High protein diets have always been controversial. Critics of the diets often predict dire consequences for those foolish enough to stay on such diets long-term.These consequences include kidney disease and bone mass loss. However, more recent analysis of such possible risks show that they exist more on paper than in reality. When examined in healthy, active adults, higher protein intakes have consistently been shown not to impose any undue risks on kidney function, bone mass, or other factors. Athletes and others engaged in regular physical activity have long been advised to ingest a higher protein intake. In some cases, the level of protein intake is extreme. Some bodybuilders have stated that they regularly ingest as much as 600 grams of protein a day. It's doubtful that this degree of protein intake contributes anything useful to their goal of boosting muscle mass. Most excess protein is merely degraded and oxidized in the liver.
But two alarming new studies, both published in the March 4, 2014 issue of the journal, Cell Metabolism, assert that a higher protein intake is not only not necessary,but could shorten lifespan if consumed during middle-age. The first study analyzed data from a nationwide nutrition study, and specifically looked at the protein intake of 6,831 middle-aged adults.The data showed that adults with an average age of 50 who consumed a diet that contained more than 20% of calories as protein were 4-times more likely to die of cancer or diabetes, and more than twice as likely to die from any cause in the next 18 years. Even a moderate protein diet of 10 to 19% protein was still associated with a 3-fold increase in death from cancer. Interestingly, the effect was only associated with consumption of animal proteins. Consuming protein from plant sources, such as beans, did not result in any negative effects on health. Even more intriguing was the finding that this effect was reversed in people over age 65; that is, those consuming a higher protein diet showed a 28% reduced risk of mortality from any cause, and a 60% reduced risk of dying from cancer. The effects of consuming a higher protein diet during middle-age on mortality were comparable to smoking!
This, of course, is very bad news for anyone who ingests a high protein diet, especially those who are middle-age. But let's take a closer look at these findings. What, for example, is it about a high protein diet that seems to increase mortality? According to the study authors, the likely explanation is that a high protein (and higher calorie) diet boosts levels of a hormone called Insulinlike growth-factor-1 or simply, IGF-1. IGF-1 is produced both locally in muscle, where it functions as a major arbiter of promoting muscle growth, and in the liver, where it provides systemic body effects. These effects include helping to preserve lean mass, bone, neurons in the brain, and heart muscle. Without sufficient IGF-1, these tissues and organs degenerate. But IGF-1 has also been implicated in the cancer process because it promotes mitosis, or cellular division. Cancer involves uncontrolled cell division. But scientists still quibble over the precise role that IGF-1 plays in cancer. Among other effects, IGF-1 prevents a process called apoptosis, a type of cellular suicide. One theory suggests that tumors upgrade local IGF-1 synthesis as means of survival.Other theories say that it's the circulating IGF-1 itself that promotes cancer spread. On the other hand, IGF-1 travels in the blood bound to six different binding proteins, with IGFBP-3 being the predominant form. An important point is that IGF-1 can only interact with cells when it is unbound, or free. Bound IGF-1 is basically inert.So the question then arises: what can cause IGF-1 to be released from its binding protein? One thing that does this is insulin, as well as estrogen. When these two hormones are released in greater amounts in the blood, you also get a higher level of free IGF-1, which may be capable of interacting with existing tumors.
An important point to consider about this new study is that no mention is made of what other nutrients the subjects ingested. If they had excess bodyfat, which is linked to higher levels of estrogen, that would account for their elevated IGF-1 levels. If they consumed excess carbohydrates, and were also pre-diabetic, this, too, would lead to higher free IGF-1 levels. The study authors implicated protein because protein is known to boost IGF-1 levels, but not necessarily the free or active form. But the mere fact that the data was derived from an epidemiological survey brings the findings into question, since such surveys are notoriously unreliable.
The study authors note that mice on restricted protein diets show a 45% decrease in tumor mass after two months. But they also say that consuming a higher protein diet protects people over age 65. This relates to the prevention of frailty associated with a lack of IGF-1, which is a major cause of death in older people. Yet, who has the highest rates of cancer? People over age 65. So why would a high protein diet, which is known to boost IGF-1, lead to less mortality in the older people? According to the study authors' suggestion, the higher IGF-1 induced by a higher protein intake should result in a greater incidence of cancer in an older population, especially since such older people usually have an abundance of damaged DNA in their cells--a scenario highly favorable to cancer onset. Would this same information apply to active people, who use or metabolize a higher protein intake differently compared to those who are sedentary?
The other study exclusively used mice as subjects, and found that a low protein, high fat diet was most detrimental to health. But they also found that a very high carbohydrate intake of 70% of ingested calories, along with a low protein intake, was most conducive to longevity! The most surprising aspect of the study, however, was the finding that reducing calories had no effect on longevity. This is contrary to dozens of previously published studies, which did find increased lifespan among various species who ingested a lower caloric intake. On the other hand, the stated mechanism for the increase in longevity linked to the high carb, low protein diet was a decrease in mTOR. mTOR is a protein that is crucial to protein synthesis, and is increased by a higher protein intake. But it is also associated with faster aging and spread of cancer in later years. But mTOR can easily be controlled by far less extreme measures than restricting protein while shoveling in high amounts of carbohydrates. The latter is disastrous for the estimated 50 million Americans who have insulin insensivity or "pre-diabetes," and would, without a doubt, result in an increase in mortality, rather than longevity, if ingested. The study authors did note that the mice who consumed a low protein, high carb diet not only consumed far more calories, but were also significantly fatter than mice who consumed a higher protein, lower carb intake. How being fat and overeating can boost lifespan is a type of metabolic magic that I doubt that anyone can explain, but it may work for mice, certainly not for humans!
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