This request reminded me of a chapter from Melanie Warner’s excellent analysis of the food industry, “Pandora’s Lunchbox.” I had pulled a quote from my iBook version of that book and pondered writing a blog post on breakfast cereal as an update to my previous breakfast post.
The quote was:
“Walk down a cereal aisle today or go onto a brand’s Web site, and you will quickly learn that breakfast cereal is one of the healthiest ways to start the day, chock full of nutrients and containing minimal fat. “Made with wholesome grains,” says Kellogg’s on its Web site. “Kellogg’s cereals help your family start the morning with energy by delivering a number of vital, take-on-the-day nutrients—nutrients that many of us, especially children, otherwise might miss.” It sounds fantastic. But what you don’t often hear is that most of these “take-on-the-day” nutrients are synthetic versions added to the product, often sprayed on after processing. It’s nearly impossible to find a box of cereal in the supermarket that doesn’t have an alphabet soup of manufactured vitamins and minerals, unless you’re in the natural section, where about half the boxes are fortified.”
The Kellogg’s and General Mills of the world strongly promoted the concept that you shouldn’t skip breakfast because they had developed products that stayed fresh on shelves for incredibly long periods of time. They could be mixed with easily accessible (low-fat, no doubt) milk to create inexpensive, very quickly and easily made, ostensibly healthy breakfasts.
Unfortunately, the processing required to make these cereals last forever involved removing the healthy components.
As Warner writes about W.K. Kellogg:
“In 1905, he changed the Corn Flakes recipe in a critical way, eliminating the problematic corn germ, as well as the bran. He used only the starchy center, what he referred to as “the sweetheart of the corn,” personified on boxes by a farm girl clutching a freshly picked sheaf. This served to lengthen significantly the amount of time Corn Flakes could sit in warehouses or on grocers’ shelves but compromised the vitamins housed in the germ and the fiber residing in the bran”
This is a very familiar story in the world of food processing; Warner covers, nicely, the same processes occurring with cheese and with milk, among other things.
I ended my 2013 post with these words:
My advice to overweight or obese patients:
Eat when you’re hungry.
Skip breakfast if you want.
If you want to eat breakfast, feel free to eat eggs or full-fat dairy (including butter).
These foods are nutrient-dense and do not increase your risk of heart disease, even if you have high cholesterol.
You will be less hungry and can eat less throughout the day than if you were eating sugar-laden, highly processed food-like substances.
At the time, this seemed like horribly contrarian advice, but in the last year and a half, more and more authorities are agreeing with these concepts.
What if all that exercise that authorities have been recommending is not helping to stem the rising tide of obesity?
What if all calories don’t have the same ability to add fat?
These twin heresies fly in the face of the usual dogma on the cause of obesity: more calories in (gluttony) than calories out (sloth). The skeptical cardiologist has been pondering these possibilities for some time, since reading Gary Taubes book Good Calories, Bad Calories.
I have been advising my patients through this blog and during office visits that added sugar and refined carbohydrates are much more of a culprit in their weight gain than fat, thus embracing the concept that there are good calories and bad calories
Exercise and Obesity
But I also spend a lot of time during my office visits discussing activity levels and encouraging my patients to engage in moderate aerobic physical activity for at least 150 minutes per week.
I do this because there is good evidence that regular physical activity is associated with lower cardiovascular risk, cancer risk, mortality, and improved brain, muscle, and bone function. Exactly what level and type of exercise is needed to reap these benefits is still up for debate.
I, personally, engage in regular moderate exercise and I think it helps maintain my weight where I want it.
Throwing Down the Gauntlet
A recent editorial in the British Journal of Sport Medicine stridently makes the claim that exercise is not useful for weight loss as conventional wisdom teaches and that the food industry has been promoting exercise while simultaneously promoting junk food and sugar-sweetened beverages (The link I provided is no longer active because the journal has removed the editorial -“This paper has been temporarily removed following an expression of concern.”)
The authors wrote:
“members of the public are drowned by an unhelpful message about maintaining a healthy weight through calorie counting, and many still wrongly believe that obesity is entirely due to lack of exercise. This false perception is rooted in the Food Industry’s Public Relations machinery, which uses tactics chillingly similar to those of big tobacco. “
Root Causes of Obesity
It would appear that science cannot tell us with total certainty what the cause of our current obesity epidemic is.
After publishing a paper in 2014 that suggested Americans had become less active over the last 20 years, Ladabaum, et al admitted this:
“Although there is no clear answer at this time regarding the relative contribution of energy intake or physical activity (or other variables including dietary components, patterns of activity, and environmental factors, including the gut micro biome) to the public health problem of obesity, we believe that public health messages should continue to emphasize the importance of both a healthy diet and remaining physically active throughout life.”
Is Exercise Amount A Cause or Effect?
In my own practice, I have observed a tendency for those patients who regularly exercise or have very physically active jobs to stay thin whereas those who don’t exercise, especially if they have sedentary jobs or are retired, tend to be obese and gain weight.
But, I also note that those patients who take my recommendations on exercise to heart are also listening to my advice in other areas, including diet and medications and are, in general, much more proactive about their health.
