Disease Proof : Disease Proof : Health & Nutrition News & Commentary : Dr. Joel Fuhrman

       Prostate cancer is the second most common cancer in men (second to skin cancer). It is well established that the death rate from prostate cancer is quite low:

• Men in the U.S. have a 16% lifetime chance of being diagnosed with prostate cancer, but only a 3% chance of dying from it.[1]
• The five-year and ten-year relative survival rates for prostate cancer are over 99% and 91%, respectively. [2]
• The primary causes of death of men with prostate cancer are cardiovascular disease and other cancers.[3]

After treatment for prostate cancer (either radiation or prostatectomy), prostate-specific antigen (PSA) levels continue to be monitored. If PSA begins to increase, this is called “biochemical recurrence” (BCR) of prostate cancer.

Biochemical recurrence and mortality

A study in U.S. veterans attempted to figure out how biochemical recurrence affected risk of dying from prostate cancer. Six hundred twenty three men were followed for 15 years after being treated for prostate cancer. In this study, 37% of men who were treated with prostatectomy and 48% of men who were treated with radiation experienced BCR.

Overall, a total of 387 men had died within 15 years – 48 of these men died of prostate cancer, representing 12% of total deaths. For men who underwent prostatectomy and experienced BCR, the total rate of death within five years was 34%, and the rate of prostate cancer death was 3%. For radiation and BCR, death rate within five years was 35%, and prostate cancer death rate was 11%.[4, 5]

In short, the researchers came to the conclusion that the probability of dying from prostate cancer, even after biochemical recurrence, is relatively small. They mention that their findings are in agreement with the often quoted phrase “most men die with prostate cancer, not of it.”

Since BCR is defined as an increase in PSA following treatment, this data also suggests that PSA levels may not be an accurate predictor of risk after treatment. Further studies will likely examine this issue.

Routine PSA screening

Routine PSA screening is known by the scientific community not to be as accurate or valuable as the public is led to believe. About 70% of men with elevated PSA do not actually have cancer, and PSA screening is not thought by scientists to reduce prostate cancer-related deaths.[6-8] Richard J. Ablin, who originally discovered PSA in 1970, recently called PSA screening a “hugely expensive public health disaster” in a New York Times editorial. Dr. Ablin supports his assertion with these facts:

• FDA approval of PSA tests occurred largely in response to a study that found that PSA screening was only able to detect 3.8% of cancers, and that blood PSA levels may be elevated due to a number of factors, such as drug use, infections, and benign prostatic hyperplasia (BPH).
• The U.S. Preventive Services Task Force, the American College of Preventive Medicine, and the American Cancer Society do not recommend routine PSA screening. However, PSA screening is still routinely used.[1]

Men should not rely on PSA screening as a method of “early detection” to prevent prostate cancer. Rather they should avoid the cause of prostate cancer. Diets high in vegetables (especially cruciferous vegetables and tomato products) and fruit, and low in dairy products, meat, and processed foods, are known to be protective.[9-11] Living and eating healthfully protects against prostate cancer, as well as the other chronic diseases common to Americans (such as heart disease, strokes, and colon cancer) – the same diseases that kill most men with prostate cancer. For those who already have prostate cancer, a healthy, plant-based diet is effective at halting progression of the disease.[12-15]

References:

1. Ablin, R.J., The Great Prostate Mistake, in New York Times. 2010. p. 27.
2. American Cancer Society. What are the key statistics about prostate cancer? 06/30/2010 09/02/2010]; Available from: http://www.cancer.org/Cancer/ProstateCancer/DetailedGuide/prostate-cancer-key-statistics.
3. Ketchandji, M., et al., Cause of death in older men after the diagnosis of prostate cancer. J Am Geriatr Soc, 2009. 57(1): p. 24-30.
4. Uchio, E.M., et al., Impact of biochemical recurrence in prostate cancer among US veterans. Arch Intern Med, 2010. 170(15): p. 1390-5.
5. Harding, A. Even when prostate cancer returns, most survive. Reuters Health 08/25/10; Available from: http://www.reuters.com/article/idUSTRE67O4RR20100825?feedType=nl&feedName=ushealth1100.
6. Esserman, L., Y. Shieh, and I. Thompson, Rethinking Screening for Breast Cancer and Prostate Cancer. JAMA: The Journal of the American Medical Association, 2009. 302(15): p. 1685-1692.
7. Coldman, A.J., N. Phillips, and T.A. Pickles, Trends in prostate cancer incidence and mortality: an analysis of mortality change by screening intensity. CMAJ, 2003. 168(1): p. 31-5.
8. Andriole, G.L., et al., Mortality results from a randomized prostate-cancer screening trial. N Engl J Med, 2009. 360(13): p. 1310-9.
9. Steinbrecher, A., et al., Dietary glucosinolate intake and risk of prostate cancer in the EPIC-Heidelberg cohort study. Int J Cancer, 2009. 125(9): p. 2179-86.
10. van Breemen, R.B. and N. Pajkovic, Multitargeted therapy of cancer by lycopene. Cancer Lett, 2008. 269(2): p. 339-51.
11. Ma, R.W. and K. Chapman, A systematic review of the effect of diet in prostate cancer prevention and treatment. J Hum Nutr Diet, 2009. 22(3): p. 187-99; quiz 200-2.
12. Frattaroli, J., et al., Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology, 2008. 72(6): p. 1319-23.
13. Ornish, D., et al., Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci U S A, 2008. 105(24): p. 8369-74.
14. Ornish, D., et al., Intensive lifestyle changes may affect the progression of prostate cancer. J Urol, 2005. 174(3): p. 1065-9; discussion 1069-70.
15. Fuhrman, J., Dr. Joel Fuhrman Case Study Series: Prostate Cancer.

