Dr. Steve Chaney, Author at Health Tips From The Professor

Do B Vitamins Reduce Heart Disease Risk?

February 23, 2016 by Dr. Steve Chaney

What Role Do B Vitamins Play in a Heart Healthy Lifestyle?

Author: Dr. Stephen Chaney

Two weeks ago I shared some studies that challenge the claim that vitamin E doesn’t reduce heart attack risk. To close out “Heart Health” month, I want to share some information that may change how you think about B vitamins and heart disease risk. Once again, you’ve seen the headlines: “B Vitamins Do Not Reduce the Risk of Heart Disease”. In fact, these headlines have been repeated so many times that virtually every expert thinks that it has to be true. Once again, I’m going to share some information with you that I learned from a seminar by Dr. Jeffrey Blumberg who disagrees with this commonly held belief.

Dr. Blumberg is a Professor in the Friedman School ofNutrition Science and Policy at Tufts. Dr. Blumberg has over 200 publications in peer-reviewed scientific journals. He is considered one of the world’s top experts on supplementation, and his specialty is conducting and analyzing clinical studies. He believes that the media has seriously misinterpreted the studies on B vitamins and heart disease risk. You might call this “The Rest of the Story” because you (and your doctor) definitely did not hear this part of the story in the news.

Do B Vitamins Reduce Heart Disease Risk?

The study in question is called the “Heart Outcomes Prevention Evaluation-2“. In that study a group of middle aged men and women received 2.5 mg of folate, 50 mg of vitamin B6 and 1 mg of vitamin B12 versus a placebo and were followed for an average of 5 years.

The headlines that you may have seen said “B vitamins do not reduce the risk of major cardiovascular events in patients with vascular disease”. But, the headlines did not tell the whole story.

In the first place, that was only true for heart attacks and cardiovascular death. Strokes were reduced by 25%. I don’t know about you, but I consider strokes to be fairly major.

However, even when we focus on heart attacks and cardiovascular deaths the headlines didn’t tell the whole story. You see, even the best intentioned studies sometimes contain fatal flaws that aren’t obvious until after the study has been completed.

The Flaws In The Study

There were two major flaws in this study.

Flaw #1 was that 70% of the study subjects were eating foods fortified with folate and had adequate levels of that nutrient in their bloodstream before the study started.

For those people who were already getting enough folate in their diet, B vitamin supplementation didn’t make much of a difference. However, for those people not getting adequate levels of folate in their diet, B vitamin supplementation decreased their risk of heart disease by ~15%.

Flaw #2 was that ~90% of the people in the study had a history of coronary artery disease and most of them were already on cholesterol lowering medications.

To understand why this is a problem you have to understand both the proposed mechanism by which B vitamin supplementation has been proposed to lower the risk of heart disease AND how the cholesterol lowering drugs work.

Deficiencies of folate, B6 and B12 are thought to increase the risk of heart disease because the B vitamin deficiency causes an increase in homocysteinelevels in the blood, and high homocysteine levels are thought to increase inflammation – which is a risk factor for heart disease. So supplementation with folate, B6 and B12 has been proposed to decrease heart disease risk by decreasing inflammation.

The problem is that the most commonly used cholesterol lowering medications also decrease inflammation.So you might not be surprised to learn that those people who had a history of coronary artery disease(and were taking cholesterol lowering medication that reduces inflammation) did not receive much additional benefit from B vitamin supplementation.

For those people in the study who were not taking cholesterol lowering medication, B vitamin supplementation also reduced their risk of heart attacks by ~15% – but there were too few people in that group for the results to be statistically significant.

So the headlines from this study really should have said “B vitamins do not reduce the risk of heart attacks or cardiovascular deaths in people who are already getting adequate folate from their diet or in people who are taking drugs that reduce the bad effects of B vitamin deficiency”. But that kind of headline just wouldn’t sell any newspapers.

What Does This Study Mean For You?

There are two very important take-home lessons from this study.

Lesson #1: Once again this study makes the point that supplementation makes the biggest difference when people have an increased need. The studies discussed in Vitamin E and Heart Disease two weeks ago illustrated increased need because of age, pre-existing disease, and genetic predisposition. This study illustrated increased need because of inadequate diet.

Lesson #2: This study also illustrates a problem that is becoming increasingly common in studies of supplementation. It is considered unethical to not provide participants in both groups with what is considered the standard of care for medical practice. In today’s world the standard of care includes multiple drugs with multiple side effects, and some of those drugs may have the same mechanism of action as the supplement.

I have discussed this problem in the context of omega-3 fatty acids and heart disease in a previous “Health Tips From the Professor,” Is Fish Oil Really Snake Oil? In many cases it is no longer possible to ask whether supplement X reduces the risk of a particular disease. It is now only possible to ask whether supplement X provides any additional benefit for patients who are taking multiple drugs, with multiple side effects. That’s not the question that many of my readers are interested in.

The Bottom Line

Headlines have proclaimed for years the “B Vitamins Do Not Reduce Heart Disease Risk”. Dr. Jeffrey Bloomberg of Tufts University has reviewed one of the major studies behind this claim and found the headlines to be misleading.

For example, the study showed that B vitamin supplementation reduced strokes by 25%, which is a pretty significant finding in itself.

When he analyzed the portion of the study looking at heart attacks, he found two major flaws:

#1: 70% of the people in the study were already getting adequate amounts of B vitamins from their diet and would not be expected to benefit from supplementation. For the 30% who weren’t getting adequate amounts of B vitamins from their diet, supplementation reduced their risk of heart attack by 15%.

#2: 90% of the people in the study were taking a drug that masks the beneficial effects of B vitamin supplementation. For the 10% who weren’t taking the drug, supplementation with B vitamins also reduced their risk of heart attack by 15%, but there were too few people in that group for the results to be statistically significant.

Obviously, there were only a handful of people in the study who weren’t getting enough B vitamins from their diet AND weren’t on medication, so we have no idea what the effect of B vitamin supplementation was in that group.

Once again this study makes the point that supplementation makes the biggest difference when people have an increased need. The studies discussed in “Health Tips From the Professor” two weeks ago illustrated increased need because of age, pre-existing disease, and genetic predisposition. This study illustrated increased need because of inadequate diet.

This study also illustrates a problem that is becoming increasingly common in studies of supplementation. It is considered unethical to not provide participants in both groups with what is considered the standard of care for medical practice. In today’s world the standard of care includes multiple drugs, some of which may have the same mechanism of action as the supplement.

In many cases it is no longer possible to ask whether supplement X reduces the risk of a particular disease. It is now only possible to ask whether supplement X provides any additional benefit for patients who are taking multiple drugs, with multiple side effects. That’s not the question that many of my readers are interested in.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Plantar Fasciitis Causes and Treatment

February 16, 2016 by Dr. Steve Chaney

You Can Enjoy Pain Free Living From Home

Author: Julie Donnelly, LMT –The Pain Relief Expert

Editor: Dr. Steve Chaney

Recently a woman came in to see me who was suffering from severe plantar fasciitis pain, her arch hurt so much she could barely walk. She’d been to several specialists and has so far bought three pair of orthotics (at $400 each!). Plantar fasciitis is getting to be a commonplace condition in my office. I love working with athletes, but I’m finding this isn’t only a problem for athletes.

Because of driving a car for long distances her right foot was worse than her left, which makes sense since the muscles that enable you to press down on the gas and brake pedals, are the same ones that are the cause of plantar fasciitis.

Plantar Fasciitis Causes: Are Muscles The Culprit?

Muscles are seldom considered when searching for the answer to plantar fasciitis pain. Instead the foot is considered to be the problem, instead of the symptom, and orthotics are commonly recommended. In many cases, when muscles are the cause of the plantar fasciitis symptoms, the orthotics will cause more pain.

The analogy I always use is, if you pull your hair at the end, your scalp will hurt. But you don’t need to massage your scalp, you don’t need to take pain-killers for the headache, and you don’t need brain surgery — you just need to let go of your hair! It’s the same with joint pain. Muscles pull on tendons, and the tendons insert into a joint. When the muscle is tight you will feel the pain at the joint. But you don’t need to rub the joint, or take pain-killers, or have surgery—you need to release the spasms in the muscle fibers.

In the case of plantar fasciitis, the muscles are in your lower leg, and the insertion of the tendon is in your arch – so when the muscles are tight your arch will hurt.

