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.

 

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Blood Sugar…shrinks the brain?

Check out this week old study! Subjects had their brain volume examined through MRI four years ago to evaluate changes that may occur prospectively.

“The aim of this study was…to investigate in cognitively healthy individuals, who did not have T2D, whether higher fasting plasma glucose levels falling in the normal range as defined by the World Health Organization were associated with declines in hippocampal and amygdalar volumes.”

The results?

Plasma glucose levels were found to be significantly associated with hippocampal and amygdalar atrophy and accounted for 6%–10% in volume change after controlling for age, sex, body mass index, hypertension, alcohol, and smoking.

High plasma glucose levels within the normal range (<6.1 mmol/L) were associated with greater atrophy of structures relevant to aging and neurodegenerative processes, the hippocampus and amygdala. These findings suggest that even in the subclinical range and in the absence of diabetes, monitoring and management of plasma glucose levels could have an impact on cerebral health. If replicated, this finding may contribute to a reevaluation of the concept of normal blood glucose levels and the definition of diabetes

Pretty fascinating stuff. Keep in mind that diabetic/prediabetic/normo ranges for blood glucose are usually changing. They used WHO guidelines in this study but a range of <6.1 nmol/L is usually the beginnings of pre diabetes for many other guidelines.

From the mayo clinic – Fasting blood sugar test. A blood sample will be taken after an overnight fast. A fasting blood sugar level less than 100 mg/dL (5.6 mmol/L) is normal. A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes

However, the study took this into consideration:

…subanalyses using even tighter inclusion criteria for fasting glucose (<5.6 mmol/L) and for BMI (<25 kg/m2) produced essentially identical findings or, in the case of BMI, slightly stronger findings. This result suggests that the effect of plasma glucose on cerebral structural integrity is not restricted to the upper normal range.

Update: Another study this week showing the differences between Teens with Metabolic syndrome and those that don’t in regards to cognitive function. As expected, cognitive scores were lower in the teens with metabolic syndrome.

References:

Higher normal fasting plasma glucose is associated with hippocampal atrophyThe PATH StudyNicolas Cherbuin, PhD, Perminder Sachdev, MD, PhD, FRANZCP and Kaarin J. Anstey, PhD. Neurology September 4, 2012 vol. 79 no. 10 1019-1026

Obesity and Metabolic Syndrome and Functional and Structural Brain Impairments in AdolescencePo Lai Yau, PhDa, Mary Grace Castro, BSa, Adrian Tagania, Wai Hon Tsui, MSa, and Antonio Convit, MD doi: 10.1542/peds.2012-0324

 

Interesting New Meta Analyses Out on BP and Low Carb. Response from Egg Study

In case you haven’t heard, last week the Cochrane Hypertension Group released some compelling updates on Blood pressure medications (1). But before we get to that, you may be wondering what the heck the Cochrane Collaborative is. While TheFatNurse can’t comment on all nursing schools, during TheFatNurse’s time as a wee little nursing student, one of the buzzwords was Evidence Based Practice in school. As a result, one of the organizations to help increase the use of evidence based practice is the Cochrane collaboration.

The Cochran Collaboration consists of over 28,000 volunteers in more than 100 countries that saw a need to organize the medical literature in a way that was easy to understand and evaluate. The goal is to allow evidence based practice to make its way into the healthcare setting. They go about doing this through systematic reviews of randomized control trials. So what did they findout about hypertension and blood pressure?

The Cochrane group set out to see what the literature showed about individuals with anti hypertension medications and mild hypertension (systolic of 140-159 or diastolic of 90-99) but no prior related issues involving cardiovascular diseases/events. They wanted to examine Randomized Control Trial studies that had at least 1 year duration. Specifically, the outcomes from the literature they were examining were all hypertension related such as coronary heat disease, stroke, mortality, total cardiovascular events and adverse effects from medications causing withdrawals. So what did they conclude? In the author’s own words:

In this review, existing evidence comparing the health outcomes between treated and untreated individuals are summarized. Available data from the limited number of available trials and participants showed no difference between treated and untreated individuals in heart attack, stroke, and death. About 9% of patients treated with drugs discontinued treatment due to adverse effects. Therefore, the benefits and harms of antihypertensive drug therapy in this population need to be investigated by further research.