Therefore, I can’t say for sure whether it is the exercise or the other aspects of a healthy lifestyle (including diet) being followed in any individual patient that is keeping the pounds off. How much my patients move during the day when they are not specifically exercising may also be playing a role and is hard for me to assess.
There is also the mind-boggling possibility, as Gary Taubes has written about (here and in his book Why We Get Fat) that our genetics are driving both our activity levels and our food consumption:
“Ultimately, the relationship between physical activity and fatness comes down to the question of cause and effect. Is Lance Armstrong excessively lean because he burns off a few thousand calories a day cycling, or is he driven to expend that energy because his body is constitutionally set against storing calories as fat? If his fat tissue is resistant to accumulating calories, his body has little choice but to burn them as quickly as possible: what Rony and his contemporaries called the “activity impulse”—a physiological drive, not a conscious one. His body is telling him to get on his bike and ride, not his mind. Those of us who run to fat would have the opposite problem. Our fat tissue wants to store calories, leaving our muscles with a relative dearth of energy to burn. It’s not willpower we lack, but fuel. “
I’m not ready to accept the heresy that exercise and activity have nothing to do with weight gain or loss. I, like most cardiologists, walk the walk and talk the talk of regular vigorous exercise for health benefits, extended longevity, cardiovascular fitness and for helping in weight control.
Exercise is not the be all and end all of weight control because increased consumption of bad or good calories can overcome the most prolonged and intense workouts but it is a useful adjunct.
The best way we have of estimating a patient’s risk of stroke if they have atrial fibrillation (AF) is by the CHA2DS2-VASc scale.
This scale take the factors we know that increase the risk of stroke and assigns 1 or 2 points. The acronym comes from the first letter of the factors that are known to increase risk as listed to the left.
Most of the factors get 1 point, but prior stroke (S) and age>75 (A) get 2 points.
We then add up your points and use another chart (or app) to calculate the risk of stroke per year.
Your risk of stroke is very low if you have zero risk factor; it gets progressively higher as you reach the maximum number of 9.
Treatment with an oral anticoagulant (OAC), either warfarin, or one of the four newer anticoagulant agents (NOACS), is recommended when the risk gets above 1-2% per year.
The higher the risk, the more the benefit of these blood thinners in preventing stroke.
In lower risk patients, the bleeding risk of OAC of 1% per year may outweigh the benefits conferred by stroke reduction.
Both European and American guidelines recommend using the CHA2DS2-VASc score for initial risk stratification. The European guideline recommends OAC therapy for males with a CHA2DS2-VASc score ≥1 and for female patients with a score ≥2., whereas the American guideline recommends use of OAC if the CHA2DS2-VASc score is ≥2 for men and women.
I’ve been using the CHA2DS2-VASc scale for several years in my AF patients. I try to review the patient’s risk of stroke and their risk of bleeding during every office visit, and decide whether they should be on or off an OAC.
Initially, it was helpful typing all those capital letters and number twos (although I never took the time to make the twos a subscript) because it helped remind me of the factors.
However, I now view this acronym as a big pain in the neck and I am sick of typing it into my electronic medical records. It is also, really hard to say. Do you say “chad -two-D-S-two-vasc?” That is six syllables! I could have told my patient that warfarin is rat poison during that time.
And, what is with the Sc? Sex category? Why not just an S?
An Easier Term For The Stroke Risk Estimator: The Lip Score
I would like to formally request that this be termed the Lip stroke risk score in honor of Dr. Gregory Y. H. Lip who developed it at the University of Birmingham (UK).
because (per his bio):
“The CHA2DS2-VASc and HAS-BLED scores for assessing stroke and bleeding risk, respectively were first proposed and independently validated following his research, and are now incorporated into major international management guidelines.”
If the Lip score should somehow be unacceptable, then let’s go with the Birmingham score (recognizing, of course, that this is Birmingham, England and not Birmingham, Alabama). After all, this is what the app I use terms itself and I can type Birmingham a lot faster than CHA2DS2-VASc (even without the subscripts).
The Lip Score will be a great advance in the world of stroke risk estimation for AF patients. It will make all of us doctors creating EMR notes much more efficient, shaving precious minutes off the work day. It will be easier to communicate to patients, medical students and other medical personnel.
Finally, it gives, credit where credit is due, to Dr. Lip, who, according to his bio: “In January 2014, was ranked by Expertscape as the world’s leading expert in the understanding and treatment of AF,”
(I have no knowledge of Expertscape but you can be sure I will be investigating them soon)
Giving Lip service to stroke and atrial fibrillation,
In the last year, several of my patients have asked me whether it is safe for them to take testosterone for “low T.” They were responding to media reports suggesting that testosterone therapy raised heart attack risk by one-third.
I must admit, I had been skeptical of the legitimacy of the “low T” diagnosis. Many of the symptoms attributed to testosterone (T) deficiency, it seemed, were just part of normal male aging: decreased libido, fatigue, weight gain, and loss of muscle mass.
