Tag Archive for: CVD

Do Calcium Supplements Harm Your Heart?

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Over the past few years, concern has grown about the relationship between heart disease and calcium intake. A couple of studies have shown a possible association between calcium intake and cardiovascular disease. In an article also published this month in the Journal of Women’s Health (1), two clinicians reported on a number of studies including one that examined calcium intake and heart disease. Their purpose was to update clinical guidelines for physicians and internists who regularly treat women and heart disease.

They selected a study that included a meta-analysis of studies on calcium intake from food and supplements (2). You know my position on meta-analysis and its overuse and limitations, but in this case, the researchers wanted to establish positions for both the National Osteoporosis Foundation and the American Society for Preventive Cardiology on calcium intake and heart disease. I think the use of this statistical method was warranted.

After an exhaustive review of the studies and re-analysis of the data, researchers found that calcium intake, from either food or supplements, at levels up to 2,000–2,500 mg per day are not associated with CVD risks in generally healthy adults. Although they found a few trials that reported increased risks with higher calcium intake, the risks were small and not considered to be clinically important even though they were statistically significant. The results applied to women and men.

At this point, with data from tens of thousands of subject, taking calcium from food or supplements will not harm your heart if you’re healthy. Does that mean you should limit calcium if you’re not healthy? No. There just isn’t sufficient data to know. In my opinion, if you take 800–1,000 mg of calcium per day, I think you’ll be fine but you should always check with your physician. You need calcium for many reasons, including bone and blood health and conducting signals between nerves. Especially if you don’t consume a lot of dairy, take your calcium supplement.

What are you prepared to do today?

Dr. Chet

 

References:
1. J Women’s Health DOI: 10.1089/jwh.2018.6932
2. Ann Intern Med 2016;165:856–866.

Treating a Woman’s Heart Disease

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The paper I’ve been using as a primary source for this week’s Memos is titled “Sex Differences in Ischemic Heart Disease. Advances, Obstacles, and Next Steps”; the purpose of this paper is to provide the current state of the science to clinicians when it comes to preventing and treating heart disease in women. A team of experts combed the medical literature to let their colleagues know where we stand in treatment and where future research should go, and you could look at it as a roadmap for improving prevention and treatment. You could also look at this as an indictment for less-than-quality care for women with heart disease.

There were seven categories of treatment options for various phases of heart disease, from diagnosing heart disease to mortality. I’m going to talk about just two but understand that even though the mortality from heart disease has decreased over the past 30 years, there are still gaps in treatment between men and women.

The first was a 30-minute delay in restoring the flow of blood to the heart in women who were having a heart attack with ST- segment elevation, a distinct change in the EKG. The time from the onset of symptoms and arrival at the hospital as well as time from arrival at the hospital to needle insertion for a percutaneous coronary intervention was 30 minutes or longer compared to men. That means women don’t get to the hospital early enough, so that’s on them. Ladies, you need to make that 911 call a little quicker. But it also means that once they’re there, it takes longer to get the arteries open again. That creates the possibility of more damage.

One of the problems is getting the correct diagnosis. There are 11 other conditions that can cause ST-segment elevation including takotsubo syndrome also known as broken heart syndrome. Still, 30 minutes seems way too long and needs to be improved.

The second is the one that really stunned me: fewer women are given recommendations for cardiac rehabilitation after a heart attack. Not only that but fewer women register to take part in cardiac rehab. They also attend fewer sessions than men do. When I read that, I was almost apoplectic. The heart is a muscle that can be damaged by a heart attack. When it’s time to rehabilitate that muscle, it’s not like restoring range of motion after knee surgery. If this muscle isn’t rehabbed and then trained for the rest of a women’s life, the death rate increases for those women.

