Protein Is Essential to Our Health, But

There is no doubt that protein is essential for our health. It’s not only the main building block for our muscles and bones, but also a structural component of enzymes, cellular receptors, and important signaling molecules. Protein also performs transport carrier functions, and the amino acid components serve as precursors to hormones and vitamins. But as we have all heard before, you can get too much of a good thing. It’s important that we understand that there is an upper limit to how much protein will actually benefit us. For example, if we consume more protein than the body needs, our kidneys are tasked with removing more nitrogen waste products from the blood. This added stress will task the kidneys with more work and could worsen kidney function if you already have kidney disease.1 To understand why eating too much protein is a bad idea we need a basic understanding of a few concepts: Calorie restriction, Insulin, Insulin-Like Growth One (IGF-1), and The Mammalian (or mechanistic) Target of Rapamycin (mTOR) Pathway.

4 Important Concepts

Calorie restriction

This is where you simply lower your calorie intake while still eating enough to prevent malnutrition. Which has been the “gold standard” in preserving health, extending life, and slowing down the aging process in animal studies for over 60 years. This is because calorie restriction in known to alter the expression of hundreds to thousands of genes. Some of which are related to longevity and some play a role in metabolism, cell growth, reproduction, immune response, and other biological processes. While these have mostly been seen in animal studies there is also strong evidence that suggests caloric restriction has a similar effect on human lifespan as well.2  Though many think that  the effects are mainly due to the fact they are decreasing total calorie intake. There is recent research that has begun to tease out that it’s not a lack of total calories that trigger the beneficial effects of calorie-restricted diets. Instead, the some of the latest science suggests that this phenomenon may actually result more from the reduced protein intake, specifically the reduced intake of methionine (an amino acid) which there are high levels of in meats.3   But it would not be wise to eliminate methionine entirely, as it is a methyl donor for one of our most important antioxidants, glutathione. Many just need to lower the amount they consume.

Insulin

Next up is Insulin, a hormone that is present in most biological lifeforms, from worms and flies all the way to humans. In humans, Insulins role is to control nutrient storage – storing energy (nutrients) during times of abundance to buffer those times when food (energy) is scarce. In simplified terms, its job is to help convert excess carbohydrates into fat. Insulin also play a role in regards to aging. When our bodies perceive food as abundant, insulin will send the all-clear message to reproduce. This means all our bodily processes are geared toward creating new life and away from preserving our own. On the flip side, if our body perceives it’s in a famine state an array of protective and regenerative mechanisms get switched on. This is to ensure that our species survives through lean times. In general, the lower average insulin level and better our insulin sensitivity is, the slower we age. In fact, according to studies of the planet’s oldest living people, lower insulin levels and higher insulin sensitivity are associated with longer lifespan.4

Insulin-Like Growth Factor One (IGF-1)

Now that we have looked at insulin let’s move on to Insulin-Like Growth Factor One (IGF-1). Excess protein that is not utilized by the body stimulates the production of IGF-1. As the name would suggest IGF-1 is a close relative of insulin and it plays a somewhat similar role. In fact, they are so similar that they even cross-react with each other’s receptors. Human growth hormone also plays an important role as it acts as a messenger for IGF-1. Once HGH is release by our pituitary gland, HGH stimulates the manufacture and release of IGF-1.  Most of the anabolic and growth affects seen with IGF-1 are attributed to HGH. Essentially, IGF-1 tells our bodies to grow by instructing cells to reproduce.  But this process, which results in a stronger organism, comes with a high price tag. Similar to insulin, IGF-1 is a powerful stimulus of aging. Studies have shown evidence that animals that produce less IGF-1 live significantly longer and live less disease-ridden lives compared to those that produce high levels of this hormone.5,6

