The 2015-2020 Dietary Guidelines for Americans (DGA) have finally been released and I’m sure that most of you could care less what they say. You may think that they can’t be trusted because you believe the original science-based recommendations have been altered by political, food and agribusiness forces. Perhaps you don’t trust science to guide us in food choices. Perhaps, like the skeptical cardiologist, you realize that the DGA has created, in the past, more problems than they have corrected.
This time, the skeptical cardiologist believes they have made a few strides forward, but suffer from an ongoing need to continue to vilify all saturated fats.
As such, the DGA no longer lists a recommended limit on daily cholesterol consumption (step forward) but persists in a recommendation to switch from full fat to non fat or low fat dairy products, which is totally unsubstantiated by science, (see my multiple posts on this topic here).
By now you should have gotten the message that a healthy diet consists of lots of fruits, vegetables, nuts, legumes, fish, olive oil and whole grains. The DGA emphasizes this.
There is general consensus that processed foods and added sugar should be limited.
Most of the controversy is about what to limit and how much to limit foods that are considered unhealthy.
Red meat and processed meat remain in the crosshairs of the DGA (although not stated explicitly), but eggs and cholesterol have gotten a pass, something which represents a significant change for the DGA and which I have strongly advocated (here and here).
But hold on, my professional organization, the American College of Cardiology says otherwise.
Misleading Information From the American College of Cardiology
The American College of Cardiology sent me an email and posted on their website the following horribly misleading title:
The first paragraph of the ACC post reads as follows:
“Physiological and structural functions of the body do not require additional intake of dietary cholesterol according to the 2015 Dietary Guidelines released on Jan. 7 by the U.S. Departments of Health and Human Services (HHS) and of Agriculture (USDA). As such, people should practice healthy eating patterns consuming as little dietary cholesterol as possible. – ”
While technically these statements can be found in the document (by digging way down) the executive summary (infographic below) says nothing about limiting cholesterol.
The “Key Recommendations” list eggs as included under a “healthy eating pattern” along with other protein foods.
In addition, there is no mention of cholesterol under what a healthy pattern limits.
In the same section on cholesterol that the ACC inexplicably has chosen to emphasize, is this sentence:
“More research is needed regarding the dose-response relationship between dietary cholesterol and blood cholesterol levels. Adequate evidence is not available for a quantitative limit for dietary cholesterol specific to the Dietary Guidelines.”
So the DGA recommends no specific limit on dietary cholesterol.
This is consistent with what the DG advisory committee recommended when they wrote “dietary cholesterol is no longer a nutrient of concern.”
The DGA goes on to state:
“A few foods, notably egg yolks and some shellfish, are higher in dietary cholesterol but not saturated fats. Eggs and shellfish can be consumed along with a variety of other choices within and across the subgroup recommendations of the protein foods group.”
The Vegan Agenda
I have a theory on why the ACC went so wildly astray in reporting this information: they are led by a vegan.
The current president of the ACC, Kim Williams, is an evangelical vegan, unrepentant, as this NY times article points out. Apparently, he tries to convert all his patients to the “plant-based diet.”
He is quoted extensively in the ACC blurb on the DGA and is clearly attempting to put a bizarre vegan spin on the new guidelines, ignoring the evidence and the progressive shift from the 2010 guidelines.
Can any information from the ACC be trusted if such basic and important science reporting was so heavily distorted by its President?
No wonder Americans tune out dietary advice: it can so easily be manipulated by those with an agenda.
Why is death from coronary heart disease declining in the US at the same time that obesity and diabetes rates are climbing?
Two editorials recently published in The Lancet show the widely varying opinions on the optimal diet for controlling obesity , diabetes and coronary heart disease that experts on nutrition, diabetes and heart disease hold.
The first paper contains what I would consider the saturated fat “traditionalist” viewpoint. This is a modification of the misguided concept that was foisted on the American public in the 1980s and resulted in the widespread consumption of industrially produced trans-fats and high sugar junk food that was considered heart healthy.
The traditionalists have shifted from condemning all fats to vilifying only saturated and trans fats. They would like to explain at least part of the reduction in coronary heart mortality as due to lower saturated fat consumption and the accompanying lowering of LDL (“bad”) cholesterol.
The SFA traditionalists fortunately are in decline and more and more in the last five years, prominent thinkers, researchers and scientists working on the connection between diet and the heart believe saturated fats are neutral but sugar and refined carbohydrates are harmful in the diet.
Darius Mozzafarian, a highly respected cardiologist and epidemiologist, who is dean of the School of Nutrition Science and Policy at Tufts, wrote the second editorial and is what I would term a saturated fatty acid (SFA) progressive.
He makes the following points which are extremely important to understand and which I have covered in previous posts. I’ve included his supporting references which can be accessed here.
Fat Doesn’t Make You Fat, Refined Starches And Sugar Do
"Foods rich in refined starches and sugars—not fats—seem to be the primary culprits for weight gain and, in turn, risk of type 2 diabetes. To blame dietary fats, or even all calories, is incorrect
Although any calorie is energetically equivalent for short-term weight loss, a food's long-term obesogenicity is modified by its complex effects on satiety, glucose–insulin responses, hepatic fat synthesis, adipocyte function, brain craving, the microbiome, and even metabolic expenditure Thus, foods rich in rapidly digestible, low-fibre carbohydrates promote long-term weight gain, whereas fruits, non-starchy vegetables, nuts, yoghurt, fish, and whole grains reduce long-term weight gain.1, 2, 3
Overall, increases in refined starches, sugars, and other ultraprocessed foods; advances in food industry marketing; decreasing physical activity and increasing urbanisation in developing nations; and possibly maternal–fetal influences and reduced sleep may be the main drivers of obesity and diabetes worldwide".
