Animal protein raises IGF-1 more than other foods, but this doesn’t mean meat is bad for you, or is “as bad as smoking cigarettes” as some headlines have proclaimed.
When IGF-1 levels are too high, some forms of cancer grow more easily (mainly prostate and breast). However, when IGF-1 levels are low, risk of cardiovascular disease, dementia, Alzheimer’s, and sarcopenia are all much higher. In fact, death to cancer is also much more common with low IGF-1 too, possibly due to increased risk of cachexia (muscle wasting).
While diseases associated with high IGF-1 levels are scary, the truth is that low IGF-1 levels are more likely to be of concern for many people. If you are worried about IGF-1 levels, perhaps the best action you can take is to exercise frequently. Frequent exercise cuts the risk of cancers associated with IGF-1 to a much greater extent than cutting animal protein does, and also doesn’t predispose you to the diseases associated with low IGF-1. In fact, the risk of all of the diseases associated with low IGF-1 are also reduced when you exercise frequently.
We encourage you to read the entire article below. This is part 2 of a 3 part segment. You’ll get loads of great information about exactly what IGF-1 does, how it affects our health, and how we can be sure to do IGF-1 “the right way”–the way where we live a long, strong, disease-free life!
IGF-1 and Cardiovascular Disease
Cancer is a scary disease, but cardiovascular diseases (CVD) consistently outrank all cancers combined as the leading cause of death in the United States. When examining the relationship between IGF-1 levels and CVD, we actually witness an inverse relationship, meaning that risk of CVD increases as IGF-1 decreases.
Studies in rats show that when rats are fed a heart-damaging diet extremely high in fat, the rats with low IGF-1 levels suffered more and greater ill effects from that diet than the control rats with normal IGF-1 levels. Not only do the IGF-1 deficient rats have increased blood glucose levels and impaired ability to clear glucose from the blood (problems associated with diabetes), but they also had significantly higher inflammation, which is coming to be understood as a root cause in CVD!
In humans, we’ve witnessed that IGF-1 is directly beneficial on a number of factors involved in CVD risk. IGF-1 reduces oxidative stress on the blood vessels, reduces the number of blood vessel cells that die, reduces inflammation, and improves the stability of plaques already formed, making them less likely to cause dangerous clots that can cause problems like strokes. In this way, keeping IGF-1 levels normal protects against CVD and CVD mortality.
Cardiovascular disease is the #1 killer of both men and women in the US. Being in the bottom 20% for IGF-1 levels dramatically increases your risk of death due to stroke and heart attack.
When we look at how CVD kills, strokes are one of the two major events. Again, we witness that IGF-1 actually protects against mortality. Mice with overexpressed IGF-1 levels have significantly better long-term recovery from strokes, and in humans, we see better outcomes for stroke patients when they have higher IGF-1 levels. We also see significantly more strokes in individuals with low IGF-1 levels!
The other major events associated with CVD are heart attacks. As with strokes, risk of heart attacks appears to be increased when IGF-1 levels are low. Researchers have noted a 38% increased risk of death for every drop in IGF-1 levels of 40 ng/mL (from ischemic heart disease, the type of heart disease most responsible for heart attacks). For individuals in the lowest 20% of IGFBP-1 (another IGF-1 binding protein), risk was 311% greater compared to those with higher IGF-1 levels.
It gets worse, though…
IGF-1 and the Brain
Beyond playing a role in keeping our cardiovascular system in good shape, IGF-1 also protects the brain. One way it does this is by helping to control something called “hippocampal neurogenesis”—essentially, growing new cells in the hippocampus, a region of the brain which is heavily involved in both short and long-term memory. Maintaining high levels of hippocampal neurogenesis helps the brain stay “plastic”, or flexible and able to learn.
Increased IGF-1 levels appear to improve cognitive function in the elderly. It’s possible that declining IGF-1 levels play a significant role in the loss of mental function frequently associated with aging!
