Saturated Fat, Cholesterol & Carbohydrates all over the World & Updates

Hello again! It’s been a long 5 months since TheFatNurse’s last post! I’ve been finishing up the last semester of my Family Nurse Practitioner Program and getting ready for the Boards. This means I’ve been spending less time focusing on fat related issues and more time diving into other areas of health. As result, I’ve had less time to focus on the blog. I do plan to get back into updating more regularly once the year is over.

However, the past couple of weeks has had several developments that are too note worthy to not mention! Starting in Australia:

ABC has an investigative show called Catalyst in Australia. Last week they aired a controversial report on saturated fat and cholesterol’s weak association with heart disease. This generated the obvious controversy…but the show followed it up with an episode about statins that generated even more controversy!

The basic premise of this episode was the overprescription of statins based off faulty guidelines and research on primary prevention groups (this is important to keep in mind). In addition to the literature on statins and heart disease, the show also covers some of the research process/designs when drug trials are conducted that can lead to flawed conclusions.

The expected controversy even lead the Australian Advisory Committee to urge ABC to pull the episode from airing since they believed it could have lead people to stop taking their medications – leading to death. Today Dr. Kerryn Phelps, a former Australian Medical Association president, added to the controversy by writing:

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Both episodes are worth a look to understand what the discussion is all about as many people are probably going to be confused with all this conflicting advice.

Moving onto Italy:

Apparently Pasta consumption has dropped 23% in the past decade. Why is this?

Worried about its fattening effects, she and her husband eat it no more than a few times a week, favoring couscous, meat and vegetables instead. “Metabolism changes when you approach 40,” she says, “and pasta is out of the question.”

The share of women between 26 and 30 years old who believe pasta is fattening increased 26% from 2008 to 2012, according to a Nielsen survey. And among 26- to 30-year-old men, the number who think pasta makes people fat increased 16%.

Reminds me of this episode of Portlandia:

Now to Britain:

Looks like the amount of saturated fat that will be in Britain will be decreased and taken out of the food supply:

Almost half of the food manufacturing and retail industry has signed up to the Responsibility Deal Saturated Fat Reduction Pledge by agreeing to reduce the amount of saturated fat in our food and change their products to make them healthier.

Cutting the amount of saturated fat we eat by just fifteen per cent could prevent around 2,600 premature deaths every year from conditions such as cardiovascular disease, heart diseaseand stroke.

Check out the link to the story which details what companies are planning to do. Such as:

Nestlé – which will remove 3,800 tonnes of saturated fat from over a billion Kit Kat bars per year by reformulating the recipe

And whatever they end up replacing the saturated fat will make kit kats “healthier?” Sigh…

And in Sweden:

Apparently, “Sweden has become the first Western nation to develop national dietary guidelines that reject the popular low-fat diet dogma in favor of  low-carb high-fat nutrition advice.”

I’ve heard in the past that a huge portion of the population in Sweden follows a Low Carb High Fat diet so this is not too surprising.

We’ll end with China

I’ve covered in the past how asians are often used in popular press to demonstrate how carbohydrates cannot be fattening since Asians are so skinny…despite being healthy and skinny not being the same thing.

Apparently a new study was released last month showing increased carbohydrate consumption being tied to coronary heart disease in the Chinese.

I won’t get into too much about this particular study since it’s observational and relies on questionnaires – which have faults in generating conclusive evidence. However, these study designs were used in the past to demonize dietary fat. So even if this study is not conclusive, it’s worth noting since it produced different results using similar methods in the past. Some notable observations:

These associations were robust and independent of several known CHD risk factors, including socio economic status, centralobesity, smokingstatus, hypertension, and saturated fat intake.

In a Japanese cohort, the average intakes of raw white rice were 170 g/day in women and 180 g/day in men. In that study, white rice intake was found to be inversely associated with death from cardiovascular disease in men but not in women (49). The reasons for the apparent conflicting results between that study and ours are not clear.

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Perspectives on Obesity Between the Clinician and Patient Pt.2

In part 1 we went over some data that showed some clinicians may have negative attitudes about their obese patients – which sadly reflect the same negative attitudes society has on the obese (lacking willpower and etc). We explored clinician beliefs on the causes of obesity and provided contradicting data that did not support some of the beliefs clinicians had on why people gain weight. In the end, while some clinicians may have negative attitudes towards the obese, it is not clear if these negative attitudes are due to some intrinsic prejudice or were formed due to frustration in not being able to treat obesity efficiently. In this post we will go over one of the dogmas in healthcare that contributes to this frustration: “calories in & calories out”

You may already be familiar with the arguments against this concept and there are certainly other experts out there who are actively challenging this belief. Instead of going through an in depth review of the literature, I’ll provide a perspective on how this belief has influenced my formal education as a nurse, how it can effect the clinicians perspective when interacting with an obese patient and some responses I’ve received from people who felt they were treated differently by their providers due to their weight.

The basic concept of “calories in and calories out” is that eating more calories than you burn will lead to caloric excess and when you build up 3500 calories you’ll gain a pound of fat. Pretty straight forward and this concept was pounded into my brain while studying for my licensure:

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Review Material for the RN licensure that Pretty Much Sums up What you Learn in Nursing School

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Two things should jump out at you. The first is that nutrition only comprises a small portion of an RN’s formal education. The second point is that the education you need to pass the NCLEX in regards to nutrition is very thin. Additionally, most of the education on nutrition is focused on specific physiologic/pathophysiologic states and not necessarily on health promotion/prevention. The parts that are focused on health promotion are based on the usual “calories in & calories out” model in conjunction with advice such as limiting dietary fat (especially saturated dietary fats).

A lack of nutrition education extends to medical schools as well [1]

Researchers from the University of North Carolina at Chapel Hill asked nutrition educators from more than 100 medical schools to describe the nutrition instruction offered to their students. While the researchers learned that almost all schools require exposure to nutrition, only about a quarter offered the recommended 25 hours of instruction, a decrease from six years earlier, when almost 40 percent of schools met the minimum recommendations. In addition, four schools offered nutrition optionally, and one school offered nothing at all.

For those schools who do offer the minimum hours in nutrition It is likely that the calories in and calories out model is used for weight maintenance. The simplicity of this model is a big contributor to what causes so much frustration for not only the patient, but the clinician as well.

When I was still deciding on pursuing a career as a family nurse practitioner, one of the books I read was Unforgettable Faces a memoir of an FNP from her point of view while treating patients with a variety of diseases. It gives a nice personal view of what goes on in a clinicians head when interacting with patients who are suffering a host of physical, mental and socioeconomic issues. There is a section where the author talks about treating obesity that is worth a visit.

In the book, the author meets a male patient who if 5’1″ and 330 lbs. He is clearly described as obese and the author comments that obesity is one of the hardest medical problems to deal with. Flipping over his chart, the clinician notices the patient has been skipping out on appointments:

He was supposed to lose ten pounds on a new diet. Instead, he gained fourteen more pounds! Most people who seriously diet will lose weight in seven days from water loss alone. He stepped down off the scale like a boy who’s gotten a bad report card and trailed me into my room.

The patient came in originally to apply for disability related to his hypertension (which was under control with meds according to the author) and difficulty with physical labor which puts him out of breath. However, the clinician informs the patient that his shortness of breath was related to his weight and that he needed to lose weight not apply for disability.

As i looked at the morbidly obese, thirty-five-year-old man, galvanized by a strong sense of denial, I realized that the real problem was motivation. Without superior motivation on the part of everyone concerned, nothing could be accomplished. It was clear to me that this patient was malingering.

“Do you think you’d feel better if you could lose some weight?”

“Maybe,” Mr. White said indifferently with a shrug of his shoulders.

In that exchange from the clinician’s perspective, it seemed that the clinician felt the patient was unmotivated in addressing his weight. That may be true…but this tells us absolutely nothing about WHY the patient is unmotivated. The next part of the story involves the harm of using “calories in & calories out.”

“Are you sticking to your diet?”

“I try to.”

I worked out the incriminating math…The result was impressive, but did not surprise me. Leaving aside his weight gain, he was ingesting at least three-thousand-nine hundred sixty calories a day. Some diet!

His [BMI] was almost twice that level, drug treatment is necessary, but it would not be successful without dieting. If Mr. White didn’t take the matter seriously, he might be facing surgery.

“I don’t think you’re sticking to your diet. I calculate that you are eating two or three times more than you should be eating.”

He sat with his arms folded and looked straight ahead, avoiding my eyes. His face turned expressionless.

This is where “calories in & calories out” is extremely unfair to both parties. The clinician in this case calculated the patient’s theoretical daily calories based off his weight and used it as an assumption of how the patient is eating. Based on this assumption, the clinician then makes another assumption that the patient doesn’t view the matter seriously. This is all possible of course if the story is all about the quantity of “calories in & calories out,” but this simplistic view ignores the quality of where these calories come from.

This perspective is already changing a bit with people such as Dr. Lustig informing the public about how the differences in calories from sugar impact the body. Last year, another study showed how the composition of a diet can create different responses despite being isocaloric [2]

…because metabolic pathways vary in energetic efficiency, dietary composition could affect energy expenditure directly by virtue of macronutrient differences or indirectly through hormonal responses to diet that regulate metabolic pathways.

Acutely, reducing dietary glycemic load diet may elicit hormonal changes that improve the availability of metabolic fuels in the late postprandial period, and thereby decrease hunger and voluntary food intake.

In otherwords, while calories in & out tells us how much we need to eat and how much we need to expend, it tells us absolutely nothing about how the foods that make up these calories effect our metabolism and psychologic satiety. So what the study did was take overweight individuals and semi-starved them to achieve an average weight loss of 13.6% from their baseline. As clinicians, when we inform a patient to cut the calories and lose weight, there are a lot of patients who are initially successful but then eventually gain the weight back (sometimes gaining more weight than initially lost!).