The two muscles are the tibialis anterior and the peroneal. The tibialis anterior runs along the entire length of the shin bone and then the tendon inserts onto the first metatarsal (the long bone that is on the inside of your arch and goes up to your big toe), while the peroneal runs along the entire outside of your lower leg, goes behind your ankle, and the tendon inserts on the fifth metatarsal (the bone on the outside of your foot) and also on the first metatarsal at the same point as the insertion of your tibialis anterior. This is important to visualize so you can see how the tendons pulling on the bones will put pressure on your arch and cause the arch muscles to be strained — causing plantar fasciitis pain in the bottom of your foot.

Self-Treatment For Plantar Fasciitis Pain

There are several muscles that all impact your arch and cause the pain of plantar fasciitis. This picture is doing the treatment for the muscle that runs down the outside of your lower leg, called peroneal. The peroneal is neglected by most therapists when searching for an answer to foot pain, yet it is often one of the key muscles that needs to be treated to get relief.

Sit as shown in the picture and use either the Julstro Perfect Ball, or a new tennis ball, and press the outside of your leg directly onto the ball. You’ll find a very tender point at the same level as shown in this picture.

When you find it, hold the pressure steady, and then slightly move your leg so the ball rolls up and down the outside of your leg. Use your hand as shown to press down on your leg to increase the pressure.

You’ll be thrilled when you see how quickly you’ll feel relief! You’ll be able to go back out and enjoy your life pain-free!

Plantar fasciitis causes are often centered around muscles in the legs, therefore plantar fasciitis pain relief is also.

Wishing you well,

Julie Donnelly

About The Author

Julie Donnelly is a Deep Muscle Massage Therapist with 20 years of experience specializing in the treatment of chronic joint pain and sports injuries. She has worked extensively with elite athletes and patients who have been unsuccessful at finding relief through the more conventional therapies.

She has been widely published, both on – and off – line, in magazines, newsletters, and newspapers around the country. She is also often chosen to speak at national conventions, medical schools, and health facilities nationwide.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Check It Out!

If you would like easy to follow instructions on how to relieve joint pain and muscle tightness from head to toe click here (http://www.triggerpointyoga.com/product/triggerpoint-yoga-full-body-kit/?ap_id=SteveChaneyTips) to check out Julie Donnelly’s Trigger Point Yoga instruction kit today. Whenever, I have pain and stiffness I use her techniques. They work!

Vitamin E And Heart Disease

February 9, 2016 by Dr. Steve Chaney

Does Vitamin E Reduce Heart Attack Risk?

Author: Dr. Stephen Chaney

Since February is “Heart Health Month”, I thought I would share some information with you that might change how you think about vitamin E and heart disease risk. You’ve seen the headlines: “Vitamin E Does Not Reduce the Risk of Heart Disease”. In fact, these headlines have been repeated so many times that virtually every expert thinks that it has to be true. Let me share the opinion of one expert who disagrees. This week I’m going to share some information with you that I learned from a seminar by Dr. Jeffrey Blumberg from Tufts University.

But first let me tell you who Dr. Blumberg is. Dr. Blumberg is a Professor in the Friedman School of Nutrition Science and Policy at Tufts. Dr. Blumberg has over 200 publications in peer-reviewed scientific journals. He is considered one of the world’s top experts on supplementation.

Now back to what I learned at his seminar. Dr. Blumberg’s specialty is conducting and analyzing clinical studies, and his perspective on some very influential clinical studies is a bit different from what you may have heard from media reports. He believes that the media has seriously misinterpreted several recent studies. You might call this “The Rest of the Story” because you (and your doctor) definitely did not hear this part of the story in the news.

Does Vitamin E Reduce Heart Disease Risk In Women?

Let’s start with vitamin E and the risk of cardiovascular disease in women. The most influential study on this subject was the Women’s Health Study (Lee et al., JAMA, 294:56-65, 2005). This was a major study in which 39,876 women were given either 600 IU of vitamin E every other day or a placebo and followed for 10 years.

The headlines said “Vitamin E Supplements Do Not Reduce Risk Of Cardiovascular Death, Heart Attack And Stroke In Women”. That was true if you looked at the total population of women in the study.

But Dr. Blumberg pointed out that when you looked at women who were 65 or older in that study vitamin E supplementation caused a…

24% decrease in cardiovascular deaths,

26% decrease in major cardiovascular events,

21% decrease in venous thromboembolism (blood clots forming in the veins),

…and all of these decreases were statistically highly significant. That’s important because the risk of heart disease in pre-menopausal women is extremely low. It’s the over 65 group who have a high risk of heart disease.

Perhaps the headlines should have said: “Vitamin E reduces the risk of cardiovascular disease and cardiovascular deaths in those women at high risk of heart attacks”. But, of course, they didn’t. Perhaps that wasn’t considered newsworthy.

Other Studies On Vitamin E and Heart Disease Risk In Women

If this were the only study suggesting the vitamin E might benefit women at high risk of having a heart attack or stroke, it might be easy to dismiss it, but it’s not the only study showing this effect.

For example, a subsequent study called the “Women’s Antioxidant Cardiovascular Study” looked at the effect of 600 IU of vitamin E every other day on cardiovascular events in 8171 women health professionals (Cook et al, Archives of Internal Medicine, 167:1610-1618, 2007).

Once again the headlines said that vitamin E supplementation had no effect on cardiovascular events in women. But, when the authors looked at those women who already had cardiovascular disease at the beginning of the study (and were, therefore, at high risk of suffering a cardiovascular event during the study) vitamin E supplementation caused a 23% decreased risk of heart attack, stroke and cardiovascular death.

Another important study was the HOPE (Heart Outcomes Prevention Evaluation) study (Levy et al, Diabetes Care, 27: 2767, 2004). The overall study results were similar to several other recent trials – no significant effect of vitamin E supplementation on cardiovascular health in the population group as a whole.

However, by the time that study was performed it was clear that a particular genetic variation in the haptoglobin gene called the haptoglobin 2-2 genotype lead to a significant increase in oxidative damage to the vascular wall (the professor will collect your quizes at the end of this email).

When the data were reanalyzed by genotype, it became clear that people with the haptoglobin 2-2 genotype experienced a significant decrease in both heart attack and cardiovascular death with vitamin E supplementation. This finding has been confirmed by a subsequent double-blind, placebo-control study specifically designed to look at the cardioprotective effects of vitamin E in people with different haptoglobin genotypes (Milman et al, Arterioscler. Thromb. Vasc. Biol., 24: 136, 2008).

In short, the headlines from all three studies should have said: “Vitamin E reduces the risk of cardiovascular disease and cardiovascular deaths in those women at high risk of heart attacks” – and, it doesn’t appear to matter whether the increased risk is due to age, pre-existing disease, or genetic predisposition.

Does Vitamin E Reduce Heart Disease Risk In Men?

For men the most influential study was called the “Physician’s Health Study II” (H. D. Sesso et al, JAMA, 300: 2123-2133, 2008). In this study male physicians aged 40-84 were invited to participate in a double-blind clinical trial in which they were randomly assigned into groups who were given 400 IU of vitamin E every other day or placebo. They were followed for an average of 8 years during which data on both total mortality and cardiovascular mortality were obtained.

Once again, the headlines read “Vitamin E Does NotPrevent Cardiovascular Disease in Men”. But let me tell you what Dr. Blumberg said so that you understand “The Rest of the Story”. It starts by looking at the selection process for the Physician Health Studies.

Dr. Sesso and his colleagues sent out a letter asking 261,248 male physicians in the US if they would be willing to participate in the study. Only 112,528 responded and, of those responding, only 59,272 indicated that they were willing to participate. Of those who said that they were willing to participate only 32,223 met the selection criteria.

The exclusion criteria eliminated anyone who already had suffered a heart attack, stroke, angina or was on a blood thinner – in other words those people who were at greatest risk of suffering a heart attack or stroke during the study.

Finally, the study had an 18 week “run in” period to eliminate those people who were unwilling or unable to comply with the study protocol. This eliminated another 10,000 participants, leaving only 22,071 participants – less than 10% of the original.

This is where it gets really interesting. Dr. Sesso and his colleagues used publicly available databases to evaluate total and cardiovascular mortality in each group (H. D. Sesso et al, Controlled Clinical Trials, 23: 686-702, 2002). It turns out that at each stage of the selection process the incidence of both total and cardiovascular mortality during the 8-year period decreased.

In fact, the doctors who were actually included in the study were 67% less likely to die from all causes and 73% less likely to die from cardiovascular disease than the male physician population as a whole.

The bottom line is that the selection process eliminated almost all of the physicians at significant risk of having a heart attack or stroke during the study. The only ones who were actually enrolled in the study were those physicians who were at very low risk for having a fatal heart attack or stroke – or dying from any cause – during the study.