There Are Many Different Kinds of Saturated Fats With Markedly Different Health Effects: It Makes No Sense to Lump Them All Together
"SFAs are heterogeneous, ranging from six to 24 carbon atoms and having dissimilar biology. For example, palmitic acid (16:0) exhibits in vitro adverse metabolic effects, whereas medium-chain (6:0–12:0), odd-chain (15:0, 17:0), and very-long-chain (20:0–24:0) SFAs might have metabolic benefits.4 This biological and metabolic diversity belies the wisdom of grouping of SFAs based on a single common chemical characteristic—the absence of double bonds. Even for any single SFA, physiological effects are complex: eg, compared with carbohydrate, 16:0 raises blood LDL cholesterol, while simultaneously raising HDL cholesterol, reducing triglyceride-rich lipoproteins and remnants, and having no appreciable effect on apolipoprotein B, 5 the most salient LDL-related characteristic. Based on triglyceride-lowering effects, 16:0 could also reduce apolipoprotein CIII, an important modifier of cardiovascular effects of LDL and HDL cholesterol. SFAs also reduce concentrations of lipoprotein(a) ,6 an independent risk factor for coronary heart disease."
The Effects of Dietary Saturated Fats Depend on Complex Interactions With The Other Ingredients in Food
"Dietary SFAs are also obtained from diverse foods, including cheese, grain-based desserts, dairy desserts, chicken, processed meats, unprocessed red meat, milk, yoghurt, butter, vegetable oils, and nuts. Each food has, in addition to SFAs, many other ingredients and characteristics that modify the health effects of that food and perhaps even its fats. Judging the long-term health effects of foods or diets based on macronutrient composition is unsound, often creating paradoxical food choices and product formulations. Endogenous metabolism of SFAs provide further caution against oversimplified inference: for example, 14:0 and 16:0 in blood and tissues, where they are most relevant, are often synthesised endogenously from dietary carbohydrate and correlate more with intake of dietary starches and sugars than with intake of meats and dairy.4"
Dietary Saturated Fat Should Not Be a Target for Health Promotion
"These complexities clarify why total dietary SFA intake has little health effect or relevance as a target. Judging a food or an individual's diet as harmful because it contains more SFAs, or beneficial because it contains less, is intrinsically flawed. A wealth of high-quality cohort data show largely neutral cardiovascular and metabolic effects of overall SFA intake.7 Among meats, those highest in processing and sodium, rather than SFAs, are most strongly linked to coronary heart disease.7Conversely, higher intake of all red meats, irrespective of SFA content, increases risk of weight gain and type 2 diabetes; the risk of the latter may be linked to the iron content of meats.2, 8 Cheese, a leading source of SFAs, is actually linked to no difference in or reduced risk of coronary heart disease and type 2 diabetes.9, 10 Notably, based on correlations of SFA-rich food with other unhealthy lifestyle factors, residual confounding in these cohorts would lead to upward bias, causing overestimation of harms, not neutral effects or benefits. To summarise, these lines of evidence—no influence on apolipoprotein B, reductions in triglyceride-rich lipoproteins and lipoprotein(a), no relation of overall intake with coronary heart disease, and no observed cardiovascular harm for most major food sources—provide powerful and consistent evidence for absence of appreciable harms of SFAs."
Dietary Saturated Fats May Raise LDL cholesterol But This Is Not Important: Overall Effects On Obesity and Atherosclerosis Are What Matters
"a common mistake made by SFA traditionalists is to consider only slices of data—for example, effects of SFAs on LDL cholesterol but not their other complex effects on lipids and lipoproteins; selected ecological trends; and expedient nutrient contrasts. Reductions in blood cholesterol concentrations in Western countries are invoked, yet without systematic quantification of whether such declines are explained by changes in dietary SFAs. For example, whereas blood total cholesterol fell similarly in the USA and France between 1980 and 2000, changes in dietary fats explain only about 20% of the decline in the US and virtually none of that which occurred in France.11Changes in dietary fats11 simply cannot explain most of the reductions in blood cholesterol in Western countries—even less so in view of the increasing prevalence of obesity. Medication use also can explain only a small part of the observed global trends in blood cholesterol and blood pressure. Whether decreases in these parameters are caused by changes in fetal nutrition, the microbiome, or other unknown pathways remains unclear, thus highlighting a crucial and greatly underappreciated area for further investigation."
Dietary Saturated Fats Are Neutral For Coronary heart Disease Risk
Finally, SFA traditionalists often compare the effects of SFAs only with those of vegetable polyunsaturated fats, one of the healthiest macronutrients. Total SFAs, carbohydrate, protein, and monounsaturated fat each seem to be relatively neutral for coronary heart disease risk, likely due to the biological heterogeneity of nutrients and foods within these macronutrient categories.7Comparisons of any of these broad macronutrient categories with healthy vegetable fats would show harm,12 so why isolate SFAs? Indeed, compared with refined carbohydrates, SFAs seem to be beneficial.7
The overall evidence suggests that total SFAs are mostly neutral for health—neither a major nutrient of concern, nor a health-promoting priority for increased intake.
Focusing On Reducing Saturated Fats Leads To Unhealthy Dietary Choices
"Continued focus on modifying intake of SFAs as a single group is misleading—for instance, US schools ban whole milk but allow sugar-sweetened skim milk; industry promotes low-fat foods filled with refined grains and sugars; and policy makers censure healthy nut-rich snacks because of SFA content.13 "
It is extremely hard to change most people’s opinions on dietary fat.