What seems to happen is that metabolism decreases in these individuals to adjust for the weight lost. So this study wanted to see is if this metabolic compensation occurs with the same amount of calories but with different compositions of dietary fat, protein and carbohydrate after the initial 13.6% weight loss. To test this, the study evaluated a low carb high fat diet, a low GI diet and a low fat diet. Or another way to put it: a restricted carbohydrate diet, modified carbohydrate diet, and high carbohydrate diet. So what did they find?

This study was covered in large depth by the media when it was released a year ago so you can read over it yourself if you want a little more information. I would also recommend reading the actual study as well since there are some limitations to the study (it is written in an easy to understand manner) if you have time. But the basic finding was “calories out” differed between diets despite “calories in” being the same between all 3. The calories out were so dramatic between two of the diets (the low fat vs low carb high fat) that the author’s note:

…differed by approximately 300 kcal/d between these 2 diets [in favor of the low carb] , an effect corresponding with the amount of energy typically expended in 1 hour of moderate-intensity physical activity.

Not only was the calories out different between the three diets, but other metabolic markers differed significantly between all three despite “calories in” being the same. Again, the calories in & calories out model tells us nothing about what certain foods are doing to us metabolically and psychologically. Let’s get back to our story.

When we last left our story, our clinician had just informed the patient he must have been overeating based off calculating their weight maintenance from the calories in and calories out model. As we went over briefly, a positive caloric balance is influenced by more than how much a person simply eats. The quality of where those calories are coming from can influence a person’s metabolism. Was it really okay for the clinician in this case to accuse the patient of over eating? The clinician then continues:

“If you eat right – plenty of whole grains, fruits, and vegetables – you can still eat pretty well and it won’t seem like a diet. Do you want to talk to the dietician again?”

He thought for a moment. That face again.  “No.”

“Okay, then let’s start over and set a weight management goal. If you could lose five pounds in a month, that would be something we can work with. If you could lose anymore weight, you’d feel good that you are doing something about this.”

So there are two things to keep in mind about this conversation. How does the clinician know the patient isn’t already eating “plenty of whole grains, fruits, and vegetables?” In the previous study it was shown that restricting carbohydrate (low carb) or modifying carbohydrate (low GI diet) both yielded better metabolism and metabolic markers than a low fat high carbohydrate diet. The second and most important thing to notice is that not once did the clinician ask the patient what he was doing at home. Instead the clinician starts informing the patient that he needs to lose weight. This tells the patient absolutely nothing.

A patient who is obese has already been told that they need to lose weight from previous providers. And if they haven’t, have probably been told by friends/family and society to lose weight (sometimes unfairly). Why didn’t the clinician simply ask what sort of foods the patient was eating or if the patient thought the diet was working? And if the diet wasn’t working…how come? How did the diet that was previously recommended make him feel? Did the clinician simply conclude further exploration wasn’t necessary because the patient was obviously non compliant due to her previous calculations of calories in and calories out? The frustration from the clinician’s side starts to become more apparent:

My inner voice was less optimistic. I wondered why I bothered going through the motions. We both knew that nothing was going to happen.

Like a mother trying to coax a recalcitrant child, I felt foolish.

Without warning, Daniel White stood up. The chair creaked and groaned as if in pain as he did so…His parting words were to the point: “Dieting sucks.”

At this point the frustration from both parties was pretty clear. I think the patient’s last words are very telling of what went wrong in this meeting. Dieting for this patient does suck…but why? Were they constantly hungry all the time? Was dieting simply not working? What exactly did “dieting” for this patient mean? It just seemed the patient was informed to lose weight by the clinician. Was it not worth exploring these issues further? It could just be the patient is non-compliant, but without asking these questions we’ll never know. Ultimately, this is the greatest harm of the calories in & out model – it can lead providers to conclude that weight gain is nothing more than a patient being non compliant/weak-willed/undisciplined.

After reading this post please do not view the clinician from this book as incompetent or mean. In fact, from reading the book, she is actually a very good provider and cares very much for her patients. Her case study was used to simply highlight and explore a bigger issue – a systemic issue on why some healthcare providers may feel frustration towards obese patients. The book was also written in 1999 when a lot of the research on obesity was still new and calories in and out was still king (for many providers it still is).

However, the frustration that some patients have with the interactions from their providers for obesity related issues is still very much prevalent. After sharing part 1 of my exploration into provider attitudes with some of the communities I’m a part of, I received a touching amount of stories from people who felt their providers treated them with negative attitudes based off their weight. If you’re a provider it would be great to always remember the patient’s point of view. While it can’t be confirmed that provider mistreated them due to their weight, a patient should never leave an office visit feeling disrespected for any reason.  [Some passages altered for identifying factors and to keep the content related to obesity]

1) I last saw a Dr about six months ago. He was the perfect example of robust health. I look to be the polar opposite of him. He ignored everything I said gave me some exercises to do and left. His demeanor was condescending and aloof. I have not been back nor will I.

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2)  I had a doctor once tell me “put the fork down,” instead of running blood work for a genetic problem that’s caused everyone in my family to become grossly overweight. I went to see them because over the course of a few months had become horribly tired all the time, had issues with my monthly visitor, started noticing my skin was getting grey-ish and I was gaining weight when I was usually quite active and hadn’t changed eating habits. It’s horrible how they treat people that are overweight.

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3) I went in to ask to get my thyroid tested and she {my doctor} was an ass. I was trying to talk to her about it and she said “I’ll order the test but I don’t get paid to discuss nutrition with you”…I was trying to talk about my inability to lose weight {along with other symptoms} despite my restrictive diet and working out 3 times a week…

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4) I had a doctor (a back-up doctor, not my regular doctor) who seriously thought that all she had to do was point to a red dot on a height-weight chart and glare at me for a few seconds and I would magically become thin. I’d tell her, “I know I’m fat, but you pointing to that chart doesn’t make me thin. I know I should eat less, but I’m hungry all the time. So, give me a pill that makes me less hungry, or tell me what to eat so that I won’t be so hungry.”

She was absolutely no help whatsoever. I had to figure it all out myself – through relentless self-experimentation along with trial-and-error. (Hint: a lot of the foods which made me less hungry turned out to be nutritionally-dense whole-foods which were high in natural fat and quality protein).Eventually I lost about 40 pounds. And I see this same doctor. And I’m all excited about my progress. And she points to another red dot on the same damn height-weight chart, about 2 inches away from the previous red dot, and glares at me just as much as before.

So I show her my belt, which has about 12 notches cut into it from all the lost weight, and I show in my medical file how I used to weigh a lot more. She leaves the room, and this time she comes back with a photocopy of the USDA Food Pyramid and some advice on chewing more slowly. Now, I’ve lost even more weight – 87 pounds in total, and I’ve been taken off 80% of my meds, and the doctors are amazed. I’m sure she’ll take full credit for my health improvements, and get a fat bonus for all of that work she did, pointing at a red dot and Xeroxing the Food Pyramid

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5) 2 years ago, I went to my doctor. I couldn’t understand why I kept gaining weight while eating a low (no) fat vegetarian/vegan 1200 calorie diet. I did everything by the book. Ate little and burned 500 cal/day on the elliptical and I still gained. She asked me how heavy I was, then she asked how tall I was. She calculated my bmi and said:”your bmi is high enough for a gastric bypass”.

She didn’t say she felt for me, she didn’t listen to the fact that I already ate little calories. She just assumed that I was lying, ate too much and that limiting the size of my stomach would be the best option. It seriously was the first thing she said to me after I sat there telling my story in frustration and tears. I then went a little crazy and yelled at her that she was the most incompetent person I had ever come across and left her office to never return. I don’t go to doctors anymore. Not for advice anyway.

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6) Frequently. For most of my life, the fact I could walk several miles without tiring, could lift-and-carry 100-200 pounds, but couldn’t run a quarter mile without my lungs seizing meant I was “out of shape and fat,” not asthmatic. Funny. I can even jog, if I get to take my inhaler. I’ve not had an inhaler of my own for long, about a year — I still remember the first time I had my very own inhaler. I was 1) giddy from oxygen as it was a nasty bout of bronchitis, 2) I cried for a couple of hours out of sheer relief-joy. No longer did I have to hope/beg to borrow an inhaler from my sisters or a friend.

I didn’t know that a five mile walk or a quarter mile jog wasn’t supposed to take two days to recover one’s breathing, only 5-10 minutes to “catch my breath.” But — despite having a sympathetic pulmonologist who has heard me on a bad day — I still have a couple of doctors who sneer at me, and tell me I don’t REALLY have asthma, or I don’t REALLY have an ear/sinus infection, I just need to lose fifty pounds…

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7) Not only do some doctors have a prejudice against fat patients, they automatically assume that 1) the fat is YOUR fault and 2) because you’re fat, you must be sick (diabetic, etc). My daughter’s doctor is notorious for this. She even had me go get blood work done on her. Being a concerned mom, I was worried that something was really wrong. After all, doctor knows best, right? Wrong. Her blood work came back perfectly healthy. 

I think a lot of doctors forget that THEY work for US. Some are really arrogant. But I, too, live in a small town. So, if a doctor doesn’t do something the patients like, the patients will talk. It’s nothing to hear a group of mothers/parents talk about which doctors they like and which ones they don’t.