Perhaps, I thought, men should just be more willing to exercise regularly and lose weight and accept the indignities of aging that result despite our best efforts.
On the other hand, in the back of mind was the idea that perhaps I, as a sixty-something male with declining strength and endurance, could somehow forestall the ravages of aging by taking T.
I googled “low T” and immediately found some sponsored sites, including “is it low T.com,” which appears to be an educational site for patients. However, the one treatment option that they provide links to is made by Abbvie, the somewhat hidden host of the site. Abbvie is a pharmaceutical company that makes Androgel, the most widely prescribed testosterone cream.
I answered yes to the 3 questions I thought were just uniform consequences of aging:
1. Reduction in strength and/or endurance.
2. Loss of height.
3. Deterioration in your ability to play sports.
After taking the quiz, I was told that answering yes to 3 of the 10 questions strongly suggests you have low T.
In addition, according to the site, if you answered yes to question 1 (decreased libido) or 7 (less strong erections) you have low T.
Based on this quiz, I and 99% of men my age must have low T!!
In the last 10 years, the use of testosterone therapy has quadrupled, driven by better formulations for testosterone delivery and by direct-to-consumer marketing campaigns that suggest that treating low T will reverse these normal consequences of aging.
As a result, in 2013, 2.3 million American men received testosterone therapy and 25% of these men had no baseline testosterone levels tested.
A year ago, the New York Times editorial board opined on the dangers of overprescribing testosterone and the influence of pharmaceutical companies in over-promoting the drug, in a piece entitled “Overprescribing testosterone, dangerously.” Articles like this are what have raised patients’ concerns about T therapy and increased risk of heart attack.
Testosterone and Mortality
There is a large body of evidence that shows an association between lower T levels and increased mortality and coronary artery disease. Lower T levels are also associated with higher risk of diabetes and the metabolic syndrome. Studies also show that T therapy in T-deficient men increase lean mass and reduce fat mass and are associated with a reduction in mortality. A recent review article by Morgenthaler, et al in Mayo Clinic Proceedings, provides a detailed and meticulous summary of these studies and data.
Two recent studies contradict this large body of evidence and gained enormous media attention. The first, by Vigen et al in JAMA 2013, was a retrospective analysis of VA patients which has received extensive criticism for its statistical technique and has been corrected twice. The second study was by Finical, et al in PLoS One 2014, suggesting increased mortality in patients for 90 days after receiving their prescription for T. This study also contains methodologic issues and is hardly conclusive.
Is it Safe to Take T for low T
My recommendation to patients who want to take T after looking at all the data is as follows:
-Make sure that you really have low T. Your total T levels should be less than 300 ng/dL done in a reliable, certified lab.
-At this time, I don’t see solid evidence that taking T, if you definitely have T deficiency, increases the risk of cardiovascular complications or death.
As with all medications, the shortest duration and smallest effective amount is what you should take. All medications have side effects, some that we know and some that we don’t know. Most of the studies that have been published were on small numbers of patients for short periods of time.
-If you are overweight and/or sedentary, there is good evidence that losing weight and exercising will improve many of the symptoms ascribed to low T. These will also improve your life expectancy and lower your risk of heart attack.
…And you won’t have to worry about any side effects!
Do I have low T? Like all sixty-somethings my T levels are lower than when I was 30. My endurance is less. I’m losing height. Fat wants to build up in my abdomen, despite my best efforts.
It’s only going to get worse, but I’m willing to accept these as normal consequences of the aging process, rather than introduce external T into my system with its unknown consequences.
I will not go gentle into that good night but will continue to rage against the dying of the light without the wonders of pharmaceutical grade T.
Over the years I’ve had a number of patients tell me that they prefer to take over the counter (OTC) dietary supplements containing “natural” cholesterol lowering ingredients rather than the statin drug I have prescribed.
Red yeast rice (RYR) is a common ingredient in these supplements and is promoted widely and enthusiastically across the internet and in supplement or natural food stores for the purpose of lowering cholesterol and heart disease risk.
RYR has been used for centuries in China for coloring, food and medicine. It is made by fermenting red rice with a specific type of yeast (Monascus purpureus).
Red yeast rice contains chemicals that are similar to prescription statin medications. One of these, called monacolin K, is chemically identical to the statin drug lovastatin (brand name Mevacor).
The History Of Statin Drug Development
The history of the discovery and isolation of lovastatin, the first FDA approved statin, is worthy of a digression here as I think it illustrates the process of discovery, isolation and characterization of a chemical that becomes a safe and effective treatment.
Akin Endo,whose research over decades was crucial to discovering statins, writes that he was inspired by Alexander Fleming, who discovered penicillin in the blue-green mold belonging to the genus Penicillium in 1928.
He writes; “Although no metabolites that inhibited any enzymes involved in cholesterol synthesis had been isolated previously, I speculated that fungi like molds and mushrooms would produce antibiotics that inhibited HMG-CoA reductase. Inhibition of HMG-CoA reductase would thus be lethal to these microbes.”
Endo began analyzing thousands of molds and fungi for biologically active chemicals that would inhibit HMG-CoA reductase.