My patients have been hearing the SFA traditionalist dogma for decades and thus it has become entrenched in their minds.
When I present to them the new progressive and science-based approach to fat and saturated fat some find it so mind boggling that they become skeptical of the skeptical cardiologist!
Hopefully, in the next few years, the progressive SFA recommendations will become the norm and maybe , some day in the not too distant future, the inexplicable recommendations for low-fat or non fat dairy will disappear.
As more data accumulates we may become SFA enthusiasts!
For another viewpoint (?from an SFA enthusiast) and a detailed description of both editorials see Axel Sigurdsson’s excellent post here.
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.
A year ago one of my patients began experiencing chest pain when he walked up hills. Subsequent evaluation revealed that atherosclerotic plaque (95% narrowing of a major coronary artery ) was severely reducing the blood flow to his heart muscle and was the cause of his chest pain. When this blockage was opened up with a stent he no longer had the pain.
Along with other medications (aspirin and plavix to keep his stent open) I had him start atorvastatin, the generic version of Lipitor, a powerful statin drug that has been shown to prevent progression of atherosclerotic plaque and thereby reduce subsequent heart attacks, strokes and death in patients like him
I saw him in the office the other day in follow up and he was feeling great . He asked me “Doc I read your post yesterday.s Since you say that cholesterol in the diet doesn’t matter anymore, does that mean I don’t have to take my cholesterol drug anymore.?”
His question gets at the heart of the “diet-heart hypothesis”. The concept that dietary modification, with reduction of cholesterol and fat consumption can reduce coronary heart disease.
The science supporting this hypothesis has never been strong but the concept was foisted on the American public and was widely believed. It was accepted I would say because it has a beautiful simplicity which can be summarized as follows:
“If you eat cholesterol and fat it will enter your blood stream and raise cholesterol levels. This excess cholesterol will then deposit in your arteries, creating fatty plaque , clogging them and leading to a heart attack.”
This concept was really easy to grasp and simplified the public health recommendations.
However, cholesterol blood levels are determined more by cholesterol synthesized in the liver and predicting how dietary modifications will effect these levels is not easy.
Since the public has had the diet-heart hypothesis fed to them for decades and given its beautiful simplicity it is hard to reverse this dogma. My patient’s question reflects a natural concern that if science/doctors got this crucial question so wrong, is everything we know about cholesterol treatment and heart disease wrong?
In other words, are doctors promoting a great cholesterol hoax?
Evidence Strongly Supports Statins in Secondary Prevention
For my patient the science supporting taking a cholesterol-lowering statin drug is very solid. There are multiple excellent studies showing that in patients with established coronary artery disease taking a statin drug substantially reduces their risk of heart attack and dying.
These studies are the kind that provide the most robust proof: randomized, prospective and blinded.
When cardiologists rate the strength of evidence for a certain treatment (as done for lifestyle intervention here) we use a system that categorizes the evidence as Level A, B, or C quality.
LeveleA quality (or strong) evidence consists of multiple,large, well-done, randomized trials such as exist for statins in patients with coronary heart disease.
Level B Evidence comes from a single randomized trial or nonrandomized studies.
Level C evidence is the weakest and comes from “consensus opinion of experts, case studies or standard of care.”
When treatment recommendations are based on Level C evidence they are often reversed as more solid data is obtained. Level A recommendations almost always hold up over time.
The level of evidence supporting restricting dietary cholesterol and fat to reduce heart attacks and strokes has always been at or below Level C and now it is clear that it is insufficient and should be taken out of guideline recommendations.
Evidence Strongly Supports Atherogenic Cholesterol is Related to Coronary Heart Disease
There are other lines of evidence that strongly support the concept that LDL cholesterol (bad cholesterol) or an atherogenic form of LDL cholesterol is strongly related to the development of atherosclerosis. If you are born with really high levels you are at very high risk for coronary heart disease, conversely if you are born with mutations that cause extremely low levels you are highly unlikely to get coronary heart disease.
Thus, the cholesterol hypothesis as it relates to heart disease is very much till intact although the diet-heart hypothesis is not.
Conflating the Diet-Heart Hypothesis and the Cholesterol Hypothesis
There is an abundance of misinformation on the internet that tries to conflate these two concepts. Sites with titles like “The Great Cholesterol Lie” , “The” Cholesterol Hoax”, The Cholesterol Scam” abound .
These sites proclaim that cholesterol is a vital component of cell membranes (it is) and that any attempt by diet or drugs to lower levels will result in severe side effects with no benefit
Doctors, according to these types of sites, in collusion with Big Pharma, have inflated the benefits of statin drugs and overlooked the side effects in the name of profit. Often, a “natural” alternative to statins is promoted. In all cases a book is promoted.
The Great Cholesterol Truths
It’s unfortunate that nutritional guidelines have promoted restriction of cholesterol and fat for so long. These guidelines (like most of nutritional science) were based on flawed observational studies. They should not have been made public policy without more consensus from the scientific community. The good news is that ultimately the truth prevails when enough good scientific studies are done.
It is right to question the flimsy foundation of nutritional recommendations on diet and heart disease but the evidence for statin benefits in patients with established coronary heart disease is rock solid.
Hopefully, the less long-winded explanation I provided my patient in the office will persuade him to keep on taking his atorvastatin pills while simultaneously allowing him to eat eggs, shrimp and full fat dairy without guilt.