So the headlines describing this study should have read “Vitamin E Does Not Prevent Cardiovascular Disease in Men Who Are At Very Low Risk Of Heart Attack And Stroke”.The irony is that there was nothing wrong with the design of the study. It’s probably just a male ego thing. Guys who were unhealthy just didn’t want to participate in a study that might show how unhealthy they really were.

What Does This Mean For You?

These studies illustrate the true story of supplementation. For those of us who are at low risk of disease, supplementation is just a form of health insurance. But for those of us at high risk of disease, supplementation can make a huge difference in our health. That increased risk can be due to many things, as we have seen in the studies above. It can be due to poor diet, age, pre-existing disease, and/or genetic predisposition.

The problem is that most of us don’t really know whether we are at low risk or high risk until it’s too late. For millions of Americans the first sign of heart disease is sudden death.

The Bottom Line

The experts have been saying for years that vitamin E does not reduce the risk of heart disease. That claim is true, if you look at the general population, most of which is at low risk of developing heart disease – at least during the time frame of the clinical studies. However, when you look at people who are at high risk of developing heart disease, the answer is different.

For example, when you look at clinical studies with women, vitamin E significantly decreased the risk of heart attacks in women who…

Were over 65,

Had pre-existing heart disease at the beginning of the study,

Or, had a genetic predisposition to heart disease.

The headlines from these studies should have read “Vitamin E reduces the risk of cardiovascular disease in those women at high risk of heart attacks”, but they didn’t.

For men the story is a bit different. The Physician’s Health Study is considered the definitive study on the subject. However, most of the unhealthy male physicians either didn’t enroll in the study or dropped out before its completion. In fact, the doctors who were actually included in the study were 67% less likely to die from all causes and 73% less likely to die from cardiovascular disease than the male physician population as a whole. The headlines describing this study should have read “Vitamin E Does Not Prevent Cardiovascular Disease in Men Who Are At Very Low Risk Of Heart Attack And Stroke”.

These studies illustrate the true story of supplementation. For those of us who are at low risk of disease, supplementation is just a form of health insurance. But for those of us at high risk of disease, supplementation can make a huge difference in our health. That increased risk can be due to many things, as we have seen in the studies above. It can be due to poor diet, age, pre-existing disease, and/or genetic predisposition.

The problem is that most of us don’t really know whether we are at low risk or high risk until it’s too late. For millions of Americans the first sign of heart disease is sudden death.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Do Calcium Supplements Prevent Bone Fractures? – Part2: Preventing Osteoporosis

February 2, 2016 by Dr. Steve Chaney

Creating A “Bone Healthy” Lifestyle

Author: Dr. Stephen Chaney

$prevent bone fractures$ A recent study (Tai et al, British Medical Journal, BMJ/2015; 351:h4183 doi: 10.1136/bmj.h4183)reported that calcium supplementation for women over 50 resulted in only a very small increase in bone density, which translated into a very small (5-10%) decrease in the risk of bone fractures. They concluded that the standard RDA recommendation of 1,000 – 1,200 mg/day of calcium for adults over 50 is unlikely to help in preventing osteoporosis or reducing the risk of bone fractures.

In last week’s issue of “Health Tips From the Professor,” I discussed the many flaws of the study. In brief:

The study was a meta-analysis of 51 published clinical studies. Normally, meta-analyses are very strong, but they have an “Achilles Heel” – something called the Garbage-In, Garbage-Out Simply put, this means that the meta-analysis is only as strong as the individual studies that went into it. The authors included 40 years of clinical studies in their meta-analysis, and most of those studies had an inadequate design by today’s standards.

The study also made a number of what I would call apples to oranges comparisons that were of questionable validity.

In this week’s issue of “Health Tips From The Professor”, I would like to explore the other side of the coin. I would like to consider the possibility that the study might be correct and discuss what that might mean for you.

What Is A “Bone Healthy” Lifestyle?

Despite the concerns I just mentioned, let’s assume for a minute that the study might just be correct in spite of its many flaws. Let’s assume that the “one size fits all” RDA recommendation of 1,000 – 1,200 mg/day of calcium if you are over 50 may actually be flawed advice. If so, perhaps it’s time to say good riddance! It may finally be time to put away the “magic bullet”, “one size fits all” thinking and start seriously considering holistic approaches.

Now that I have your attention, let’s talk about what you can do to prevent osteoporosis – and the role that supplementation should play. Let’s talk about a “bone healthy” lifestyle.

#1: Let’s start with supplementation: Bone is not built with calcium alone. Bone contains significant amounts of magnesium along with the trace minerals zinc, copper and manganese – and all of these are often present at inadequate levels in the diet. Most of us know by now that vitamin D is essential for bone formation, but recent research has shown that vitamin K is also essential (Kanellakis et al, Calcified Tissue International, 90: 251-262, 2012). An ideal calcium supplement should contain all of those nutrients.

#2: Next comes diet: Many of you probably already know that some foods are acid-forming and other are alkaline-forming in our bodies – and that it is best to keep our bodies on the alkaline side. What most of you probably don’t know is that calcium is alkaline and that our bones serve as a giant buffer system to help keep our bodies alkaline. Every time we eat acid-forming foods a little bit of bone is dissolved so that calcium can be released into the bloodstream to neutralize the acid. (My apologies to any chemists reading this for my gross simplification of a complex biological system).

Consequently, if we want strong bones, we should eat less acid-forming foods and more of alkaline-forming foods. Among acid-forming foods, sodas are the biggest offenders, but meat, eggs, dairy, and grains are all big offenders as well. Alkaline-forming foods include most fruits & vegetables, peas, beans, lentils, seeds and nuts. In simple terms, the typical American diet is designed to dissolve our bones. Calcium from diet or supplementation may be of little use if our diet is destroying our bones as fast as the calcium tries to rebuild them.

#3: Test your blood 25-hydroxyvitamin D level: 25-hydroxy vitamin D is the active form of vitamin D in our bloodstream. We need a sufficient (20-50 ng/mL) blood level of 25-hydroxy vitamin D to be able to use calcium efficiently for bone formation. We now know that some people who seem to be getting adequate vitamin D in their diet still have low 25-hydroxyvitamin D levels. In fact, various studies have shown that somewhere between 20-35% of Americans have insufficient blood levels of 25-hydroxy vitamin D. You should get your blood level tested. If it is low, consult with your health professional on how much vitamin D you need to bring your 25-hydroxy vitamin D into the sufficient range.

#4: Beware of drugs:The list of common medications that dissolve bones is a long one. Some of the worst offenders are anti-inflammatory steroids such as cortisone & prednisone, drugs to treat depression, drugs to treat acid reflux, and excess thyroid hormone.

I’m not suggesting that you avoid prescribed medications that are needed to treat a health condition. I would suggest that you ask your doctor or pharmacist (or research online) whether the drugs you are taking adversely affect bone density. If they do, you may want to ask your doctor about alternative approaches, and you should pay a lot more attention to the other aspects of a “bone healthy” lifestyle.

#5: Exercise is perhaps the most important aspect of a bone healthy lifestyle:Whenever our muscles pull on a bone it stimulates the bone to get stronger. I’ll put the benefits of exercise in perspective in the next section.

Exercise Is A Critical Part of Preventing Osteoporosis

Instead of just quoting more boring studies, I’m going to share a couple of stories that help put the importance of exercise into perspective.

The first is my wife’s story. She ate a very healthy diet with minimal meat and lots of fruits and vegetables for years. She took calcium supplements on a daily basis. She walked 5 miles per day and took yoga classes several days each week. Yet when her doctor recommended a bone density scan in her early sixties she discovered she had low bone density. She was in danger of becoming osteoporotic!

Her doctor prescribed Fosamax. My wife tried it for one day and decided the side effects were worse than the disease. So she started asking holistic health practitioners what she should do. They recommended she find a personal trainer and start pumping iron. That was not an easy solution, but it was the right one. When she went in for her second bone scan 3 months later, her doctor excitedly announced that her bone density had increased by 7%. Her doctor said “We never get results that good with Fosamax”. When my wife told her she wasn’t taking Fosamax, her doctor became even more excited. (Most doctors actually do prefer holistic approaches. They just don’t recommend them.)

The moral of this story is that you can be doing everything else right, but if you’re not doing weight bearing exercises – if you’re not pumping iron, everything else you are doing may be for naught. Weight bearing exercise is an absolutely essential part of a “bone healthy” lifestyle!