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8) I was fortunate in that when I was told I needed to lose weight I already knew that LCHF worked for me, my problem was just doing it, all my doctor really did was have the nurse hand me some Xerox’d sheet telling me to eat less fat

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9) My ob/gyn, yesterday, blew me off. The VERY first thing out of her mouth was “you’re fat, and you need to change your diet.” She did not, in any way, shape, or form, ask me what is a normal day’s worth of meals for me. [The sneer and look she gave me, quite full of disgust, indicated she has the belief I only eat fast food/junk food. Grr.]…

…I’m getting very, very tired of the memorized rote script doctors, who cannot accept patients are individuals, and might actually KEEP RECORDS and DATA of their own, and might actually have more than one doctor. If I wanted a completely useless answer in response to a question, I would call Dell’s tech support in India. It’d certainly be more -amusing-. Needless to say, I won’t be going back to her. She doesn’t appear to value my -life- more than the fact I’m fat.

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10) As a patient I hope whoever I see understands I am in front of them so I can improve my health. My hope is that he/she is open minded and willing to listen to what I have to say understanding that just because I have no titles after my name I am knowledgeable enough to take part in improving my health. Most often what I encounter are busy people with huge workloads that stereotype people while making a snap judgement.

By the time I see someone I have waited for 2-4 hours passed tons of bureaucratic hurdles and exhausted my patience. I always feel rushed when I am talking to any primary care nurse or physician. I try and cover everything about why I am in front of that person in the 5-10 minutes we have. It never works out well for either of us. Having tried this many times over the years I have simply given up. I find it easier to work on my health alone.

Summary: This post explored additional issues on clinician perspective in dealing with issues on obesity. Patients are more than just calories in and calories out. Using this model to calculate and make assumptions about a patient’s lifestyle is detrimental for both the provider and patient – leading to both parties being frustrated at one another. 

References:

1) http://www.nytimes.com/2010/09/16/health/16chen.html

2) Ebbeling, C. B., Swain, J. F., Feldman, H. A., Wong, W. W., Hachey, D. L., Garcia-Lago, E., & Ludwig, D. S. (2012). Effects of Dietary Composition During Weight Loss Maintenance: A Controlled Feeding Study. JAMA: the journal of the American Medical Association307(24), 2627.

 

Perspectives on Obesity Between the Clinician and Patient Pt.1

As healthcare providers, we often spend more time focusing on the cardiometabolic effects of obesity and forget about the psychologic aspects. It should be obvious to anyone in America that there is a huge prejudice against the overweight/obese in society. This isn’t surprising, but you may be surprised to find this same sort of prejudice in the clinical setting – a place where patients expect their clinicians to treat them with empathy and respect.

For example, primary care providers were asked about their attitudes on the obese (defined as BMI > 40 in one sample and BMI > 30 in the other to see differences in attitude related to BMI). What did they find? [1]

More than 50% of physicians viewed obese patients as awkward, unattractive, ugly, and noncompliant…Primary care physicians view obesity as largely a behavioral problem and share our broader society’s negative stereotypes about the personal attributes of obese persons.

Surprisingly, we found few differences based on physician characteristics (including BMI and gender) or how obesity was defined in the survey. Among those that were detected, the mean differences were very small, raising doubts about their clinical significance.

This perspective may even be more prevalent in younger primary care providers: [2]

We found higher prevalence of negative attitudes toward obese patients than reported by others. For example, almost 80% of our respondents reported that patients frequently or almost always lacked discipline, and 52% felt patients lacked motivation to lose weight.

The high prevalence of negative attitudes may hinder primary care physicians from discussing weight loss with extremely obese patients. It was interesting that older age and higher patient volume were independently associated with less negative attitudes. Perhaps, physicians with more experience or who are more successful develop a “tolerance” toward patients with extreme obesity.

There was a high prevalence of negative attitudes, particularly in younger physicians and those with lower patient volume. Increased knowledge of weight-loss diets was associated with less dislike in discussing weight loss (P < 0.0001), less frustration (P = 0.0001), less belief that treatment is often ineffective (P < 0.0001), and less pessimism about patient success (P = 0.0002)…further research is needed to determine if interventions to increase knowledge of physicians will lead to less negative attitudes toward weight loss and extremely obese patients.

It’s hard to say why some clinicians may feel this way towards the obese. Do the negative attitudes occur because of societal beliefs? Or do they occur due to frustration at not seeing weight loss from patients after intervention? I would argue it’s a combination of both with one belief reinforcing the other. However, is the difficultly in helping patients lose weight really a result of low “will power” or “discipline?” Perhaps providers have the wrong beliefs about causes of obesity in the first place – which influences the interventions they are likely to tell their patients. From the first study on primary care provider beliefs:

 Physical inactivity (mean rating of 4.3) was rated significantly more important than any other cause of obesity (p < 0.0009). Two other behavioral factors—overeating and a high-fat diet— received the next highest mean ratings (3.9 and 3.8, respectively; 3, moderately important; 4, very important; 5, extremely important).

So primary care providers seemed to rate physical inactivity as the leading cause of weight gain in obesity. It definitely is true that exercise can help a person lose weight, but exercises’ effect on weight loss is more dramatized than reality. In Identifying the difference between exercise + diet versus diet alone in randomized control trials by the Cochrane Collaboration, the difference with the addition of exercise was: [3]

In the group exercise plus diet versus diet alone fourteen trials involving 1049 participants included data regarding weight loss that were suitable for meta-analysis. Participants in both groups lost weight across trials. The pooled effect for interventions with a follow-up between 3 and 12 months was a reduction in weight of 1.1 kg (95% confidence interval (CI), 0.6 to 1.5) in the exercise and diet group compared with the diet alone group.

So the difference these RCTs found with the addition of exercise + diet versus diet alone was an average of 2.4 lbs lost in favor of exercise with diet. Again, the addition of exercise does help with more weight loss but hardly the amounts that all those late night exercise gadget infomercials portray. This is not to say that one shouldn’t bother with exercise if they are already eating right – exercise has other obvious benefits.

Going back to the study on primary care provider attitudes on obesity, you’ll notice that the next two highest rated beliefs providers have on causes of obesity are: overeating and a high fat diet. One of these points is not supported by the literature. If you look at the National Health and Nutrition Examination Survey (NHANES) from the CDC you’ll see this:

Image From Dr. Feinman

Image From Dr. Richard D. Feinman professor of biochemistry at SUNY

It is definitely true that both Men and Women are eating more calories since the 80’s…but is it from a high fat diet? Men have actually decreased their total fat and saturated fat calories while women have increased both. However, both men and women have increased their dietary carbohydrate by vast margins at + 23.4% and + 38.4% respectively! If one is to believe a high fat diet is one of the independent causes of obesity, how can they discount the increase in carbohydrate as a factor as well?

Additionally, the increase in carbohydrate consumption likely contributes to the increases in overeating/calories. This requires a paradigm shift from viewing a calorie is a calorie and focusing on the hormonal, physiologic and psychologic effects that macronutrients have on the body and mind. By doing so, we can see that a patient’s inability to lose weight has nothing to do with a lack of discipline, laziness or willpower to reduce/count calories. Instead, it may just be that they’ve been receiving the wrong advice in the first place.

BTW, before this post ends, it should also be pointed out that negative attitudes/beliefs to the obese applies to clinicians from the patient’s perspective as well. From a study last month: [4]

Respondents reported more mistrust of physicians who are overweight or obese, were less inclined to follow their medical advice, and were more likely to change providers if the physician was perceived to be overweight or obese, compared to normal-weight physicians who elicited significantly more favorable reactions.

These weight biases remained present regardless of participants’ own body weight. Stronger weight bias led to higher trust, more compassion, more inclination to follow advice, and less inclination to change doctors when the physician was presented as normal weight. In contrast, stronger weight bias led to less trust, less compassion, less inclination to follow advice and higher inclination to change doctors when the physician was presented as obese.

This study suggests that providers perceived to be overweight or obese may be vulnerable to biased attitudes from patients, and that providers’ excess weight may negatively affect patients’ perceptions of their credibility, level of trust and inclination to follow medical advice.

At the end of the day, after all this talk of health and weight, let’s just treat individuals as individuals irrespective of their weight.

 Summary: The prejudice that the obese face in society is very prevalent, but this negative attitude may also be present in the healthcare setting from clinicians. It’s hard to say if these attitudes from clinicians originated with the same prejudice from society in general, or if they are from clinicians developing negative attitudes due to lack of success in treating their obese patients. Interestingly enough, patients have negative attitudes about their providers if the provider is obese. In the end, let’s just get respect one another whether a person is obese or not.

ObeseAttitudes

1) Foster, G. D., Wadden, T. A., Makris, A. P., Davidson, D., Sanderson, R. S., Allison, D. B., & Kessler, A. (2003). Primary care physicians’ attitudes about obesity and its treatment. Obesity Research11(10), 1168-1177.

2) Ferrante, J. M., Piasecki, A. K., Ohman-Strickland, P. A., & Crabtree, B. F. (2009). Family physicians’ practices and attitudes regarding care of extremely obese patients. Obesity, 17(9), 1710-1716.

3) Shaw, K., Gennat, H., O’Rourke, P., & Del Mar, C. (2006). Exercise for overweight or obesity. Cochrane Database Syst Rev4.

4) Puhl, R. M., Gold, J. A., Luedicke, J., & DePierre, J. A. (2013). The effect of physicians’ body weight on patient attitudes: implications for physician selection, trust and adherence to medical advice. International Journal of Obesity.