That has to change today. If you have any type of coronary event, from atrial fibrillation to a full blown heart attack, the first question you ask is “When can I begin cardiac rehab?” I understand that every insurance plan may be different but you need to understand any limitations, how to exercise after a heart attack, and how to progress. That’s important, not just for the muscle, but also for the nervous system, the lungs, increasing the number of blood vessels, and even to reduce the depression that occurs after a heart attack.

And then you’re going to do it until you get every session you qualify for and get a plan to take home with you to keep improving. When that’s done, you’re going to get a plan from your physician as to how to progress from that point. These are non-negotiable. This has to change and it has to change today. The quality of your life depends on it.

Next Tuesday I’ll finish American Heart Month with a question I get a lot: does taking my calcium supplements increase calcification in my coronary arteries? I’ll let you know on Tuesday.

What are you prepared to do today?

Dr. Chet

 

Reference: Circ Cardiovasc Qual Outcomes. 2018;11:e004437.

 

Emerging CVD Risk Factors for Women

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The paper I referred to in Tuesday’s Memo provided a list of emerging risk factors for heart disease that apply only to women. But first, I wanted to define exactly what a risk factor is and what it means.

As defined by the World Health Organization, a risk factor is any attribute, characteristic, or exposure of an individual that increases the likelihood of developing a disease or injury. The key word is likelihood. It does not mean cause and effect, and that includes genetic tendencies. Lifestyle contributes close to 80% when it comes to raising or lowering risk. You’re not doomed; you just have to be aware and take action.

There were several emerging risk factors for cardiovascular disease (CVD):

  • Gestational diabetes: your risk of getting type 2 diabetes increases four-fold later in life; type 2 diabetes is a risk factor for heart disease.
  • Hypertension during pregnancy: hypertension and preeclampsia increase the risk of heart disease three-fold.
  • Early menopause: women’s hormones are protective against heart disease. When they change during menopause, the risk of heart disease begins to increase; the earlier that happens, the sooner the risk rises.
  • Autoimmune disease: diseases such as rheumatoid arthritis and lupus increase the risk of heart disease. Autoimmune diseases increase inflammation, and that may partially explain this connection.

You can see why these emerging risk factors are primarily associated with women. While depression is also associated with an increased risk in women, it may be that women seek help more than men.

Keep in mind that these conditions don’t make heart disease a given, just a risk. But if that gives you the oomph you need to get to the gym today or skip that sweet roll, I’m okay with that.

What happens after a woman has heart disease or a heart attack? We’ll take a look at that on Saturday including one thing that stunned me and has to change.

What are you prepared to do today?

Dr. Chet

 

Reference: Circ Cardiovasc Qual Outcomes. 2018;11:e004437.

 

It’s American Heart Month

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February was declared American Heart Month by President Lyndon Johnson in December 1963. As I’m searching the recent research in preparing to update the Women’s Heart Health audio, I’ve found new research on women’s hearts. I’m not ignoring men, but the research on women has lagged behind what we know about the risk of heart disease in men, because women’s bodies react differently to heart issues. Now we’re starting to catch up on women’s hearts.

Let’s look at the same risk factors for heart disease and see the differences between men and women. In a paper published this month, researchers looked at the differences in how risk factors for heart disease are managed in women. Here’s what they found:

  • Blood lipids: after menopause, women are less likely to achieve goals in reducing triglycerides and LDL-cholesterol and increasing HDL-cholesterol.
  • Blood pressure: as women get older, those with hypertension are less likely to lower blood pressure; only 29% achieve healthy blood pressures.
  • Exercise: 25% of all women get no regular exercise.
  • Obesity: carrying extra weight impacts the risk of heart disease more in women than men—64% compared to 46%.

There are more risk factors, but what makes these four important is that they can be improved through changes in lifestyle. Eating less. Eating better. Moving more. Even a 10% change can help reduce a women’s risk of getting heart disease.

Some new risk factors are emerging that are unique to women. I’ll cover those on Thursday.

What are you prepared to do today?

Dr. Chet

 

Reference: Circ Cardiovasc Qual Outcomes. 2018;11:e004437.

