGR is in turn controlled by a protein called LXR alpha, and the researchers thought that naringenin could be having its effect on HMGR by interacting with LXR alpha. Cholesterol-lowering statin drugs work by targeting HMGR.
To investigate the interactions reported in previous studies, the researchers took took samples of human cells (including liver cells) grown in the laboratory and treated them with naringenin. They looked at the effects on LXR alpha and the PPAR alpha and gamma proteins targeted by fibrate and glitazone drugs.
LXR alpha and both PPAR proteins are involved in controlling the activity of certain genes in the cell, so the researchers then looked at whether naringenin affected the activity of genes controlled by PPAR alpha and LXR alpha.
Finally, the researchers tested the effect of naringenin on freshly extracted rat liver cells.
What were the basic results?
The researchers found that naringenin did make PPAR alpha and PPAR gamma more active in human cells grown in the laboratory. They found that naringenin affected PPAR activity in liver cells in a similar manner to the drug ciglitazone. Naringenin inhibited the activity of the LXR alpha protein in human cells grown in the laboratory.
Treating liver cells with naringenin increased the activity of those genes involved with fatty acid oxidation that are controlled by PPAR alpha. Treatment also reduced the activity of genes controlled by LXR alpha. These changes in gene expression suggested that the cells were shifting from making fats and cholesterol to breaking down fats.
Finally, the researchers found that treating freshly extracted rat liver cells with naringenin for 24 hours reduced their production of a type of fat called triglycerides, and also reduced their production of bile salts.
How did the researchers interpret the results?
The researchers concluded that: “Our findings explain the myriad effects of naringenin and support its continued clinical development. Of note, this is the first description of a non-toxic, naturally occurring [LXR alpha] inhibitor.”
Conclusion
This complex laboratory research suggests that naringenin can affect proteins and genes involved in fat metabolism in liver cells. Although the effect that it has on the cells is similar to the effects of drugs such as the fibrates and glitazones, this does not necessarily mean that naringenin could be used to treat the same conditions as the fibrates and glitazones. In the body different drugs interact with different subsets of the numerous proteins and molecules in the body in different ways. It is these complex interactions which will determine their overall effects. This study has only assessed interactions of naringenin with a small number of proteins in cells in the laboratory, and cannot tell us what the overall balance of positive and negative effects will be on the whole body.
Further points to consider:
* This study focused on the fat-metabolising effects of narangenin, suggesting a potential for treating people with high cholesterol rather than diabetes, as was reported in newspapers.
* The reported link to diabetes is more tenuous considering that the only association that has been made in this study is likening the action of naringenin to the effect of glitazone drugs. These are not the drugs of choice in diabetes; they are only used in certain circumstances. Importantly, they have been identified to carry cardiovascular risk and are used under close supervision.
* This study cannot tell us whether eating grapefruit or drinking grapefruit juice would provide sufficient naringenin to act upon cells in the same way as observed in this lab experiment.
* Although the authors of the current research describe an uncontrolled study of naringenin in people with high cholesterol, further randomised controlled studies in people with this or other conditions would be required to determine what its beneficial and adverse effects might be.
Grapefruit is also known to interact with enzymes in the body that break down many drugs. This can mean that consuming too much grapefruit (e.g. by drinking grapefruit juice) can interfere with people’s drug treatment and cause harmful effects. For example, people taking the statin simvastatin to control their cholesterol levels are advised to avoid drinking grapefruit juice as it can increase the chance of side effects from the drug. Grapefruit also is known to interact with a range of cardiovascular drugs and other medicines.
Diabetics or other individuals taking medications should not increase their consumption of grapefruit or grapefruit juice based on this study’s findings.
An Aussie research team has identified a new risk factor for developing breast cancer.
According to the study conducted jointly by the Peter MacCallum Cancer Centre, the University of Melbourne and the University of Queensland, the risk factor involves a modification (DNA methylation) to the BRCA1 gene.
BRCA1 is known for its involvement in breast and ovarian cancer. Women with mutations in this gene, which inactivates its function, are predisposed to these diseases.
The DNA methylation modification is known as an epimutation and acts to turn off the BRCA1 gene from its normal protective function against breast cancer.
The study involved women diagnosed with breast cancer before the age of 40 years for whom BRCA1 mutations had not been identified.
The epimutation was found in the blood of some women with breast cancer, especially those who develop the same type of breast cancer that develops in women with a BRCA1 mutation.
However, unlike mutations in the BRCA1 gene, these epimutations appear not to be inherited and the relatives of women with epimutations are not at increased risk of breast or ovarian cancer.
The paper has been published online in the journal Cancer Prevention Research.