Can We Prevent Sarcopenia?

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Based on the research presented in Thursday’s Memo, the earlier we address the possibility that sarcopenia will affect us, the more likely we’ll succeed (1). I use fudgy words such as “likely” because we don’t know for sure, but based on the current status of research, here’s what we can do to prevent sarcopenia.

Use It or Lose It

In the study I talked about Thursday, the men who exercised regularly had a lower rate of decline in muscle function. The researchers speculate that chronic exercise helps preserve the motor units, thus preserving the ability of the nerve cells to send out nerve fibers to attach to muscle fibers.

That’s all well and good, but how can we make sure that we preserve the potential and perhaps increase our motor unit activity if we’ve lost some? Research shows that weight training will help. In several studies, resistance training increased muscle strength in the elderly; strength will improve balance and quality of life.

What kind of exercise will work best? It seems to be high intensity exercise. In a study on elderly mice, high intensity interval training (HIIT) increased the muscle mass, muscle fibers, and the number of mitochondria (2). This was a small study and it was on rodents, so the application to humans isn’t assured. To me, it means use your muscles as you mean to keep using them. The harder you exercise within your physical limitations, the better.

Focus on Protein

Retaining muscle mass is not only about exercise. For some reason, as we get older, we decrease our protein intake, but research shows that increasing protein intake can help retain muscle mass. If you don’t have protein in muscle cells, retaining or adding connections to those cells won’t matter much.

How much protein should people try to get? The current recommendation is 0.8 grams per kilogram body weight per day or a third of a gram per pound body weight; someone who weighs 200 pounds would need about 66 grams of protein per day. But research shows that bumping that up to 1.1 grams per kilogram body weight or a half gram per pound may be better as we get older. That’s 100 grams for a 200-pound person (3). That’s easy for even those who are math-challenged: whatever your goal weight, divide by 2, and that’s your daily goal for grams of protein.

It also seems better to stretch protein intake out throughout the day rather than a big slug at one time. Balanced intake will produce a sustained level of amino acids available for muscle repair throughout the day.

The research is far from complete in this area but it seems that as we age, our protein needs revert to when we were younger: we need more of it.

The Bottom Line

Sarcopenia can result in loss of strength and mass, but more important is the loss of quality of life. We don’t think balance while standing or moving is important until we fall; we don’t think brute strength is important until we need to move something and can’t. This week’s Memos give you an idea of how to prevent and perhaps improve nerve and muscle function.

Don’t think this is for only retirees; once you hit 40, it’s a downward trend. Starting early may help minimize the decline. One thing is clear: if you expect to be mobile when you get older, you need to work on it earlier rather than later.

What are you prepared to do today?

Dr. Chet

 

References:
1. J Physiol. 2018 Mar 11. doi: 10.1113/JP275520.
2. J Gerontol A Biol Sci Med Sci. 2018 Mar 14;73(4):429-437.
3. Nutrients 2018, 10, 360; doi:10.3390/nu10030360.

 

Research Update on Sarcopenia

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We know what sarcopenia is, but what can be done about it? Recent research may give us a clue.

Researchers in the United Kingdom examined a variety of variables related to sarcopenia in a group of men. Remember, a motor unit is a nerve and all the muscle fibers to which it attaches. They looked at the differences between the size of the motor units and the total units between 48 young men, 13 non-sarcopenic elderly men, 53 pre-sarcopenic, and 28 sarcopenic men.

The motor unit potential was greater in non-sarcopenic and pre-sarcopenic men than in young men. Why would that be? The researchers suggested that the nerves are still sending out nerve shoots trying to recruit more muscle fibers. This was not the case with the sarcopenic men; their motor unit potential was much lower. That could mean that once connections are lost, there’s no way to recover muscle function including strength.

While the researchers could not answer that final question with certainty, it’s apparent that preventing potential motor unit loss is critical. How? We’ll talk about that on Saturday.

What are you prepared to do today?

Dr. Chet
Reference: J Physiol. 2018 Mar 11. doi: 10.1113/JP275520.

 

So You Lose a Little Muscle—So What?

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Any of my former students who read the Memo should remember the following definition quite well:

A motor unit is a nerve and all the muscle fibers to which it attaches.

