Protein: Underappreciated Role in Optimal-Active Aging - Part 1 |
By Hector Lopez, MD, MS(c), CSCS and Joseph Jimenez, MD, MBA, CSCS
First published at www.MohrResults.com, August 2007
Sarcopenia is the unintentional and involuntary loss of lean body mass (muscle and bone mass), functional strength and power associated with aging. Typically, age-related decreases in muscle mass may begin as early as age 25. Between 30 to 60 years of age, muscle mass decreases at a rate of 0.3%– 0.8% per year, and by age 80 a substantial loss of muscle mass of up to 25–40 percent would have accrued because the rate of loss accelerates dramatically after age 60. The prevalence is in the range of 10% -15% in women in their 60s to as high as 18% - 28% in men in their 80s. The muscle wasting correlates with a substantial loss of functional strength necessary to competently and confidently perform ADL (activities of daily living, such as regular housework, self-care, or lifting tasks in the home, etc.) This often leads to decreases in weight-bearing physical activities and hence energy expenditure. From this perspective, one can see how sarcopenia is intimately linked to osteoporosis, increased risk of falls, fractures, hospitalizations, and, as a consequence, expensive orthopedic procedures, which pose unique challenges in the rehabilitation setting either in the pre-surgical or post-surgical period. This loss of muscle tissue can also be accompanied by an increase in body fat, particularly in the visceral area, which is the adipose tissue known to be most influential to cardiovascular and metabolic disease.
The negative change in body composition has implications for increased risk in cardiovascular disease, insulin resistance, and type 2 diabetes. Hence, you have the emergence of the “fat-frail” population, characterized by sarcopenia and obesity (this could be termed “diabesity”). The “fat-frail” syndrome is really part of the spectrum of dysfunctional metabolic syndromes including diabetes, hypertension, hypercholesterolemia, and gout. Consequently, this population of obese-sarcopenics is prone to worse medical outcomes than their non-obese and frail counterparts. The cumulative impact on the health care costs related to sarcopenia is 2.5% of the total health care costs for the year 2000 alone. Interestingly, reducing the prevalence of sarcopenia by 10 percent would yield a staggering $1.7 billion in savings per year for the U.S. It is important to note that these are direct costs of the disability, which means that the study did not account for many other medical complications associated with sarcopenia and dysfunctional metabolic syndrome, such as increased risks of metabolic, renal and cardiovascular conditions. In this article, we will discuss strategies to help prevent sarcopenia and slow its progression. The following strategies build on each other and are by no means an answer to sarcopenia and age-related dysfunctional metabolic syndrome in isolation. We will provide a rationale for using a comprehensive, integrative approach as the optimal strategy for attenuating and/or preventing sarcopenia.
A High Protein Meal a Day Keeps Sarcopenia Away
Sarcopenia, in the classic non-obese, frail elderly population, is a consequence and manifestation of chronic energy deficit and malnourishment coupled with decreased physical activity. The question is, if this population is not eating enough, what macronutrients (carbohydrates, fats, protein) are preferred as the source of calories? Can nutritional interventions be recommended to prevent sarcopenia? What is clear from the available data is that diets high in carbohydrates and low in protein (i.e., protein intake as recommended by the RDA) consistently fail to prevent muscle wasting, and providing enough calories to theoretically maintain bodyweight still often results in negative nitrogen balance (a marker of protein/muscle breakdown). In contrast, higher protein intake in the elderly tends to result in more positive nitrogen balance (a marker of muscle anabolism or preservation). Preliminary studies suggest that seniors need higher protein daily intake in the range of 0.8–1.4 grams/kg per day. So if you weigh 150 lbs, this equals 68 kg (to calculate your weight in kg, divide your weight in pounds by 2.2, so 150/2.2 = 68). This translates to about 70 grams of protein per day to 105 grams per day in this example. Increasing protein intake however, is only a starting point, and, as we will see, the source of protein, timing and possibly frequency of protein intake are often underappreciated, yet critical factors in this population.