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A recent flurry of news articles have reported on a recent study that showed that treatment of pancreatic cancer cells with fructose increased cell proliferation – uncontrolled proliferation is a hallmark of cancer. This follows on the heels of another study that linked fructose consumption from added sugars to elevated blood pressure. The bad press on fructose is making people question the safety of the ubiquitous commercial sweetener, high fructose corn syrup (HFCS).

Due to the introduction of HFCS, fructose intake has increased dramatically in the U.S. since the 1970s. Between 1970 and 2000, HFCS intake increased by 100-fold, and total fructose intake increased by 30%.¹

Fructose makes up half of the sucrose molecule (with glucose), but may also be present in “free” form. Abosrption of fructose and glucose, and the differences between fructose in natural foods and fructose in HFCS are explained in this post.

These authors investigated whether cancer cells could use fructose for energy, because they are known to use glucose – cancer cells are known to have a greater number of glucose transporters and metabolize glucose more rapidly than normal cells because their rapid proliferation requires greater amounts of energy.²

Although different transport mechanisms are used to get fructose and glucose into cells, their metabolism is thought to be similar once they enter cells. However, these scientists found that in human pancreatic tumor cells, metabolism of fructose and glucose occurs via different pathways, both leading to cell proliferation. Keep in mind that both sugars led to increased cell proliferation at similar rates – that is, this study did not show that fructose is “worse” than glucose, just that they stimulate proliferation by different mechanisms. Glucose was used by the cancer cells for energy production, whereas fructose was used to generate nucleic acids (DNA and RNA). This study was the first to show that cancer cells could differentiate between fructose and glucose, and that they could use fructose as efficiently as glucose to fuel cell growth.^3,4

Sucrose intake, fructose intake, and high glycemic load have all been associated with pancreatic cancer in epidemiological studies, and diabetes also increases risk.^5,6  

The message of this study and others on the negative effects of fructose is that added sugars, abundant in the Western diet, are detrimental to health and should be minimized, but sadly this is not the message that is getting through to the public. 

With the recent media frenzy around HFCS, the conventional wisdom seems to have become that sugar is superior to HFCS because it is more ‘natural’ – prompting many companies to switch from HFCS to sugar for sweetening their products. Meanwhile, the high fructose, low glycemic index sweetener agave nectar, once elevated to health food status, is now being doubted because of the negative press on fructose. 

Comparing sweetener to sweetener is missing the point. All sweeteners have negative health effects, regardless of their relative quantities of fructose, glucose, and sucrose. 

Some sweeteners spike blood glucose, others raise triglycerides and form advanced glycation end products (AGEs), and all provide excess calories and are devoid of nutrients. This is not a question of which sweeteners are healthy and which are unhealthy. None are healthy. All are merely concentrated sugars – contributing to obesity and all its consequences – and therefore should all be minimized or completely avoided in a health-promoting diet.

References:

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Synthetic food dyes are used in many processed foods, such as colored breakfast cereals, candy, and “fruit-flavored” beverages and snacks. A total of 15 million pounds of dyes are added to the U.S. food supply each year. Our consumption of food dyes has increased 5-fold since 1955 as our nation has consumed more and more packaged foods.¹

These synthetic dyes have been linked to a wide variety of health concerns including behavioral problems, hyperactivity, allergic reactions, and even cancers. The Center for Science in the Public Interest (CSPI), an organization that advocates for nutrition and food safety, is calling for a ban on these synthetic dyes. Food-based dyes such as beet juice and turmeric are readily available, but are more expensive and often less bright, making synthetic dyes more attractive to food manufacturers.

Food dyes and allergic reactions:

Blue 1, Red 40, Yellow 5, and Yellow 6 have been reported to cause allergic reactions in some people.