The other night I had the best cioppino I have ever had. I’ve had variations of this wonderful tomato-based seafood stew all over the world (including the legendary bouillabaisse in Marseilles) but I left my heart with the Dungeness crab cioppino served at Sotto Mare Oysteria and Seafood restaurant in North Beach, San Francisco. It makes sense, since cioppino was invented by Genoan fishermen from the SF Bay Area in the 19th century who threw together the freshest catch from their day at sea.
The recipe for Sotto Mare’s cioppino is actually available online as follows:
¼ cup olive oil
1 tsp. crushed red chile flakes
8 cloves garlic, finely chopped
3 cups fish stock
1 ½ cups whole peeled tomatoes in juice, crushed
10 leaves basil
1 lb. cod, cut into 2″ chunks
1 lb. cleaned calamari, bodies cut into ½″-wide rings
12 oz. medium shrimp, deveined
12 oz. bay scallops
16 clams, cleaned
16 mussels, cleaned
2 2-lb. Dungeness crabs or snow crab legs, halved
Kosher salt and freshly ground black pepper, to taste
It involves a lot of shellfish: calamari, shrimp, scallop, clams, mussels, crabs and I think a large part of what made it so good was the freshness of the shellfish obtained from the nearby Pacific Ocean.
Shellfish, Dietary Cholesterol and Cardiovascular Risk
Shellfish contain a lot of cholesterol and many of my patients have been told to minimize or avoid shellfish, especially shrimp, due to concerns they will exceed the (completely arbitrary) 300 mg daily limit suggested by the American Heart Association and the USDA nutritional guidelines.
There is no scientific basis for being concerned about the amount of cholesterol one consumes when eating shellfish (or for any food for that matter, as I previously wrote about with regard to eggs here)
But there are definitely warnings out there on the internet and traditional new media from seemingly responsible authorities.
“Since our bodies make plenty of cholesterol for our needs,we do not need to add any in our diet. Cholesterol is found in all foods that come from animals: red meat, poultry, fish, eggs, milk, cheese, yogurt, and every other meat and dairy product. Choosing lean cuts of meat is not enough; the cholesterol is mainly in the lean portion. Many people are surprised to learn that chicken contains as much cholesterol as beef. Every four-ounce serving of beef or chicken contains 100 milligrams of cholesterol. Also, most shellfish are very high in cholesterol. All animal products should be avoided for this reason. “
The Physician Committee for Responsible Medicine appears to be a front for vegan-promotion. They go on to state that every 100 mg of cholesterol you consume raises your cholesterol by 5 mg/dl and that
“Every time you reduce your cholesterol level by 1 percent, you reduce your risk of heart disease by 2 percent. For example, a reduction from 300 mg/dl to 200 mg/dl (i.e., a one-third reduction) will yield a two-thirds reduction in the risk of a heart attack”
A Fox News publication simultaneously extolls the virtues of shrimp consumption (noting that “three ounces of shrimp (or about seven medium-sized shrimp) has a mere 84 calories, 1g of fat, and an impressive 18g of lean protein” and that they are a great source of selenium, “an antioxidant that fights cancer-causing free radicals in your body”) and warns you against eating it (“If you are watching your cholesterol, it’s best to go easy on shrimp because four large shrimp have 42.5mg of cholesterol”)
Other publications advise those with high cholesterol or higher risk of heart disease to choose low-cholesterol varieties of shellfish over shrimp.
The Science Supporting Shrimp
Let’s look at what is actually known about consuming shrimp and shellfish.
A study of over 13,000 subjects (the ARIC study) found no increased risk of cardiovascular disease in the high shellfish consumers versus the low shellfish consumers.
A study in 1996 compared consuming a diet with 300 grams (about 10 oz.) of steamed shrimp/day (providing 590 mg of cholesterol daily) versus a baseline diet of 107 mg/ cholesterol in 18 individuals without cholesterol problems. The shrimp consumers compared to baseline had a 7% higher LDL or bad cholesterol but a 12% higher HDL or good cholesterol. Thus, the ratio of total to good cholesterol went down. We now know that this ratio is a much more important risk marker for cardiovascular disease than the total cholesterol. Triglycerides dropped significantly when subjects were consuming shrimp versus the baseline, low cholesterol diet.
A 1990 study looked at multiple different types of shellfish substituted for meat, cheese and eggs, and found that oyster, clam, crab and mussel diets (with lower cholesterol and higher omega-3 fatty acid profiles) lowered VLDL triglycerides and VLDL cholesterol. These shellfish diets, except for the mussel diet, also lowered LDL and total cholesterol. Shrimp and squid had no effect on the lipid profiles.
Benefits of Shrimp and Shellfish Consumption
I’ve focused on shrimp in this post because it has the highest cholesterol content of all shellfish and therefore is the most likely to be considered bad for heart patients or patients with high cholesterol. I’m presuming if I can convince you that shrimp are heart healthy, then you will believe that all shellfish are.
Take a look at this chart of the nutrient composition of shrimp and you can understand that, once you eliminate unsubstantiated fears of the cholesterol content, this a great food.
I am not a big advocate of examining the macronutrient composition of foods in order to predict their health benefits. This approach to nutritional science resulted in the development of highly processed low-fat monstrosities that currently sit in boxes and bags and line the most prominent parts of supermarket shelves. The overall effect of foods on the cardiovascular system depends on an incredibly complicated interaction of food components, bacteria in the gut and genetic predispositions: areas we are only beginning to understand. However, for those readers who are concerned about such things there is reassurance.