Sarcopenia in the “frail and obese” population or in the context of the aforementioned dyfunctional metabolic syndrome, may benefit from increasing protein intake for reasons mentioned above and realize the added advantage of fat loss and body composition improvements. Studies show that the higher protein diets promote greater weight loss/fat loss and improved markers of lipid and carbohydrate metabolism relative to low protein diets. Therefore, for this population of dysfunctional metabolic patients, strategic protein intake can not only help preserve lean body mass, but also decrease body fat. Some of the attributes of protein that may explain the results of improved overall body composition and metabolic health include:
- increased sensation of fullness with protein
- improved insulin sensitivity and more stable blood sugars throughout the day
- improved nitrogen balance
- increased metabolism secondary to the thermic effects of protein
Here Are Some Useful Points With Regard To Protein:
- Before you start on a higher protein diet, ask your physician first if you have a chronic liver or kidney condition related to diabetes and/or high blood pressure. Higher protein diets may be a contraindication. Otherwise, increasing protein intake can be done safely, particularly when using strategic nutrient timing, supplementation with specific amino acid profiles, and protein of high quality. There are also other strategies to enhance the impact and anabolic efficiency of a protein meal that involves “fortification” with certain amino acids.
- Increase your protein intake to the above recommendations of 0.8 grams to 1.4 grams protein/kg of bodyweight and increase your caloric intake to help prevent progression of sarcopenia, but this is only a starting point. There will be certain situations where more than 1.2 grams protein/kg of bodyweight is clinically beneficial.
- Diets with moderate carbohydrate and moderate protein intake (40–55 percent of calories from carbohydrates, 20–30 percent of calories from protein, and 15–25 percent of calories “healthy fats”) are a great start to decreasing body fat and maintain lean body mass. Although, the elderly have a reduced capacity or “amino acid resistance”, they do still show responsiveness of muscle protein synthesis to diet, so it may be that maximizing the protein:energy ratio of food, while keeping the total amount of energy intake down to minimize fat gain is a reasonable strategy. Additionally, increasing the ratio of protein consumption in the diet helps to maximize the anabolic efficiency of their meals on a per gram and per volume basis. Increasing caloric/food volume intake is at times an insurmountable challenge in the aging patient with decreasing appetite. We also posit that because there is a synergistic effect between exercise (particularly progressive resistance exercise) and feeding in stimulating muscle protein synthesis, elderly individuals could maximize their muscle mass by integrating a program of resistance exercise, with feeding concentrated in the immediate “peri-exercise” period.
- If you are currently on a high carbohydrate/low protein diet, replace your mid-day meal or snack with a high protein meal containing 20–35 grams of protein. Protein rich meals, even if consumed just once a day have been shown to benefit whole body protein status, prevent muscle protein catabolism, and stimulate muscle protein synthesis in the elderly.
To recap, sarcopenia and dysfunctional metabolic syndrome exist in a vicious cycle of interdependent factors, all the while increasing the risk for developing multiple medical complications and co-morbidities. The vicious sarcopenic cycle, which comes full circle involves: loss of metabolically active skeletal muscle mass > decreased physical activity > decreased responsiveness of skeletal muscle to nutritional and hormonal stimuli > further decrement in skeletal muscle mass > further decline in physical activity, functional capacity, and mobility, etc. Since the elderly already have limited reserves of muscle mass, strength and function, it follows that even a modest catabolic response from acute or chronic disease could have a devastating impact on activities of daily living, quality of life, and wellness.
Summary
In part 1 of this two-part article, we have explored the importance of establishing a sound nutritional foundation to develop metabolic momentum toward “breaking the vicious sarcopenic cycle.” The second installment will focus on exercise, strategic protein supplementation, and integrating several modalities to optimize a sarcopenic prevention and management regimen.
Sarcopenia is the unintentional and involuntary loss of lean body mass (muscle and bone mass), functional strength and power as a person ages. . . . The negative change in body composition has implications for increased risk in cardiovascular disease, insulin resistance, and type II diabetes. Hence, you have the emergence of the “fat-frail” population, characterized by sarcopenia and obesity ( this could be termed “diabesity” ).
Joseph Jimenez, MD, MBA, CSCS and Hector Lopez, MD, MS(c),CSCS are physicians training in the specialty of Physical Medicine and Rehabilitation. They are co-founders of Physicians Pioneering Performance, LLCTM.
Dr. Lopez is part of the Mohr Results, Inc Board of Advisors.
References:
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- Manninen A. High-Protein weight loss diets and purported adverse effects: Where is the evidence? Sports Nutrition Review Journal 2004: 1(1): 45–51.
- Morley J, Baumgartner R., Roubenoff R., Mayer J, Nair K. Sarcopenia. J Lab Clin Med 2001; 137–143.
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