Food dyes and hyperactivity:

Food dyes are of particular concern for children, since many colored foods are marketed to children, and their smaller body size makes them more susceptible to potential toxins. Hyperactivity in children following ingestion of food dyes is well-documented in placebo-controlled studies. Furthermore, a 2004 meta-analysis of 16 studies in children who were already hyperactive showed that their hyperactive behavior increased in response to food colorings.² In a study published in Lancet in 2007, researchers tested two different mixtures of food dyes vs. placebo in children of two age groups – one mixture increased hyperactivity in 3 year old children, and both mixtures increased hyperactivity in the 8-9 year-olds.³ This study sparked a reaction by the British government. They instructed food manufacturers to eliminate all of these synthetic dyes by the end of 2009. In fact, starting later this month, a warning notice will be required on dyed foods in Europe stating that these foods “may have an adverse effect on activity and attention in children.”⁴  As a result, several international food companies now produce products with food-based dyes or no dyes in the U.K., but continue to include synthetic dyes in their U.S. products.

Food dyes and cancer:

There are eight commonly used synthetic dyes in the U.S., and all have undergone toxicity and tumorigenicity testing in animals. CSPI summarized the results of cancer-related studies in a recent report¹:

• Red 3 was acknowledged by the FDA to be a carcinogen in 1985 and was banned in cosmetics and externally applied drugs. However Red 3 is still used in ingested drugs and foods.
• The three most widely used dyes (Red 40, Yellow 5, Yellow 6) which account for 90% of dyes in the U.S. are contaminated with low levels of chemical carcinogens, as byproducts of the manufacturing process. Although the FDA places limits on the concentrations of these contaminants in the final dye products, they still may pose risks.
• Citrus Red 2 added to the diet resulted in bladder tumors.
• Red 3 resulted in thyroid tumors and caused DNA damage.

In their report, CSPI noted flaws in many of the animal cancer studies on Yellow 6, Yellow 5, Red 40, Green 3, and Blue 2, including bias – most studies were either commissioned or conducted by dye manufacturers, short duration, and lack of exposure to dyes during fetal development. Additional studies are likely needed to determine whether these dyes are safe.

The simplest and most effective way to avoid the potential harmful effects of synthetic dyes is to avoid processed foods.   Unrefined plant foods contain health promoting phytochemicals, not empty calories and synthetic additives of questionable safety. When buying the occasional packaged food, check the ingredient list to avoid synthetic dyes.

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The weather is warm, school is out, and summer is upon us. Because of depletion of the ozone layer that protected against harmful radiation in earlier times, today’s sun exposure is not truly natural, and is more damaging. As we plan to spend more time outdoors, we must also avoid excessive sun exposure to protect ourselves from the free radical damage and wrinkling that can ensue and to minimize the risk of skin cancer. First we should be sure to seek shade often, wear protective clothing, and avoid noon time sun. When choosing a sunscreen or sunblock is important to use the safest and most effective methods of sun protection – the SPF number does not tell the whole story.

Exposure to sunlight triggers vitamin D production. However, according to the American Academy of Dermatology there is no safe amount of unprotected UV exposure that can allow for sufficient vitamin D production without increasing the risk of skin cancer. Supplementation is the safest method of maintaining sufficient vitamin D levels.¹

Melanoma, the deadliest form of skin cancer, has been steadily on the rise since, its prevalence increasing approximately 2.9% per year since 1981.² It is essential to protect your skin from the sun’s rays.

UVA and UVB rays

UVB rays are the rays that cause sunburn. They bind DNA and can cause mutations that lead to skin cancer. UVA rays penetrate more deeply into the skin, causing oxidative damage that can lead to skin aging and skin cancer.³

Both types of radiation are believed to contribute to melanoma, but many sunscreens block only UVB.

Types of sun protection

• Sunscreen absorbs and deflects the sun’s rays away from the skin through a chemical reaction. Sunscreens vary in their ability to protect against UVB and UVA rays depending on the ingredients used. Common sunscreen ingredients include oxybenzone, octisalate, and avobenzone.
• Sunblock creates a physical barrier between the UVA and UVB rays and the skin.⁴ Titanium dioxide and zinc oxide are the most common sunblocks. Physically blocking sunlight from penetrating the skin is the most effective way to block UVA radiation.

Which type of sun protection is safer? Which is more effective?

