This post by @tednaiman led to some questions about protein safety that were kindly answered by @mackinprof. High protein diets are often promoted for weight loss, muscle hypertrophy, and prevention of sarcopenia. What are the safety questions and what does the research show?
Concern #1. Protein is bad for the kidneys.
No. The basic thought was that since the kidneys “process” the protein, if you eat more, they work harder, so high protein diets are hard on the kidneys. That is not what the evidence shows.
Zhu et al., 2018 showed no benefit in diabetics with kidney disease (unhealthy patients) when put on a low protein diet.
Longland et al., 2016 also showed that a higher protein diet actually improved kidney function measures (GFR in healthy patients, unclear if a benefit but certainly did not worsen function).
One noted nephrologist at a conference had us repeat “there is no such thing as a renal diet!”
Concern #2. Protein is bad for the bones.
No. Shams-White et al., 2017 reviewed several studies and found high protein intakes did not have any negative effects on bone health and there was actually a trend towards improved bone health.
Concern #3. Increased protein is bad for the liver and cholesterol.
No. Antonio et al., 2016 showed high protein diet for a year had no negative impact on liver functions or cholesterol.
(Just FYI, only a few days of a bad diet can change liver functions and cholesterol, so 4 months is a good length of time to study this).
Concern #4. You only need so much protein and the rest (up to 50-60%) is turned to sugar.
No. Multiple studies have shown no increase in blood glucose after protein intake.
Yes, the body can make glucose from protein but even after as 12 hour fast (body needs glucose) when fed 23g protein only around 4g sugar is made (Fromentin et al., 2013). A teaspoon of sugar is 5g.
So what is the primary care perspective? Protein can assist in weight loss, muscle gain, and prevention of muscle loss. In a world of obesity and sarcopenia, a higher intake of protein may be quite beneficial and appears quite safe but nothing is taken for granted.
Sarcopenia, the age-related loss of muscle mass and strength, is a major concern for health and mobility in older adults. But muscle decline can begin much earlier, often as soon as our 30s and 40s.
Here's why building and maintaining muscle strength is crucial at every stage.
Muscle Strength Over the Life Course 📊
Research shows muscle strength peaks in our 20s and early 30s, remains steady in midlife, and declines at about 1-2% per year post-50.
By age 70, that rate can accelerate sharply, making age-related muscle loss (sarcopenia) more noticeable. Why is Muscle Decline a Concern?
Have you read “Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review”
You should!
Follow along as we discuss this paper.
@dabonillao @RBKreider @ExphysPhD @daforerog @chadkerksick @DrMikeRoberts @EricRawsonPhD @Creatine4Health @darrencandow @DrCreatine Creatine’s role goes beyond athletic performance—it’s central to cellular energy in various tissues. This review shows how creatine supports high-energy systems like muscles, heart, and brain, helping cells meet energy demands when they need it most.
@dabonillao @RBKreider @ExphysPhD @daforerog @chadkerksick @DrMikeRoberts @EricRawsonPhD @Creatine4Health @darrencandow @DrCreatine Our brain cells, including astrocytes and neurons, depend on creatine to support energy needs for survival, ion transport, and possibly neurotransmitter signaling. This may mean creatine helps neurons stay functional, especially under stress.
Iron deficiency without anemia (IDNA) is more common than most people realize. Many think anemia is the first sign of low iron, but often, deficiency starts well before that.
You can be iron deficient without having low hemoglobin. This means your oxygen-carrying capacity might be affected before you have "anemia."
Symptoms of iron deficiency without anemia (IDNA) can include:
Fatigue
Reduced exercise capacity
Restless legs
Poor focus
Persistent hypothyroid symptoms (even if treated)
What can we do to avoid lean mass loss with weight loss?
Check out this recent paper with me:
Strategies for minimizing muscle loss during use of incretin-mimetic drugs for treatment of obesity
@DrCarlaPrado @imwmhealth @DrZhaopingLi @heymsfield @DrNadolsky Background: Incretin-mimetic drugs (IMDs) like semaglutide and tirzepatide have shown remarkable efficacy in treating obesity. However, rapid weight loss can lead to skeletal muscle loss, impacting long-term health and metabolic outcomes.
@DrCarlaPrado @imwmhealth @DrZhaopingLi @heymsfield @DrNadolsky This review explores strategies for preserving muscle mass during IMD therapy.
Safety and Side Effects:
Water Retention: While short-term water retention due to increased intracellular volume is possible, long-term supplementation doesn't significantly impact total body water relative to muscle mass.
“Exercise-Specific Adaptations in Human Skeletal Muscle: Molecular Mechanisms of Making Muscles Fit and Mighty”
If you have then awesome b/c it’s a lot to discuss.
Too much for one thread. I’d like to share some concepts that I found interesting. I’ll stick to one at a time.
Let’s look at the molecular mechanisms behind getting "fit" vs. getting "mighty".
work by: Aaron Thomas @_ConnorStead, @ExercProteomics @mackinprof
The first concept to discuss is Initial Response: Both AT and RT induce a generic "exercise stress" response in untrained individuals, characterized by broad transcriptional and translational changes.