A Tale of Two Lipid Panels

Awhile ago, TheFatNurse noticed something strange while reviewing some Lipid panels. Normally, when you receive a lab result, a reference range is given and any numbers above or below the reference range is flagged. What was strange about some of these lipid panels was the lack of flags for patient numbers that were clearly in the high risk range. For example, Let’s take a hypothetical patient:

Total Cholesterol: 165
HDL: 35
LDL: 105
Triglycerides: 244

If you’ve read through the critique of LDL Cholesterol as an indicator of risk you’ll know that LDL cholesterol can sometimes be inaccurate in gauging heart disease risk. However, that is a different problem all together (addressed later in the post) and for the purposes of this post let’s just use the standard numbers provided by the ATP-III clinical guidelines:

So according to the clinical guidelines, this patient’s total cholesterol would be classified as “desirable,” his HDL cholesterol would be “low,” his LDL cholesterol  is pretty much at “optimal,” and his triglycerides are “High.” Therefore, on a lipid panel  you may assume that his Triglycerides and HDL will be flagged. However, depending on what reference ranges a lab uses, this can differ. Here are two example:

ReferenceRange1

This patient is within “range” according to this reference

ReferenceRange2

This patient is not within “range” according to this reference

Before going on, it should be made clear that one should never make the mistake of thinking a reference range is the same thing as target goals (which change according to an individual’s risk category) for a patient. A reference range is simply the distribution of values that are seen in the folks of a given population. However, patients can make the mistake of comparing their numbers to the reference range (and sadly sometimes even clinicians make this mistake) and therefore think they are at low risk when the opposite is really true.

In the first panel, the numbers from our hypothetical patient would not be flagged and a person may think they are at low risk. In the second panel, the numbers from HDL and Triglyceride would be flagged as abnormal. Therefore, it’s more important to go by target goals rather than what a lab supplies as a reference range. As a side note, the advance lipid panels such as the NMR, VAP, and Ion Mobility advance lipoprotein tests, suggest a reference range for triglycerides at <150 mg/dL. The reference range supplied by the first lab at <250 is obviously way too high to be viewed as a target goal and should never be viewed as such.

However, as mentioned in a previous post, even reaching the target goals of LDL cholesterol can be inaccurate to risk. This is even mentioned in the ATP-III where it is suggested to use Non-HDL cholesterol as a target goal if triglycerides are above 200 like our hypothetical patient. However,  Non-HDL isn’t always supplied in a lipid panel and many clinicians do not understand its purpose nor do they know how to calculate it even if they wanted to use it. The same dilemma holds true for looking at the TG/HDL ratio as well. In this scenario, our hypothetical patient’s TG/HDL ratio of 6.97 indicates a high likely hood of increased small and total LDL particles which means he’s at risk for atherosclerosis despite being at target for his LDL cholesterol. If we could advance test everyone with LDL particle testing that could solve a lot of confusion but that would be very expensive  and it’s not always an appropriate test if the regular lipid panel is concordant. With this in mind and everything else we’ve discussed so far on reference ranges and target goals, it’s not hard to imagine a situation where the interpretation of risk between the patient and the clinician and another clinician is vastly different between each party.

TL:DR; Different labs provide different reference ranges which are not the same as target goals. Some of the supplied reference ranges can be vastly outside what would typically be considered a target goal. This can lead to different interpretations of a lipid panel where risk may be judged inaccurately.

Lipids: What School Did and Did Not Teach

Hello again world! It’s been a long two months since TheFatNurse last posted due to busy events in TheFatNurse’s life. However, since that time, TheFatNurse finally had the lecture on lipids and heart disease in TheFatNurse’s nursing school. It had it’s highs, lows and also a few surprises as well. This post should offer you some insights into some of the formal education that some health care professionals may receive regarding lipids.

 Cholesterol is the most highly decorated small molecule in biology. Thirteen Nobel Prizes have been awarded to scientists who devoted major parts of their careers to cholesterol. Ever since it was isolated from gallstones in 1784, cholesterol has exerted an almost hypnotic fascination for scientists from the most diverse areas of science and medicine…

 -Michael Brown and Joseph Goldstein Nobel Lectures (1985)

I. Going Over The Basics

The lecture began with a quick overview of lipids. Specifically, the instructor explained that cholesterol was “made in the liver” and “absorbed in the gut.” This is only somewhat true; while the liver is most known for cholesterol synthesis, cholesterol is also made de novo in extrahepatic cells (made outside the liver) where it is often trafficked in pathways that cross/involve the liver.

The instructor also commented about cholesterol being absorbed in the gut…but did not make it clear where that cholesterol came from and could make one think he was referring to dietary cholesterol. However, most of the cholesterol that is absorbed in our gut is actually biliary in origin rather than diet.

TheFatNurse has gone over the basics of lipid metabolism in previous posts so won’t go over it again too much in this post but if you need a quick refresher a good review of the subject matter can be found here in this review in Nature [1]

Not everyone has an academic journal account so you can also gleam most of the basics of cholesterol in these two comics from the TheFatNurse comic collection

Cover

Click here for a review about the history of lipoproteins & cholesterol!

Click here for a review on what HDL and Triglycerides Do!

Click here for a review on what HDL and Triglycerides Do!

If you’re craving more in depth details then I would highly recommend reading Dr. Dayspring’s “Lipid and Lipoprotein Basics” [2] which contains not only a comprehensive overview of all the dynamic relationships involving everything lipid but also helpful diagrams that help visualize the whole process.

The instructor then proceeded to mentioned particles and explained, “cholesterol is found in HDLs, LDLs and IDLs.” This is somewhat correct, but cholesterol is also carried by Chylomicrons and VLDLs (although both to a lesser degree). The instructor also went over triglycerides and informed the class that they could be used for energy but were associated with higher cardiovascular risk and were carried by Chlyomicrons and VLDLs. Again, this is only somewhat true, since triglycerides can be found in HDLs, LDLs, and IDLs as well. This is important because the variations in how much triglycerides these lipoproteins have is associated with many dynamic changes on how many lipoproteins you have, their sizes, and ultimately even your cardiovascular risk. You can see a breakdown of their percentages of cholesterol and triglycerides below:

LP-Density-Wiki

The biggest critique TheFatNurse had with the intructors’ explanation of cholesterol was the lack of separation in explaining the differences between lipoproteins and cholesterol. For example, the instructor would mention “LDL cholesterol” and “HDL cholesterol” various times as if these were two different types of cholesterol. Cholesterol is cholesterol and it’s either in an unesterified form or esterified form. When we mention measurements of “HDL-cholesterol” or “LDL-cholesterol” we are hoping that the cholesterol we find on these lipoproteins tells us how many lipoproteins there are. This confusing language was mentioned in Frederickson, Levy and Lee’s landmark 5-part series on lipids in The New England Journal of Medicine [3] back in the 60’s.

Even then, Fredrickson, Levy and Lees pointed out that it may be more appropriate to use the terms dyslipoproteinemia and hyperlipoproteinemia rather than dyslipidemia and hyperlipidemia since the focus was on the lipoproteins rather than the lipids themselves. The lack of using this terminology in today’s world can be attributed to much of the confusion about cholesterol and lipoproteins in general (If there is still some confusion, there’s some pictures that provide an analogy of cholesterol vs the lipoproteins further down this post as well as more clarification in the cholesterol comics posted earlier).

II. Going Over Clinical Lipid Values

The instructor then informed the class that we could get these measurements through a fasting lipid panel to evaluate the total cholesterol and LDL cholesterol which would inform us of our risk and give us a target to shoot for. This created a transition to introduce the ATP-III guidelines [4] for us. However, at this point TheFatNurse put up a raised hand to point out the importance of how elevated triglycerides can effect the estimation of LDL-cholesterol (calculated by the Friedewald equation). [5] The ATP-III guidelines are old and definitely has problems, but what was disturbing was the lack of any mention on looking at non-HDL cholesterol which is actually mentioned in the guidelines!

Many persons with atherogenic dyslipidemia have high triglycerides
(≥200 mg/dL). Such persons usually have an increase
in atherogenic VLDL remnants, which can be estimated clinically by measuring VLDL cholesterol. In persons with high triglycerides, the combination of LDL cholesterol + VLDL cholesterol (non-HDL cholesterol) represents atherogenic cholesterol. Non-HDL cholesterol thus represents a secondary target of therapy (after LDL cholesterol) when triglycerides are elevated.

YUNONONHDL

Indeed, Non-HDL-Cholesterol  (Total Cholesterol – HDL-Cholesterol) is often a better predictor of risk than LDL-cholesterol. A simple search through pubmed will provide you with all sorts of studies for different populations. Here’s a small sample:

“Non-HDL cholesterol and apoB are more potent predictors of CVD incidence among diabetic men than LDL cholesterol” [6]

“Non-HDL-C was more strongly associated with subclinical atherosclerosis than all other conventional lipid values. These data suggests that Non-HDL-C may be an important treatment target in primary prevention.” [7]

“We reconfirmed non-HDL-C as a predictor of the risk for CAD and a residual risk marker of CAD after LDL-C-lowering therapy” [8]

“For participants with triglycerides <2.26 mmol/L (<200 mg/dL), the overall misclassification rate for the CVD risk score ranged from 5% to 17% for cLDL-C methods and 8% to 26% for dLDL-C methods when compared to the RMP…For participants with triglycerides ≥2.26 mmol/L (≥200 mg/dL) and <4.52 mmol/L (<400 mg/dL), dLDL-C methods, in general, performed better than cLDL-C methods, and non-HDL-C methods showed better correspondence to the RMP for CVD risk score than either dLDL-C or cLDL-C methods.” [9]

“The discrimination power of non-HDL-C is similar to that of apoB to rank diabetic patients according to atherogenic cholesterol and lipoprotein burden. Since true correlation between variables reached unity, non- HDL-C may provide not only a metabolic surrogate but also a candidate biometrical equivalent to apoB, as non- HDL-C calculation is readily available.” [10]

“…among statin-treated patients, levels of LDL-C, non–HDL-C, and apoB were each strongly associated with the risk of major cardiovascular events, but non–HDL-C was more strongly associated than LDL-C and apoB. Given the fact that many other arguments for the clinical applicability of non–HDL-C and LDL-C are identical, non–HDL-C may be a more appropriate target for statin therapy than LDL-C.” [11]

“CHD risk associated with ↓HDL-C in women was >2- to 4-fold elevated depending on TG levels. Non-HDL cholesterol was a significant predictor of CHD in men.” [12] *of note this study reported findings that “Non-HDL cholesterol was significantly related to CHD in men but not in women.”