Many sunscreens do not protect against UVA rays. The SPF listed on these products refers only to UVB protection. The FDA has no standards for measuring how well a sunscreen blocks UVA rays. Ironically, a product with a high SPF, and no UVA protection, could promote unsafe sun exposure behaviors – you may falsely believe that you can safely stay in the sun longer, overexposing yourself to UVA rays even though you avoid sunburn from the UVB rays.⁵

The Environmental Working Group has reported this troubling news about sunscreens: Vitamin A is often listed on sunscreen labels as an antioxidant that can fight skin aging. Vitamin A is an antioxidant, but in isolation it could be dangerous, both in supplements and for the skin. Sunscreens may actually promote the progression skin cancer if they contain vitamin A – vitamin A applied to the skin has been shown by FDA studies to accelerate the growth of skin tumors in animals.⁶

Sunscreens may also damage your skin. Common sunscreen ingredients can generate free radicals, causing oxidative damage. The sunscreen itself and how often it is applied determines whether it releases or absorbs more free radicals.⁷

Chemical sunscreen ingredients, including oxybenzone, can potentially disrupt hormonal systems in the body, which could have long-term health implications.⁸

In addition, a number of studies have linked allergic reactions to chemical sunscreens, particularly oxybenzone.⁹ Little is known about the potential harm of chronic sunscreen use and the systemically absorbed chemicals deposited after topical application.¹⁰

These sunscreen ingredients are potentially harmful and should be avoided:¹¹

• Oxybenzone (found in 60% of sunscreen products)
• Octisalate (found in 58% of sunscreen products)
• Octyl methoxycinnamate (OMC; found in 40% of sunscreen products)
• Padimate O

Mineral sunblocks contain either titanium dioxide or zinc oxide, and these are preferable to chemical sunscreens. These minerals do not penetrate as deeply into the skin as chemical sunscreens. They lie on top of the skin and penetrate only into superficial layers, reflecting UV rays before they cause damage. Mineral sunblocks are the only method of sun protection that blocks UVA rays.

Nanoparticles in sunscreens

There are concerns about certain sunblock products that use small particles of titanium dioxide and zinc oxide produced via nanotechnology. The purpose is to make the sunblock more easily absorbed by the skin and therefore more transparent. These tiny nanoparticles, however, can penetrate biological membranes and easily reach cells. Nanoparticles are smaller than anything humans have put into commercial products before.  Preliminary investigations have found only a limited ability of mineral nanoparticles to penetrate the skin¹², but oxidative stress and DNA damage to skin cells have been observed. Also, upon inhalation these particles reach the bloodstream and several organs.^11,13 Additional studies are needed in order to definitively determine whether these products are safe.

Mineral sunblock is the safest choice.

Overall, the physical sunblocks, with titanium dioxide and zinc oxide, are the safest choices for sun protection. They are the least irritating, and they safely provide protection against both UV-A and UV-B rays. According to the Environmental Working Group, mineral sunblocks containing nanoparticles are still a safer option than chemical sunscreens. Unfortunately, sunblock labels most often do not disclose whether the product contains nanoparticles. We've done our research and found a product-line which uses nonmicronized zinc oxide that is safe and effective. Our GreenScreen line protects against both UV-A and UV-B without the use of nanoparticles or harmful chemicals.

Remember, sun protection products must be applied liberally to insure you receive the SPF protection claimed on the label. Most people apply 25-75% less sunscreen than the amount used when the manufacturers test their products.¹⁴

Make the summer sunshine a safe, fun, and healthy experience for you and your family!

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In his book Disease Proof Your Child, Dr. Fuhrman states that the biggest contributor to adult cancers is an unhealthy childhood diet.¹

Cancer takes years and years to develop. In fact,  a woman's diet during pregnancy is known to influence the risk of childhood cancers in her children.² A woman’s risk of breast cancer similarly is influenced during fetal development by her mother’s dietary habits.³ But breast cancer risk may begin even earlier than this.

A recent animal study suggests that breast cancer risk may be transmitted even from previous generations – that a grandmother’s unhealthy diet may translate into increased breast cancer risk for her granddaughters. 

The researchers conducted their study as follows:  A generation of female rats (grandmothers) was fed either a normal or high-fat diet during pregnancy - the high-fat diet provided an excess amount of omega-6 fat, attempting to partially mimic the standard American diet, with its abundance omega-6-rich animal products and oils.  Mother and granddaughter rats were fed a normal diet, and granddaughter rats either had two normal diet grandmothers, two high-fat diet grandmothers, or one of each. “Granddaughter” rats were given a chemical carcinogen to initiate breast cancer, and researchers recorded whether or not they developed tumors.⁴

These were their findings:

• 50% of the rats with two normal diet grandmothers developed breast tumors
• 68% of the rats with one high-fat diet grandmother developed breast tumors
• 80% of the rats with two high-fat diet grandmothers developed breast tumors⁵

Based on these results, an unhealthy diet may cause inheritable changes in gene expression, causing subsequent generations to be more susceptible to breast cancer-initiating factors such as chemical carcinogens. Family-related risk of breast cancer is usually thought to be related only to specific genes, such as BRCA1 and BRCA2, which are known to increase breast cancer risk. However, this study points to non-genetic, but family-related transmission of risk via dietary habits.

