We all know we are supposed to eat our fruits and vegetables (FV), that they are good for us and all that. Hell, some people even claim that doing so might prevent cancers from growing in our bodies. The direct evidence for that claim is lacking, but a new study suggests we are getting closer.
A new article just released online connects the intake of more FV in healthy young adults with lower levels or pro-inflammatory chemical markers in the body. While this does not directly demonstrate a cancer prevention activity, nearly all of the pro-inflammatory markers that are reduced with higher FV intake are associated with cancer progression (and reduced risk of coronary artery disease and heart disease).
Not only that, but we also know that obesity increases ALL of these pro-inflammation markers, that these markers are associated with metabolic syndrome (leading to type-II diabetes), and that inflammation is thought to be the cause of many diseases (including cardio vascular disease, Alzheimer's Disease, several forms of cancer, insulin resistance, inflammatory-bowel diseases (IBDs), inflammatory arthritis, sepsis, and even the aging process itself).
After looking at the research, I will offer dietary suggestions. Now on to the study.
Fruits and vegetables are important sources of fiber and nutrients with a recognized antioxidant capacity, which could have beneficial effects on the proinflammatory status as well as some metabolic syndrome and cardiovascular disease features. The current study assessed the potential relationships of fruit and vegetable consumption with the plasma concentrations and mRNA expression values of some proinflammatory markers in young adults.
One-hundred and twenty healthy subjects (50 men/70 women; 20.8+/-2.6 y; 22.3+/-2.8 kg/m2) were enrolled. Experimental determinations included anthropometry, blood pressure and lifestyle features as well as blood biochemical and inflammatory measurements. The mRNA was isolated from peripheral blood mononuclear cells (PBMC) and the gene expression concerning selected inflammatory markers was assessed by quantitative real-time PCR. Nutritional intakes were estimated by a validated semi-quantitative food-frequency questionnaire.
The highest tertile of energy-adjusted fruit and vegetable consumption (>660 g/d) was associated with lower plasma concentrations of C-reactive protein (CRP) and homocysteine and with lower ICAM1, IL1R1, IL6, TNF-alpha and NF-kappa-B1 gene expression in PBMC (P for trend <0.05),>19.5g/d) from fruits and vegetables (P for trend <0.05).>11.8 mmol/d) of dietary total antioxidant capacity showed lower plasma CRP and mRNA values of ICAM1, IL1R1, IL6, TNF-alpha and NF-kappa-B1 genes (P for trend <0.05).>
A higher fruit and vegetable consumption was independently associated not only with reduced CRP and homocysteine concentrations, but also with a lower mRNA expression in PBMC of some relevant proinflammatory markers in healthy young adults.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
In 1988, Reaven2 noted that several risk factors (eg, dyslipidemia, hypertension, hyperglycemia) commonly cluster together. This clustering he called Syndrome X, and he recognized it as a multiplex risk factor for CVD. Reaven and subsequently others postulated that insulin resistance underlies Syndrome X (hence the commonly used term insulin resistance syndrome). Other researchers use the term metabolic syndrome for this clustering of metabolic risk factors. ATP III used this alternative term. It avoids the implication that insulin resistance is the primary or only cause of associated risk factors.More to the point, metabolic syndrome is associated with a variety of conditions, including polycystic ovary syndrome, fatty liver, cholesterol gallstones, asthma, sleep disturbances, and some forms of cancer - and type II diabetes.
Grundy outlines the components of metabolic syndrome as follows:
ATP III1 identified 6 components of the metabolic syndrome that relate to CVD:I bring this up only to demonstrate that the findings from the new article above have implications beyond the reduced risk of CVD. One of the primary proinflammatory markers is Il-6. In a 2008 paper, Naugler & Karin, in "The wolf in sheep’s clothing: the role of
These components of the metabolic syndrome constitute a particular combination of what ATP III terms underlying,major, and emerging risk factors. According to ATP III, underlying risk factors for CVD are obesity (especially abdominal obesity), physical inactivity, and atherogenic diet; the major risk factors are cigarette smoking, hypertension, elevated LDL cholesterol, low HDL cholesterol, family history of premature coronary heart disease (CHD), and aging; and the emerging risk factors include elevated triglycerides, small LDL particles, insulin resistance, glucose intolerance, proinflammatory state, and prothrombotic state. For present purposes, the latter 5 components are designated metabolic risk factors.
- Abdominal obesity
- Atherogenic dyslipidemia
- Raised blood pressure
- Insulin resistance ± glucose intolerance
- Proinflammatory state
- Prothrombotic state
interleukin-6 in immunity, inflammation and cancer" (Trends in Molecular Medicine:474; 11 Pages), the authors look at IL-6 and its relationship to cancer.
For years, IL-6 has been known to have a key role in the maturation of B cells, as well being as a member of the trio of cytokines [tumor necrosis factor (TNF)-a and IL-1 complete the triumvirate] that drives the acute inflammatory response. More recent reports have shown how dysregulation of IL-6 signaling contributes to inflammation-associated disease conditions, including obesity and insulin resistance, inflammatory-bowel diseases (IBDs), inflammatory arthritis, sepsis and even the aging process itself.I want to offer one more passage from this article because I think it is related to the main article above, and because I think it offers a pathway for understanding the re-emergence of some forms of cancer years after the original tumor was removed.