But, can exercise do it alone? Some people seem to think so. That brings up my second story. About 30 years ago one of my UNC colleagues, who was an expert on calcium metabolism, was doing a bone density study on female athletes at UNC. One of the tennis players was nicknamed “Tab.” Tab was a popular soft drink at that time, and Tab was all she drank – no milk, no water, only Tab. When my colleague measured the bone density of her playing arm, it was normal for a woman of her age. When he measured the bone density of her non-playing arm, it was that of a 65 year old woman. The reason is simple. When we exercise a particular bone, our body will add calcium to that bone to make it stronger. If we are not getting enough calcium from our diet, our body simply dissolves the bones elsewhere in our body to get the calcium that it needs.

The moral of this story is that exercise alone is not enough. In terms of bone health, we absolutely need exercise to take advantage of the calcium in our diet, and we absolutely need sufficient calcium in our diet to take advantage of the exercise.

This is the most glaring deficiency of the meta-analysis I described last week. None of those studies included exercise. No wonder the increase in bone density was minimal!

Putting It All Together – A “Bone Healthy” Lifestyle

If you seriously want to minimize your risk of osteoporosis, there are a few simple steps you can take (simple, but not easy).

Consume a “bone healthy” diet that emphasizes fresh fruits and vegetables, minimizes meats, and eliminates sodas and other acidic beverages. For more details on whether your favorite foods are acid-forming or alkaline-forming, you can find plenty of charts on the internet.

Minimize the use of medications that adversely affect bone density. You’ll need to work with your doctor on this one.

Get plenty of weight bearing exercise. This is an absolutely essential part of a bone healthy lifestyle. Your local Y can probably give you guidance if you can’t afford a personal trainer. Of course, if you have physical limitations or have a disease, you should consult with your health professional before beginning any exercise program.

Get your blood 25-hydroxy vitamin D level tested. If it is low, take enough supplemental vitamin D to get your 25-hydroxy vitamin D level into the sufficient range – optimal is even better. Sufficient blood levels of 25-hydroxy vitamin D are also absolutely essential for you to be able to utilize calcium efficiently.

Consider a calcium supplement. Even when you are doing everything else correctly, you still need adequate calcium in your diet to form strong bones. “I’m not necessarily recommending a “one-size fits all” 1,000 to 1,200 mg/day. Supplementation is always most effective when you actually need it. For example:

If you are not including dairy products in your diet (either because they are acid-forming or for other health reasons), it will be difficult for you to get adequate amounts of calcium in your diet. You can get calcium from other food sources such as green leafy vegetables. However, unless you plan your diet very carefully you will probably not get enough.

If you are taking medications that decrease bone density, that may increase your need for supplemental calcium. Unfortunately, we don’t yet have guidelines on how much is needed.

If you do use a calcium supplement, make sure it is complete. Don’t just settle for calcium and vitamin D. At the very least you will want your supplement to contain magnesium and vitamin K. I personally recommend that it also contain zinc, copper, and manganese.

Unfortunately, we don’t really have good guidelines for how much calcium you need. Studies like the one described above are challenging the old RDAs, but we don’t yet have enough studies to know how much calcium we need to build strong bones when we are following a “bone healthy” lifestyle that includes proper diet, sufficient 25-hydroxy vitamin D blood levels and plenty of exercise.

What About Medications For Preventing Bone Loss?

The danger is that, as the conclusions of this meta-analysis get widely publicized and doctors stop prescribing calcium supplements, they probably aren’t going to recommend a holistic approach. They probably won’t recommend a “bone healthy” lifestyle. Instead, they will most likely recommend drugs to prevent bone loss. In fact, the authors of the study described last week specifically praised the use of bisphosphonate drugs (Fosamax and Zometa), and a related drug (Xgeva) that works by a similar mechanism because they increased bone density by 5-9% over 3 years.

However, these drugs have a dark side, and it’s not just the acid reflux, esophageal damage and esophageal cancer that you hear about in the TV ads. These drugs all act by blocking bone resorption, the ability of the body to break down bone. In the short term, this prevents the bone loss associated with aging and reduces the risk of bone fractures.

However, you might remember from last week’s article that bone resorption is also an essential part of bone remodeling, the process that keeps our bones young and strong. When these drugs are used for more than a few years you end up with bones that are dense, but are also old and brittle. Long term use of these drugs is associated with jaw bones that simply dissolve and bones that easily break during everyday activities. This is yet another example of drugs with side effects that look a lot like the disease you were taking the drug for in the first place.

The Bottom Line

A recent study has reported that the RDA recommendation of 1,000 – 1,200 mg/day of calcium for people over 50 provides only a minimal increase in bone density (0.7-1.8%) over the first year or two. This translates into a very small (5-10%) decrease in risk of bone fractures. It did not matter whether the calcium came from dietary sources or from supplementation. The authors concluded that adding extra calcium to the diet, whether from foods or supplements, was not a very efficient way to increase bone density and prevent fractures.

2. This study suffers from some serious flaws, which I discussed in last week’s “Health Tips From the Professor”

3. Unfortunately, many doctors are likely to take this study to heart. They are likely to stop recommending calcium and other natural approaches and start relying even more heavily on drugs to preserve bone mass. That’s bad news because, while the most frequently proscribed drugs do increase bone mass and prevent fractures short term, they also cause your bones to age more rapidly. After a few years you end up with bones that are dense, but are also incredibly brittle and fracture very easily. That’s right. If you use these drugs long enough, they will cause the very condition you were trying to prevent.

4. We should also consider the possibility that this study may just be correct. Let’s assume for a minute that the RDA recommendation of 1,000 – 1,200 mg/day of calcium for everyone over 50 may actually be flawed advice. If so, it may finally be time to put away the “magic bullet” thinking and start seriously considering holistic approaches to preserving bone mass.

5. A far better choice is to follow a “bone healthy” lifestyle.

Start with a “bone healthy” diet. Avoid acid-forming foods like sodas, meats, eggs, dairy, and grains. Instead choose alkaline-forming foods like most fruits & vegetables, peas, beans, lentils, seeds and nuts.

Check on the medicines you are using. If they are ones that adversely affect bone density, ask your health professional if there are bone-healthier options.

Check your blood level of 25-hydroxy vitamin D on a regular basis. If it is low, consult with your health professional on the amount of vitamin D you need to take to bring your 25-hydroxy vitamin D into the optimal range.

Get plenty of weight bearing exercise. This means pumping iron. It is an absolutely essential part of a bone healthy lifestyle. Of course, if you have physical limitations or have a disease, you should consult with your health professional before beginning any exercise program.

If you are not getting sufficient calcium from your diet, consider a complete calcium supplement. In addition to calcium and vitamin D, a bone-healthy calcium supplement should at the very least contain magnesium and vitamin K. I also recommend it contain zinc, copper, and manganese.

Just don’t rely on a calcium supplement alone to keep your bone density where it should be. If your 25-hydroxy vitamin D isn’t where it should be and/or you aren’t doing weight bearing exercise on a regular basis, your calcium supplement may be almost useless. All the aforementioned may aid in preventing osteoporosis. In my opinion, that may be the biggest take-home lesson from the recent meta-analysis.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Do Calcium Supplements Prevent Bone Fractures? – Part1

January 26, 2016 by Dr. Steve Chaney

Why The Recent Headlines May Be Misleading

Author: Dr. Stephen Chaney

Does calcium help prevent bone fractures? Osteoporosis is a debilitating and potentially deadly disease associated with aging. It affects 54 million Americans. It can cause debilitating back pain and bone fractures. 50% of women and 25% of men over 50 will break a bone due to osteoporosis. Hip fractures in the elderly due to osteoporosis are often a death sentence.

For that reason, the RDA for calcium has been set at 1,000 to 1,200 mg/day to reduce the risk of osteoporosis, and calcium supplements are often recommended to reach that target.However, recent headlines are proclaiming that calcium supplements do not actually prevent bone fractures and might increase your risk of a heart attack. Are the RDA recommendations wrong? Should you throw out your calcium supplements?

In this article I will review the article behind the study and help you put it into perspective. After all, you don’t really want to know whether calcium supplementation is beneficial for the average adult. You want to know whether it will be beneficial for you.

Let me start by putting the heart attack myth to rest. I have covered this in detail in a previous “Health Tips From The Professor” article, Calcium Supplements Increase Heart Attack Risk . If you don’t want to go to the trouble of reading my previous article, the short version is that:

Most of the studies suggesting an increased risk of heart attacks are flawed.

A very large study (74,000 women followed for 24 years) has shown fairly convincingly that calcium supplements do not increase heart attack risk. If anything, they decrease heart attack risk.

Unfortunately, like most other nutrition myths, this one is still being repeated – even after it has been refuted by subsequent studies.