 

How Long Does Fitness Last?

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Does exercise when you’re young have any impact when you’re older? That’s the question researchers sought to answer in a very unique study. They recruited men who competed in running events in the 1968 Olympics and evaluated fitness variables to see how they had changed since then. The subjects were tested in 1993 and retested in 2013. Did their fitness and cardiovascular measures decline at the same rate as their age would predict?

Maximal heart rate is calculated by subtracting your age from 220. There are formulas that make it a little more precise, but the shortcut is close enough for most purposes. At every retest, the runners measured max heart rate was significantly higher than predicted. The maximal amount of oxygen they used was also higher than would be expected for their age.

What does this mean? The fitness you attain when you’re younger can impact your fitness when you’re older. This study shows that there are some measures related to the cardiovascular system that can be sustained. You may never have trained like an Olympian, but even if you start later, the fitness you gain may yield benefits years later. Improving your fitness now will still pay dividends twenty or thirty years ahead when you may have more physical restrictions than you have now.

That raises another question: will being fit help you live longer? We’ll tackle that on Saturday.

If you want the best way to combine a change in your diet with an exercise program to maximize fat loss, no matter what your current fitness level may be, make sure you sign up for the Super Bowl Webinar.

What are you prepared to do today?

Dr. Chet

 

Reference: Med Sci Sports Exerc. 2018 Jan;50(1):73-78.

 

Why Do Statins Fight with Grapefruit?

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One of the most complicated medication-food interactions is grapefruit and statins, the popular cholesterol-lowering drug. The goal of this Memo is to make sense of the research to date by answering a couple of questions.

Before I begin, let me briefly explain how a statin works. One of the many enzymes required to produce cholesterol in the body is called HMG CoA reductase. In fact, it’s the rate-limiting enzyme; it controls how much cholesterol is made. Interfere with the enzyme, and you can block the production of cholesterol. That’s what most types of statins do; they block HMG CoA reductase, thus limiting the amount of cholesterol made. If your cholesterol is too high, it goes down.

How Does Grapefruit Juice Interact with Statins?

While this is some complicated biochemistry, let’s see if I can explain it simply. There’s a series of naturally occurring enzymes produced in the small intestine called CYP 450 3A4 that modifies the statin before it’s released into the bloodstream; it controls the amount and the form of the statin that gets into your body. Grapefruit juice contains phytonutrients that interfere with the CYP 450 3A4 action, letting more of the statin get into the bloodstream more quickly. Rather than fighting, it was more of a case of helping too much.

Is that good or is it bad? The research never really specifies. The logical expectation is that it would lower cholesterol too much or because it’s not in the correct form, maybe not enough. I couldn’t find an answer to that question. The original research on grapefruit juice began in the late 1980s and seemed to end about 2004. Since then, the recommendation is if you take a statin, no grapefruit juice.

What Is the Real Concern with the Interaction?

This question perplexed me for years, but I finally found an answer: with too much of the statin available due to the interference of the phytonutrients with the CYP 450 3A4, the overabundance could lead to an increased risk of rhabdomyolysis, a breakdown of muscle tissue. Muscle pain is a frequent side effect of taking statins, so the concern makes sense. The problem is that it was never really tested in any research I could find.

On top of that, the primary studies on grapefruit juice and statins used double-strength grapefruit juice in high amounts and a high dose of statins in healthy subjects. Yes, they found that the statin levels increased. But no other measures were checked such as impact on cholesterol production or markers of muscle damage. That was the state of research for the past decade.

What If You Wanted to Boost Your Statin?

In a recently published review paper, researchers theorized on the impact of grapefruit juice on cholesterol levels and the risk of cardiovascular disease. They found that if a statin such as simvastatin was taken at the same time as grapefruit juice, it increased the absorption 260% but if taken 12 hours apart, absorption was up only 90%. With atorvastatin, the increase was 80% no matter when the grapefruit juice was taken.