These findings imply that what mothers eat during pregnancy not only affects their children, but their children’s children as well.

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Part 2:

Angiotensin receptor blockers - anti-hypertensive drugs – linked to lung cancer and heart-related deaths

Angiotensin-receptor blockers (ARBs) are used to to treat hypertension, heart failure, and diabetic nephropathy (kidney dysfunction). They work by blocking a hormone system that regulates vascular tone and water and salt balance to control blood pressure.

Because angiotensin can affect cell survival and angiogenesis (formation of new blood vessels), two important factors in tumor growth, angiotensin is thought to play a role in cancer progression.¹ To determine whether taking ARBs affected cancer risk, scientists performed a meta-analysis of several studies to uncover any possible links between ARBs and cancers. They determined that ARBs carry a increased risk of new diagnosis of any cancer (8%), and a significantly higher risk of lung cancer (25%).²

One ARB in particular, olmesartan (Benicar), is now under scrutiny by the FDA for potential cardiovascular risks. In a clinical trial testing olmesartan’s efficacy for slowing kidney damage in diabetics, there were increased rates of sudden cardiac death and death from heart attack and stroke in the subjects taking the drug compared to those taking placebo.³

In my practice, and from results recorded from members at DrFuhrman.com, even people with dramatically high blood pressure readings and dramatically high cholesterol levels have successfully returned their levels to normal without medications. In fact, as published in the medical journal Metabolism, the nutritarian diet is the most effective method to lower high cholesterol, even more effective than drugs.⁴ If people were very informed of these results and the risks involved with taking medications many more would certainly embrace nutritional excellence as therapy. High cholesterol and high blood pressure are lifestyle-created conditions, and the safest and most effective treatment is a high nutrient diet and exercise.

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A study in Sweden examining the effects of zinc and the omega-3 fatty acid DHA on mortality in prostate cancer patients was presented at the American Association for Cancer Research annual meeting in April. Five-hundred twenty-five men with prostate cancer were followed for twenty years after being diagnosed with prostate cancer.  Baseline dietary habits, stage of cancer at diagnosis, and deaths over the twenty years were recorded and analyzed.¹

The authors chose to investigate these two nutrients because zinc and omega-3s share the common action of attenuating the inflammatory response, and chronic systemic inflammation may fuel prostate cancer progression. Importantly, zinc and DHA are both difficult to obtain on a plant-based diet.

Zinc is especially concentrated in the prostate, but zinc levels become depleted in cancerous cells. Addition of zinc to cultured prostate cancer cells leads to cell death, possibly by suppressing the activity of inflammatory molecules. A previous study found that long-term zinc supplementation was associated with reduced risk of advanced prostate cancer.²

In the current study, the researchers organized the study participants into quartiles according to their intakes of zinc and DHA. In men who were diagnosed at with early stage cancers, the highest quartile of zinc intake (15.7 mg zinc daily or more) was associated with a 74% reduction in risk of death from prostate cancer compared to the lowest quartile (12.8 mg zinc daily or less). Absorption of zinc tends to be low on a vegan diet – beans, whole grains, nuts, and seeds have high zinc content, however these foods also contain substances that inhibit the aborption of zinc.³ A 2009 study of vegetarians found a high prevalence of zinc deficiency.⁴ To correct for bioavailability, the zinc requirement for vegans may be as much as 50% higher than that of omnivores.⁵

I recommend zinc supplementation with a multivitamin and mineral to ensure sufficient zinc intake in vegans or those who minimize animal foods.

The connection between omega-3 intake and prostate cancer is somewhat complex. For example, flaxseed oil was found to increase prostate cancer risk, whereas whole flaxseed, EPA, and DHA were found to be protective.^6,7,8 EPA and DHA are known to have anti-cancer and anti-inflammatory properties.⁹ In this study, the highest quartile of DHA intake was associated with 30% reduced risk of overall prostate cancer mortality, and a 45% risk reduction in men diagnosed at early stages, supporting the idea that DHA is protective against prostate cancer. Plant foods contain ALA, which can be elongated to DHA, but the major food source of DHA is fish, which often contains pollutants and is not acceptable for vegetarians and vegans. For these reasons, I recommend a laboratory cultivated DHA supplement made from micro-algae, which is also a more environmentally sustainable option than fish or fish oil.