Start with the fact that there are no carbohydrates in shellfish: since carbs and added sugar are likely the biggest culprits in our obesity epidemic, shrimp and shellfish are great tools in helping to manage weight. Shrimp have a very high percentage and quality of protein content for muscle building.
Some avid shrimp promoters insist that shrimp should be consumed regularly to reduce the risk of both cancer and heart disease. The fat in shrimp is mostly polyunsaturated fat with a high ratio of omega-3 to omega-6 which is considered optimal . Eating 100 ounces of shrimp daily gives you 180 mg of EPA and DHA (considered the most important of the omega-3 fish oils for heart health) daily, close to the 250 mg daily the USDA recommends for most adults.
Astaxanthin has been found to be a potent natural antioxidant, exceeding ten times the antioxidant activity of β-carotene and 500 times that of α-tocopherol. The astaxanthin level of wild shrimps has been reported to vary between 740 and 1400 μg/100 g in edible meat portions.
If I were a vegan or vegetarian I would consider slipping shrimp into my dishes instead of tofu.
The cioppino recipe above doesn’t add a lot to the shellfish and fish: a little olive oil and tomatoes, basil and garlic-these things are not going to jack up the calories, sugar or fat content.
Depending on how you cook shrimp, the resulting dish will have markedly different nutrient composition compared to the raw nutrients listed above.
Breading and deep frying the shrimp takes 3 oz from 60 calories to 206 and the fat grams from 1 to 10. I suspect that you or your body will figure this out and eat less later. Given the fairly low fat and carbohydrate content of the Sotto Mare cioppino, I am ashamed to admit, I ate that whole bowl pictured above (which the menu said could be shared between two).
The SOSC doesn’t share my love of cioppino; she ordered the linguine with clam sauce. Three ounces of clams have only 26 mg of cholesterol but it seems to me the majority of calories in this dish are coming from the carbs in the pasta and whatever the composition of the sauce is. In any event, the SOSC pronounced it the best she has ever had.
Mercury in Shellfish
The level of mercury is a concern in all the fish that we consume. Fortunately a recent study from Maine University found that shrimp is very low in mercury. This included varieties from Thai shrimp farms, Maine shrimp farms and the Gulf of Mexico. In comparison to other types of fish, shellfish are universally on the low end of the mercury level graph as shown below.
Fear neither the cholesterol nor the mercury in shrimp and consume your cioppino with gusto and without guilt!
The updated AHA/ACC Cardiovascular Prevention Guidelines (CPG) which include the excessively wordy “The Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults Risk” were published late last year and immediately were the center of controversy.
After working with them for 9 months and using the iPhone app to calculate my patients’ 10 year risk of atherosclerotic cardiovascular disease (ASCVD, primarily heart attacks and strokes) it has become clear to me that the new guidelines will recommend statin therapy to almost all males over the age of 60 and females over the age of 70.
As critics have pointed out, this immediately adds about 10 million individuals to the 40 million or so who are currently taking statins.
Should we be starting all elderly Americans on statin drugs?
My simple answer is no. It doesn’t make sense to do this, because clearly not all elderly individuals have atherosclerosis or will ever develop its consequences of heart attack and stroke. Many have inherited the genes that allowed their parents to live free of heart disease into their 90s and will not benefit at all from long term statin therapy; they may actually suffer the expense and side effects instead.
How can we better decide who among the elderly will benefit from statin therapy?
If you have read my previous posts on searching for subclinical atherosclerosis here and here you probably know the answer. Let’s look at a specific case and apply those principles.
Robert is 69 years old. I see him because, in 2010, the posterior leaflet of his mitral valve ruptured, resulting in the mitral valve becoming severely incompetent at its job of preventing back flow from the left ventricle into the left atrium. I sent him to a cardiac surgeon who repaired the ruptured leaflet. Although he has a form of “heart disease,” this is a form that has nothing to do with cholesterol, hypertension or diabetes and is not associated with ASCVD.
However, it is my job to assess in him, like all individuals, the risk of developing coronary heart disease or ASCVD.
He has no family history of ASCVD and he feels great since the surgery, exercising aerobically 4-5 times per week.
His BMI is 23.87 which is in the normal range. His BP runs 116/80.
His total cholesterol is 210 and LDL or bad cholesterol is 142. Good or HDL cholesterol is 56 and triglycerides 59. The total and LDL cholesterol levels are considered “high,” but they could be perfectly acceptable for this man.
When I ran his 10 year ASCVD risk (risk of developing a heart attack or stroke over the next 10 years), it came back as 14%. The new guidelines would suggest having a conversation with him about starting a statin if his risk is over 7.5%. His risk is double this and statins are definitely recommended in this intermediate risk range. Interestingly, I cannot enter a cholesterol level or blood pressure for a man of this age that yields a risk less than 7.5%.
When I had my discussion with him about his risk for ASCVD, I plugged his numbers into my iPhone and showed him the results and gave him the guideline recommendation.
Lifestyle Changes to Lower Cholesterol
The new Cardiovascular Prevention Guidelines have a section devoted to Lifestyle Management to Reduce Cardiovascular Risk. Unfortunately, none of the lifestyle changes they recommend have been shown to reduce ASCVD risk in an individual like Robert. He already exercises the recommended amount, is at his ideal body weight and eats a healthy diet. If we were to tighten up on his diet by, say reducing red meat, eggs and high fat dairy, all we would accomplish would be to lower his LDL and HDL cholesterol levels and make his life and meals less satisfying. The lower total cholesterol and LDL cholesterol would not lower his risk of ASCVD and the calculated 10 year ASCVD risk would still be in the range where statins are recommended.