Bone Metabolism and Osteoporosis

Before you can truly understand osteoporosis and how to prevent it, you need to know a bit about bone metabolism. We tend to think of our bones as solid and unchanging, much like the steel girders in an office building. Nothing could be further from the truth. Our bones are dynamic organs that are in a constant change throughout our lives.

Cells called osteoclasts and osteoblasts constantly break down old bone (a process called resorption) and replace it with new bone (a process called accretion). Without this constant renewal process our bones would quickly become old and brittle (I’ll discuss more about this next week when I talk about the side effects of drugs commonly used to increase bone density).

When we are young the bone building process exceeds bone resorption and our bones grow in size and in density. During most of our adult years, bone resorption and accretion are in balance so our bone density stays constant. However, as we age bone the bone building process (accretion) slows down and we start to lose bone density. Eventually our bones look like Swiss cheese and break very easily. This is called osteoporosis.

We should also think of our bones as calcium reservoirs. We need calcium in our bloodstream 24 hours a day for our muscles, brain, and nerves to function properly, but we only get calcium in our diet at discrete intervals. Consequently, when we eat our body tries to store as much calcium as possible in our bones. Between meals, we break down bone material so that we can release the calcium into our bloodstream that our muscle, brain & nerves need to function.

If we lead a “bone healthy” lifestyle, all of this works perfectly. We build strong bones during our growing years, maintain healthy bones during our adult years, and only lose bone density slowly as we age – maybe never experiencing osteoporosis. We always accumulate enough calcium in our bones during meals to provide for the rest of our body between meals.

What is a “bone healthy” lifestyle, you might ask. Because calcium is a major component of bone, the medical and nutrition communities have long focused on calcium as a “magic bullet” that can assure bone health. Once the importance of vitamin D was understood, it was added to the equation. For years we have been told that if we just get enough calcium and vitamin D in our diets, we would build strong bones when we were young, maintain bone density most of our adult years, and lose bone density as slowly as possible as we age.It is this paradigm that the current study challenges.

Do Calcium Supplements Prevent Bone Fractures?

$prevent bone fractures$ Let’s start by looking at the study behind the headlines (Tai et al, British Medical Journal, BMJ/2015; 351:h4183 doi: 10.1136/bmj.h4183). This was a meta-analysis that included 15 studies (1533 participants) looking at dietary sources of calcium and 51 studies (12,257 participants) looking at calcium supplementation in women.

The results of the meta-analysis were thought provoking, but do not exactly support the headlines you have been reading. For example:

The headlines say “Calcium Supplements Do Not Prevent Broken Bones”.

This study did not actually look at calcium supplementation and the risk of bone fractures. That was a previous study (Boland et al, BMJ 2015, 351:h4580) by the same authors.
This study showed that calcium supplementation increased bone density by 0.7-1.8%, which the authors concluded was sufficient to reduce fracture risk by about 5-10%. That’s a disappointingly small effect, but it is not zero – as the headlines suggested.

The headlines say “It’s better to get your calcium from food than from supplements”.

This study showed that it did not matter whether the calcium came from food or from supplements. The increase in bone density was identical.

Garbage-In, Garbage-Out

Meta-analyses such as this one can be very strong, but they can also suffer from the “garbage-in, garbage-out” phenomenon. In short, if most of the studies that went into the meta-analysis were poorly designed, the conclusions of the meta-analysis will be unreliable.

The problem is that many of the individual studies were conducted 10, 20, 30 or 40 years ago when our knowledge of bone metabolism was incomplete.

Thirty or 40 years ago it was “state of the art” to just use a calcium supplement. Then we learned that adequate vitamin D was essential for efficient calcium utilization.

Most of the studies included in this meta-analysis looked at calcium supplementation without vitamin D. Only 13 of the studies (25%) included vitamin D.

Ten or 20 years ago it was “state of the art” to just use a calcium supplement with vitamin D. Then we learned that the blood level of 25-hydroxyvitamin D (the active form of vitamin D in the bloodstream) did not necessarily reflect vitamin D intake from the diet. In today’s world a study in which the 25-hydroxy vitamin D level is not measured should be considered sub-standard.

Only 18 (35%) of the studies measured baseline 25-hydroxy vitamin D levels.

If dietary calcium intake at baseline is already adequate, it is illogical to expect additional calcium to significantly increase bone density.

The baseline calcium intake was <800 mg/day (clearly inadequate) in only 26 (51%) of the studies. Baseline calcium intake was either not determined in the other studies or was already in the adequate range prior to supplementation.

In the future, we will probably want to include exercise as a component in the study (more about that next week). None of the studies included exercise as a component

In short, by today’s standards many, if not most, of the studies included in the meta-analysis had an inadequate design.

If I had designed the meta-analysis, I would have been a lot more restrictive in the studies I included.

I would have started by including only studies in which the baseline intake of calcium was <800 mg/day. If you want to critically evaluate whether calcium supplementation has a beneficial effect, you need to start with people who have an inadequate dietary intake of calcium. If their diets are already calcium sufficient, supplementation is unlikely to have any benefit.

At the very least I would only include studies that used calcium supplements containing 400-800 IU of vitamin D as well. In fact, based on the latest data, I would make sure that the calcium supplement I used also contained adequate levels of magnesium, vitamin K, zinc, copper and manganese. All of those have been shown to be important for bone formation and we cannot assume they are present at sufficient levels in their diet (more about that next week).

I would only include studies that measured blood levels of 25-hydroxy vitamin D at baseline and following supplementation with vitamin D so that we knew that the 25-hydroxy vitamin D level was sufficient to support optimal calcium utilization.

Finally, I would only include studies that specifically measured the effect of exercise on calcium utilization or included exercise as an integral part of their study.

The number of studies included in the meta-analysis would be much less, but they would all be high quality studies.

Finally, the authors also noted that a number of studies in the supplement group showed significantly greater (2.5 – 5.0%) increase in bone density. They dismissed them as outliers. I would have preferred a closer look at those studies to see if there was anything about the population group or study design that might explain the greater bone density increase in those studies.

Apples and Oranges

Because the authors included a wide variety of clinical studies, they were able to state that “Increases in bone mineral density were similar in trials of calcium monotherapy [calcium by itself] versus co-administered calcium and vitamin D…and in trials where baseline dietary calcium intake was <800 [clearly insufficient] versus >800 [probably sufficient] mg/day.” This could be considered a strength of their meta-analysis, but they are only valid comparisons if other important features of the studies being compared were uniform – i.e. they were comparing apples to apples.

But what if they were comparing apples and oranges?

For example, we know that vitamin D is required for efficient calcium utilization. When the authors compared studies having a baseline calcium intake of <800 mg/day with studies having a baseline calcium intake of >800 mg/day, they did not even check to see whether use of vitamin D was evenly distributed between the two groups. If most of the studies with a baseline calcium intake of <800 mg/day did not include vitamin D with their calcium supplements, the authors would be comparing apples and oranges. The comparison would be invalid.

Similarly, we also know that if calcium intake at baseline is adequate, adding more calcium is unlikely to increase bone density significantly. When the authors compared studies with and without vitamin D, they did not even check to see whether baseline calcium intake was evenly distributed between the two groups. If the participants in most of the studies utilizing supplements providing both calcium and vitamin D were already consuming sufficient calcium at baseline, they would be comparing apples to oranges. Again, the comparison would be invalid.

The authors of the meta-analysis simply did not provide the detail needed to determine whether their comparisons were apples to apples or apples to oranges. Thus, what seemed to be a strength of their study is actually a major weakness.

The Bottom Line

A recent study has reported that the RDA recommendation of 1,000 – 1,200 mg/day of calcium for people over 50 provides only a minimal increase in bone density (0.7-1.8%) over the first year or two. This translates into a very small (5-10%) decrease in risk of bone fractures. It did not matter whether the calcium came from dietary sources or from supplementation. The authors concluded that adding extra calcium to the diet, whether from food or supplements, was not a very efficient way to increase bone density and prevent fractures.

This study suffers from some serious flaws. It is a meta-analysis of previous clinical trials looking at the effects of calcium on bone density. Meta-analyses can be very strong studies because they average the effects of many individual studies. However, meta-analyses can also suffer from the “garbage-in, garbage-out” phenomenon. Simply put, the quality of the meta-analysis is only as good as the studies that go into it. In this case the meta-analysis included many clinical studies that were done 10, 20, 30 and even 40 years ago. Based on what we now know about bone metabolism, the design of many of those early studies was clearly inadequate (details are given in the article).