“non-HDL-C remains an important target of therapy for patients with elevated TGs, although its widespread adoption has yet to gain a foothold among health care professionals treating patients with dyslipidemia.” [13]

“…in a Dutch population-based cohort…Both men and women with increasing levels of apoB and non-HDL-c were more obese, had higher blood pressure and fasting glucose levels, and a more atherogenic lipid profile….data support the use of first apoB and secondly non-HDL-c above LDL-c for identifying individuals from the general population with a compromised CV phenotype.” [14]

“Future guidelines should emphasize the importance of non–HDL-C for guiding cardiovascular prevention strategies with an increased need to have non–HDL-C reported on routine lipid panels.” [15]

There was honestly a lot more out there so TheFatNurse thought it was a little disturbing that the only lipid parameter that was covered was Total Cholesterol and LDL-Cholesterol, especially since Non-HDL (unlike Apo-B, LDL-particle count or Lipoprotein sizes) does not require advance lipid testing and is readily available with some simple math on a basic lipid panel.

Another free lipid marker that was not covered is the Triglyceride/HDL ratio. Again, there is plenty of evidence suggesting that this ratio should be evaluated due to it’s predictive value for metabolic syndrome which increases one’s cardiovascular risk significantly. Metabolic syndrome is elevated BP, increased trunk obesity, elevated triglycerides, decreased HDL, and impaired fasting glucose. You need 3 out of the 5 for the official diagnosis:

“The Tg/HDL-C ratio could be a useful index in identifying children at risk for dyslipidemia, hypertension, and MS.” [16]

“Among women with suspected ischemia, the TG/HDL-C ratio is a powerful independent predictor of all-cause mortality and cardiovascular events.” [17]

“We evaluated the predictive value of a surrogate maker of insulin resistance, the ratio of triglyceride (TG) to high-density lipoprotein (HDL), for the incidence of a first coronary event in men workers according to body mass index (BMI)… In conclusion, the TG/HDL ratio has a high predictive value of a first coronary event regardless of BMI.” [18]

“A triglyceride/HDL cholesterol ratio of 3.8 divided the distribution of LDL phenotypes with 79% (95% confidence interval [CI] 74 to 83) of phenotype B [more atherogenic] greater than and 81% (95% CI 77 to 85) of phenotype A less than the ratio of 3.8. The ratio was reliable for identifying LDL phenotype B in men and women.” [19]

“…results add further support to the notion that the TG/HDL-C ratio may be a clinically simple and useful indicator for hyperinsulinemia among nondiabetic adults regardless of race/ethnicity.” [20] *of note, there is some research suggesting that the TG/HDL marker may not be as good of a predictive marker for insulin resistance for African-American women in other studies.

“The triglyceride/HDL ratio, a simple, readily available and inexpensive measure, can be a useful surrogate to identify those with insulin resistance as well as those with more atherogenic small LDL particles in nondiabetic patients with schizophrenia.” [21]

“…findings of this study demonstrate that the triglyceride-to-HDL cholesterol ratio is associated with insulin resistance measures in White Europeans and South Asian men; this relationship appeared to be less established in South Asian women.” [22]

“The TG/HDL-C ratio may be a good marker to identify insulin-resistant individuals of Aboriginal, Chinese, and European, but not South Asian, origin.” [23]

“An elevated TG/HDL-C ratio appears to be just as effective as the MetS diagnosis in predicting the development of CVD.” [24]

“Adolescents with an elevated TG/HDL ratio are prone to express a proatherogenic lipid profile in adulthood. This profile is additionally worsened by weight gain.” [25]

“The TG/HDL-C ratio is associated with IR mainly in white obese boys and girls and thus may be used with other risk factors to identify subjects at increased risk of IR-driven morbidity.” [26]

The importance of predicting insulin resistance is  associated with it’s impact on the lipoprotein profile and thus cardiovascular risk:

“…progressive insulin resistance was associated with an increase in VLDL size (r = −0.40) and an increase in large VLDL particle concentrations (r= −0.42), a decrease in LDL size (r = 0.42) as a result of a marked increase in small LDL particles (r = −0.34) and reduced large LDL (r = 0.34), an overall increase in the number of LDL particles (r = −0.44), and a decrease in HDL size (r = 0.41) as a result of depletion of large HDL particles (r = 0.38) and a modest increase in small HDL (r = −0.21; all P < 0.01). These correlations were also evident when only normoglycemic individuals were included in the analyses (i.e., IS + IR but no diabetes), and persisted in multiple regression analyses adjusting for age, BMI, sex, and race.” [27]

*of note: “When compared with IS [insulin sensitive], the IR [insulin resistant] and diabetes subgroups exhibited a two- to threefold increase in large VLDL particle concentrations (no change in medium or small VLDL), which produced an increase in serum triglycerides; a decrease in LDL size as a result of an increase in small and a reduction in large LDL subclasses, plus an increase in overall LDL particle concentration, which together led to no difference (IS versus IR) or a minimal difference (IS versus diabetes) in LDL cholesterol” as well as “these insulin resistance-induced changes in the NMR lipoprotein subclass profile predictably increase risk of cardiovascular disease but were not fully apparent in the conventional lipid panel.”

YUNOLDL

The focus on LDL-cholesterol and Total cholesterol is nothing new. In speaking with doctors TheFatNurse has encountered, medical as well as PA & NP schools are lagging a bit behind when it comes to more current lipoprotein research. And while targeting LDL-Cholesterol remains the “gold standard.” The associations between LDL-cholesterol and heart disease aren’t as strong as you might think. In this study of 231,986 hospitalizations from 541 hospitals of CAD hospitalizations from 2000 to 2006 with documented lipid levels in the first 24 hours of admission, [28] they found

“mean lipid levels were LDL 104.9 +/- 39.8, HDL 39.7 +/- 13.2, and triglyceride 161 +/- 128 mg/dL.”

In otherwords, the average person admitted actually had Near optimal/above optimal LDL-cholesterol! However, you’ll notice that the average HDL was below target

And what about Triglycerides? You’ll see that they were elevated:

Triglycerides on average were borderline high in this group (although the standard deviation was pretty wide). So while LDL-Cholesterol, “the primary target of therapy,” was pretty good, perhaps just as much emphasis should be placed on HDL cholesterol and Triglycerides or even the evaluations of other lipid parameters such as the Non-HDL cholesterol and TG/HDL ratio we discussed earlier.

That’s not to say LDL-Cholesterol is worthless, it can have good predictive value for those who are concordant. Versus those who are discordant. TheFatNurse talks about this briefly and why it’s important in this other comic from TheFatNurse’s comic series. Here’s a little snippet on why discordance is not good:

ConDis

What is LDL-P? These are the actual number of LDL lipoproteins themselves! Apo-B measurements are also a way to get LDL-P numbers and the Non-HDL marker we discussed earlier can act as a surrogate for Apo-B and LDL-P (although Non-HDL is not as accurate). When we get a regular lipid panel, we are only looking at the cholesterol in the lipoproteins and not the lipoproteins themselves! Here are some pictures to illustrate. For example, say your doctor informs you that you have 16 oz of Cholesterol as you can see below:

Screen Shot 2013-03-01 at 12.35.28 AM

16 Oz of Thai Ice Tea *Ahem* TheFatNurse means 16 oz of cholesterol

In order to get that 16 oz measurement, the lab needed to break apart the lipoproteins that were carrying the cholesterol in the first place. Usually the amount of cholesterol can correlate with the number of lipoproteins…but not always. For example, was this 16 oz of cholesterol carried in lipoproteins the size of shot glasses?

Screen Shot 2013-03-01 at 12.36.20 AM

The 16 oz of cholesterol spread over six smaller shot glasses *Ahem* Lipoproteins

Or was it carried in the form of rock glasses?

Screen Shot 2013-03-01 at 12.36.49 AM

The same 16 oz of cholesterol carried in larger Rock *Ahem* I mean larger lipoproteins

As you can see it’s impossible to really know the characteristics of the lipoproteins based off just the cholesterol itself! In the first example, the 16 oz of cholesterol was carried in 6 small shot glasses/lipoproteins. In the second example, the 16 oz of cholesterol was carried in 2 larger rock glasses/lipoproteins. The first example is more atherogenic while the second one is less. You can see two different characteristics emerge at this point: size and number. Whether it’s the size or the total number of lipoproteins that is more atherogenic is hotly debated, but either characteristic is a much better predictor of risk than just looking at just the cholesterol itself. In many people LDL-cholesterol correlates (what is known as concordance) well with the number of LDL particles but not always. When LDL-cholesterol doesn’t correlate well, it’s said to be discordant.