Therefore, I am not going to tell Robert that he should reduce his saturated fat consumption (he already has incorporated that into his diet since he’s been bombarded with the low fat mantra for 30 years).
Searching for Subclinical Atherosclerosis
I’m going to tell Robert that we need to know if he has atherosclerosis, the disease that we are attempting to modify.
We started with an ultrasound to look at the lining of the large arteries in his neck that supply blood to the brain, the carotid arteries (a process I describe in more detail here). Although severe atherosclerotic blockages in these arteries put one at risk of a stroke, I was much more interested in the subtle changes in the arteries that precede symptoms and are an early harbinger of atherosclerosis.
Careful ultrasound recording and measurement of the main common carotid arteries from both the left and right side showed that the IMT or thickness was lower than average for his age, gender and ethnicity. His carotid IMT was at the average for a 60 year old, therefore, his so-called vascular age was 60 years, younger than his chronological age. If I plug that age into the ASCVD risk estimator, I get an 8.2% 10 year risk, just barely above the statin treatment cut-off.
Careful scrutiny with ultrasound of the entire visible carotid system in the neck on both sides did not reveal any early fatty plaques or calcium in the lining of the carotid arteries. He had no evidence for atherosclerosis, even very subtle early forms, in this large artery, a finding which is usually predictive of what is going on in the other large arteries in the body, including the coronary arteries, which supply blood to the heart.
At this point, I think, we could have stopped the search for subclinical atherosclerosis and agreed that no statin therapy was warranted. However, Robert wanted further reassurance that his coronary arteries were OK, therefore we set him up with a coronary calcium study (see my full description of this test here).
Searching for Subclinical Atherosclerosis: The Calcium Score
Robert’s coronary calcium score came back at 21 (all in the LAD coronary artery) , which put him at the 26th percentile compared to normal men of his age and gender. A score of 21 is average for a 59 year old man and 82% of men aged 69 have a score greater than zero. Robert had much less calcium in his coronaries than men his age, another factor putting him in a low risk category.
Given the low risk findings from both the vascular screening and the coronary calcium, I felt comfortable recommending no statin therapy and going against the guidelines.
Statins: Better Targets for The Two-edged Sword
This is not an unusual scenario; many of my older patients without heart attacks, strokes or diabetes fall into the risk category that would warrant statin therapy and if they have no clinical or subclinical evidence of atherosclerosis, I don’t advise statin therapy. My patients are free to follow the guidelines and take statin drugs after this advice, but most are very grateful that another pill (which they likely have heard bad things about on the internet or from friends with adverse experiences) can be avoided.
Statins are wonderful drugs when utilized in the right population, but they also carry a 9% increased risk of diabetes and about a 10% real world risk of developing muscle aches and weakness (myalgia).
I think it is essential to aim these two-edged swords at the right targets if we are to maximize the overall health benefits.
For most of the last 25 years I have told patients when I recommend a statin drug to them that they should take it in order to lower their bad cholesterol (and raise the good cholesterol) thereby lowering their risk of future heart attacks.
I based this statement on my understanding of large statin trials which demonstrated reduction in heart attacks seemingly closely tied to drops in the bad cholesterol level.
Although I was aware of the so-called “pleiotropic” (meaning effecting multiple pathways leading to atherosclerosis) of statins it was easier to point to the cholesterol lowering effects and unify that message with the recommendation to reduce fat and cholesterol in the diet , thereby lowering cholesterol in the blood and arteries and cut heart attack risks.
Thus emerged a very simple (and likely false) paradigm: Fat in the diet causes fat in the blood which causes fat in the arteries which causes fatty plaques in the coronary arteries which causes heart attacks when they get too big and block off the blood flow.
I, like most cardiologists and lay people mistakenly assumed that since lower bad cholesterol levels associated with taking a statin drug were associated with lower heart attack risks then dietary changes aimed at lowering bad cholesterol levels would also lower heart attack risk.
It turns out that we don’t really know how the statins reduce heart attacks . As a recent review points out:
some of the cholesterol-independent or “pleiotropic” effects of statins involve improving endothelial function, enhancing the stability of atherosclerotic plaques, decreasing oxidative stress and inflammation, and inhibiting the thrombogenic response. Furthermore, statins have beneficial extrahepatic effects on the immune system, CNS, and bone. Many of these pleiotropic effects are mediated by inhibition of isoprenoids, which serve as lipid attachments for intracellular signaling molecules. In particular, inhibition of small GTP-binding proteins, Rho, Ras, and Rac, whose proper membrane localization and function are dependent on isoprenylation, may play an important role in mediating the pleiotropic effects of statins.
Supporting the non cholesterol lowering effects of statins on reducing CVD are the following observations
-Most heart attack victims don’t have elevated bad cholesterol levels and dietary reduction of bad cholesterol doesn’t seem very effective at preventing heart attacks.
-Drugs, like Zetia or ezetimibe which lower cholesterol level by other mechanisms don’t seem to prevent atherosclerosis even though they substantially lower bad cholesterol levels.
-Statin drugs reduce heart attacks in patients who have normal or low bad cholesterol levels
What Causes Atherosclerosis?
An article (Innate and adaptive inflammation as a Therapeutic Target in Vascular Disease) published in JACC recently by Tousoulis,et al. summarizes the current understanding of how atherosclerosis develops and the multiple ways that statins may affect that process. They write
Atherosclerosis, once thought to be a lipid storage disease, is now considered a chronic low-grade inflammatory condition that affects the vascular wall. It is characterized by the deposition of cholesterol and lipids followed by infiltration of T cells and macrophages, all as a result of an endothelial injury response.
