Tag Archive for: CVD

An Aspirin a Day

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In Tuesday’s Memo, I talked about biohacking. Specifically, I talked about the idea of having everyone over a certain age take a pill that can impact the risk factors for CVD: high blood pressure, cholesterol, high heart rate, and blood cell stickiness. The idea is that taking that single pill in low doses every day might help reduce CVD events such as strokes and heart attacks.

Researchers in Australia and the U.S. decided to test one component of the polypill: aspirin. The study was called the Aspirin in Reducing Events in the Elderly (ASPREE) trial. They recruited over 19,000 people 70 and older or 65 if they were Black or Hispanic in the U.S. They randomly assigned half the subjects to take 100 mg of enteric-coated aspirin while the other half got a similar looking placebo. The subjects were tracked for an average of 4.7 years. The researchers examined many variables including mortality and the incidence of disease.

The results were published in three separate papers in a recent issue of the New England Journal of Medicine. The study was terminated after five years by the primary funding organization, the National Institute on Aging. The results were not exactly what was hoped. We’ll get into the details on Saturday. If you’d like to read the studies, all are available online at the links in the references.

What are you prepared to do today?

Dr. Chet

 

References:
1. DOI: 10.1056/NEJMoa1800722.
2. DOI: 10.1056/NEJMoa1803955.
3. DOI: 10.1056/NEJMoa1805819.

 

Yes, Supplements Matter

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The study that was published in the Journal of American Academy of Cardiology created several issues that go beyond the headlines of supplements being of no benefit. Let’s first take a look at the published results of the study.

The researchers found that most supplements such as multivitamins, vitamin D, calcium, and vitamin C do not have a significant effect on cardiovascular disease or overall mortality. On the other hand, folic acid had a significant beneficial effect on reducing stroke and overall CVD, and B-complex, a vitamin with a variety of B vitamins in it, also helped reduce the incidence of stroke. However, the study showed antioxidants had a negative effect on all cause mortality as did niacin. Whether beneficial or not, the results, while statistically significant, were not clinically significant.

The researchers stated that they expected beneficial effects on the reduction of cardiovascular disease and overall mortality. The fact that they did not find those benefits resulted in the headlines that supplements don’t matter.

Here are just three of the issues with the study. They included studies with different nutrients as well as studies that didn’t have the same amount of nutrients. The RCTs included in the analysis did not have the exact same amounts of any given nutrient in the supplement; three of the studies on antioxidants and cancer mortality had different amounts of beta-carotene and vitamin E. Another way of putting it was they not only were comparing apples to oranges, but they also compared three oranges to a dozen apples.

Another issue was adherence to the study rules. The subjects did not necessarily take all the supplements they were given, and compliance varied between the studies. Positive or negative effects could be determined by whether subjects took all of their supplements or took them only when they remembered or felt like taking them. The adherence to supplement use varied by study.

Here’s one more issue. Every RCT used supplements as a potential treatment for a disease—in this case, diseases related to the heart and the death rate from heart disease or other diseases. It’s the treatment model used by physicians: the pill, whether pharmaceutical or supplement, must reduce the incidence of or cure the disease. While desirable, that’s not what nutrition is all about.

The Bottom Line

While we would like to see research results that prove that we can live longer or better by taking supplements, that isn’t really the point in my opinion. We take supplements to fill the gaps in our diet. As the researchers point out, if everyone ate more plant-based foods, we could meet the minimal amounts of nutrients our bodies needs. That hasn’t happened in the 30 years I’ve looking at this issue, and I don’t see it changing any time soon.

Taking vitamin and mineral supplements serves as nutritional insurance to support your body’s processes and to make sure you don’t open the door for deficiency diseases; supplements are more like shotguns than rifles. Supplements do matter and I’m going to continue to take mine every day.

There are so many issues with this research paper—much too long for this Memo—that I recorded a Straight Talk on Health about them. If you’re a Member or Insider, you can listen to Research Update on Supplements any time. If you’re not, now is a good time to join.

What are you prepared to do today?

Dr. Chet

 

References: Jenkins, D.J.A. et al. J Am Coll Cardiol. 2018;71(22):2570–84.

 

The Truth Behind the Obesity Paradox

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

Study One: Dialysis, BMI, and Mortality

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

Study Two: The Rotterdam Study

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

Study Three: BMI and Mortality

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

Study Four: A Broader Look

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

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

The Bottom Line

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

What are you prepared to do today?

Dr. Chet

 

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

 

What Is the Obesity Paradox?

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Did you ever hear something that didn’t seem to make sense? That seemed to go against everything you thought to be true? One example of this is something called “The Obesity Paradox.” I’ve seen a few headlines this week that have talked about it, so it’s time to address it in the Memo.

One of the variables that we would think is related to the development of cardiovascular disease would be body weight. It seems logical: as weight increases, so does the strain on pumping the blood through the additional blood vessels required to feed the extra fat and muscle. People who are overweight may eat the wrong foods, consume too much food, and move too little.

But since the early 2000s, several studies have been published seeming to show that body weight wasn’t necessarily a risk factor for CVD or an early death. They showed that those who were overweight, a BMI between 25.0 and 29.9, had lower mortality rates than those who were normal weight. Some showed that stage-one obesity, a BMI between 30.0 and 34.9, was also not related to mortality. Thus the term “The Obesity Paradox” was coined. But is it true? We’ll take a look at the research the rest of the week.

What are you prepared to do today?

Dr. Chet

 

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.