It’s called a unit because both sides of that equation are important. Muscle fibers contract when stimulated by a nerve. Reduce the number of fibers that the nerve can attach to, and the muscle won’t generate as much force. Losing a little strength is no big deal, right? How about walking up a flight of stairs? Or even being able to maintain balance while standing? Yes—it’s a big deal.

Sarcopenia is the progressive loss of muscle strength and function as people age. How much loss? Just look at the picture from the Journal of Physiology: the loss of muscle is obvious and with that, a loss of function. Let that sink in. I’ll talk about whether anything can be done about it the rest of the week.

What are you prepared to do today?

Dr. Chet

 

Reference: J Physiol. 2018 Mar 11. doi: 10.1113/JP275520.

 

Exercise: It All Counts

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Here’s something to ponder the rest of the week: why do you exercise? If you don’t, what would your purpose be if you did? I think there are two primary reasons. First, burning calories helps lose weight. Second, if you exercise regularly, you might live longer. But then you hit those exercise recommendations: 150 minutes per week—30 minutes a day five days a week. Who has that much continuous time? Maybe it doesn’t have to be continuous.

A recent published study used data from the NHANES database to determine whether exercise had to be continuous or whether it could be done in shorter segments they called bouts in order to have benefit. They looked at a single outcome: mortality. The subjects wore accelerometers to determine activity levels throughout the day. It turns out that whether you do your 30 minutes of exercise continuously or break the 30 minutes into bouts or segments lasting at least five minutes at a time, there was no difference in the reduction in mortality. Of course, the more total minutes per week were associated with continuing decreases in mortality, but it didn’t matter whether it was in shorter bursts or continuous minutes.

If you want to exercise to live longer, just get moving at least five minutes at a time several times per day. Whether bouted exercise will get you fitter is a different question, but if you want to live longer, get moving.

I know you’ll be busy buying chocolate this weekend no matter what your religious affiliation, so no memo on Saturday. I’ll be back next Tuesday.

What are you prepared to do today?

Dr. Chet

 

Reference: J Am Heart Assoc. 2018;7:e007678. DOI: 10.1161/JAHA.117.007678.

 

Freeze Your Way to Weight Loss?

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If you pay any attention to the news, you may have heard about a recent pilot study: researchers exposed the vagus nerve to freezing temperatures—the nerve that controls hunger. They apparently didn’t freeze it solid, but just enough to slow down the transmission of signals. Without any other interventions, the 10 subjects lost an average of 3.6% of their initial body weight in 90 days. The purpose of the study was to make sure there were no hazardous side effects. The comments by scientists were what they always are: “Interesting, but much research has to be done.”

No, it doesn’t. This is not normal! Does anyone think that exposing oneself to magnetic waves while a needle is inserted into a nerve to freeze that nerve to lose weight is normal? Looking at the study’s average weight loss for someone 5’4” tall with a BMI of 35, that would be about seven pounds. Over 13 weeks. And at the end, no one has learned how to change his or her lifestyle to maintain whatever weight was lost, as minimal as it was. I know we’re always looking for an easy way out, but there are much better and safer ways to lose a half pound a week. Let’s move on.

What are you prepared to do today?

Dr. Chet

 

Reference: Annual Scientific Meeting of the Society of Interventional Radiology. Los Angeles, CA. 03-21-2018.

 

Guidelines for Type 2 Diabetes: EBM in Practice

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The American College of Physicians (ACP) has established guideline statements for the management of HbA1c in non-pregnant adults using medication. They considered the research behind guidelines set by four other major physician organizations for treating type 2 diabetes. After reviewing that data, they have proposed four guidelines for use when treating patients. These are non binding guidelines; the choice is always left to the physician and the patient. But I think they get back to what evidence-based medicine should have always been about: use the best science and research and work with the patient to see what they want to do. Let’s take a look.

ACP Guideline Statements

These are the statements:

Guidance Statement 1
Clinicians should personalize goals for glycemic control in patients with type 2 diabetes on the basis of a discussion of benefits and harms of pharmacotherapy, patients’ preferences, patients’ general health and life expectancy, treatment burden, and costs of care.

Guidance Statement 2
Clinicians should aim to achieve an HbA1c level between 7% and 8% in most patients with type 2 diabetes.

Guidance Statement 3
Clinicians should consider de-intensifying pharmacologic therapy in patients with type 2 diabetes who achieve HbA1c levels less than 6.5%.

