Chapter 23
How to Lower IGF-1 Levels Through Diet
Because of their lifelong IGF-1 deficiency, people with Laron syndrome are not only short, but also practically cancer-proof. Among nearly 500 affected individuals, only a single case of (nonfatal) cancer has been described. This cancer rate is 100 times lower than in people without Laron syndrome—and with not a single death from cancer. Most malignant tumors are covered with IGF-1 receptors. Without IGF-1, the tumors probably could not grow and spread.
As children, we needed growth hormones to get big, but what if we could get all the growth hormones we need as children to grow to normal height, and then as adults downregulate hormones like IGF-1? Turning off excess growth signals could preserve our cellular balance, which determines life and death, prevent cancer, put us steadily into repair-and-maintenance mode, and thereby extend our lives. As it turns out, we can. We can suppress IGF-1 activity—not through surgery or drugs, but through simple changes in eating habits.
How to Lower IGF-1 Levels Through Diet
Not surprisingly, pharmaceutical companies have put out a number of chemical IGF-1 blockers, including ones with funny names like figitumumab and less funny side effects, such as “early fatal toxicity.”
How can we lower IGF-1 levels naturally?
Yes, with total fasting. If you consume nothing but water for five days, it can temporarily cut the levels in half. Do not do this without medical supervision, though. That is why cancer patients often fast for a few days before and after chemotherapy. The IGF-1 reduction can weaken cancer cells, making them easier to destroy. But how do we know that the benefit of fasting is due to the reduction of IGF-1? Because the cancer cells revive as soon as IGF-1 reaches the same level as before the starving.
Fasting, however, is the epitome of an unsustainable condition. If you fast long enough, you will definitely stop the aging process—because you will be dead. With the goal of avoiding this fatal end of long-term fasting, diets were developed that mimic fasting and thereby lower IGF-1 levels. They leave out the key component of the diet that drives it up in the first place: animal protein.
In rodents, calorie restriction alone lowers IGF-1 levels, but in humans even strict calorie restriction does not work unless protein is restricted as well. Scientists were only able to budge subjects’ IGF-1 levels by pushing the protein intake of subjects who were already restricting calories from typically American amounts closer to the recommended levels.
At an intake that far exceeds the recommended consumption, protein from plant and animal sources raises IGF-1 levels equally, but at a more reasonable level, animal protein appears to be the main culprit. Men and women who avoid proteins from meat, eggs, and dairy products have significantly lower IGF-1 levels, even if they slightly exceed protein recommendations. When people switch to a plant-based diet, their IGF-1 levels can drop significantly in less than two weeks. Yet it may also not help if you simply eat more plant foods, avoid meat, or switch to fish. But this is not all or nothing. A study of women with a BRCA mutation and thus a high risk of breast cancer found that IGF-1 levels could be reduced by participants generally eating fewer animal products, but not giving them up entirely.
Even with a single serving of chicken breast per day, you would expect it to significantly increase IGF-1 amounts in the blood. Chicken may worsen IGF-1 more than beef, but that is only known from studies in rats; it still needs to be tested in humans. More than a dozen randomized controlled trials showed that dairy products increase IGF-1 within as little as a week. Perhaps the most curious experiment was a study from Denmark in which IGF-1 levels were successfully lowered when subjects switched from 2.5 liters of milk, which they drank daily for ten days, to 2.5 liters of Coca-Cola. I think this is truly the only study in which people benefited from drinking 25 liters of Coke!
The relationship between milk consumption and IGF-1 is so reliable that the association reaches a p-value of 10–27. In science, the p-value refers to the probability of obtaining such an extreme result that it really should not happen. It is used to describe how great the probability would be of getting the same results by chance. How small is a chance of 10–27? The probability that the connection between milk consumption and IGF-1 is just a fluke is lower than the probability of winning the lottery not just once or twice, but three times in a row and then subsequently being struck dead by lightning.
IGF-1 could provide an explanation for the relationship between the consumption of dairy products and prostate cancer, but the fact that the biggest milk drinkers seem on average to live shorter lives and are more likely to die of cancer may have more to do with animal fat than with animal protein, since these results did not occur with low-fat milk.
The surge in IGF-1 after consuming dairy products may be partly attributable to the intake of preformed IGF-1 that is already in the milk. After all, the purpose of milk is to put a few hundred pounds on a calf in a few months; it should not be surprising that it contains large quantities of growth hormones. Bovine IGF-1 is identical to human IGF-1 and is not affected by pasteurization. While IGF-1, taken orally, has been shown to enter the bloodstream of rats, pigs, and presumably calves, similar studies in humans still need to be conducted. Regardless, milk protein can trigger a strong rise in our own IGF-1 production, which is less likely when we consume protein from plant sources.
Animal vs. Plant Protein
The different effect of animal and plant protein seems to be attributable to different amino acid profiles—the building blocks of proteins. Did you also love playing with construction sets as a child, like I did? I still remember how excited I was on my sixth birthday when I unpacked a big set. I dumped the whole load of the new building material onto the floor in front of me and could hardly wait to put it together. Our liver reacts just as exuberantly when it is confronted with a big batch of protein building blocks.
Although various tissues produce some IGF-1 locally, the liver is responsible for about 75 percent of the IGF-1 that circulates through the body. So what happens when we eat a load of protein? The liver begins to spit out IGF-1 to tell all body cells that it is time to grow, to use up the surplus. With so much protein as working material, the liver sends signals to the cells to be fertile and multiply.
The problem is that some of the newcomers spurred on by the growth hormone could be tumors. When you are an adult, you want to slow cellular growth, not speed it up. The goal, therefore, would be to consume protein appropriately, not in excess. But animal protein seems to give the liver a different signal than most plant proteins. Why is protein from an animal associated with elevated IGF-1 levels, but plant protein is not? Let’s return to our construction set.