Pretty interesting. Another new study out last week was a meta analysis on low carb diets (2). Here were the results:

A total of 23 reports, corresponding to 17 clinical investigations, were identified as meeting the pre-specified criteria. Meta-analysis carried out on data obtained in 1,141 obese patients, showed the LCD to be associated with significant decreases in body weight (−7.04 kg [95% CI −7.20/−6.88]), body mass index (−2.09 kg m−2[95% CI −2.15/−2.04]), abdominal circumference (−5.74 cm [95% CI −6.07/−5.41]), systolic blood pressure (−4.81 mm Hg [95% CI −5.33/−4.29]), diastolic blood pressure (−3.10 mm Hg [95% CI −3.45/−2.74]), plasma triglycerides (−29.71 mg dL−1[95% CI −31.99/−27.44]), fasting plasma glucose (−1.05 mg dL−1[95% CI −1.67/−0.44]), glycated haemoglobin (−0.21% [95% CI −0.24/−0.18]), plasma insulin (−2.24 micro IU mL−1[95% CI −2.65/−1.82]) and plasma C-reactive protein, as well as an increase in high-density lipoprotein cholesterol (1.73 mg dL−1[95%CI 1.44/2.01]). Low-density lipoprotein cholesterol and creatinine did not change significantly

Again, very interesting stuff. Also David Spence, the author behind the egg yolk as deadly as cigarette smoking study (as some in the media dubbed it), responded to Nutritionist Zoe Harcombe’s critique of his study in her blog’s comments. Just scroll down until you find it.  It’s a good debate between Dr. Spence and Zoe Harcombe.

Picture by Coldbourne from ClipArt. Creative Commons Attribution-Share Alike 3.0

TheFatNurse hopes this is where the future of research is heading towards where debate can occur openly and freely for people to observe and put in their analysis. What would make this better is if all studies were open to the public and not just the abstracts. For example, the two studies TheFatNurse mentioned are not accessible with TheFatNurse’s university account which means TheFatNurse and others can only rely on the abstract to see what the study is about. This is a start, but the abstract tells us nothing about the details on how the experiment was setup, potential confounding factors and other information to allow an honest critique. By having open debate, it’ll be much more productive in moving towards the truth and confirming the validity of studies whether they are for or against the existing paradigm of fat.

References:

(1) Pharmacotherapy for mild hypertension

  1. Diana Diao1,*,
  2. James M Wright2,
  3. David K Cundiff3,
  4. Francois Gueyffier4

Editorial Group: Cochrane Hypertension Group

Published Online: 15 AUG 2012

Assessed as up-to-date: 1 OCT 2011

DOI: 10.1002/14651858.CD006742.pub2

(2) Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors

  1. F. L. Santos1,
  2. S. S. Esteves2,
  3. A. da Costa Pereira3,
  4. W. S. Yancy Jr4,5,
  5. J. P. L. Nunes3,*

Article first published online: 20 AUG 2012

DOI: 10.1111/j.1467-789X.2012.01021.x

LowCarb/HighFat or Low Fat + medication on blood pressure

One of the things TheFatNurse has noticed about eating a reduced carb and high fat lifestyle is the drop in blood pressure TheFatNurse is experiencing. Seriously, TheFatNurse has gone from an average of 124/75ish  to…110/62…what the hell…time to look into this mofo.

This is an older study in the Arch of Intern Med from 2010 that is pretty interesting (1). It compared a low carb diet to a low fat diet + Orlistat. This drug works by preventing the absorption of fat and therefore reduce calories. Of course if you ain’t absorbing it…it’s gotta come out somewhere right? Thus, one of the potential “treatment effects” is fat oily and foul smelling stools known as steatorrhea.