mTOR

I’m guessing that a number of people have heard of insulin and IGF-1 before, but I assume not many have heard of “The Mammalian (or mechanistic) Target of Rapamycin (mTOR).” Even most physicians learn very little or most often nothing about this vital pathway, which has only recently been discovered in the late 1960s. mTOR7 is a complex protein that serves as our body’s most important and incredibly complex signaling pathway. It is the key muscle-building mechanism is all mammals. When mTOR is not stimulated, it instructs the cell to turn on the multiple repair and maintenance processes at its disposal. These include autophagy (cleaning up cellular debris), DNA repair, and activating intracellular antioxidants and heat-shock proteins (HSPs). When mTOR is activated (stimulated), typically due to excess protein, it signals the cell grow and proliferate while it also suppresses most cellular and mitochondrial repair and regeneration mechanisms.  If we maintain low levels of glucose, excess amino acids (protein), insulin, and growth factors (like IGF-1), we will inhibit mTOR. Inhibiting mTOR allows for the up-regulation of gene expression that promotes cellular and mitochondrial maintenance or repair. There are many nutrient that stimulate mTOR but amino acids, which are derived from protein, are the most potent. Therefore, stimulating mTOR by eating large amount of protein is one of the quickest ways to suppress cellular and mitochondrial autophagy. This prevents the body from effectively cleaning out debris and damaged cells. Activation of this mechanistic pathway is not only associated with decreased lifespan but also with virtually all cancers.8

Why Can’t we Just Completely Suppress this mTOR Pathway?

At this point you may be saying “alright stimulating mTOR seems to be bad so the solution is to just suppress mTOR as much as possible.” But, chronically suppressing mTOR would not be a wise decision. Remember this pathway is the key muscle building mechanism in mammals. Thus, if we chronically suppress it’s activation we are going end up weak and frail. This is why there is a protein paradox and how much you consume is based on what stage of life you are in and what your goals are. Are you young and want to be strong and fit then a higher protein intake (within reason) could be for you.  Or maybe you’re a little bit older and want to focus on optimizing yourself for longevity. If so a lower protein diet could be a good idea.Now that we have looked at insulin let’s move on to Insulin-Like Growth Factor One (IGF-1). Excess protein that is not utilized by the body stimulates the production of IGF-1. As the name would suggest IGF-1 is a close relative of insulin and it plays a somewhat similar role. In fact, they are so similar that they even cross-react with each other’s receptors. Human growth hormone also plays an important role as it acts as a messenger for IGF-1. Once HGH is release by our pituitary gland, HGH stimulates the manufacture and release of IGF-1.  Most of the anabolic and growth affects seen with IGF-1 are attributed to HGH. Essentially, IGF-1 tells our bodies to grow by instructing cells to reproduce.  But this process, which results in a stronger organism, comes with a high price tag. Similar to insulin, IGF-1 is a powerful stimulus of aging. Studies have shown evidence that animals that produce less IGF-1 live significantly longer and live less disease-ridden lives compared to those that produce high levels of this hormone.5,6

  1. http://www.pkdiet.com/pdf/proteingfr.pdf
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2692623/
  3. http://www.cell.com/cell-metabolism/pdf/S1550-4131(14)00062-X.pdf
  4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319489/
  5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074016/pdf/nihms-594842.pdf
  6. http://www.biochemsoctrans.org/content/ppbiost/40/4/721.full.pdf
  7. http://jcs.biologists.org/content/joces/122/20/3589.full.pdf
  8. http://sabatinilab.wi.mit.edu/Sabatini%20papers/mTOR_cancer-NRC-2006.pdf

Fact of the week

 A 2014 study done on mice published in Cell Metabolism,9 showed that longevity and health were boosted when carbohydrates replaced proteins in the diets of the mice. This suggests that reducing protein inhibits the mTOR pathway more than reducing carbohydrates.

While this study was

done on mice, not humans, it still gives us valuable results that are likely to be similar in humans. It’s also worth noting that the researchers didn’t test a high-fat diet, but only focused on carbohydrate versus protein. If these were your only two choices then protein restriction may in fact be more important than carb restriction. However, there can be, for many  people, long-term drawbacks to eating excessive carbohydrates.

  1. http://www.cell.com/cell-metabolism/pdf/S1550-4131(14)00065-5.pdf