Some support for looking at other markers besides LDL-cholesterol due to discordance can be found below:

“For individuals with discordant LDL-C and LDL-P levels, the LDL-attributable atherosclerotic risk is better indicated by LDL-P.” [29]

“…significant discordance between LDL and non-HDL cholesterol levels in diabetes patients with high triglycerides or the MS. This might explain patients’ high residual CV risk despite having achieved their desirable LDL cholesterol levels.” [30]

“Discordance analysis demonstrates that apoB is a more accurate marker of cardiovascular risk than non-HDL-C.” [31]

“Four-hundred twenty-eight (18%) of children were in the LDL-P < LDL-C subgroup and 375 (16%) in the LDL-P > LDL-C subgroup. Those with LDL-P > LDL-C had significantly greater body mass index, waist circumference, homeostatic model of insulin resistance, triglycerides, systolic and diastolic blood pressure… a discordant atherogenic phenotype of LDL-P > LDL-C, common in obesity, is often missed when only LDL-C is considered” [32]

“Many patients with type 2 diabetes mellitus (T2DM) have relatively normal levels of low-density lipoprotein (LDL) cholesterol yet have increased risk for cardiovascular events…despite attainment of LDL cholesterol <50 mg/dl or non-HDL cholesterol <80 mg/dl, patients with diabetes exhibited significant variation in LDL particle levels, with most having LDL particle concentrations >500 nmol/L, suggesting the persistence of potential residual coronary heart disease risk.” [33]

“Both men and women with increasing levels of apoB and non-HDL-c were more obese, had higher blood pressure and fasting glucose levels, and a more atherogenic lipid profile…Less clear differences in CV risk profile and subclinical atherosclerosis parameters were observed when participants were stratified by LDL-c level. Furthermore, apoB but not LDL-c detected prevalent CVD, and non-HDL-c only detected prevalent CVD in men…Our data support the use of first apoB and secondly non-HDL-c above LDL-c for identifying individuals from the general population with a compromised CV phenotype.” [34]

“A recent large meta-analysis with >60,000 patients in statin trials found that when LDL-C was low (LDL-C <100 mg/dl), but non–HDL-C was elevated (non–HDL-C >130 mg/dl) there was an increase in cardiovascular events compared with those with both elevated LDL-C and non–HDL-C…Although both lipid profiles represent a patient at high residual risk for a major adverse cardiac event, the patient with the low LDL-C (<100 mg/dl), but with a discordantly high non–HDL-C (>130 mg/dl), is the type of patient who may slip through the cracks because the at-goal LDL-C may mislead the clinician into believing the patient is adequately treated…Should non–HDL-C replace LDL-C as the main target of therapy? The advantages appear clear: non–HDL-C is a better risk predictor, can be performed in a nonfasting state, and does not incur any additional costs to the healthcare system.” [35]

Perhaps highlighting the imporatnace of the awareness of these other lipid markers: 44% of clinical providers could not calculate Non-HDL when given a standard lipid panel and there was confusion amongst not just primary care providers, but cardiologists as well. [36]

“…non-HDL-C appears to be an indirect way of estimating apoB. We argue that we should integrate the information from non-HDL-C and apoB for better risk assessment and a better target of therapy” [37]

“This meta-analysis is based on all the published epidemiological studies that contained estimates of the relative risks of non-HDL-C and apoB of fatal or nonfatal ischemic cardiovascular events. Twelve independent reports, including 233 455 subjects and 22 950 events, were analyzed…Whether analyzed individually or in head-to-head comparisons, apoB was the most potent marker of cardiovascular risk (RRR, 1.43; 95% CI, 1.35 to 1.51), LDL-C was the least (RRR, 1.25; 95% CI, 1.18 to 1.33), and non-HDL-C was intermediate (RRR, 1.34; 95% CI, 1.24 to 1.44)…We calculated the number of clinical events prevented by a high-risk treatment regimen of all those >70th percentile of the US adult population using each of the 3 markers. Over a 10-year period, a non-HDL-C strategy would prevent 300 000 more events than an LDL-C strategy, whereas an apoB strategy would prevent 500 000 more events than a non-HDL-C strategy.” [38]

In most studies, both apo B and LDL-P were comparable in association with clinical outcomes. The biomarkers were nearly equivalent in their ability to assess risk for CVD and both have consistently been shown to be stronger risk factors than LDL-C. We support the adoption of apo B and/or LDL-P as indicators of atherogenic particle numbers into CVD risk screening and treatment guidelines. [39]

III. Going Over Dietary Cholesterol and Fat

For individuals who are not at LDL cholesterol goal, the instructor recommended that cholesterol should be limited to <200 mg/day and total saturated fat reduced to less than 7% of daily caloric intake. However,despite the instructor’s recommendations, there has been some debate on whether the guidelines on dietary cholesterol are that effective or even necessary.

“The European countries, Australia, Canada, New Zealand, Korea and India among others do not have an upper limit for cholesterol intake in their dietary guidelines. Further, existing epidemiological data have clearly demonstrated that dietary cholesterol is not correlated with increased risk for CHD. Although numerous clinical studies have shown that dietary cholesterol challenges may increase plasma LDL cholesterol in certain individuals, who are more sensitive to dietary cholesterol (about one-quarter of the population), HDL cholesterol also rises resulting in the maintenance of the LDL/HDL cholesterol ratio, a key marker of CHD risk.” [40]

Sincerely, Sugar

Sincerely, Sugar

Physiologically, as we mentioned earlier, most of the cholesterol we absorb is biliary in origin rather than dietary. Therefore, would decreasing cholesterol consumption down to <200 mg/day even have a meaningful impact? The focus on dietary cholesterol can also take attention away from dietary plant sterols (phytosterols). The difference between these plant sterols and cholesterol (sterols from animals) is that plant sterol absorption is minimized compared to cholesterol:

“Dietary cholesterol comes exclusively from animal sources, thus it is naturally present in our diet and tissues. It is an important component of cell membranes and a precursor of bile acids, steroid hormones and vitamin D. Contrary to phytosterols (originated from plants), cholesterol is synthesised in the human body in order to maintain a stable pool when dietary intake is low…conversely, phytosterols are poorly absorbed and, indeed, rapidly excreted. Dietary cholesterol content does not significantly influence plasma cholesterol values, which are regulated by different genetic and nutritional factors that influence cholesterol absorption or synthesis. Some subjects are hyper- absorbers and others are hyper-responders, which implies new therapeutic issues. Epidemiological data do not support a link between dietary cholesterol and CVD.” [41]

Without going into too much detail (save that  for a future post), people who are hyperabsorbers may end up absorbing phytosterols into the plasma where some evidence is showing that they can be atherogenic if not more so than cholesterols in the artery wall. After all, there is a disease called phytosterolemia (also known as sitosterolemia) [42] that causes individuals to die at an early age from heart disease due to elevated absortion of these phytosterols. Remember, atherosclerosis occurs when a sterol is deposited into the arteries to elicit an inflammatory response; this can be a cholesterol or a phytosterol. Most people don’t have to worry about this tho and this point on phytosterols was only mentioned to show that there are other sterols out there than just cholesterol which can impact atherosclerosis. As expected, there was no mention of hyper absorbers in the class which is fair since this is newer emerging data.

And what about the saturated fat limitation? TheFatNurse has beat to death the notion that dietary saturated fat (and total fat) is responsible for coronary heart disease, but here’s a couple of meta analyses that you can look over yourself:

“Meta-Analysis of Cohort Studies of Total Fat and CHD…Intake of total fat was not significantly associated with CHD mortality…Intake of total fat was also unrelated to CHD events”

“Meta-Analysis of Cohort Studies of SFA and CHD…Intake of SFA was not significantly associated with CHD mortality…Similarly SFA intake was not significantly associated CHD events…no significant association with CHD death.”

“Randomized Controlled Trials of Dietary Fat and CHD…Meta-Analysis of Randomized Controlled Trials of Fat-Modified Diets and CHD…the low-fat diets did not affect CHD events”

“The available evidence from cohort and randomised controlled trials is unsatisfactory and unreliable to make judgement about and substantiate the effects of dietary fat on risk of CHD.” [43]

“…there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.””More data…needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.” [44]

“Compared with participants on low-fat diets, persons on low-carbohydrate diets experienced a slightly but statistically significantly lower reduction in total cholesterol (2.7 mg/dL; 95% confidence interval: 0.8, 4.6), and low density lipoprotein cholesterol (3.7 mg/dL; 95% confidence interval: 1.0, 6.4), but a greater increase in high density lipoprotein cholesterol (3.3 mg/dL; 95% confidence interval: 1.9, 4.7) and a greater decrease in triglycerides (-14.0 mg/dL; 95% confidence interval: -19.4, -8.7).” [45]

“No clear effects of dietary fat changes on total mortality or cardiovascular mortality “”There are no clear health benefits of replacing saturated fats with starchy foods (reducing the total amount of fat we eat).” [46] *

There are other interesting individual studies challenging the notion of saturated fat and heart disease, but instead of continuing the onslaught of posting studies, it may be more interesting to go over the mechanisms of dietary fat. After all, it seems like it would be common sense that ingestion of saturated fats would lead to more fats in the blood stream right? However, this does not happen and.its more likely one would find increased levels of lipids, in particular, triglycerides in your blood stream with the consumption of carbohydrate. You can see in one of the meta-analysis above from Hu et al 2012 that low carb diets often yielded less total cholesterol, less LDL-cholesterol, more HDL-cholesterol and less triglycerides. How can this be?

The best way to view this is to break apart from the conventional “a calorie is a calorie.” While a calorie is a calorie is true by its definition to raise the temperature of 1 gram of water through 1 °C, this view often leads to people not realizing that calories from different sources have different effects hormonally and on the body’s regulatory system. Carbohydrates, for example, stimulate insulin secretion and effects the availability of energy sources such as free fatty acids.

IV. Going Over Metabolism of Fat in The Body

While the metabolic processes of dietary fat can be complex, the basic concepts can be broken down into a few key ideas. The main idea, as mentioned before, is to stop viewing, “a calorie is a calorie.” A calorie from fat, protein or carbohydrate can exert different hormonal and therefore regulatory effects on the body independent of its energy content.