In 1971, after studying 3800 different strains of fungi he found a promising candidate: citrinin. Unfortunately,
“Citrinin strongly inhibited HMGCoA reductase and, furthermore, lowered serum cholesterol levels in rats. However, the research was suspended because of its toxicity to the kidneys. ”
End spent another 10 years isolating another promising HMG-CoA reductase inhibitor, “compactin, ” from mold and studying it in rats and other animals. Compactin demonstrated marked cholesterol lowering properties in dogs and monkeys and in the few humans who received it but the pharmaceutical company he worked for shut down the project after it appeared that in doses 200 x what were considered appropriate, it increased lymphoma risk in dogs.
The large pharmaceutical company, Merck, got wind of Endo’s studies with compactin, studied his data and realized the potential of similar but safer HMG-CoA reductase inhibitors. Drugs which inhibited HMG-coA reductase were now being termed statins.
Merck set out to find its own statins and in February 1979 isolated a statin very similar to compactin in chemical structure, called mevinolin, from the fungus Aspergillusterreus.
Endo, working separately and also in February 1979, isolated another statin (named monacolin K) from cultures of Monascusruber.(RYR).In the fall of the same year, it was confirmed that monacolin K and mevinolin were the same compound (later both changed to lovastatin).
The drug showed dramatic activity in lowering LDL cholesterol, with very few side effects. This led Merck to begin large-scale clinical trials of lovastatin in patients at high risk and long-term toxicity studies in dogs in 1984. The drug dramatically reduced cholesterol levels and was well tolerated. No tumors were detected. In 1987, Merck gained FDA approval and lovastatin became the first commercial statin.
Since then, six other statin drugs, some of which are synthesized in the laboratory rather than isolated from mold, have been approved for human therapy. These drugs have prevented thousands of heart attacks and contributed to the dramatic drop in cardiovascular deaths seen in developed countries over the last 30 years.
Ryr And Cholesterol Lowering
This brings us back to RYR and its ability to lower cholesterol. Small studies using a version of RYR that contained lovastatin have demonstrated a reduction in cholesterol compared to placebo.
However, because many red yeast rice supplements contained lovastatin (also called monacolin)In May 1998, the FDA ruled that Cholestin (the RYR product used in the studies showing cholesterol lowering benefit) was not a dietary supplement but an unapproved drug.
As a result, Pharmanex removed RYR from Cholestin. Since that ruling, the FDA has written warning letters to several other dietary supplement manufacturers to remove drug claims or eliminate red yeast rice with high lovastatin levels from their products, including Heart and Cholesterol (Mason Vitamins, Miami Lakes, Florida) Cholestrix (Sunburst Biorganics, Baldwin, New York), Red Yeast Rice and Red Yeast Rice/Policosanol Complex , and Red Yeast Rice (Nature’s Way Products Inc, )
A study in 2010, found levels of monacolins varying one-hundred fold in 12 RYR preparations available commercially (total monacolins (0.31-11.15 mg/capsule), monacolin K (lovastatin) (0.10-10.09 mg/capsule), and monacolin KA (0.00-2.30 mg/capsule).
Even more worrisome was that four products had elevated levels of citrinin. You remember citrinin, don’t you? That is the chemical that Endo initially identified as a candidate for cholesterol lowering drug but rejected because it was causing kidney failure in his rats.
Because of limited government oversight and variable manufacturing processes, one can also expect that the same manufacturer will have marked variation of monacolin content and citrinin from batch to batch or bottle to bottle.
Problems With Alternative Medicine In General
These problems with RYR supplements are typical of all supplements.As the the authors wrote
“Our results highlight an important issue with red yeast rice and many other alternative medicines: the lack of standardization of active constituents. Standardization of ingredients is difficult for several reasons: (1) There are variable growth and/or culture conditions and differences in harvesting and processing among manufacturers; (2) medicinal agents from natural sources are complex substances with many chemical constituents, many of which have unclear roles in their pharmacologic activity; and (3) different manufacturers may standardize products to amounts of 1 or 2 chemicals thought to be active ingredients, while other constituents are not standardized and may also have biologic and pharmacologic activity.”
One has to ask, given this background, why would a patient choose to take a “natural” OTC supplement containing an unknown amount of both a). Effective cholesterol lowering chemicals and b)potentially toxic extraneous chemicals over the precisely formulated, carefully regulated, fully studied, pure statin drug available by prescription.
It’s especially baffling to me when one considers that lovastatin comes from RYR. Thus it would have to be considered “natural.”
Akira Endo spent decades carefully identifying the effective and safe chemical portion of RYR. It is now available as a generic costing pennies per pill.
We know exactly how many milligrams you are consuming. We know what benefits to expect and what side effects can occur based on studies in hundreds of thousands of patients who have taken a similar dosage.
You are much better off taking the prescribed statin drug than RYR.
When I was a child in small town Oklahoma, I collapsed walking home from school one day after eating pecans. Apparently I had never encountered pecans in England where I grew up and I had a very severe, life-threatening allergic reaction (anaphylaxis.)
