You probably know that a steady intake of food-based antioxidants is important to protecting your DNA and lowering risk of diseases.
What you may not realize is that one important plant antioxidant is commonly consumed—but poorly absorbed by the body!
Lycopene is a carotenoid with a unique structure that drives its intense free-radical-trapping activity. Lycopene also operates by additional mechanisms to provide health-giving benefits in the form of cellular communication and cell cycling.
The problem is that the fiber content in lycopene-rich foods such as tomatoes interferes with lycopene absorption and bioavailability. Eating concentrated tomato-based foods like pasta sauce with olive oil provides far greater absorption. Supplementation with lycopene also boosts absorption into the bloodstream, especially when taken with the heaviest meal of the day.
In this article, you’ll learn about controlled studies showing that increased lycopene levels result in broad cellular benefits and reduced incidences of cancer, diabetes, Alzheimer’s, and cardiovascular disease!
Lycopene is a member of the carotenoid family of plant pigment molecules. Carotenoids give vegetables and fruits their yellow, red, and orange colors; they are part of the plant’s natural mechanism for processing and protecting themselves from the sun’s energy. Carotenoids, and especially lycopene, are extremely powerful antioxidants.
By capturing reactive oxygen species, lycopene prevents damage to fats, proteins, and DNA strands that we now recognize to be the causes of aging and other chronic diseases, including cardiovascular and neurological diseases, diabetes, cancer, and even osteoporosis.
In addition to its antioxidant characteristics, lycopene has at least four other important health-promoting mechanisms:
Humans are incapable of producing carotenoids, so we rely on our diet to obtain sufficient amounts. Tomatoes are our main dietary source of lycopene, but lycopene from fresh tomatoes is less bioavailable than that from processed tomato products.
There’s no question that boosting your lycopene intake has major protective effects.
Higher lycopene intake and higher blood lycopene levels are strongly associated with reduced risk for a variety of cancers, as well as cardiovascular diseases and the metabolic syndrome.
Cancer is the second leading killer of adult Americans, resulting in more than 527,000 deaths annually in the US.10 Because cancer is closely associated with a lifetime burden of oxidative stress, lycopene, with its strong antioxidant effects, is a subject of keen interest to oncologists and public health workers. As we’ve seen, lycopene has additional mechanisms that add to its cancer preventive powers.
Prostate cancer is the disease that is best known as a target for prevention by lycopene. In addition to reducing oxidant stress in prostate tissue, lycopene also reduces inflammatory signaling, prevents DNA damage, modulates the expression of important endocrine growth factors, and enhances communication between cancer cells at “gap junctions,” helping them stop growing out of control.6 Lycopene also slows the new blood vessel growth that prostate cancers need to support their development.
Human studies of lycopene and prostate cancer are encouraging. Lycopene intake is correlated with lower prostate cancer development and with slower progression if it does develop. Lycopene supplementation also reduces cancer-related symptoms such as pain and urinary tract symptoms.
In one well-publicized investigation, men with newly-diagnosed prostate tumors were supplemented with lycopene 15 mg twice daily for three weeks prior to surgical removal of diseased tissue. In supplemented patients, the tumors were found at surgery to be significantly smaller and less invasive than those in control patients. The tumors were also significantly more likely to be lower-grade in supplemented than in control patients. Levels of the tumor marker called prostate specific antigen (PSA) fell substantially in supplemented patients, while they rose by about the same rate in control patients. Other human studies have shown similar effects, including slowing the rate of PSA increase.
Breast cancer is the leading cause of cancer death in women. It too may yield to lycopene’s preventive effects. After treatment with lycopene, human breast cancer cells in culture showed genetic changes resulting in improved DNA repair, slowing of cell replication, and increased death by apoptosis. Both alone and in combination with melatonin, lycopene sharply reduces markers of oxidant stress in breast tissue, while enhancing the breast’s natural antioxidant enzyme protection systems.
Lycopene may help reduce the risk of cervical cancer as well; women with the highest lycopene concentrations in blood are 56% less likely to have persistent infection with human papillomavirus, the main cause of cervical malignancies.
