Chapter 25
A Rejection of Cancer
To protect ourselves from cancer, our body releases, among other things, a cell-binding protein into the blood to disable foreign IGF-1. Think of it like an emergency brake. Let’s say you’ve managed to dial down the production of new IGF-1 through diet. But isn’t all that excess IGF-1 from the eggs and bacon you ate yesterday still floating around? No problem: The liver sends out a strike team of binding proteins to take it out of circulation.
When you change your diet and eat plant-based, after just a few weeks you substantially strengthen your blood in the fight against cancer. The explanation for this could be the secretion of IGF-1 that animal protein triggers. If you cut back on animal protein for only eleven days, your IGF-1 levels can drop by 20 percent, and your level of IGF-1-binding protein can shoot up by 50 percent. After study participants ate plant-based for less than two weeks, researchers dripped some of their blood onto cancer cells in a petri dish and found that it suppressed cancer growth 30 percent better than before. This applied to both prostate cancer and breast cancer cells. The diet change altered IGF-1 and thus strengthened cancer defense. How do we know? If you give the cancer cells back the IGF-1 that the plant-based diet had suppressed, the cancer cell growth kicks back in. The participants in this intervention also added walks to their program, but when it comes to binding IGF-1 and killing cancer cells, apparently not even 3000 hours in the gym can compete with a few plant-eaters out for a stroll.
The cancer-suppressing effect is apparently so strong that Dr. Ornish and colleagues, in a randomized controlled trial, managed to slow, halt, and even reverse the progression of early-stage nonaggressive prostate cancer without chemotherapy, surgery, or radiation—using only a plant-based diet and lifestyle changes. After one year, the subjects’ blood could suppress the growth of cancer cells almost eight times better. Biopsies showed a downregulation of the crucial cancer genes—the expression of the cancer-growth genes was effectively switched off. But if, for example, you eat a lot of dairy products with prostate cancer, you have a 76 percent higher risk in all-cause mortality and a 141 percent higher risk of dying of that cancer. Lowering IGF-1 by reducing the consumption of animal protein could explain why vegans—people who eat no meat, no eggs, no dairy products, or other animal products—have less cancer of any kind overall.
An edible that lowers IGF-1
Are there foods that actively lower IGF-1? A retrospective snapshot study raised the question of whether tomato consumption might be associated with lower IGF-1 levels. Hopes had been raised by a study (funded by a lycopene supplement manufacturer) using lycopene, the red tomato pigment, in colon cancer patients. But six further studies to date were a bust. Lycopene supplementation does not appear to affect IGF-1 levels in general.
Flaxseed reduces IGF-1 in rats, but it failed in experiments in humans. Green tea had a similar effect in mice, but neither green tea nor green tea supplements managed that in us. Seaweed, however, may be useful. When postmenopausal women were given just 5 grams of winged kelp (Alaria esculenta) daily, the IGF-1 rise triggered by a protein load of 67 grams was reduced by 40 percent.
IGF-1 and Life Expectancy
Epidemiological studies found that both high and low IGF-1 concentrations are associated with a shorter lifespan, which made headlines like: “IGF-1: Miracle cure or poison?” In see.nf/igf1 I go into the data in detail and show that the correlation between IGF-1 levels and mortality can be a case of reverse causation, since both acute and chronic illnesses can lower IGF-1, creating a false impression of harm.
With the help of Mendelian randomization methods, you can tease that apart, because they examine what happens when people are practically sorted from birth into whether they genetically have a lower or higher lifelong IGF-1 setpoint. Such studies show that IGF-1 does in fact increase the risks for age-related diseases such as heart disease, osteoarthritis, and diabetes. That helps explain, in part, why the risk for type 2 diabetes rises with the consumption of animal protein but falls with plant protein.
As we will see in Part IV (“Dr. Greger’s Anti-Aging Tips”), protein restriction alone can increase life expectancy, but it is possible to disentangle the effects of IGF-1 and protein intake. As I noted earlier in the chapter, those who won the genetic lottery and have lower IGF-1 levels, without having to do anything for it, are more likely to live past 90, even make it through that decade, and overall have a higher life expectancy.
Beyond genetics, intervention studies show that reducing protein intake to the recommended amount and/or switching from animal to plant protein sources greatly benefits metabolism. However, the prospective study by Longo and colleagues, which established the positive association between reduced protein intake and lower mortality in middle age, showed that at around age 65 it flips into the negative. Here we may be dealing with reverse causation—for example, frail adults are more likely to be undernourished. Nevertheless, the researchers recommended for those over 65 a protein intake of at least 10 percent of calories, which in a diet of 2000 calories per day would amount to 50 grams, and those should ideally come from plant sources.
Food for Thought
Insulin-like growth factor 1 is attributed extraordinary importance for the spread of cancer, so dialing down IGF-1 activity not only has the potential to slow the aging process but could be a way to deploy anti-aging genes against cancer. IGF-1 is revved up by protein-rich diets, especially animal protein. This is one explanation for the benefits of a plant-forward diet and also the reason why a diet with a relatively low protein content is considered crucial for lifelong health.
To help slow this pathway of aging, you should daily:
Inflammation
One of the most medically significant discoveries of recent years has been the role of inflammatory processes in many chronic diseases, including at least eight of the ten leading causes of death. The significance of this new understanding is comparable to the discovery of bacteria hundreds of years ago, which revolutionized the prevention and treatment of infectious diseases.
For most of our existence on this earth, infections were the main cause of death and disease. Without soap, sewage systems, or water treatment, we were under constant attack. From the inside, we were plagued by chronic parasite infestations, and from the outside, we were attacked by dangerous microbes. Without antibiotics, a scraped knee could be fatal, which is why, in the course of evolution, our immune system has learned to remain in a constant state of high alert and to react too strongly rather than too weakly. But sometimes that can harm us more than help us. For example, a skull trauma may destroy hundreds of thousands of brain cells, but the subsequent inflammatory response may kill millions of brain cells—or the patient himself.
Metainflammation
Inflammation is a good thing. For example, if you get a splinter in your finger and the area turns red and warm, hurts, and swells, that inflammation is the body’s natural response to tissue damage or irritation. Its purpose is to trigger healing; it is not a disease.
The body’s response to the splinter is an example of an acute infection, a localized, temporary, direct response to an infection or injury and focused on solving a problem. Chronic inflammation, also called metabolic inflammation or metainflammation for short, by contrast is systemic, persistent, and nonspecific and seems to perpetuate a disease state. It is low-grade and smolders, and blood tests show an abnormally high level of inflammatory markers such as C-reactive protein (CRP).