My pediatrician was promptly called, drove over, picked me out of the street and (legend has it) with one hand on the steering wheel and the other jabbing me with epinephrine drove me to the local hospital (apparently ambulances were not invented at this time). There I spent several days in an oxygen tent recuperating.
Since then I had, until recently, concluded (based on my own multiple food reactions and research) that I was allergic to “tree nuts.”
I would patiently explain to the uninitiated that I could eat almonds because they are in the peach family and I could eat peanuts because they are in the legume family: neither one of these, therefore, were true “tree nuts.”
To all whom I gave this seemingly erudite explanation I owe an apology for I have learned the earth-shattering truth that pecans are drupes! They are no more a nut than an almond is!
In fact, even walnuts are not nuts as hard as that is to believe.
Pecans, walnuts and almonds are all drupes.
Why, you may wonder, is any of this botanical folderol of any relevance to cardiology?
Nuts and Cardiovascular Death
For those paying attention to media reports on the latest food that will either kill you or make you live for ever you may already know the answer. This paper published in JAMA made big headlines.
It turns out, however, that most of what the 136,000 Chinese were eating and half of the “nuts” the 85,000 low income Americans were eating in that JAMA study were legumes: peanuts or peanut butter. The authors wrote:
“Our findings … raise the possibility that a diet including peanuts may offer some CVD (cardiovascular) protection. We cannot, however, make etiologic inferences from these observational data, especially with the lack of a clear dose-response trend in many of the analyses. Nevertheless, the findings highlight a substantive public health impact of nut/peanut consumption in lowering CVD mortality, given the affordability of peanuts to individuals from all [socioeconomic status] backgrounds.”
These findings follow another large observational study published in 2013 which also found (in American doctors and nurses) an inverse relationship between nut consumption and mortality.
“compared with participants who did not eat nuts, those who consumed nuts seven or more times per week had a 20% lower death rate. Inverse associations were observed for most major causes of death, including heart disease, cancer, and respiratory diseases. Results were similar for peanuts and tree nuts, and the inverse association persisted across all subgroups.”
We also have a very good randomized trial (the PREDIMED study) that showed that the Mediterranean diet plus supplementation with extra-virgin olive oil or mixed nuts performed much better than a control diet in reducing cardiovascular events.
Participants in the two Mediterranean-diet groups received either extra-virgin olive oil (approximately 1 liter per week) or 30 g of mixed nuts per day (15 g of walnuts, 7.5 g of hazelnuts, and 7.5 g of almonds) at no cost, and those in the control group received small nonfood gifts (I wonder what these were?)
After 5 years, those on the Med diet had about a 30% lower rate of heart attack, stroke or cardiovascular death.
Nuts versus Drupes versus Legumes
The evidence supporting “nut” consumption as a major part of a heart healthy diet is pretty overwhelming. But what is a nut and which nuts or nut-like foods qualify?
Let’s lay out the basic definitions:
Nut-Generally has a hard outer shell that stays tightly shut until cracked open revealing a single fruit inside. Examples are hazelnuts and acorns.
Drupe-Has a soft, fleshy exterior surrounding a hard nut. Classic drupes are peaches and plums with interior nuts so hard we won’t eat them. Examples are pecans, almonds, walnuts and coconuts.
Legume-generally has a pod with multiple fruit which splits open when ready. Examples are peas, carob, peanuts, soybeans and beans.
What Nuts Were Consumed in Studies Showing Benefits of Nuts?
Initially participants were given a questionnaire and asked
” how often they had consumed a serving of nuts (serving size, 28 g [1 oz]) during the preceding year: never or almost never, one to three times a month, once a week, two to four times a week, five or six times a week, once a day, two or three times a day, four to six times a day, or more than six times a day.”
After initial surveys, the questionnaires split out peanut consumption from “tree nut” consumption and whether you ate peanuts or nuts the benefits were similar.
Thus, for the most part, participants were left to their own devices to define what a nut is. Since most people don’t know what a true nut is, they could have been eating anything from almonds (drupe related to peaches) to hazelnuts (true nut) to a pistachio “nut” (drupe) to a pine “nut” (nutlike gymnosperm seed).
Nutrient Content of Nuts
The nutrient components of these nuts varies widely but one consistency is a very high fat content. For this reason, in the dark days when fat was considered harmful, nuts were shunned.
Please repeat after me “Fat does not cause heart disease or make you fat.”
A one ounce portion of pecans contains 20.4 grams of fat (11.6 arms monounsaturated and 6.1 polyunsaturated) so that 90% of its 204 calories come from fat.
Nuts, of course, also contain numerous other biologically active compounds that all interact and participate in the overall beneficial effects that they have on cardiovascular disease and mortality.
They are a whole, real food which can be eaten intact without processing and these are the foods we now recognize provide the best choices in our diets, irrespective of fat or carbohydrate content.
They are also convenient, as they are easy to store and carry with you, providing a perfect snack.
If You Think It’s A Nut, It’s A Nut
Hazelnut Death Experiment (Don’t try this at home!) A single hazelnut was partitioned into halves, quarters, slivers and little tiny bits. Progressively larger portions were consumed at 5 minute intervals. An Epipen (right) was available in case of anaphylaxis.