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Overweight/obesity is a significant risk factor for breast cancer.¹ The American Institute for Cancer Research estimates that 17% of breast cancers (this equates to 33,000 new cases per year) are due to excess weight alone, and women who are obese when diagnosed are more likely to die from breast cancer after diagnosis.²

A study of 72,000 postmenopausal women presented at this year’s American Association for Cancer Research annual meeting took into account body mass index (BMI) at age 20 and at their current age (55-74), and compared breast cancer risk between those who gained weight and those who did not. They found that a 5 point increase in BMI during these years doubled the likelihood of postmenopausal breast cancer compared to women whose BMI remained stable.³

Although excess weight has been consistently associated with breast cancer risk, the scientists undertook this study because previous studies investigating BMI or body weight during early adulthood were not conclusive. Rather than look simply at BMI at age 20, they looked at the change in BMI over time. Their results clearly indicate that weight gain puts women at risk for breast cancer, and confirms the importance of maintaining a healthy weight for cancer protection.

How much weight gain is risky?

Weight gain of 30 lbs. in a 5’4” woman would produce a 5 point increase. This may seem like a large amount of weight, but over thirty years, it would be a barely noticeable amount – a steady weight gain of 1 pound per year. This study suggests that even 1 pound per year is a dangerous amount of weight gain. And it turns out that this dangerous amount of weight gain is quite common - 60% of the women in the study had increased their BMI by at least 5 points since age 20.⁴  This tells us that most American women likely do gain this much weight during adulthood, doubling their risk of breast cancer.

Read more about Dr. Fuhrman’s strategy for breast cancer prevention.

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You’ve probably seen these headlines on the internet or television recently, claiming that fruits and vegetables provide very little protection against cancer. Of course something like this makes big news – it makes eaters of the typical Western diet feel validated in their unhealthy choices. But is it true? Do fruits and vegetables really offer only weak protection against cancer? Let’s look at the details of the study.

Researchers analyzed data from the European Prospective Investigation into Cancer and Nutrition (EPIC), a large study of over 400,000 people. Subjects reported dietary intakes and were followed for approximately 8 years. The researchers reported the associations between fruit and vegetable intake and risk of total cancer. Two-hundred grams of combined fruits and vegetables (approximately 2 servings) offered a 3% decrease in risk that was statistically significant.¹ 

According to the lead scientist, Dr. Paolo Boffetta, from Mount Sinai Medical Center, “The bottom line here is that, yes, we did find a protective effect of fruit and vegetable intake against cancer, but it is a smaller connection than previously thought. However, eating fruits and vegetables is beneficial for health in general and the results of this study do not justify changing current recommendations aiming at increasing intake of these foods.”²

A tiny amount of plant food offers a tiny amount of benefit.

Yes, 3% is a tiny reduction in risk – but 200 grams is also a tiny amount of fruits and vegetables! One medium apple is approximately 180 grams, one cup of blueberries is 150 grams, and 1 cup of chopped raw broccoli is 90 grams. So keep in mind all these people did is eat the standard cancer-causing diet and add one apple or two cups of vegetables with dinner, they did not follow a vegetable-centered diet. They were still eating all the cancer-causing processed foods and animal products as their major source of calories.

The median daily intake in this study was 335 grams of fruits and vegetables combined per day – only about three servings. According to the CDC, only one-third of U.S. adults eat two or more servings of fruit per day, and only one-quarter of adults eat three or more servings of vegetables per day.³ These minimal amounts cannot be expected to provide disease protection. I recommend a far more substantial intake of fruits and vegetables with 90 percent of calories coming from nutrient rich plant material, lots of it raw and green. I recommend about two pounds of vegetables per day (approximately 900 grams) and at least 4 fresh fruits per day (which adds another 600 grams). Most importantly, attention should be paid to the highly cancer-protective plant foods, greens, onion, berries, beans and seeds. 

The more fruits and vegetables the subjects ate, the more cancer protection they got.

Many of the news stories on this subject neglected to mention the fact that the researchers found a dose-response relationship between fruit and vegetable intake and cancer risk – this means that as the number of servings increased, rates of cancer decreased. Those eating five servings per day reduced their risk by 9% compared with those eating 2.5 or less, and those eating more than eight servings per day reduced their risk by 11%.⁴ The benefits of lifestyle changes are proportional to the changes made. As we add more vegetable servings, we increase our phytochemical intake and leave less room in our diet for harmful foods, enhancing cancer protection even further. 

Different fruits and vegetables offer different levels of protection.

In this study, all fruits and vegetables were lumped together in one category – this could have diluted the results. Leafy greens and potatoes have nutrient profiles that are quite different, but in this study, they are both treated the same.   The participants did not eat an extra 200 grams of raw greens - French fries and ketchup counted as a vegetable.