Two of the most exciting recent advances involve inflammation-associated carcinogenesis and the innate–adaptive immunity interface, in both of which IL-6 has an important role. The inflammatory process is increasingly linked to carcinogenesis, most notably to the promotion and progression of cancers. Several new reports of different experimental models of cancer show a requirement for IL-6 signaling and several epidemiological reports linking IL-6 signaling to human cancers have appeared.
Chronic inflammation describes a state in which inflammatory cells are recruited to a site, undergo expansion and differentiation and are prevented from undergoing apoptosis. Apoptosis normally limits inflammation but becomes dysregulated in states of chronic inflammation. A key regulator of these effects is NF-kB , which integrates stress stimuli and, depending on the cell-type studied, prevents apoptosis or initiates signals that enhance or perpetuate the inflammatory process.One of the known ways in which prostate cancer kills men is that the cancer cells (generally stem cells) migrate to an area in the body where there is active bone marrow and take up residence, essentially escaping detection and any impact of chemo or radiation therapies.
The emergence of neoplasia requires several elements, including self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, evasion of apoptosis, limitless replicative potential, tissue invasion and metastasis and sustained angiogenesis . Most of these functions occur through the activation of NF-kB . IL-6 is a growth signal and blocks apoptosis and, as such, is one of the effector signals of activated NF-kB in the promotion of neoplasia. IL-6 signals through STAT3, which is in turn activated in diverse cancers .
The obvious cancer in which to find IL-6 involvement is multiple myeloma (MM), a neoplasm of terminally differentiated B-cells (plasma cells), which is dependent on IL-6. Although it was thought initially that MM cells produced their own IL-6, which perpetuated the malignancy through autocrine action, it was later discovered that bone marrow stroma was the main source of IL-6 in this tumor .
The fact that IL-6 is also associated with bone marrow suggests a mechanism for understanding why the cancer cells seek out active marrow - the feed off of the inflammatory response. So, and I am speculating here, if we can control the production and expression of IL-6 through diet (and exercise, among other ways, including meditation), we might be able to delay or suppress the re-emergence of these cancer stem cells. Doing so effectively saves the lives of those who die from prostate cancer since few men actually die from the original tumor but, rather, from the metastatic spread of the cancer stem cells into the lower back (the only site of active bone marrow in middle aged men) and then into the rest of the body.
So What Do We Do?
Based on the feature article and other research I have done, I can make the following suggestions. Do as many of these as you can and your health will improve, your weight will go down, and you'll feel better, not to mention reducing all inflammation related illnesses, including cancer.
We'll start with foods we need LESS OF in our diets:
Avoid ALL sugar, especially high fructose corn syrup.
Avoid ALL trans-fats (deep-fried foods, margarine, processed foods).
Avoid pro-inflammatory fats (saturated fats contain arachidonic acid, which we need, but too much causes inflammation responses in the body). Also limit or or avoid butter, cream, cheese and other full-fat dairy products; unskinned chicken and fatty meats; and products made with coconut and palm kernel oils.
Avoid most vegetable oils: regular safflower and sunflower oils, corn oil, cottonseed oil, and mixed vegetable oils.
Limit all refined grains and non-fruit/vegetable carbohydrates in general. Carbohydrates are basically sugars, and sugars increase insulin levels, and higher insulin levels increase inflammation.
Now some foods we need MORE OF in our diets:
We need to eat more fruits and vegetables. Among the most studied for their anti-inflammatory benefits:
- all dark berries
- tart cherries
- cruciferous vegetables (horseradish, kale, collard greens, cabbage, brussels sprouts, broccoli, cauliflower, bok choy, and others)
- higher fiber vegetables (pumpkin, yams)
Include avocados and nuts, especially walnuts, cashews, almonds, and nut butters made from these nuts. (Peanuts are less healthy.)
Try to eat 40 grams of fiber a day. This is easy to do by increasing your consumption of fruit (especially berries and apples), vegetables (especially pumpkin, cruciferous veggies, and to a lesser extent, beans), and unrefined whole grains (whole grain rice, quinoa, and steel cut oats).
Consume more omega-3 fatty acids: eat salmon (preferably fresh or frozen wild or canned sockeye), sardines packed in water or olive oil, herring, and black cod (sablefish, butterfish); omega-3 fortified eggs; hemp seeds and flaxseeds (preferably freshly ground); or take a fish oil supplement (see below), pumpkin seeds, and walnuts.
Eat plain dark chocolate in moderation (minimum cocoa content of 70 percent), and moderation means an ounce or two a day.
Eat organic as much as possible.
For more info on the anti-inflammation diet, see Dr. Andrew Weil - and ignore his high carbohydrate recommendations. Protein intake (lean meats, fish, chicken, turkey, low-fat dairy, and eggs) should be 40% of calories, healthy fats should be 30%, carbohydrates (mostly from fruits and vegetable) should be 30%.