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Shoulder Muscle Pain Relief

January 19, 2016 by Dr. Steve Chaney

You Can Enjoy Pain Free Living From Home

Author: Julie Donnelly, LMT –The Pain Relief Expert

Editor: Dr. Steve Chaney

Yesterday I was at my sailing club and a man was sitting watching the water, rubbing his shoulder and clearly in pain. I asked him what was wrong and he said he had a sore shoulder for the past three months and he desperately wanted to find some pain relief. He loves to sail and this shoulder muscle pain was preventing him from going out on the water. He said he had already been to a massage therapist, a physical therapist, and a chiropractor. He finally went to an orthopedic surgeon and was told that surgery was the only way to relieve the pain of his sore shoulder, but he had decided that he didn’t want to take that path…yet.

Shoulder Muscle Pain Cause

I use an analogy that makes it so clear why spasms in will cause joint pain. If you pull your hair your scalp will hurt, but you don’t need to massage your scalp, or take aspirin for your headache, and you definitely don’t need brain surgery. You simply need to let go of your hair!

Your shoulder has more muscle attachments than any joint in your body.

Each muscle pulls your shoulder in a different direction, but as the muscle gets tight it puts pressure on the bone. Your shoulder muscle pain is the end result – just like pulling your hair hurts your head.

To get relief, all you need to do is release the tension in the muscles. ‘

Stretching WON’T Help Relieve Sore Shoulder Pain!

It is important to untie the knots (spasms) in the muscles before stretching. Think of what happens if you take a 12″ length of rope, tie enough knots in it so it is 11″ long, and then try to stretch it back to 12″ without first untying the knots. This is what will happen to your muscle fibers if you stretch without first releasing the spasms.

My years of working with athletes who not only have sore shoulder pain, but also have pain in every joint caused by their repetitive strain. Working with athletes showed me that it was vital to teach them how to do self-treatments they could use during a race or competition.

This led to several books and DVD programs, including my Focused Flexibility Training. On one DVD, I demonstrate how to self-treat every muscle from your head to foot, and then on two DVDs (1 Upper Body and 1 Lower Body) Ana Johnson, a fantastic yoga instructor, leads you through self-treating the muscles you will be stretching, and then a 30-minute yoga program. It works to quickly eliminate sore shoulder pain, as well as pain and stiffness throughout your body.

There are several treatments for sore shoulder pain, each addressing a different group of muscles that pull your shoulder and arm in the wide range of motions you make every day without even thinking about it.

Self-Treatment For Shoulder Muscle Pain

The photo to the left show you how to treat your Infraspinatus muscle. This muscle brings your shoulder back, like you’re taking a tennis serve. When your Infraspinatus muscle is in spasm, it will cause shoulder muscle pain as you try to bring your arms forward.

Place the Perfect Ball as shown in the picture, and lean your weight into the ball. Look for the “hot spot,” which will be tender. As you lean into the ball, then take the pressure off, and then lean again, you’ll find the muscle becoming less and less painful.

Move the ball to different areas of your shoulder, finding the various painful points. Each one is a spasm that is causing your sore shoulder pain. You can enhance this treatment by slowly drawing your arm across your body while you are still pressing into the ball. Since the spasms have been released, this movement will safely stretch the muscle fibers. As you release each spasm, and then stretch, you’ll find pain relief, and you’ll know how to stop pain quickly and easily should it return.

As for the man I mentioned at the beginning of this blog, I’m happy to say that today he told me he slept through the night for the first time in weeks, and he’s getting better every time he does the self-treatments I taught him. That is so fulfilling — I LOVE my work!

With some knowledge of how to find spasms, how to self-treat them, and how to stretch properly, you can Stop Pain FAST!

Wishing you well,

Julie Donnelly

About The Author

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Should You Eat Often to Lose Weight?

January 12, 2016 by Dr. Steve Chaney

6 Small Meals a Day Plan?

Author: Dr. Stephen Chaney

Should you eat often to lose weight? A friend, your doctor, or your favorite health guru may have told you with some conviction that eating 6 small meals a day, as opposed to 2 or 3 large meals, can help you lose weight. If you are like most people, you are probably wondering whether something so simple might be the secret to permanent weight control. Should you really eat like a bird?

The advocates of eating frequent, small meals argue that large meals cause a much larger spike in insulin resulting in more of the calories being stored as fat. They also argue that a long time between meals leads to excessive hunger and overeating when you do sit down to a meal. The opponents of this idea claim that those arguments are nonsense and that eating frequent meals can cause you to lose track of the calories you have consumed.

The clinical studies on this subject have not been much help. Some studies show that more frequent food consumption during the day is associated with lower body weight, while other studies find no association between frequency of food consumption and weight.

Your friend may have also told you that consuming your calories earlier in the day will help prevent weight gain. You’ve probably heard the saying: “Eat breakfast like a king, lunch like a prince, and dinner like a pauper”. This hypothesis is on a bit stronger footing, but there are far too few studies on the subject.

With both of those concepts in mind, a recent study provides an excellent perspective.

Should You Eat Often to Lose Weight?

A recent study (Aljuiraban et al., Journal of the Academy of Nutrition and Dietetics, 115: 528-536, 2015) used data from the International Study on Macro/Micronutrients and Blood Pressure to evaluate the relationship between frequency of eating and time of eating with caloric density (calories/serving), nutrient quality and BMI (a measure of body weight). The study included 2,696 men and women aged 40 to 59 years from both the United States and England. The dietary data were obtained from each participants on two consecutive days at the beginning of the study and again 3 weeks later.

The results of the study were:

BMI was significantly less for those individuals consuming >6 meals per day than for those consuming <4 meals/day.

BMI was also significantly less for those individuals consuming their calories early in the day than for those consuming most of their calories late in the day.

What Is The “Rest Of The Story”?

Those of you old enough to have heard the Paul Harvey radio show might remember that he would tell a fairly ordinary story. Then, after the commercial break, he would come back and tell “The Rest Of The Story”, and that was always the most interesting part of the story. This study is no different.

If this study had just measured associations with BMI, it would have been just another boring food frequency study that just happened to show an association between more frequent food consumption and lower body weight. However, it also evaluated the association of food frequency and food timing with many other parameters. This was the most interesting part of the study. This was “the rest of the story”.

Those individuals consuming >6 meals/day had higher intakes of low fat dairy products, fruits and vegetables and lower intake of alcohol and red meats than those consuming <4 meals/day.

Those individuals consuming >6 meals/day also consumed less energy dense foods, fewer total calories, and more nutrient rich foods than those individuals consuming <4 meals/day.

Those individuals consuming >6 meals per day were much less likely to have their evening meal at a restaurant or cafeteria than those individuals consuming <4 meals/day.

Similarly, those individuals consuming the majority of their calories early in the day also had higher intake of low fat dairy products, fruits and vegetables and lower intake of alcohol and red meat than those consuming the majority of their calories late in the day. They also consumed less energy dense foods, fewer total calories, and more nutrient rich foods.

Although the difference was not statistically significant, it is perhaps worth noting that individuals consuming >6 meals/day tended to eat a higher percentage of their calories early in the day compared to individuals consuming <4 meals/day.

In other words, it was not necessarily the frequency or time of eating that was associated with body weight. It could simply have been the quality of the diet that determined body weight. It’s no secret that eating fewer calories, more fresh fruits and vegetable, eating lower fat dairy products, and consuming less alcohol and red meat is associated with a lower body weight. In today’s world of supersized portions, it’s also not surprising that frequently eating your dinner at restaurants is associated with higher weight.

What’s not clear from this study is why there was such a strong association between consuming a healthy, low calorie diet and frequency/timing of eating. It’s also not clear whether this is a universal association, or whether it was unique to this clinical study.

The Bottom Line

A recent study has shown that BMI was significantly less for those individuals consuming >6 meals per day than for those consuming <4 meals/day. BMI was also significantly less for those individuals consuming the bulk of their calories early in the day compared to those consuming their calories late in the day.

In both cases, it turns out that the individuals with lower BMI were also consuming healthier diets as measured by lower calorie intake, greater consumption of fruits, vegetables and low fat dairy and reduced consumption of alcohol and red meats.

Consequently, it isn’t clear from this study whether low BMI is associated with frequency of eating, timing of eating, or simply the quality of the diet.

The jury is still out on whether consuming frequent, small meals can help you lose weight. This just may be one of those approaches that works better for some people than for others.

The preponderance of evidence suggests that consuming the bulk of your calories early in the day may help you lose weight, but the evidence is far from definitive at this point.