It turns out, that my attempts to put pecans and walnuts in to a specific family of nuts that increased my risk of dying if I consumed them were misguided.
I’m allergic to drupes.
In fact, I did an experiment recently and consumed a true nut (a hazelnut) and found I had no reaction.
I’m not allergic to nuts!!!
In the world of allergic reactions, thus, there is no particular value to partitioning nuts from drupes from legumes.
Similarly, for heart healthy diets, it doesn’t matter if you are consuming a true nut or a drupe as long as you think of it as a nut.
Consume them without concern about the fat content and consume them daily and as along you are not allergic to them they will prolong your life.
I am Board Certified by the American Board of Internal Medicine (ABIM) in both Cardiovascular Disease and Internal Medicine.
Recently the ABIM has changed the rules and started a Maintenance of Certification (MOC) Program which is chock-full of useless forms, fees and tests.
I, and thousands of other doctors have rebelled against this program, recognizing that there is no evidence it will improve doctors care, patient outcomes or overall quality of medical care but that it will fill the coffers of bureaucrats and bureaucratic institutions and fritter away valuable time we could be spending on patients.
I did not pay my several hundred dollar fee the ABIM demanded for 2015.
As a result, I received this morning an email from ABIM telling me that “your MOC status has changed”. I logged in and found that I was listed as “Certified, Not Participating in MOC.”
I’m still the clinical cardiologist I was yesterday and I still spend hours weekly reading about the latest developments in cardiology that impact clinical care, teaching residents, and giving conferences but I wonder what the ramifications of this will be.
Dr. Wes, a cardiologist who has been a vociferous opponent of MOC is alerting physicians that one ramification is that the SGR bill the Senate is considering would tie doctor evaluations to MOC status.
You can read his comments here. He includes sample letters to send to Congress.
If the federal government puts their weight behind sanctifying MOC, then all physicians will be forced to participate.
I strongly all urge all physicians to consider weighing in on this with your local congresspeople.
My role models and mentors during my medical training taught me what I considered to be the proper appearance and demeanor of the professional physician.
The male doctor wore a dress shirt and a tie. The doctor wore a white coat over his/her regular clothes. The more senior the doctor was in the medical hierarchy the longer the white coat and the more impressive the words written on the coat.
Presumably, this professional appearance of the doctor increased the confidence that the patient had in the professionalism of the doctor.
Upon encountering a patient in the hospital room or office exam room, the doctor extends his right hand, greets the patient and smiles and shakes hands.
I wore a tie and a white coat and shook hands consistently during the first 20 years of my practice but gradually these markers of a good doctor have fallen under scrutiny.
The Physician Necktie as Disease Vector
Beginning about 15 years ago studies were published suggesting the physician necktie could become colonized with bacteria and serve as a vector for transmitting bacteria. Some authors, as a result, have called for an end to doctors wearing neckties (bow ties may be an exception).
In the UK, the tie has been banned for those involved in patient care because
“Ties are rarely laundered but worn daily. They perform no beneficial function in patient care and have been shown to be colonised by pathogens.”
After reading about ties as vectors I gradually stopped wearing them at work. Initially, I felt uncomfortable, as if I were not being professional. Somehow, I felt my patients would respect me less. Over time, however, I have reached a point where I only wear a necktie on Wednesdays.
A logical reader might ask why I still wear them at all. I don’t have a good answer for that. Perhaps, I feel a need to wear the dress shirts and ties I have accumulated over the years. Perhaps I don’t really feel the tie is a big contributor to nosocomial infections. Perhaps I want my patients to see that Dr. Pearson can dress professionally on occasion but he chooses not to the majority of the time.
The White Coat As Disease Vector
I’ve been wearing a white coat to make hospital rounds since I was a medical student starting on the wards 37 years ago (Yikes! Has it been that long?). The coat gave me an immediate power and respect and identified me as a caregiver.
My two oldest daughters have both undergone a “white coat ceremony,” recognizing the important and exciting transition from pre clinical studies to actual patient interactions in the health care field.
The white coat serves other purposes for doctors. I keep my billing cards in one pocket and in another I have a case with my business cards. The lapel serves as a convenient spot to clip my hospital ID badge. I used to carry around EKG calipers or rulers in my breast pocket but as EKGs have increasingly gone electronic I no longer do this.
Presumably the white coat helps keep dirt and vomit and phlegm from patients from sullying the “street” clothes of the physician.
However, the down side of all that stuff landing on the white coat and not on the street clothes may be that the white coat is accumulating bacteria that can then be transmitted to other patients.
In a 2009 study, the white coats of 23% (34 of 149) of medical and surgical Grand Round attendees at a teaching hospital were contaminated with S. aureus, 18% (6 coats) of which were resistant to methicillin.
As a result of studies demonstrating bacterial contamination of white coats, the Society for Health Care Epidemiology of America SHEA recently recommended
White Coats: Facilities that mandate or strongly recommend use of a white coat for professional appearance should institute one or more of the following measures:
HCP should have two or more white coats available and have access to a convenient and economical means to launder white coats (e.g. on site institution provided laundering at no cost or low cost).