Guidance Statement 4
Clinicians should treat patients with type 2 diabetes to minimize symptoms related to hyperglycemia and avoid targeting an HbA1c level in patients with a life expectancy less than 10 years due to advanced age (80 years or older), residence in a nursing home, or chronic conditions (such as dementia, cancer, end-stage kidney disease, or severe chronic obstructive pulmonary disease or congestive heart failure) because the harms outweigh the benefits in this population.

EBM and Guideline Statements

I think the Guideline Statements reflect what EBM was always supposed to be about: consider the patient and what they want. I have spoken to many adults with type 2 diabetes who become frustrated with their inability to reach the HbA1c goals their physician has set. If they can’t reach it, more medication seems to be the only solution, and that’s not what they want.

I think these guidelines bring the patient or their caregiver into the equation. What price does the patient have to pay with their body? How much will it affect their life positively or negatively? Are there real improvements in quality of life if the HbA1c is 6.5% versus 7.0%? What is the cost of emotional stress?

The new guideline statements are a great addition to a physician’s repertoire: treat the patient as an individual. The patient comes before statistics and hazard ratios.

The Bottom Line

While not all organizations are going to adopt these guidelines, they’re important. There has been significant pushback from other organizations, all suggesting that there are new medications that may prevent some of the negative effects of prior treatment. “New medications”—they’ve learned nothing.

The one opportunity I see is that there’s hope for all of us who want to work at getting control of our lifestyle and reduce the dependence on medications as recommended by statement three. You say you don’t want to take medication? Excellent! Here is your chance to prove it.

Eat less. Eat better. Move more.

What are you prepared to do today?

Dr. Chet

 

Reference: Ann Intern Med. doi:10.7326/M17-0939.

 

What Is Evidence-Based Medicine?

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The term evidence-based medicine (EBM) dominates the scientific literature related to the treatment of disease. In short, the use of EBM is intended to treat patients based on the best available science and research; only the largest, best designed, and strongest studies are used when setting up the standards for treatment. That seems to make sense. That applies to the use of medications for the treatment of type 2 diabetes in adults as well as other diseases.

In the past, physicians primarily depended on their training. It doesn’t mean they didn’t use science to guide their decisions, but where and how physicians were trained influenced their treatment decisions more than research and science. That’s why EBM was developed; the use of solid evidence when considering treatment of patients keeps treatment up to date.

The problem is that the way EBM evolved appears to have excluded one of the primary purposes of how it began: consideration of the values and preferences of the patient. Treating patients should never be a one-way street. Your doctor should be a trusted advisor, not a dictator, and should give you the most up-to-date options for treatment of your condition; then you decide together which treatment option fits your life. The clinical and research evidence guides the physician in what to do along with knowledge of your personal health history, but only in the context of what you want.

For example, if after discussing all the options, a patient decides an earlier death is preferable to extending life by taking medication and suffering horrible side effects, that’s a valid preference that the doctor must respect. Another example: if the patient’s life expectancy is less than 10 years or so, pain management may be a better option than joint replacement when all the ramifications of major surgery are considered. That kind of joint decision-making is what EBM is supposed to be all about.

Saturday I’ll look at the guidelines for HbA1c proposed by the American College of Physicians in light of EBM. It’s a Memo you don’t want to miss.

What are you prepared to do today?

Dr. Chet

 

Reference: Ann Intern Med. doi:10.7326/M17-0939.

 

A New Approach to HbA1c

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Type 2 diabetes is a significant problem in North America and it’s spreading throughout the entire world. The treatment standard has always focused on controlling blood sugar, especially HbA1c. Normal is less than 5.7%. For most individuals, reducing the HbA1c to under 6.5% has been the goal for pharmacologic treatment.

HbA1c is a protein found on red blood cells that indicates blood glucose levels over the past 90 days. It develops when hemoglobin, a protein within red blood cells that carries oxygen throughout your body, bonds with glucose in the blood. Think of it as the sugar you ate over the last three months getting stuck to your red blood cells; the higher your HbA1c, the worse your control of your blood sugar has been. For a prediabetic, that means your days of diabetes meds and finger pricks is getting closer. For a diabetic, that opens the door to many of the worst consequences of diabetes, such as heart and kidney disease, blindness, and nerve damage.