Calculating the effect on benefits and hazards, when simvastatin or lovastatin are taken at the same time as grapefruit juice, the estimated reduction in LDL cholesterol is 48%, and therefore, the decrease in heart disease is 70%. If the juice is taken 12 hours before these statins, the reductions are, respectively, 43% and 66%. For atorvastatin, the reduction in LDL cholesterol is 42% and in reducing the risk of CVD by 66% (1). Without the grapefruit juice, the reduction in LDL cholesterol is 37% with a decrease in risk of CVD of 61%.

This paper uses published data from many studies to perform these calculations. It doesn’t change the message in their conclusions. The benefits from the additional reduction in cholesterol may be worth the slight risk of rhabdomyolysis, but that doesn’t mean you’ll find any change in the grapefruit juice recommendation any time soon. But at least you now know the issues and why grapefruit is not the demon it’s been made out to be.

The Bottom Line

It’s important to understand that the drug, the statin, is the abnormal thing here, not the fruit. It doesn’t seem to make any sense to modify properties of a healthy diet just to be able to take a medication. But we live in the real world. Until the pharmaceutical industry can find a way to make medications that can help us and work with a healthy diet, be prudent. If you take a statin, talk with your cardiologist about finding a way to fit citrus in your diet. You may have to limit the amount or limit the times of day you eat or drink grapefruit, but as long as the net effect is getting your lipid levels in the desirable range, there has to be a way, especially since most statins should be taken at bedtime. The research is far from clear, so it’s a case by case basis.

What are you prepared to do today?

Dr. Chet

 

Reference: http://dx.doi.org/10.1016/j.amjmed.2015.07.036.

 

Normal BMI but Still Too Fat

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Last week the health headlines shouted “Study Shows Over 90% of All Americans Are Overfat!” The rate of overweight as assessed by Body Mass Index (BMI) is already 70%; now scientists want to say even more people are too fat? What’s going on? I’ll explain what overfat means first and then tell you about the study behind it.

For the most part, the greater the BMI, the greater the risk for cardiovascular disease, prediabetes, and hypertension. For those of you who aren’t sure of your BMI, check out your BMI in the Health Info section of our website. And if you think you’re just big boned, we show you how to prove it.

But there are people who have a normal BMI under 25.0 but still may be overfat. Considering Waist Circumference in addition to BMI may help but that could still miss some people. How? They may have lost muscle mass; the subtle loss of lean muscle with a gain of fat could lead to overfatness. That increases their risk for the diseases I mentioned earlier.

Here’s the most common example of someone who has a normal BMI but is overfat: a very sedentary elderly person who looks slim, but has very little muscle. As the saying goes “use it or lose it” and they’ve lost it.

A clinician from Arizona has taken it upon himself to redefine the terminology associated with excess body fat. He claims that overfatness gets missed in too many people. The problem he sees is that people who could begin treatment with diet, exercise, and medication if necessary are being missed. He outlined his arguments in a paper published in January 2017 (1), but it was his paper published in July that lead to headlines (2).

He and his co-authors examined the BMIs of people in countries all over the world. Using prior studies that estimated the number of normal-weight people who are overfat, ranging from 9.7% to 20%, he then applied that to the normal-weight populations (as assessed by BMI) in the top 30 developed countries in the world. That’s how they derived the headlines of over 90% overfat—not just in the U.S. but also New Zealand, Iceland, and Greece as well. To be fair, this applied only to males. Don’t rest on your laurels, ladies. All the same countries were greater than 80% for females.

 

The Problems

There are three with his approach in my opinion. First, adding another definition to replace BMI doesn’t really help people or their physicians as he implies. Confirming a person with normal BMI is overfat would require a more advanced exam or assessment of body fat. I’m not sure that’s practical.