For example, keeping calories the same but switching the amount of fat and carbohydrate changes the regulatory oxidative pathways of muscles in as few as three days, “isoenergetic high-fat/low-carbohydrate diet (HF/LCD) for 3 days with muscle biopsies before and after intervention. Oligonucleotide microarrays revealed a total of 369 genes of 18 861 genes on the arrays were differentially regulated in response to diet…” [47]

An even simpler example of this process is how dietary carbohydrates lead to a rise in insulin. Unfortunately, most of the focus on insulin is in its ability to bring blood sugar down in the body. This shouldn’t be surprising since regulation of blood sugar is such a huge treatment plan of healthcare today.

When the regulatory process of insulin and blood sugar is disrupted, say for example in the development of T2 Diabetics, issues such as hyperglycemia (high blood sugar) can occur which can eventually lead to insulin resistance and the development of the metabolic syndrome which is increased triglycerides, decreased HDL, elevated blood pressure, increased abdominal girth and impaired fasting blood sugar. How can it be that carbohydrates have the potential to impact all these 5 factors? Since this post is about lipids, we’ll limit the discussion to mostly increased triglycerides, low HDL and impaired fasting glucose (which indirectly impacts lipids and lipoproteins) for now and explore the other two elements in a latter post.

The body has an innate ability to convert excess glucose into triglycerides.  Indeed, there is a protein in the liver appropriately named carbohydrate response element binding protein (ChREBP) that stimulates lipogenesis in the liver in response to carbohydrate. [48]

When dietary carbohydrates are decreased, lipid metabolism in the body changes and fat oxidation (also known as beta oxidation which specifically refers to the breakdown of triglycerides into free fatty acids for energy) occurs irrespective of the amount of calories (such as fasting) one ingests. “Changes in plasma glucose, free fatty acids, ketone bodies, insulin, and epinephrine concentrations during fasting were the same in both the control and lipid studies…These results demonstrate that restriction of dietary carbohydrate, not the general absence of energy intake itself, is responsible for initiating the metabolic response to short-term fasting.” [49]

Not only is lipid oxidation increased, but expression of lipogenesis pathways are decreased when carbohydrates are decreased and fat increased in animal models (Although this supports the point TheFatNurse is trying to make, please remember that animal model can sometimes have limitations in applicability to humans). “Microarray analysis of liver showed a unique pattern of gene expression in KD [ketogenic diets which are high fat low carb], with increased expression of genes in fatty acid oxidation pathways and reduction in lipid synthesis pathways…these data indicate that KD induces a unique metabolic state congruous with weight loss.” [50]

Since carbohydrates (especially in the form of sugar) can have an effect on blood sugar, one of the recommended advice that we’re given is to exercise more. Indeed, one of the ways exercise helps to bring down blood sugar is the generation of what are called GLUT-4 receptors in the muscles and fat tissue of the body which allow glucose transport and therefore reducing some of the blood sugar levels in the body.

However, the consumption of carbohydrates can lead to these GLUT-4 receptors disappearing faster when compared to a consumption of lower carbohydrate after exercise. “…increases in GLUT4 mRNA and protein reversed completely within 42 h after exercise in rats fed a high-carbohydrate diet. In contrast, the increases in GLUT4 protein, insulin-stimulated glucose transport, and increased capacity for glycogen supercompensation persisted unchanged for 66 h in rats fed a carbohydrate-free diet…These findings provide evidence that prevention of glycogen supercompensation after exercise results in persistence of exercise-induced increases in GLUT4 protein and enhanced capacity for glycogen supercompensation.” [51]

So far we’ve set the stage that increased carbs can increase the blood glucose, increase insulin and therefore increase lipogenesis which increases Triglycerides. Increased triglycerides, as you know, is one of the factors of metabolic syndrome. By contrast, decreasing carbohydrate can have the opposite beneficial effect of lowering Triglyerides. How does it do this?

Again, the increase of circulating triglycerides is not from increasing consumption of fat. It’s when individuals become insulin-resistant, from the increasing consumption of excessive carbohydrates or sugar which impaires glucose to be taken up in the cells which makes the liver convert the glucose to triglycerides. This occurs irrespective of differences in obesity in an individual. What is commonly taught is that obesity leads to insulin resistance, but individuals can be insulin resistant and lean as well as shown here:

“Following ingestion of two high carbohydrate mixed meals, net muscle glycogen synthesis was reduced by ≈60% in young, lean, insulin-resistant subjects compared with a similar cohort of age–weight–body mass index–activity-matched, insulin-sensitive, control subjects. In contrast, hepatic de novo lipogenesis and hepatic triglyceride synthesis were both increased by >2-fold in the insulin-resistant subjects. These changes were associated with a 60% increase in plasma triglyceride concentrations and an ≈20% reduction in plasma high-density lipoprotein concentrations but no differences in…intraabdominal fat volume.”

“These data demonstrate that insulin resistance in skeletal muscle, due to decreased muscle glycogen synthesis, can promote atherogenic dyslipidemia by changing the pattern of ingested carbohydrate away from skeletal muscle glycogen synthesis into hepatic de novo lipogenesis, resulting in an increase in plasma triglyceride concentrations and a reduction in plasma high-density lipoprotein concentrations.” [52]

As far as how the liver actually convert glucose to triglycerides and how triglyceride production is decreased in the liver…there are several pathways by which this occurs but the main idea is the lowered inputs of Plasma Fructose, Plasma Glucose and Insulin by the consumption of dietary fat (even saturated fat) leads to decreased TGs. If you want more details on the biochemistry of carbohydrate and lipogenesis you can read more about it here: [53]

So what about HDL-cholesterol? Why is HDL-cholesterol decreased in Metabolic syndrome? As shown in the previous study, HDL-cholesterol tends to go down when Triglycerides go up. This shouldn’t be surprising since they are both measurements of metabolic syndrome. This is also why the TG/HDL ratio mentioned earlier is also a predictor of insulin resistance.

Along with decreasing Triglycerides, decreasing the amount of carbohydrates also raises the HDL cholesterol. This is important to note since policy recommends daily intakes of 30% total fat or less (with less than 10% of the saturated) and 60% carbohydrates. Studies showing the benefits of increased fat consumption and decreased carbohydrate consumption have vastly different ratios than the ones shown here obviously.

The benefits of reducing carbohydrate and increasing fat consumption are often ignored and suggestions to raise HDL are usually conventional advice like exercising more, glass of wine and losing weight. However, this increase in HDL tends to occur more to those who had elevated HDLs to begin with and not as pronounced with those who have low HDL levels to start with. This suggest that conventional wisdom may not be effective for those who already have metabolic syndrome:

“…the effects of physical activity, alcohol, and weight reduction on HDL-C levels may be, to a large extent, dependent on the initial level with the greatest improvement achieved in subjects with high HDL and the least improvement in those having low HDL-C levels.” [54]

But why exactly does HDL cholesterol tend to decrease? The answer may lie in the elevated triglycerides. One of the problems about teaching these lipid markers is that they are often portrayed as static entities rather than dynamic entities that interact with one another. In this case, elevated triglycerides can lead to decreased HDL cholesterol through catabolism in the megalin/cubillin processes in the kidney.

“…intravascular modeling of HDL bylipases and lipid transfer factors….determinant of the rate of HDL clearance from the circulation. CETP-mediated heteroechange of HDL cholesteryl ester (CE) with chylomicron and VLDL (TG-rich lipoproteins, TRL) triglycerides results in CE depletion and TG enrichment of HFL. TG-rich HDL releases lipid poor apoA-1 and HDL remnant particles. Lipid-poor apoA-1 is filtered by the renal glomerulus and then degraded by proximal tubular cell receptor such as cubili/megalin system.” [55]

There’s a lot of greater details in that quote I extracted from the study but if you’re interested in learning these details TheFatNurse’s HDL/Triglyceride comic covers most of the details in easy picture analogic fashion.

Anyways this post is starting to deviate a bit from it’s original purpose of critiquing the lipid lecture. However, the little side adventure of exploring TGs, HDLs and insulin resistance in more depth was to show that LDL cholesterol is not the only nor always the best indicator for heart disease of which insulin resistance is highly associated with. Unfortunately the class was taught to use LDL-cholesterol as a target goal which means intervention methods focused primarily on lowering LDL-cholesterol (and not necessarily the other markers as much although the instructor did mention targeting HDL and TGs but only briefly compared to LDL cholesterol).

V. An Unexpected Twist

However…things then took an unexpected turn! For example, the next slide was titled, “Lack of Evidence for LDL Goal.” Surprisingly, the instuctor pointed out that aiming for LDL cholesterol targets did not always yield reductions in events or mortality. One slide even said that trials which lowered cholesterol did not always improve outcomes! This is not surprising as we have covered, but it is surprising that it is being presented  in a formal setting.

The instructor then informed the class of additional studies that showed pharmaceutical treatment was beneficial despite the controversies on LDL cholesterol as a target goal. One of which was the HPS study which showed you can reduce all cause total mortality in 1 out of every 57 patients with simvastatin if given for at least 5 years. [56]

However, TheFatNurse had some criticism for the way the instructor presented these trials. Specifically, the instructor didn’t make it clear whether the studies were for primary or secondary prevention groups. There are benefits for pharmaceutical interventions, such as statins, for secondary prevention (in people with known CHD disease or its equivalent risk) although the benefits are not always as dramatic as their commercials may indicate. For primary groups (people without any CHD) the benefits are unclear if any at all. More on this in a bit…

If you want to look up the population being studied, you’ll have to find the paper and hope the patient population is described. But a good way to save time is to actually go to: http://www.trialresultscenter.org which describes the patient population along with any inclusions and exclusions for the methodology. They also list the end point goals of each trial. While the instructor did mention some populations, after diving in more details TheFatNurse learned other information about the populations being studied.