I’m including this figure from the article to give you some idea of how incredibly complicated the process is.
Can you imagine trying to explain this to the average patient?
My eyes glazed over once I reached MCP-1.
Thus, doctors end up giving the simple, accepted conventional wisdom that we are “treating” high cholesterol by giving statin drugs. What we are really treating is atherosclerosis. And statins are the only effective drug treatment we have identified for this ubiqitous and complex process.
It is entirely possible that the lower LDL cholesterol caused by statin drugs is totally unrelated to their ability to forestall atherosclerosis. The new cholesterol guidelines reflect this concept as they don’t recommend treating to an LDL target level.
I end with the closing comments from the article by Tousoulis, et al.
Given the fact that atherosclerosis is a multivariable disease, with several molecules involved in each stage, it is vey difficult to find an effective treatment. However, statins prove to be the most effective treatment so far because they interfere with most of the critical components of the atherosclerotic process and have been proven to have beneficial effects. Further to their well-established impact on nonspecific low-grade inflammation, statins also appear to have significant effects on innate and adaptive immunity that have been underestimated so far.
A number of readers of The Skeptical Cardiologist have pointed out to me that Time Magazine’s latest issue has a picture of butter on the cover with the headline “Eat Butter. Scientists labeled fat the enemy. Why they were wrong.”
The lead article summarizes a lot of the evidence I have been writing about which suggests that saturated fat has been inappropriately vilified (here) and that added sugar and processed food may be the real root cause of the obesity epidemic (here).
It is well-written and reasonably balanced and has some catchy graphics. It doesn’t really specifically address issues with dairy fat or butter as the title implies. I have defended high fat dairy in numerous posts over the past two years.
Hopefully this article in a well-respected mainstream newsmagazine will help correct the misinformation about diet and nutrition that has become entrenched in the consciousness of Americans.
Ah Cheese. A most wondrous and diverse real food. Of the thousands of delightful varieties, let us consider Wensleydale, the 33rd type of cheese requested by John Cleese of Ye Olde Cheese Emporium proprietor, Henry Wensleydale (Purveyor of Fine Cheese to the Gentry and the Poverty Stricken Too) in the Monty Python sketch, Cheese Shop.
The cheese I have in front of me from Wensleydale creamery (which owes its continued existence to being the favorite cheese of Wallace (of Wallace and Gromit fame)) lists the following ingredients:
pasteurized cow’s milk
annato (a natural coloring that gives cheese and other foods a bright orange hue. It comes from the Bixa orellana, a tropical plant commonly known as achiote or lipstick tree (from one of its uses))
Other than annato, the above ingredients are components of all cheese and signify that it is a non processed, nonindustrial product.
A 1 oz serving of this cheese (28 grams), like cheddar cheese (“the single most popular cheese in the world”), provides 110 calories, 80 of which are from fat (9 grams total fat, 6 grams saturated fat), 25 grams of cholesterol, 170 mg of salt and around 200 mg of calcium.
For the last 40 years, Americans have been mistakenly advised that all saturated fat in the food is bad and contributes to heart disease. Since cheese contains such a high proportion of saturated fat, it has also been targeted. Dietary recommendations suggest limiting real cheese consumption and switching to low-fat cheese.
This concept is not supported by any recent analysis of data, and as I’ve pointed out in a previous post, saturated fat does not contribute to obesity, nor is it clearly associated with increased heart disease risk. There are many different saturated fats and they have varying effects on putative causes of heart disease such as bad/good cholesterol and inflammation. In addition, the milieu in which the fats are consumed plays a huge role in how they effect the body.
Cheese vary widely in taste, texture and color and the final ingredients depend on a host of different factors including:
the type of animal milk used
the the diet of the animal
the amount of butterfat
whether the product is pasteurized or not
the strain of bacteria active in the cheese
the strain of mold active in the cheese
As a result the bioactive ingredients in cheese will vary from type to type.
Recent scientific reviews of the topic note that dairy products such as cheese do not exert the negative effects on blood lipids as predicted solely by the content of saturated fat. Calcium and other bioactive components may modify the effects on LDL cholesterol and triglycerides.
In addition, we now know that the effect of diet on a single biomarker is insufficient evidence to assess CAD risk; a combination of multiple biomarkers and epidemiologic evidence using clinical endpoints is needed to substantiate the effects of diet on CAD risk.
Some points to consider in why dairy and cheese in particular are healthy:
Blood pressure lowering effects. Calcium is thought to be one of the main nutrients responsible for the impact of dairy products on blood pressure. Other minerals such as magnesium, phosphate and potassium may also play a role. Casein and whey proteins are a rich source of specific bioactive peptides that have an angiotensin-I-converting enzyme inhibitory effect, a key process in blood pressure control. Studies have also suggested that certain peptides derived from milk proteins may modulate endothelin-1 release by endothelial cells, thereby partly explaining the anti-hypertensive effect of milk proteins.
Inflammation and oxidative stress reduction. These are key factors in the development of atherosclerosis and subsequent heart disease and stroke. Recent animal and human studies suggest that dairy components including calcium and or its unique proteins, the peptides they release, the phospholipids associated with milk fat or the stimulation of HDL by lipids themselves, may suppress adipose tissue oxidative and inflammatory response.