Institutions should provide coat hooks that would allow HCP to remove their white coat prior to contact with patients or a patient’s immediate environment.
Frequency: Optimally, any apparel worn at the bedside that comes in contact with the patient or patient environment should be laundered after daily use.
Home laundering: If HCPs launder apparel at home, a hot water wash cycle (ideally with bleach) followed by a cycle in the dryer or ironing has been shown to eliminate bacteria.
Basically, they are strongly suggesting you don’t wear a white coat but if you do, wash it every day and take it off before you interact with the patient.
I must admit it will be difficult for me to stop wearing the white coat. Sometimes I find myself having to pop into the hospital without my white coat (stethoscope around my neck (yes stethoscopes can serve as vectors for bacterial transmission but they can be cleaned between patients)) and I feel like an impostor.
The Handshake As Disease Vector
It has long been my practice to start patient encounter with a hearty greeting and a (somewhat) hearty handshake.
The handshake has a profound cultural role and serves as the international symbol of greeting and departure with connotations of respect, friendship, congratulations and formal agreement.
In the health care setting, the handshake has been shown to have the power to the improve the perception of the physician’s empathy and compassion. The handshake provides comfort and calms patients.
We’ve known for a long time that shaking hands is an excellent way to transmit diseases. Many of my patients, when they know they have a cold, will state this up front and decline my handshake. This is something that most people intrinsically understand. Studies have shown that health care workers hands are a common cause of disease transmission in the hospital and this is why hand washing or gelling is mandated in the hospital between patient visits.
Sklansky, et al wrote an editorial in JAMA in 2014 advocating that the hand shake be banned from the health care setting because despite our best efforts at hand hygiene we often fail, either due to poor compliance or limited activity of alcohol based hand rubs against some pathogens (including C. dif).
They suggested some alternative greeting including the hand wave, the bow, placing the right palm over the heart or the namaste gesture from yoga.
Since then, a study has shown that the fist bump (mysteriously termed a dap greeting) does reduce bacterial transmission.
Researchers at Aberystwyth Universityin Wales (the home country of the skeptical cardiologist!) immersed a donor participants’ sterile-gloved hand into a dense culture of E-coli (a non-pathogenic strain), and after it was dry, exchanged greetings with recipient participants, who also wore sterile gloves.
They tested the handshake, the high five, and the fist bump in a crossover design so that each “donor” and each “recipient” tested all greetings, eliminating potential for bias among the volunteers.
The results (graph to left) showed twice as many bacteria were transferred during the handshake compared with the high-five, but the fist-bump transmitted only about 10% of the bacteria a handshake did.
Is It Time To Lose the Tie, the White Coat and the Handshake?
It’s hard to teach this old dog new tricks but more and more I will be eschewing the handshake in my patient encounters.
I’m going to experiment with the fist bump (especially for my younger patients) and the bow and perhaps I’ll have signs put up in my exam rooms declaring them “No Handshake Zones.”
I don’t think I can abandon the white coat yet. It’s like a security blanket for me. I will experiment more and more with not wearing it and monitor my patient’s reactions.
I will definitely try to wear the white coat for only one day and then send it off to be laundered (I wonder what the environmental consequences of that are?)
Since realizing that sugar, and not fat, was the major problem in the modern Western diet, The Skeptical Cardiologist has been ratcheting down how much sugar he consumes to the smallest possible amount.
This has lowered what I like to call my “sugarstat,” and has made me exquisitely sensitive to the presence of added sugar in foods.
With this sensitivity comes the heightened realization that added sugar is everywhere.
The obvious sources are soft drinks and other sweetened beverages, candy, cakes, pies, cookies, donuts and fruit juices. Once you mostly eliminate such things from your diet you become aware of the “background” levels of added sugar in other foods.
For example, when I consume what many Americans probably perceive as a “healthy” granola bar (from even the most natural or organic of manufacturers), all I can taste is a sickly sugar taste overwhelming all the other ingredients.
Low-fat yogurt (which I have compared unfavorably to a Snickers Bar here) tastes like pure sugar mixed with odd chemicals and a vague dairy flavor.
Seemingly healthy sushi tastes too sweet to me as it turns out to have lots of sugar mixed in the rice and the popular eel sauce is mostly made up of sugar.
Most annoying is the current trend for restaurants to put a “balsamic glaze” loaded with sugar on perfectly good vegetables like brussel sprouts, ruining them for me.
Fructose and Processed Foods
A review article in the Mayo Clinic Proceedings (1) this month presents the case for fructose (from glucose and high-fructose corn syrup) being the major cause of our obesity and diabetes epidemics and thus, the major contributor to cardiovascular disease in the US.
Fructose is a monosaccharide that combines with the monosaccharide glucose to form sucrose, which is what most people recognize as sugar.
Processed foods commonly contain a lot of added fructose-containing sugar but also, increasingly they contain high fructose corn syrup (HFCS) which contains up to 65% fructose.