Cruciferous vegetables, such as kale, cabbage, collards, and broccoli, contain potent chemopreventive compounds called isothiocyanates (ITCs). ITCs have a variety of anti-cancer actions including inhibition of angiogenesis (blood vessel formation; important for tumor growth), detoxification or removal of carcinogens, inhibition of cancer cell growth, promotion of cancer cell death, and prevention of DNA damage by carcinogens. Epidemiological studies suggest that cruciferous vegetables, onions, and mushrooms are far more protective against cancer than vegetables overall - inverse relationships between cruciferous vegetable intake and breast, prostate, lung, and colorectal cancers have been found.⁵  For example, in one prospective study, one or more servings per week of cabbage reduced the risk of pancreatic cancer by 38%.⁶ And that was just one serving a week, demonstrating dramatic protection is available and real when a diet is ideally designed. The regular consumption of mushrooms has been demonstrated to decrease risk of breast cancer by over 60 percent.⁷ Onions, berries, seeds and beans also have dramatic beneficial effects.⁸ In other words, high nutrient plant foods work synergistically and a well designed diet can offer dramatic protection against not just cancer, but heart disease, strokes and dementia.

Healthful eating is a lifetime commitment

The EPIC study followed adult subjects for 8 years, but the foundation of adult cancers was very likely laid down in childhood or early adulthood.⁹   These researchers missed the most important tenet of nutritional research and that is—childhood diets are the major cause of adult cancers. I wrote a book about this—Disease-Proof Your Child, with all the supporting scientific references. The protective substances contained in fruits and vegetables are more effective if they are consistently present in the diet since childhood.  Making moderate changes later in life, like adding a serving of fruit and vegetables, is not likely to make much of an impact on cancer risk. For later life changes to dramatically reduce cancer risk a total dietary makeover is required, that is one of the purposes of my nutritarian diet-style, to offer people real protection from an ideally designed diet that is adopted later in life.

Conclusion

Most people are confused about nutrition, and results like these can add to the confusion. There is clear evidence that unrefined plant foods protect against chronic disease, but modest nutritional improvements offer only modest health benefits. Cutting back on cigarettes does not offer much protection against lung cancer either.  It is the total package of a well-designed, nutrient-dense diet, regular exercise, and a healthy weight that offers optimal benefit. We can win the war on cancer.

References:

1. Boffetta P, Couto E, Wichmann J, et al. Fruit and Vegetable Intake and Overall Cancer Risk in the European Prospective Investigation Into Cancer and Nutrition (EPIC). J Natl Cancer Inst. 2010 Apr 6.[Epub ahead of print]

2. Mount Sinai Study Shows Only a Weak Link Between Fruit and Vegetable Intake and Reduced Risk of Cancer. http://mountsinai.org/about-us/newsroom/press-releases/mount-sinai-study-shows-only-a-weak-link-between-fruit-and-vegetable-intake-and-reduced-risk-of-cancer

3. U.S. Centers for Disease Control. Fruit and Vegetable Consumption Among Adults --- United States, 2005. Morbidity and Mortality Weekly Report March 16, 2007 / 56(10);213-217

4. NewScientist. Short Sharp Science: Five fruit and veg a day won't keep cancer away. http://www.newscientist.com/blogs/shortsharpscience/2010/04/five-fruit-and-veg-a-day-wont.html

5. Higdon JV et al. Cruciferous Vegetables and Human Cancer Risk: Epidemiologic Evidence and Mechanistic Basis. Pharmacol Res. 2007 March ; 55(3): 224–236

6. Larsson SC, Hakansson N, Naslund I, Bergkvist L, Wolk A. Fruit and vegetable consumption in relation to pancreatic cancer: a prospective study. Cancer Epidemiol Biomarkers Prev 2006;15:301–305.

7. Zhang M, et al. Dietary intakes of mushrooms and green tea combine to reduce the risk of breast cancer in Chinese women. Int J Cancer. 2009;124:1404-1408

8. Powolny AA, Singh SV. Multitargeted prevention and therapy of cancer by diallyl trisulfide and related Allium vegetable-derived organosulfur compounds. Cancer Lett. 2008 Oct 8;269(2):305-14.

Stoner GD, Wang LS, Casto BC. Laboratory and clinical studies of cancer chemoprevention by antioxidants in berries. Carcinogenesis. 2008 Sep;29(9):1665-74.

Aune D, De Stefani E, Ronco A, et al. Legume intake and the risk of cancer: a multisite case-control study in Uruguay. Cancer Causes Control. 2009 Nov;20(9):1605-15.

Jenab M, Ferrari P, Slimani N, et al. Association of nut and seed intake with colorectal cancer risk in the European Prospective Investigation into Cancer and Nutrition. Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1595-603.

9. Maynard M, Gunnell D, Emmett P, Frankel S, Davey Smith G. Fruit, vegetables, and antioxidants in childhood and risk of adult cancer: the Boyd Orr cohort. JEpidemiol Community Health. 2003 Mar;57(3):218-25. Erratum in: J Epidemiol Community Health. 2007 Mar;61(3):271.

Fuemmeler BF, Pendzich MK, Tercyak KP. Weight, Dietary Behavior, and Physical Activity in Childhood and Adolescence: Implications for Adult Cancer Risk. Obes Facts. 2009;2(3):179-186.