One had patients with end-stage renal disease on hemodialysis, another had adults (aged 40-80 years) with coronary disease, other occlusive arterial disease, or diabetes, one trial only used MI survivors, and  another had patients with a history of cardiovascular disease, high triglycerides, and low levels of HDL cholesterol. If TheFatNurse didn’t look up any of this information, none of this demographic information would have been known! This is important because we need to ask ourselves if the results from these high-risk populations are appropriate to extract for a general primary population.

Back to the primary and secondary issue, one meta analysis found, “This literature-based meta-analysis did not find evidence for the benefit of statin therapy on all-cause mortality in a high-risk primary prevention set-up” [57] while the Cochrane Review found some minor benefits in primary populations but point out there are “shortcomings in the published trials and we recommend that caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk.” [58] This is still a hotly debated subject to this day and you can read an interesting debate/exchange between Dr. Rita Redberg from UCSF vs Dr. Roger Blumenthal of John Hopkins on the issue of statin use in primary populations. [59]

Even after showing that LDL cholesterol is not a good target the instructor ended by recommending we still continue to target LDL-cholesterol since it’s still in the guidelines. This rationale was disappointing, as mentioned earlier, since Non-HDL is also a target in the guidelines…yet it was never mentioned by the instructor. Additionally, TheFatNurse was also a little disheartened with the lack of discussion on carbohydrate control on the lipid profile. While the instructor had recommended the reduction of saturated fat and dietary cholesterol in class, TheFatNurse had a private conversation with the instructor between lectures and guess what? The instructor actually knew all about dietary carbohydrate and it’s effect on triglycerides and HDL-cholesterol. How come he didn’t mention carbohydrate reduction and make a case for eating fat then? In either case, I will give him credit for at least introducing doubt about LDL-cholesterol as the end all be all risk marker.

Summary: TheFatNurse finally had the lipid intervention lecture in school. As expected, it focused mainly on targeting LDL cholesterol. Advance lipid testing/targets were not mentioned which is to be expected as well…but the instructor didn’t even mention anything about Non-HDL cholesterol! This was rather disturbing since there was such an emphasis on LDL-cholesterol due to the ATP 3 guidelines…but even ATP 3, for all it’s flaws, mentions using Non-HDL cholesterol! The instructor also mentioned avoiding dietary saturated fat and cholesterol, which was expected and the potential benefits of carbohydrate reduction was not mentioned at all. However, the class then took a 180 with the instructor showing some studies that targeting LDL-cholesterol may not always yield the outcomes we want! TheFatNurse has to give props to the instructor for that…but then another 180 happened with the instructor saying we should still focus on reducing LDL cholesterol since it’s in the guidelines.

Some studies were then shown to the class on the support of pharamaceutical intervention. However, the instructor didn’t make it clear what the study populations were for some of the trials. This could lead to confusion in not knowing whether the results of trials were applicable to primary or secondary prevention groups. In the end, TheFatNurse was happy to at least see, even if brief, LDL-cholesterol being doubted formally in a classroom setting.

* The Cochrane group does recommend the replacement of saturated fat for unsaturated fat due to a reduction of 14% in cardiovascular events with the replacement of saturated fats with unsaturated fats, but this effect was only seen in studies of men (not those of women) lasting longer than two years and with populations that had cardiovascular risk to begin with and not the general population. They point out the effect on heart attacks and strokes individually were not clear.

Is The Paradigm Shift Starting? Media Updates and Carpal Tunnel

TheFatNurse is Alive and Well despite the lack of updates. Had to take on finals and TheFatNurse is happy to report they never stood a chance! In the meantime, lots of changes occurred since the last update in regards to the media and some new things TheFatNurse learned on carpal tunnel and diabetics.

Doctor Oz…leading the way!? If you’ve followed this blog then you’ll know TheFatNurse is no fan of Dr. Oz who often regurgitates the existing paradigm and has condemned fat as a evil. So you can imagine TheFatNurse’s surprise when Dr. Oz had not ONE but TWO shows that challenged the existing paradigm on diet! Last week Dr. Oz had Dr. Stephen Sinatra & Dr. Jonny Bowden talking about how the current view on cholesterol is all wrong, that there is nothing generally wrong with eating saturated fat, and that cholesterol in general is good for us.

WHOOOA

TheFatNurse’s reaction to this Episode

None of this is new to TheFatNurse…but seeing it on the Dr. Oz show, a huge influential media source, was too surreal! Many days and nights TheFatNurse was laughed at for questioning the existing paradigm…well perhaps no more! The show was progressing nicely until Doctor Oz attempted to use an illustration on how LDL and HDL works…something about a suitcase? Simply put, this best explains how TheFatNurse felt about it:

Let your Guests Explain How it Works!

Kudos to Dr. Oz for bringing up the subject matter, but if you’re interested in how LDL and HDL relate to heart disease check out the For All Ages FatNurse comics on Cholesterol in General and HDL/Triglycerides. However, despite the kudos, TheFatNurse was deeply disturbed by one of Dr. Oz’s comments:

I’m blown away by these side effects you’re reporting. You’re saying there’s data that statin drugs cause diabetes…

For reals? This was big news earlier in the year (February 2012) when the FDA announced they were adding warnings to statins for this very thing. It’s right here on the FDA website if you’re curious. TheFatNurse is just a little shocked Dr. Oz didn’t know that.

People being treated with statins may have an increased risk of raised blood sugar levels and the development of Type 2 diabetes.

However, TheFatNurse was happy to hear Dr. Oz ending the online segment by informing people that sugar is a bigger problem than fats in the diet. What is a bit peculiar is how the online episodes cutoff 1/4 of the show about cholesterol. The part they cutoff is the segment exonerating dietary fats and dietary cholesterol. TheFatNurse was fortunate enough to come across the missing segment tho:

The second Oz show that got TheFatNurse all excited occurred two weeks ago and challenged the paradigm of healthy whole wheat grain. This episode featured Dr. William Davis, a cardiologist, and the author behind Wheat Belly. Again, nothing new if you’ve been following this blog but to see the idea that “healthy whole grain wheat” as unhealthy being discussed so openly on Dr. Oz is just amazing.

Another media boost challenging the dominant paradigm on fat came from CBN news which did a segment on how a ketogenic diet (super low carb & high fat) could help with cancer by “starving” the center cells of glucose.

Although it wasn’t easy, Hatfield stopped eating carbohydrates, which turn into glucose inside your body. Cancer cells love glucose and need it so badly, that if you stop giving it to them, they die.

TheFatNurse hasn’t looked into the medical literature on the subject for clinical trials and what not but this is certainly something worth following up on in the future.

Speaking of blood glucose, TheFatNurse never knew how much more at risk people with impaired blood glucose such as diabetics or people with metabolic syndrome were at developing carpal tunnel syndrome. In this study,

metabolic syndrome was found to be three times more common in patients with CTS and CTS was more severe in patients with metabolic syndrome when compared with those without metabolic syndrome.

To keep it short, what happens is when glucose is elevated and around proteins such as collagen, elastin and fascia in tendons, it goes through something called glycosylation. This basically means that the glucose and proteins combine together. This impairs the function of things such as collagen, elastin and fascia. In nerves, glucose is converted to sorbitol which attracts water. Nerves also have collagen and elastin components. So as you can see in the picture below, when you have all this glycosylation occurring on the median nerve and the surrounding tendons in an enclosed space like the carpal tunnel it’s bad news.

Picture by Wilfredor

TL;DR: Looks like the media may be more friendly and picking up on information that goes against the traditional paradigm than before. Who knows what direction their influence is going to direct things in the future? Also carpal tunnel and hyperglycemia may be closely related.

New Videos from Dr. Dayspring and…Shaq? Canadian Diabetes Association approves of Juice?

If you have not seen Dr. Dayspring’s new video this week, TheFatNurse highly recommends you take a look below. TheFatNurse has mentioned Dr. Dayspring in the past so his name should be familiar. But if this is your first time hearing his name…he is a diplomate of the American Board of Internal Medicine and the American Board of Clinical Lipidology as well as a fellow of the National Lipid Association while being a professor at the New Jersey School of Medicine and the director of cardiovascular education at the Foundation for Health Improvement and Technology.

The video offers a general overview of cholesterol and heart disease – stuff you will already be familiar with if you have read TheFatNurse’s For All Ages comic series on cholesterol or any of Dayspring’s previous works on Lecturepad. However, the video offers a good layman’s explanation of cholesterol and heart disease. What interested TheFatNurse the most is Dayspring’s point about how hard it is to change medical dogma. After all, it was once considered heresy to wash your hands in the medical community. However, sanitation practices eventually changed…are we currently in the transition of another change with regards to the public’s view of cholesterol and fat? TheFatNurse hopes so!

In other news, TheFatNurse caught a video of Shaq on CNN talking about health. Shaq gives a small sample of what he eats and says he cuts down on the bread, eats an omelette in the morning, salads for lunch and steak or fish for dinner while avoiding soda and candy to keep his weight down (abdominal obesity) in order to reduce the risk for diabetes. Nice job Shaq! TheFatNurse has talked in the past about how focusing on weight shouldn’t be the only factor to be evaluated in diabetes prevention, but it is certainly a good initial step for people to target.

In other news, the latest edition of The Diabetes Communicator, which is associated with the Canadain Diabetes Association, contained some interesting news about Juices. According to the article,

Juice offers a source of a variety of vitamins and minerals and contains phytochemicals that may play a role in the prevention of cardiovascular disease

Sayyyy whhhat? So…you’re telling TheFatNurse…that you can drink juice to prevent heart disease…because somehow…sugar’s role in heart disease…doesn’t matter when it come to juices?

WHAT…TheFatNurse No Like

You can find an excellent rebuttal to this whole thing by Tony NickonChuk, a certified diabetes educator who was, “so horrified in fact that he penned a letter to the Editor-in-Chief of the publication along with the President and CEO of the Canadian Diabetes Association.” Check out his letter here.