However, there is universal agreement that eating a healthy, low calorie diet will help you lose weight. My money is with a healthy, low calorie diet.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Skinny Fat

January 5, 2016 by Dr. Steve Chaney

Overweight Vs. Obesity

Author: Dr. Stephen Chaney

Are you skinny fat? Weight loss season is upon us. Many of you are jumping on your bathroom scales so that you can decide how much weight you need to lose this year. For some the motivation for these New Year’s resolutions to lose weight is purely cosmetic. You just want to look better. For others the motivation for losing weight is better health. Obesity is a killer. It is associated with increased risk of diabetes, heart attack and stroke – and that’s just the tip of the iceberg.

But what if your bathroom scale says that you are normal weight? Are you off the hook? Maybe not. A recent study suggests that if you are normal weight but have central obesity (a fancy scientific term for belly fat), you are more likely to die prematurely than someone with normal fat distribution regardless of how overweight they are. That’s a pretty scary thought. It has even generated a new risk category called “skinny fat”.

How Can You Be Obese Without Being Overweight?

In recent years there has been some controversy about the health risks of obesity. Part of that controversy has arisen because obesity can be defined in multiple ways. Most of us simply hop on the scale and rely on actuarial tables to tell us what a healthy weight is for our height. Scientists, on the other hand use two very different measures of obesity.

#1 is Body Mass Index or BMI.BMI is a person’s weight in kilograms (kg) divided by his or her height in meters squared. By this measure:

Normal body weight is defined as a BMI of 18.5-24.9 kg/m².

Overweight is defined as a BMI of 25-29.9 kg/m².

Obesity is defined as a BMI of ≥30 kg/m².

#2 is waist to hip ratio or WHR. WHR is a measure of central adiposity (belly fat). By this measure:

Obesity is defined as excess central adiposity (excess belly fat), which is a waist to hip ratio ≥0.85 in women and ≥0.90 in men.

In general BMI and WHR correlate. However:

11% of men and 3.3% of women are normal weight according to BMI measurements, but have excess belly fat according to WHR measurements.These are the individualswho are obese according to their WHR measurements without being overweight according to their BMI measurements. These are the individuals often referred to as “skinny fat”.

There are similar percentages of men and women who are overweight or obese according to BMI measurements, but have low WHR measurements. These are often referred to as “pear shaped” obese individuals to distinguish them from the “apple shaped” obese individuals with a lot of belly fat.

Being Skinny Fat Can Kill You

Numerous studies have shown that “apple shaped” obesity is much more likely to be associated with disease and premature death than “pear shaped” obesity, but there have been very few studies comparing health outcomes for normal weight individuals who have excess belly fat (people who are “skinny fat”) with health outcomes of overweight and obese individuals. This study (Sahakyanet al, Annals of Internal Medicine, 2015 Nov 10 doi: 10.7326/M14-2525) was designed to fill that void.

These scientists analyzed data from the National Health and Nutrition Survey III (NHANES III). NHANES III collected BMI, WHR and health data from 15,184 Americans (52.8% women) aged 18 to 90 years (average age 45) and followed the study participants for 14.3 years. By that time 3222 of them had died, with 1413 of those deaths being due to heart disease. The results were enlightening:

Normal weight individuals with excess belly fat (“skinny fat” individuals) were 1.5 – 2.0 fold more likely to die during the 14.3 year follow up period than individuals who were normal weight and had little belly fat (“skinny lean” individuals). This was expected because this had been shown in several previous studies.

However, the surprising finding was that normal weight individuals with excess belly fat were also more likely to die than individuals who were overweight or obese. Specifically:

Men who were “skinny fat” were 2.2 – 2.4 fold more likely to die prematurely than men who were either overweight or obese, but did not have excess belly fat (men with a “pear shaped” fat distribution). “Skinny fat” women were 1.3 – 1.4 fold more likely to die prematurely than overweight or obese women with “pear shaped” fat distribution.

Men who were “skinny fat” were even slightly more likely to die prematurely than overweight or obese men with excess belly fat (men with “apple shaped” fat distribution). “Skinny fat” women were just as likely to die as overweight or obese women with “apple shaped” fat distribution.

When they looked at deaths due to cardiovascular disease the results were essentially the same.

These results were novel and should, perhaps serve as a wake-up call for normal weight individuals with excess belly fat.

The authors concluded:

“Our analysis of data…show that normal-weight U.S. adults with central obesity [excess belly fat] have the worst long-term survival compared with participants with normal fat distribution, regardless of BMI category.”

“To our knowledge, our study is the first to show that normal-weight central obesity, measured by WHR, is associated with an increased risk of cardiovascular mortality.”

“Our findings suggest that persons with normal-weight central obesity may represent an important target population for lifestyle modification and other preventative strategies.”

Why Is Being Skinny Fat So Dangerous?

As the authors of this study pointed out, it is well established that excess belly fat is associated with:

Insulin resistance, which can lead to diabetes and predispose to heart disease.
High triglycerides and high levels of “bad” cholesterol, which can lead to heart disease.
Inflammation, which can lead to a number of deadly diseases.

The metabolic effects of excess belly fat are sufficient to explain why someone who is “skinny fat” is more likely to die prematurely than someone who is “skinny lean”. However, the effect of excess belly fat is not sufficient by itself to explain why a “skinny fat” individual is more likely to die prematurely than someone who is overweight or obese.

To understand this we need to recognize that both fat and muscle contribute to body weight (and to BMI). The “skinny fat” individual has more fat mass AND less muscle mass than a “skinny lean” individual of the same weight. That is a huge factor because metabolically speaking muscle is protective. It opposes all of the bad metabolic effects of belly fat.

Simply put, being “skinny fat” is extremely dangerous because you have increased all the bad metabolic effects of excess belly fat, ANDyou have decreased the protective metabolic effect of muscle mass.

How Do You Go From Being “Skinny Lean” To “Skinny Fat”?

Most of us were lean in our younger years. For those of us who end up as “skinny fat” as we age, it is pretty obvious that there are two processes going on simultaneously.

#1: Loss of Muscle Mass:It would be easy to say that becoming “skinny fat” is a natural part of aging. The natural tendency is to loose muscle mass and replace it with fat mass as we age. If we “just go with the flow” all of us will end up being “skinny fat” at some point. However, the loss of muscle mass as we age is accelerated by our sedentary lifestyle and our diet (more on that below).

#2: Gain of Belly Fat:To some extent whether we store excess fat as “pears” or “apples” is genetically determined. However, what we eat can also exert a major influence. For example:

Alcohol: The term “beer belly” says it all. Excess alcohol consumption is associated with an increase in belly fat. Once you understand the metabolism of alcohol the explanation is pretty simple. Alcohol causes blood sugar to drop, which increases appetite. Alcohol also interferes with our judgement, which can cause us to make poor food choices.

Excess saturated fat tends to be stored preferentially as belly fat.

Excess sugars and simple carbohydrates are rapidly converted to fat stores and stored as belly fat.

What Can You Do If You Are Already Skinny Fat?

Let’s start with what you shouldn’t do. You should not go on a reduced calorie weight loss diet to get rid of your excess belly fat. The last thing you want to do is to end up being underweight with excess belly fat! Here is what you should do:

#1: Increase Your Muscle Mass:I said that loss of muscle mass was a natural part of aging. I didn’t say that it was an inevitable part of aging. If you want to prevent or reverse loss of muscle mass you need to:

Get really serious about exercise. I’m talking about 30 minute workouts at least 3-5 times per week. These workouts need to include strength training as well as aerobics and flexibility exercises. I would suggest you ask your health professional what kind of exercise program is best for you and start your exercise program under the guidance of a personal trainer or physical therapist.

Make sure that your diet contains enough protein and enough of the essential amino acid leucine to maximize the gain of lean muscle mass following your workouts. I have covered the latest age-appropriate recommendations in, leucine and muscle gain, a previous “Health Tips From The Professor.”

#2: Lose Your Belly Fat:To some extent you will start to lose your belly fat naturally if you follow the recommendations above. In addition, you will want to:

Drink alcohol in moderation.

Make food choices that allow you to replace saturated fat with monounsaturated fat and polyunsaturated fats, especially the omega-3 polyunsaturated fats.

Replace excess sugars and simple carbohydrates with complex carbohydrates from fresh fruits and vegetables along with modest amounts of whole grain foods.

The Bottom Line

A recent study has shown that being “skinny fat” (having normal body weight, but excess belly fat) is more likely to result in premature death than if you were overweight, or even obese.

The most likely explanation for this alarming statistic is that someone who is “skinny fat” has excess belly fat, which predisposes to a number of diseases, and a loss of muscle mass, which protects against those same diseases.

If you are overweight or obese, you need to reduce your caloric intake to lose weight. However, if you are “skinny fat”, you don’t want to reduce your caloric intake. You need to change your exercise and diet habits.