Recently, the American College of Physicians published new guidance statements for the use of medications for controlling HbA1c. A committee of physicians examined the data behind the current standards of treatment for four of the major physician organizations including the American Diabetes Association. In the simplest terms, they wanted to know what benefits or hazards occur when treating adults with type 2 diabetes with medications. Should the goal be to get the HbA1c as low as possible with drugs? Or should the individual be part of the treatment equation?

This is an important issue and the topic for this week. I’m going to review evidence-based medicine on Thursday. You can get the entire story by listening to the Straight Talk on Health on evidence-based medicine, normally available only to Members and Insiders; I cover the entire concept of how EBM began and what it was intended to be. For those of you who haven’t chosen a membership yet, get more info here.

What are you prepared to do today?

Dr. Chet

 

Reference: Ann Intern Med. doi:10.7326/M17-0939.

 

Spring Break!

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Paula and I are taking this week off for Spring Break, but as you can see we’re spending it in Michigan where it isn’t exactly beach weather. We’ll be back with more health news next week.

What are you prepared to do today?

Dr. Chet

The Truth Behind the Obesity Paradox

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In my opinion, the short answer to the obesity paradox is that it doesn’t really exist. But what fun would that be? That doesn’t teach you anything. Let’s take a look at the problems with the research that contributed to this paradox.
 

Study One: Dialysis, BMI, and Mortality

A study of dialysis patients led to the first observation that people with higher BMIs lived longer (1). After tracking over 1,300 subjects on dialysis for a year, researchers found that those who were overweight had a decreased risk of dying and had fewer hospital stays when compared to those who were underweight. This may have been the study that yielded the name The Obesity Paradox. The problem? The study lasted only one year. Trying to generalize what will happen to all overweight and obese people on dialysis from a study that lasted only one year and at only a single location isn’t realistic. It raises an intriguing question, but we’ll need a much more extensive study to really make a solid prediction.
 

Study Two: The Rotterdam Study

I described this study on Thursday (2). While the study appeared to show a protective benefit from being overweight or obese, the subjects were elderly with an average age of 77 at the study’s beginning. One risk factor that you cannot change is age: the older you are, the more likely you are to die. But that’s not the whole story. We can probably say that older people may live longer with a little extra weight, but to extend that prediction to all age groups isn’t valid.
 

Study Three: BMI and Mortality

While this study claimed to analyze the data on over two million people, it was still a meta-analysis (3), which doesn’t yield cause and effect, just a statistical association. Further, they used studies of varying lengths without necessarily knowing exact causes of deaths. They also did not have precise BMIs on everyone; some studies included metrics such as BMI under 27.5 and over 27.5. They tried to include the highest number of subjects, but the quality of data varied and that made it a mess. Researchers chose too many different types of studies in the meta-analysis, and it just doesn’t work. I wouldn’t bet my life on it.
 

Study Four: A Broader Look

The real problem with every approach is the lack of acknowledgement that people with advanced disease may have lost weight before they were included in the study; diseases such as heart failure, diabetes, or renal disease will often lead to weight loss. Those who were heavier when disease hit had the benefit of extra energy stored as fat to deal with the disease, and that could explain the outcomes of those studies. It had nothing to do with being obese; it was a matter of timing.

A study published last month appears to confirm that (4). Researchers in the Cardiovascular Disease Lifetime Risk Pooling Project obtained data from 10 different longitudinal studies, including individual-level data and accurate mortality data. They found that as BMI increased, the death rate from all forms of CVD increased. For those who carried extra weight while younger, CVD occurred earlier, making it more likely they would die before their time.
 

The Bottom Line

As I said, there really is no obesity paradox. Being overweight or obese carries with it risks of degenerative disease. Some people may have better genes and may gain protection for a few years. But in the end, being overweight or obese carries a higher risk of various diseases than the limited protection from an advanced disease you may gain by carrying extra weight. So my advice is the same as it always was: if you’re overweight, your best bet for a long, healthy life is to lose it.

What are you prepared to do today?

Dr. Chet

 

References:
1. Kidney International, Vol. 55 (1999), pp. 1560–1567.
2. European Heart Journal (2001) 22, 1318–1327.
3. JAMA. 2013; 309(1): 71–82.
4. JAMA Cardiol. doi:10.1001/jamacardio.2018.0022.