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Vitamin D insufficiency is widespread, and is now thought to contribute to a variety of disease states, including osteoporosis, cardiovascular disease, diabetes, autoimmune diseases, depression, and cancers.

Vitamin D affects calcium absorption and metabolism in the bone, kidney, and intestine, but it also acts as a regulator of gene transcription in many tissues, affecting genes that control cell growth, adhesion, differentiation, proliferation, and programmed cell death. Vitamin D’s action on such genes has been shown to suppress proliferation of human colon cancer cells and tumor growth.^1,2

Also, the cells of the colon, whether they are normal or cancerous, are capable of converting 25(OH)D to its active form 1,25(OH)₂D. It is likely that this ability has purpose – vitamin D may have yet unidentified actions specific to the cells of the colon.

Researchers analyzed data from the European Prospective Investigation into Cancer and Nutrition (EPIC) study, which has over 520,000 participants. Blood levels of vitamin D, which were measured at the start of the study, were compared between 1248 colorectal cancer patients and matched controls after diagnosis.

Circulating 25(OH)D levels of below 20 ng/ml were associated with increased risk of colorectal cancer compared with levels between 20-30 ng/ml.  When the researchers arranged the data into 5 quintiles of Vitamin D levels, they found a dose-dependent reduction in colon cancer risk; highest quintile (greater than 40 ng/ml) had 40% reduced risk compared to lowest quintile (less than 10 ng/ml). When cancers were distinguished by site, the association between Vitamin D levels and colon cancer was even stronger – the highest quintile showed a 60% risk reduction.³

This is the largest study on the subject to date, following up at least 25 previous studies since 2002. A 2009 review of these previous studies confirmed that there is indeed an inverse relationship between vitamin D levels and colorectal cancer. Even after a diagnosis of colon cancer, vitamin D levels are associated with increased survival – in colon cancer patients, higher vitamin D levels were predictive of a decreased risk of death from any cause, not only colon cancer.⁴

The 2009 review concluded that 25(OH)D levels of 32 ng/ml would be sufficient to achieve the protection against colorectal cancers seen in the literature, and the current study saw benefits with as low as 20 ng/ml. A minimum of 30 ng/ml 25(OH)D is thought to be required for vitamin D to properly exert its many beneficial effects.⁵ Accordingly, I  recommend that levels be maintained in the range of 35-55 ng/ml. 

About 50% of the U.S. population is deficient in vitamin D and cannot rely on sun exposure because of indoor jobs, skin color, and their climate. Plus, with the depletion of the ozone layer, the amount of sun most people would require to achieve these levels may result in too much skin damage and skin cancer.⁶ 

 References:

1. Ingraham BA, Bragdon B, Nohe A. Molecular basis of the potential of vitamin D to prevent cancer. Curr Med Res Opin. 2008 Jan;24(1):139-49.

2. Journal of Clinical Investigation (2009, July 7). Understanding The Anticancer Effects Of Vitamin D3. ScienceDaily. Retrieved April 6, 2010, from http://www.sciencedaily.com /releases/2009/07/090706171500.htm

Emory University (2008, April 14). Vitamin D And Calcium Influence Cell Death In The Colon, Researchers Find. ScienceDaily. Retrieved April 6, 2010, from http://www.sciencedaily.com /releases/2008/04/080413161052.htm

Rockefeller University Press (2008, November 26). Vitamin D Can Alter Color Cancer Cells In Many Ways, Through One Pathway. ScienceDaily. Retrieved April 6, 2010, from http://www.sciencedaily.com /releases/2008/11/081117091614.htm

3. Jenab M, Bueno-de-Mesquita HB, Ferrari P, et al. Association between pre-diagnostic circulating vitamin D concentration and risk of colorectal cancer in European populations:a nested case-control study. BMJ. 2010 Jan 21;340:b5500.

High vitamin D levels linked to lower risk of colon cancer. ScienceDaily. Retrieved April 6, 2010, from http://www.sciencedaily.com /releases/2010/01/100122002340.htm

4. Dana-Farber Cancer Institute (2008, June 20). Vitamin D Linked To Colon Cancer Survival. ScienceDaily. Retrieved April 6, 2010, from http://www.sciencedaily.com /releases/2008/06/080619090749.htm

5. Holick MF, Chen TC. Vitamin D deficiency: a worldwide problem with health consequences.Am J Clin Nutr 2008;87(suppl):1080S– 6S.

6. Terushkin V, Bender A, Psaty EL, et al. Estimated equivalency of vitamin D production from natural sun exposure versus oral vitamin D supplementation across seasons at two US latitudes. J Am Acad Dermatol. 2010 Apr 2. [Epub ahead of print]

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