Second, I looked at his work from every direction and couldn’t get the numbers to work. If 70% of Americans are overweight or obese and you add 20% of the remaining 30%, it adds up to 76% not 90%. Even if the numbers worked, the statistic would apply to a physician’s total number of patients. There would be no way to identify who is overfat without additional testing.

Third, there’s another group that needs to be addressed, and that would be those who are overweight according to their BMI but are metabolically healthy. In fact, that’s a significant problem today. Even after losing over 30 pounds, my BMI is still in the overweight category. By every test of metabolic fitness—blood pressure, cholesterol, HbA1c, or insulin—I’m at no additional risk of heart disease, yet I’m still classified as “at risk” due to my BMI. I think that’s a greater issue and will be more so as healthcare gets debated. Is your BMI over 25? You’ll pay more, even if your test results are stellar.

 

The Bottom Line

I agree with the concept that the author put forth: there are people with normal BMIs that are overfat, and they’re at greater risk for CVD and metabolic diseases. But new definitions aren’t necessary. What is necessary is identifying who is at risk. That will only occur when doctor and patient meet face to face. When was your last doctor’s appointment?

What are you prepared to do today?

Dr. Chet

 

References:
1. Front. Public Health 4:279. doi: 10.3389/fpubh.2016.00279.
2. Front. Public Health 5:190. doi: 10.3389/fpubh.2017.00190.

 

Chelation Therapy: Too Soon to Judge

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The results of the study on chelation therapy in subjects with diabetes showed a reduction in cardiovascular incidents during the follow-up time. No single event dominated, ranging from heart attack to stroke to death, but overall there were fewer incidents. Subjects who did not have diabetes did not experience a benefit in v incidents during the same follow-up time.

That led the researchers to speculate why. They couldn’t come up with any specific reason other than the chelation must involve a mechanism that was not yet identified. They carefully suggested that while the results were positive, this study could only suggest that larger clinical trials were necessary and the findings do not constitute enough evidence to be recommended as a treatment.


Should You Do It?

Here a few more things to consider:

  • The cost: each session costs $90 to $150 and there should be at least 30-40 of them. Add office visits and the total price could be around $5,000; none of it is covered by insurance.
  • All the subjects continued to use their typical medications for diabetes, cholesterol, and blood pressure. This was not replacing traditional treatments, it was in addition to the treatments.
  • The investment of time was significant at three-plus hours once a week or on whatever schedule the patient and doctor agree upon.


The Bottom Line

This study demonstrated a small cardiovascular benefit to the patients, reducing the risk of a cardiovascular event from 35% to 25%. In my opinion, the results are too small to justify the cost of money or time.

I know people who swear by chelation therapy, and I’m happy it worked for them, but there’s too much we don’t know. Nobody tracks what is actually changed in the body during chelation. Where do the heavy metals go? What if someone doesn’t process metals the same way to eliminate them? At this point, there are more questions than answers.

Here’s an idea. Spend the money on more vegetables and fruit for your diet. Invest the three hours per week in additional exercise. Both of those things will give you a better return on your investment than chelation therapy.

Eat less. Eat better. Move more.

What are you prepared to do today?

Dr. Chet

 

Reference: Circ Cardiovasc Qual Outcomes. 2014;7:15-24

 

Update on Chelation Therapy

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One of the questions asked during Tuesday’s Conference Call was about chelation therapy for helping with memory. I didn’t find any research to support that outcome, but a couple of studies have been published on chelation therapy with cardiovascular disease (CVD). One paper was from the Trial to Assess Chelation Therapy or TACT study.

Chelation therapy is used to eliminate heavy metals with the goal of reducing the metals that can be toxic to the body. While it’s been used for decades, the research hasn’t demonstrated a clear benefit.

For the TACT trial, researchers recruited over 1,700 subjects. In this paper, they used a sub-group of subjects from the original study who had diagnosed diabetes and had a heart attack more than six months before the study began. Half the diabetic subjects received chelation with EDTA (ethylene diamine tetraacetic acid) as well as some vitamins and minerals. The other half were infused with just saline solution. All subjects were given low doses of vitamins and minerals.