Lycopene is also showing promise in preventing lung cancer. Lung tissue has a very high exposure to oxygen, making it especially vulnerable to the oxidant stress that can lead to cancers. Lycopene reduces lung cells’ oxidant-induced DNA damage in humans, and people with the highest dietary intakes of lycopene have a 28% lower risk of developing lung cancer.
Colon cancer is the second most common cancer in adults. Like many other cancers, it is controlled in part by hormonal factors, including insulin-like growth factor-1, or IGF-1. Lycopene supplementation, 30 mg/day, in human subjects with a family or personal history of colon cancer, decreases IGF-1 concentrations while increasing levels of the IGF-1 binding protein, which has the effect of reducing IGF-1 availability to stimulate cancer cell growth.
One important note: lycopene’s antioxidant effects are so powerful that they have the potential to interfere with cancer chemo- and radiation therapy, both of which rely on producing free radicals within tumors to kill malignant cells. Experts warn that people who are undergoing either chemo- or radiation therapy for a known cancer should speak with their treating oncologist before increasing lycopene intake.
Cardiovascular diseases (heart attacks, stroke, congestive heart failure, and others) are the leading cause of death in Western societies; together they cause up to 1/3 of deaths around the globe. It has long been known that diet is strongly correlated with the risk of these diseases.
People with low blood lycopene levels suffer from increased risk for atherosclerosis; including greater thickness and stiffness of their arteries. People with atherosclerosis visible on ultrasound in their carotid arteries (those leading to the brain) have lower blood levels of lycopene than do those with normal carotids.
Conversely, those with the highest lycopene blood levels have a 45% lower risk of atherosclerosis. That group also has more flexible arteries than those in the lower lycopene group and a reduced risk of heart attack.
Lycopene protects heart and blood vessel tissue by several mechanisms, including antioxidant function. Lycopene scavenges the powerful oxidant hypochlorous acid, which is associated with atherosclerosis. Lycopene also decreases fat and LDL cholesterol oxidation, steps that occur early in the chain of events that leads to atherosclerosis.
Studies show that lycopene supplementation can decrease total cholesterol by 5.9% and LDL cholesterol by 12.9% (and by50% in animal studies). Some of this effect may be due to lycopene’s ability to inhibit cholesterol synthesis.
Lycopene supplementation has powerful effects on the inflammation that is intimately involved with atherosclerosis. Lab and human studies demonstrate that lycopene decreases production of multiple pro-inflammatory mediators and markers of inflam-mation.
One dramatic human study showed that 15 mg/day of lycopene orally improved endothelial function by 23%. At the same time the inflammatory marker, C-reactive protein (hs-CRP) fell dramatically, along with systolic blood pressure and important vascular adhesion molecules that trap platelets and immune cells to form inflammatory plaques. Some of that reduced inflammatory response is attributed to lycopene’s ability to block fat oxidation in arterial lining cells.
Intriguingly, neither diets high in tomatoes (10 ounces/day) nor diets containing 32-50 mg of lycopene from tomato-based foods have any detectable effects on inflammatory markers, though one study showed a modest 3.3% improvement in endothelial function after consumption of 2.3 ounces/day of tomato paste for 15 days.
Even lycopene supplementation at moderate doses (10 mg/day) proved incapable of changing inflammatory markers or insulin resistance, another major cardiac risk factor. Studies showing a substantial impact of lycopene intervention, instead, used 15-30 mg/day of purified lycopene extracted from tomatoes.
Diabetes, like other chronic age-related conditions, is powerfully driven by oxidation and inflammation. Not surprisingly, then, blood lycopene levels in diabetics are typically much lower than they are in healthy control patients, presumably the result of consumption of lycopene by reactive oxygen species.
Diabetics may be able to protect themselves by increasing their lycopene intake; studies show that high consumption of tomato products can improve resistance to oxidation in people with type II diabetes. Diabetics with the highest blood lycopene levels also have greater glucose tolerance than do those with lower lycopene levels.