Loss of muscle mass and gain of fat mass is a normal part of aging. However, you can slow or reverse the age-related loss of muscle mass with an exercise program and enough protein and leucine in your diet to maximize the effects of that workout program (details above).

You can prevent or get rid of excess belly fat by:

Following the exercise program and nutritional support of that exercise program described above.

Making food choices that replace saturated fats with monounsaturated fats and polyunsaturated fats, especially omega-3 polyunsaturated fats.

Replacing foods high in sugar and simple carbohydrates with fresh fruits and vegetables and whole grains in moderation.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

8 Tips on How to Eat Less

December 29, 2015 by Dr. Steve Chaney

Avoid Mindless Eating

Author: Dr. Stephen Chaney

Weight loss season is just around the corner. In just a few days you will probably be making your New Year’s resolutions, and weight loss will probably be near the top of the list. You may be considering the latest new diet fad – never mind that you’ve tried lots of diets in the past and have always regained the weight you lost.

What if you could learn just a few tricks that would help you discover how to eat less every day? Would that be of interest to you? Do you think it might help you lose some weight and keep it off?

This week I’m going to share 8 tips for eating less every single day from Professor Brian Wansink of Cornell University. He is Director of their Food and Brand Lab. He has devoted his career to studying how external clues influence our eating patterns. He is the author of the best-selling books “Mindless Eating” and “Slim by Design”. He is the world expert on this topic.

A few years ago I had the pleasure of attending a seminar he gave. Here’s a quick summary of what I learned.

8 Tips on How to Eat Less

Tip #1: The Size Of The Container Matters

In one of his research studies he gave moviegoers who had just eaten dinner either a big bag or a small bag of stale popcorn. Those given the big bag ate 34% more. Think about that for a minute. The subjects in his study weren’t hungry. They had just eaten dinner. The popcorn wasn’t particularly tasty. It was stale. Yet they ate 34% more based solely on the size of the bag!

The take home lesson is always to choose the smallest container when given a choice. This is also why you want to serve your meals on small plates and drink your beverages in small glasses or cups. If you want to snack while you watch TV, place your snack food in a very small container and store the rest out of sight.

Tip #2:Don’t Fall For Marketing Hype

He was asked to consult for a cafeteria serving health food because they weren’t attracting enough customers. He just advised them to change the names of their menu items (e.g. “Succulent Tuscany Pasta” instead of “Italian Pasta”). Sales increased by 27%.

The take home lesson is not to fall for the marketing hype. Restaurants and food manufacturers know all the tricks. They know how to make even ordinary foods sound delicious. Make your food choices based on the ingredients of the food, not on the marketing description.

Tip #3: Make Junk Food Inconvenient

In another study he put clear glass dishes of candy either on a secretary’s desk or 6 feet away on a cabinet. The secretaries consumed 125 more calories/day from candy when it was on their desk. Think about that for a minute. 125 excess calories/day could amount to around one pound of weight gain/month, 12 pound/year, 60 pounds every 5 years, and a whopping 120 pounds over 10 years!

The take home lesson is to make high calorie snacks and junk foods inconvenient. Put them in the back of your refrigerator, on the top shelf of your cabinets, or other out of the way places. Even better, don’t bring them home in the first place.

Tip #4: Watch The Refills.

When he used a refillable soup bowl (it never goes below half full) people ate 73% more soup than those given a regular bowl of soup. When he asked the people with the refillable bowl if they were full, they replied “How could I be? I only ate half a bowl of soup”.

Of course, most of us will never experience a refillable soup bowl. However, if you are having a meal with friends and enjoying the conversation, it is easy to ignore the refills – either from your waiter at a restaurant or your favorite aunt at a family gathering.

Tip #5: Low Fat Doesn’t Mean “Eat More”

When he took a batch of trail mix and labeled some as “low fat” and some as “regular” people ate 21% to 46% more calories of the “low fat” trail mix. This was not an idle exercise. In fact, many low fat foods aren’t low calorie, but people assume that they are and use that as an excuse to eat more.

The take home lesson is to not assume you can eat more just because a food is labeled low fat, gluten free or some other healthy sounding description. In many cases, it has just as many calories as the full fat version. Even if it is, in fact, lower in calories, the only way you benefit from the reduced calories is when you consume the same portion size as you would for the full fat food it replaces.

Tip #6: Health Foods Are Not Necessarily Healthy

When he showed people an Italian sandwich and told them that it was from either “Jim’s Hearty Sandwich Shop” or from “Good Karma Healthy Foods”, people estimated the calories as 24% lower if they thought it came from Good Karma.

The take home lesson is that health foods are not necessarily healthier. Food manufactures know that health food is in, and they market their products accordingly. If you walk down the aisles of your favorite health food store, you will find foods that are just as high in sugar, fat and calories as the junk food you can buy at the convenience store down the street. They may contain “natural” fats and sugars, but those have just as many calories as the “unhealthy” fats and sugars in the junk foods. You still need to read labels and choose unprocessed fruits, vegetables and whole grains whenever possible.

Tip #7: Don’t Call It Exercise

When he took students on a walk around a lake before dinner, they ate more calories at dinner if they were told that it was an exercise walk than if they were told that it was a sight-seeing walk – and most of the extra calories came from dessert. Think about that for a minute. It is a human tendency to reward ourselves for virtuous behavior, but when that reward involves eating, it becomes self-defeating.

The take home lesson is two-fold.

Reframe our virtuous behavior. If we call it exercise or a work-out, it implies that we have done something virtuous and deserve a reward. If we call it a nature walk or think of it as a sport, it becomes its own reward. If we think of substituting a salad for a dinner of fried chicken and mashed potatoes with gravy as virtuous behavior, we may think we deserve a dessert as a reward. If we think of the salad as a gourmet experience, it can become a reward in its own right.

Rethink our rewards. The reward doesn’t need to be food related. It could involve reading a book, watching a show, or whatever you favorite activity might be.

Tip #8: Knowing This Stuff Isn’t Enough.

The fascinating thing is that his research shows it doesn’t matter how intelligent or well informed you are.

He did a study with 60 graduate students. Just before winter break, he gave them a lecture on external eating cues in which he specifically told them that they would eat more from a big bowl of Chex Mix than from a small bowl. The students then spent 90 minutes in small group exercises designed to show them how to overcome external eating cues.

After winter break he invited those same students to a Super Bowl party in which he divided them into two rooms and gave them, you guessed it, either large or small bowls of Chex Mix. The ones given the large bowls ate 53% more!

He later gave the same lecture to a meeting of The American Diabetes Association (Those are the experts) and then repeated the same experiment with them – and they still ate more from the large bowls.

How Can You Avoid Mindless Eating?

Dr. Wansink’s research clearly shows that overeating is mindlessly dependent on external eating cues, AND that you can’t avoid being influenced by those external clues even if you are intelligent and motivated! How to eat less?

Dr. Wansink recommends planning ahead. For example:

Serve your food on small plates and don’t leave food lying around where you can see it or get to it easily.

If you bring home a box or bag of snack food (hopefully healthy snack food), divide it up into healthy portion sizes as soon as you bring it home.

Put the healthy food choices in the front of your refrigerator or cupboard where you will see them easily and hide the unhealthy foods in the back (or don’t bring them home to begin with).

However, the most important thing is to realize most of this behavior is mindless. It is not enough to simply understand these external eating cues at an intellectual level. We need to be constantly vigilant for external eating cues, or we will find ourselves overeating without really understanding why.

Hopefully, these tips will help you eat less and attain a healthier weight next year than you did this year. However, these 8 tips are just the tip of the iceberg. If this article has piqued your interest and you’d like to learn more, I recommend you read one of Dr. Wansink’s books.

The Bottom Line

Brian Wansink’s research has shown that overeating, to a large extent, is mindlessly dependent on external eating cues, and that you can’t necessarily avoid being influenced by those external clues even if you are intelligent and motivated!

I have distilled his research into 8 simple tips to help you eat less and attain a healthier weight next year than you did this year.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Merry Christmas

December 22, 2015 by Dr. Steve Chaney

Author: Dr. Stephen Chaney

The Christmas season is a wonderful time of year. It is a time when we get together with family and reconnect with friends. It’s a time of year when we remember the joy of giving and the joy of making the world a better place.

For those of us who are Christians, it is a time to remember that God gave us his only son. But, no matter what our religion, it is a time of year when we can focus on the common beliefs we share and the true purpose of our lives here on earth.It is a time to share the Christmas spirit of peace on earth and good will to all.

The Professor and his family wish you a blessed Christmas and happy, healthy & prosperous New Year