Large intake of fructose goes hand in hand with consumption of processed foods. Approximately 75% of all foods and beverages in the US contain added sugars. Consumption of added sugar by Americans increased from 4 lbs per person per year to 120 lbs per person per year between 1776 and 1994.
Thanks to a dramatic increase in sugar-sweetened beverages, American teenagers consume about 72 grams of fructose daily.
There are a substantial amount of observational, short-term basic science, and clinical trial data suggesting that all this added sugar, especially fructose, are posing a serious public health problem.
The article presents these data in detail and I’ll summarize the major points as follows:
Fructose is the likely component of sucrose and HFCS that promotes insulin resistance.
In animals and humans, replacement of starch (chains of glucose) with sucrose or fructose causes increase glucose and insulin levels and reduced insulin sensitivity.
Fructose stimulates epigenetic changes and metabolic alterations that shunt calories into storage depots in abdominal fat cells.
In simpler language, fructose promotes abdominal fat build-up and makes you more likely to develop type 2 diabetes.
Fruits and Fructose
I’m sure many of you are thinking, “but fructose is the major sugar in fruit, should I stop eating fruit?”
The answer is NO! The fructose in fruit is not highly concentrated. Fructose makes up 1% of the weight of a pear for example. It is combined with all of the good things, including fiber and phytonutrients and vitamins, that make fruit good for you.
Eliminating added fructose (sugar and HFCS) is by far the simplest thing you can do diet wise to improve your health. If you avoid added fructose, you will be cutting out a lot of the processed foods and sugar-sweetened beverages which have no nutritional value but contribute to obesity and diabetes.
Fructose as Toxin
Robert Lustig, a pediatric endocrinologist has talked and written extensively about fructose as a “toxin.” You can watch him here. He’s also published a lot of books on the topic including one which identifies the 56 names under which sugar masquerades.
It’s probably not worth buying that book, but keep in mind that agave and evaporated cane juice are just different forms of sugar. Makers of organic and “natural” foods are as guilty as food industry giants at adding sugar, but they try to pretend that “natural” sources of sugar are somehow better for you.
I don’t think the science on fructose is totally settled, however, and another recent review (from scientists not funded by the food industry) concluded:
“current evidence on the metabolic effects of fructose, as consumed by the majority of populations, is insufficient to demonstrate such a role in metabolic diseases and the global obesity epidemic”
Anthony C. Pearson, MD, FACC
1. Added Fructose: A Principal Driver of Type 2 Diabetes Mellitus and Its Consequences. Mayo Clin Proc. 2015:90(3);372-381. DiNicolantonio, JJ, O’Keefe, JH and Lucan SC
Yes. PCSK9 is a factor in escalating LDL cholesterol levels. The point was brought home as I rode the escalator up from the first to the top floor of the San Diego Convention Center at this year’s American College of Cardiology meetings. I suspsect if I had taken an elevator I would have seen a sign proclaming that PCSK9 is a factor in elevating cholesterol levels.
And PCSK9 signage is everywhere in this meeting.
Proprotein convertase subtilisin/kexin type 9, also known as PCSK9, is an enzyme that appears to degrade LDL receptors.
If you are born with a mutation that produces less active PCSK9 you have more LDL receptors and consequently more LDL is taken out of circulation leading to lower LDL levels.
Mutations leading to gain of PCSK9 function result in lower LDL receptors, higher LDL levels and substantial clinical evidence for premature atherosclerosis.
Amgen has produced all the PCSK9 signs that abound at the ACC meetings because they have produced a fully humanized monoclonal antibody (utilizing Chinese hamster ovaries) that inhibits PCSK9 and does a great job of lowering LDL without significant adverse effects.
At a late-breaking clinical trial session, results of longer term follow up of the company’s Osler randomized trials were presented and simultaneously published here.
The results were remarkably good. Not only did evolocumab drop LDL by 61% (from 120 down to 48) it showed significant improvement in cardiovascular outcomes.
“The rate of cardiovascular events at 1 year was reduced from 2.18% in the standard-therapy group to 0.95% in the evolocumab group (hazard ratio in the evolocumab group, 0.47; 95% confidence interval, 0.28 to 0.78; P=0.003).”
According to the biotech website fiercebiotech:
“The antibody is expected to win FDA approval by Aug. 27, trailing Sanofi ($SNY) and Regeneron’s ($REGN) alirocumab, which, thanks to some regulatory opportunism, is likely to hit the market a month or so before. Pfizer ($PFE) is in third place, working through Phase III with its bococizumab. Analysts say each treatment could bring in more than $3 billion a year at its peak…”
More study is needed of these drugs before approval in my opinion for a number of reasons. There is evidence of a small, but significant increase in neurocognitive side effects for one.
Although with evolocumab these were not related to the level of LDL achieved, there are concerns that extremely low LDL levels may interfere with neural development and such effects may not manifest for years.
The study authors did a good job of pointing out other limitations including small number of events, open-label design and patients selected who were free of adverse events. Hopefully, the FOURIER study will resolve these issues.
This post was also posted at SERMO, the physician social network. I would encourage physicians to join in the robust discussions on medicine and other topics at this site.