Eating a lycopene-rich Mediterranean diet increases lycopene levels and can reduce levels of hemoglobin A1c, the blood marker of sustained blood sugar elevations, from 7.1 to 6.8%. (Tomatoes have other beneficial compounds such aschlorogenic acid that may have accounted for these marked reductions in hemoglobin A1c.)
The most common and life-threatening complication of diabetes is cardiovascular disease; like people in the general population, diabetics may be able to reduce their risk of cardiovascular complications by supplementing with lycopene.
Consuming about 7 ounces of raw tomatoes daily for 8 weeks successfully lowered both systolic and diastolic blood pressure in diabetics. Part of that effect may arise from a reduction in activity of angiotensin converting enzyme (ACE), an effect produced by common antihypertensive drugs.
In older diabetic women, 30 mg/day of lycopene reduced total and LDL cholesterol by 12 and 16% respectively, while also lowering a common marker of tissue oxidation that contributes to atherosclerosis.
Other complications of diabetes are also less severe in those with higher lycopene levels. For example, diabetics with healthy eyes have higher levels of lycopene than do those with the blindness-inducing condition called diabetic retinopathy.
Similarly, diabetic neuropathy, a painful and debilitating nerve condition that is among the hardest of pain syndromes to treat, is substantially ameliorated in animal studies of lycopene supplementation.
Finally, cognitive decline associated with diabetes can be decreased with long-term lycopene supplementation.
Of course, diabetics are not the only people who face neurological degeneration over time. In the next section we’ll see how lycopene may improve brain health for everyone.
Oxidative stress plays a major role in the neuro-degenerative diseases of aging.
Most of the carotenoid antioxidant nutrients, including lycopene, are reduced in one or more of those diseases such as Alzheimer’s disease, vascular dementia, and Parkinson’s disease with dementia. They were recently also shown to be depleted in mild cognitive impairment.
These facts make lycopene an important dietary component for maintaining brain health.
Animal models of Alzheimer’s, Parkinson’s and Huntington’s diseases have all confirmed lycopene’s preventive potential. A lycopene-rich tomato powder supplement completely prevented destruction of essential dopamine-producing brain cells in a mouse model of Parkinson’s disease. Raw tomato supplements had similar but considerably less impressive effects.
Other studies have shown that lycopene improves brain resistance to oxidant stress in Parkinson’s disease models, and it successfully prevented the neurobehavioral deficits associated with the disease.
Huntington’s disease is less common but by no means less tragic; it produces uncontrolled motor movements coupled with dementia, and is inevitably fatal. In animal models of Huntington’s disease, lycopene reduced memory impairment while blocking the behavioral and biochemical abnormalities. The mechanism appears to be through inhibition of inflammatory nitric acid production, in addition to protective effects on brain mitochondria.
Alzheimer’s disease is practically the perfect example of brain destruction by oxidant stress. Lycopene may prevent Alzheimer’s by inhibiting formation of oxidant-producing Abeta proteins. As a result, studies show decreased death rates of neurons, especially in the memory-processing hippocampus area of the brain.
There’s also growing evidence that lycopene can prevent the inflammatory response to an acute stroke, and can reduce the total size of the damaged brain area. Finally, lycopene has also recently been shown to be protective against environmental neurotoxins and excessive levels of certain elements such as manganese, again through its antioxidant effects.
Our bodies are under continuous attack by oxidant stress, which produces inflammation and direct tissue damage. Ultimately, chronic inflammatory insult accelerates aging and other diseases that shorten life span.
Lycopene, a natural antioxidant derived from red fruits like tomatoes, has powerful antioxidant capabilities. It operates by additional mechanisms to provide health-giving benefits.
But lycopene in raw tomatoes is poorly bioavailable, and although it is more readily absorbed from processed tomato products (like tomato sauce), many people don’t eat enough of these foods to obtain an adequate supply.
Studies show that lycopene supplementation holds promise for reducing the impact of aging and many other chronic conditions, through the interactions of its many target effects. Lycopene has been shown to reduce the risk of certain cancers, cardiovascular disease, and metabolic disorders such as diabetes, and neurodegenerative decline.