Subjects were infused once per week for 30 weeks and then biweekly and bimonthly until 40 sessions were completed. Each chelation session lasted three hours. With the investment of time, did the chelation therapy result in fewer cardiovascular events over the next five years? We’ll see on Saturday.

What are you prepared to do today?

Dr. Chet

 

Reference: https://doi.org/10.1161/CIRCOUTCOMES.113.000663

 

Why I’ll Keep Using Coconut Oil

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The research that the authors of the American Heart Association Presidential Advisory on Dietary Fats and Cardiovascular Disease, specifically on coconut oil, seems to be in conflict. The authors suggested coconut oil is bad for us, but the research studies they used didn’t really seem to confirm that conclusion. What gives?

The criteria that the Advisory’s panel used were limited in scope. There’s no evidence that the regular use of coconut oil contributes to CVD, even in cultures that regularly use coconut oil. They used a part-equals-whole logic. As they reported, there were significant increases in LDL-cholesterol when subjects increased coconut oil in their diet in the studies they cited. Because a high LDL-cholesterol level contributes to CVD, therefore coconut oil must contribute to CVD. That’s why the Panel does not recommend its use.

I understand what they said. The data they used supported their conclusion. However, they used a very narrow use of the data on coconut oil to support their recommendation.

They are correct when they state that coconut oil is high in saturated fat; in fact, it has the highest percentage of saturated fat of all fats and oils including lard and butter. But it also has a very high percentage of short- and medium-chain saturated fatty acids as opposed to longer chain fatty acids. The advantage is that short- and medium-chain fatty acids can by-pass the liver and be used directly to produce energy in most organs of the body, which makes coconut oil an option for getting energy quickly.

Let’s examine the statement that LDL cholesterol increased when subjects were taking coconut oil (1). In one study, LDL rose from 166 to 171 mg/dl in men and 155 to 156 in women (2). In another study, LDL rose from 118 to 128 mg/dl in a study of men and women (3). These were studies that lasted six weeks and five weeks respectively. There’s no evidence it would continue to rise had the subjects continued to use coconut oil. An increase of 3–6% in LDL-cholesterol wasn’t translated into a risk for CVD. Statistically significant? Yes. Meaningful in the real world? No.

The panel did not recommend coconut oil because it has saturated fat and has no other health benefits, but that point is debatable. Research on other benefits of coconut oil is really just beginning. Too many health gurus are overstating the benefits, especially when it comes to Alzheimer’s disease, and that creates the hype and most likely, the reason the Panel singled out coconut oil to examine more closely.

 

The Bottom Line

The Panel suggested we keep fat intake to no more than 30% of dietary intake; of that, only 10% should be saturated fat. They recommend that we substitute poly-unsaturated and mono-unsaturated fats and oils for saturated fat. That’s not really controversial and it’s a good idea.

What they did not say was that we couldn’t use coconut oil as one of our sources of saturated fat. If we eat 2,000 calories per day, that would mean up to 200 calories per day can come from saturated fat; that’s about two tablespoons per day, and that seems to be a reasonable source of saturated fat consistent with their recommendation.

Here’s the real bottom line: if you’re going to use a sat fat as a source of immediate energy, coconut oil is a healthier choice than lard or butter. And that’s why I use coconut oil; I don’t use a lot, but it works for me and makes sense to me as a scientist.

My recommendations never change. Eat less. Eat better. Move more. And in my opinion, using coconut oil is eating better.

What are you prepared to do today?

Dr. Chet

 

Reference:
1. Circulation. 2017;135:00–00. DOI: 10.1161/CIR.0000000000000510
2. J Lipid Res. 1995;36:1787–1795.
3. Am J Clin Nutr. 2011;94:1451–1457