When rats are injected with IGF-1, hippocampal neurogenesis actually increases, and cognitive impairments are reversed. One hypothesis for why stress can cause cognitive impairment (and ultimately lead down the road towards diseases like Alzheimer’s and dementia) is that cortisol (the stress hormone) impairs IGF-1 production, lowering serum levels and affecting hippocampal neurogenesis.
When elderly mice were given IGF-1 replacement therapy, cognitive function improves, learning and memory are improved, and neurogenesis is increased. They also develop more blood vessels in the brain, and utilize blood glucose better. In essence, mice who have their IGF-1 levels artificially increased ‘recover’ from the cognitive declines we generally associate with “just getting older”.
While we can’t necessarily expect to see the same results in humans, we do have data that suggests that IGF-1 levels are inversely associated with both Alzheimer’s disease and dementia. The higher your IGF-1 levels, the lower your risk of these specific cognitive disorders. It’s not a big leap to expect overall cognitive function to be better in elderly individuals with higher IGF-1 levels.
IGF-1 and Aging
Growing old doesn’t just bring cognitive decline, we often witness a decline in physical health as well. Bones become more brittle and muscles start wasting away, and IGF-1 plays a protective role against these facets of aging as well!
Men with low levels of IGF-1 had a 45% increased risk of hip fracture for every decline of roughly 50 ng/mL. At around 150 ng/mL, the association becomes insignificant, indicating that IGF-1 levels above this level are unlikely to be protective.
Higher IGF-1 levels also predicted a lower loss of lean muscle mass in aging men. Sarcopenia, a condition where the muscles begin to waste away, becomes more and more common as you grow older, in part due to declining IGF-1 levels. When muscle is lost, so is stability and ability to provide yourself with care, causing a decrease in quality of life and potentially increasing risk of injury or death due to complications from falls.
IGF-1 and Longevity
Perhaps the most common refrain from people seeking to convince you that lowering IGF-1 levels is a healthy idea is that in some species, IGF-1 is inversely related to longevity—that is, when IGF-1 levels are lowered, the animals live longer. Unfortunately, this association simply doesn’t hold true in humans.
To begin with, humans are significantly more complicated than the species this association has been found in, such as nematodes and fruit flies. Whereas mammals typically have receptors for IGF-1 in many organs (meaning that many organs are affected by IGF-1), the simpler organisms typically only have IGF-1 receptors in their nervous system.
The importance of this is that whereas IGF-1 might only affect a single pathway in a simpler organism, in mammals it will affect numerous organs and pathways, potentially in different ways for every different receptor, and not all of them helpful. In other words, even if IGF-1 is harmful to one system, it might be completely necessary to a different system; it’s not as if you can selectively choose which system will get the IGF-1!
This is why low IGF-1 levels are actually correlated with increased risk of death, not decreased risk—despite what science shows with nematodes and fruit flies. Men in the bottom 10% of IGF-1 levels have an overall 38% greater risk of death (though by the 20th percentile, the association disappears).
To put it bluntly, longevity only matters if you don’t die of other causes. It doesn’t matter if you could have lived to 120 if you die of a stroke at 72, or if at age 84 you break a hip and die due to complications. Even if lowering IGF-1 levels could potentially extend the clock on our life, it also ironically increases our risk of dying from other causes—not a great trade-off!
In fact, low IGF-1 levels may not even be associated with longevity in humans at all. One study showed that the female offspring of centenarians had significantly higher levels of IGF-1, though they also had reduced IGF-1R levels (a receptor that IGF-1 binds to in order to cause an effect). The researchers hypothesized that the higher IGF-1 levels may have been the body’s way of compensating for reduced receptor activity, but the result is the same: IGF-1 was higher, not lower, in the female offspring of individuals who lived to be at least 100 years old.
It also demonstrates that when our body has errors in one system, it typically compensates with another, making it challenging to actually predict the effects of changing hormonal levels on longevity and health. Changes almost
never happen in isolation!