Government and health organization nutritional guidelines have had a huge and harmful impact on what the food industry presents to Americans to eat. The emphasis on reducing animal fats in food led to the creation of foods laden with processed vegetable oils containing harmful trans-fatty acids. This mistake has been recognized and corrected, but the overall unsupported concept of replacing naturally occurring saturated fats with processed carbohydrates and sugar is ongoing and arguably the root of the obesity epidemic in America.
Converting mistaken nutritional guidelines into law
The USDA in 2012 following an act of Congress stimulated by Michelle Obama, changed the standards for the national school lunch and breakfast guidelines, for the first time in 15 years.
The law was intended to increase consumption of fruits, vegetables, whole grains and promote the consumption of low-fat or nonfat milk. It seemed like a good idea and likely to counter increasing obesity in children. However, the original recommendations were modified by Congress, due to heavy food industry lobbying, to allow the small amount of tomato paste in pizza to qualify as a vegetable.
Unfortunately, the food industry has responded by providing products which meet the government’s criteria for healthy lunches, but in actuality are less healthy.
Dominos Pizza, as a recent New York Times article pointed out, is now providing a specially modified pizza to schools which is unavailable in their regular stores. Their so-called “Revolution in School Pizza” is a…
line of delicious, nutritious pizzas created specifically for schools delivered hot and fresh from your local Domino’s Pizza store. Domino’s Pizza Smart Slice is the nutritious food that kids will actually EAT and LOVE!
This pizza, in contrast to the pizza sold in Domino’s stores, utilizes a “lite” Mozarella cheese to cut fat content, a pepperoni with lower sodium and fat content, and a crust that contains 51% whole grain flour.
This “smart slice” replaces dairy fat with carbohydrates; there is no evidence that this will improve obesity rate or reduce heart disease In fact, this change may lead to less satiety and a tendency for the children to want to snack on further carbohydrate or sugar-laden products when they get home. Furthermore, as critics have suggested, it may promote the consumption of “unhealthy” versions of pizza that are sold in stores.
If we are going to make laws that promote healthy eating, we have to be absolutely certain that they are supported by scientific evidence. These School Lunch Program Standards are an example of how getting the science wrong or getting ahead of the science can lead to worse outcomes than if there were no laws regulating school diets.
Hopefully, you will continue to consume real full-fat cheese without concerns that cheese is “artery-clogging” and you will be more successful in obtaining the “fermented curd” than John Cleese’s Mr. Mousebender was below:
I reviewed in a previous post the importance of detecting subclinical atherosclerosis when trying to assess someone’s risk of heart attack and of dying suddenly. Subclinical atherosclerosis refers to the build-up of plaque in the lining of our arteries which occurs long before any symptoms of atherosclerosis occur.
Since the process tends to be diffuse, occurring in all the large arteries of the body, it makes sense that if we can easily visualize one artery this will give us a window into what is happening in other arteries (including the coronary arteries supplying blood to the heart muscle).
The vascular screening I offer in my office uses high frequency ultrasound to image the large artery, the carotid artery, that supplies blood to the brain.
Normally the lining of that artery is smooth and thin as in the example to the left. As the process of atherosclerosis works its damage on the artery lining it becomes thicker and plaque begins to develop. High frequency ultrasound is an excellent tool for identifying these early, subclinical stages of atherosclerosis because it is painless, harmless, inexpensive, and quick.
Identifying Higher Risk Patients
Mr. M is a 60 year old man who I was seeing for an abnormal heart rhythm. Using the ACC risk estimator I calculated his 10 year risk of atherosclerotic cardiovascular disease (ASCVD) as <7.5%. However, he had a brother who had cardiac stents placed in his coronary arteries (indicating coronary artery disease (CAD)). His carotid artery screening (shown below) shows a large, soft plaque
This indicates that although his known risk factors for atherosclerosis were not tremendously high, the combination of known and unknown factors (likely genetic, given his brother’s premature CAD) were damaging the lining of his arteries leaving him at a high risk for stroke and heart attack.
A patient like Mr. M I consider to have documented atherosclerotic cardiovascular disease (ASCVD)and I will strongly recommend statin therapy along with a baby aspirin
Several studies have shown in those patients who are reluctant to start statin therapy, documenting subclinical atherosclerosis serves as a strong motivational factor for lifestyle change or compliance with medications.
Identifying Lower Risk Patients
Equally important as identifying advanced subclinical atherosclerosis, imaging the carotid artery can identify those patients who are at lower risk and save them from a lifetime of unnecessary treatment.
Ms N is 64 years old whom I see h for high blood pressure and supra ventricular tachycardia (an abnormal heart rhythm). She has a total cholesterol of 219, HDL(or good) cholesterol of 74, systolic blood pressure of 130 and the ACC risk estimator gives her an 8.4% risk of ASCVD over the next 10 years. She greatly dislikes taking medications, but her mother died in her early fifties from a “massive heart attack” .
Her carotid exam shows the carotid thickness as less than average for her age and gender, equivalent to that of a 58 year old. There is no plaque anywhere in her carotid system. I feel comfortable not recommending statins to this type of patient. In many cases, I often stop cholesterol treatment in patients with no evidence for subclinical atherosclerosis who have marginal cholesterol levels and intermediate risk.
What vascular screening allows me is the ability to see if my patients do or do not have the disease that we are trying to prevent or mitigate: atherosclerosis.
As the skeptical cardiologist I must point out that national guidelines do not endorse vascular screening primarily because there are no randomized controlled trials showing that it influences outcomes. I’ll talk more about potential pitfalls of vascular screening when done by for profit ventures in a subsequent post and we’ll discuss the other good way of assessing for subclinical atherosclerosis: coronary calcium.