Yea…TheFatNurse has random thoughts…Deal with it!

The researchers were looking to see what sort of metabolic, body weight and adverse effects these two diets would have in a 48 week period in overweight subjects with some having obesity related problems such as diabetes, lipid issues and hypertension. However, despite the low fat diet having a leg up with medication versus the low fat diet, the researchers still predicted the low carb diet would make participants lose more weight.

One of the things TheFatNurse always checks when experiments are testing low carb diets is what they mean by “low carb.”. Depending on who’s doing the study, low carb can be defined anywhere from 10 to 40 percent of one’s daily caloric intake. Even a 40% carb diet can technically be classified as low carb since the USDA Dietary Guideline For Americans actually recommends upwards of 65% of your daily diet being from carbs. The diets in this study seemed to reflect the more hardcore low carb community diet:

Participants were instructed to restrict carbohydrate intake initially to less than 20 g/d using pocket guides and hand- outs. Participants could eat unlimited meat and eggs, 112 g of hard cheese, 0.48 L of low-carbohydrate vegetables (eg, leafy greens), and 0.24 L of moderate-carbohydrate veg- etables (eg, broccoli, asparagus) daily; calorie intake was not restricted.

And the low-fat diet with orlistat:

Participants were instructed to restrict intake of total fat (<30% of daily energy), saturated fat (<10% of daily energy), cholesterol (<300 mg daily), and calories using pocket guides, hand- outs, and individualized goals.13,14 Recommended calorie in- take was 500 to 1000 kcal below a participant’s calculated weight maintenance intake.15 In addition, a 30-day supply of orlistat (120 mg before meals 3 times a day) was provided monthly.

Notice something? The low-carb diet had no restriction in calories but the low fat diet followed the usual protocol of eating below your maintenance caloric intake (along with the usual less than 10% saturated daily fat and less than 300 mg daily cholesterol. So what were the results?

Despite the different diets, both groups lost similar weight with no statistical differences. Additionally, triglycerides, LDL-C, HDL-C improved in both groups with no statistical differences either (remember tho, the LDL/HDL  cholesterol isn’t the true benchmark, its the particles but no lipoprotein particle testing was done here). Additionally, TheFatNurse thought the Hemoglobin A1c1% change was pretty interesting. A1C1 measures your sugar levels for the past 3 months and in this study the percent of change was -0.30 (CI; -0.52 to -0.09) for the low carb diet compared to the -0.06 (CI; -0.36 to +0.14) for the low fat diet with orlistat. That’s a pretty good change, although it wasn’t statistically significant (P=0.10); This means there’s a 10% probability that the differences were due to chance. Just an interesting observation.

Perhaps the most interesting portion was the Blood pressure readings. The low carb diet won out with a difference of (in mm Hg)  -7.44 (CI;-11.12 to -3.75) systolic and -4.97 (CI;-7.64 to -2.29) diastolic. with P values for both <.001. People eating the low fat diet with Orlistat actually increased their blood pressure on average.

When one thinks about the diet composition of the low carb group with the results its pretty interesting. Remember the instructions, “eat unlimited meat and eggs.” This translated to the low carb group eating not only more calories in general, but almost double the amount of total fat on a daily basis. As for saturated fat? The low carb group ate a little bit more than double the saturated fat on average daily than the low fat group. Cholesterol intake? Well over double on average compared to the low fat group.

Contrast that with what’s in TheFatNurse’s review textbook that TheFatNurse used for the nursing licensure exam on reducing hypertension:

“Consume a diet low in fat, saturated fat, and cholesterol.”

Hmm…quite the opposite results we got in this study? So why is this? Well the lower carbohydrates consumed will effect the body’s insulin levels. insulin has an effect on the kidneys. It causes your kidneys to retain salt and therefore lead to increased blood pressure. Is this new to you? TheFatNurse thinks it might be for a lot of people, but it shouldn’t be considering “the sodium-retaining effects of insulin have been known for a long time [since 1953].” (2)

Bottomline: TheFatNurse is not against low fat per se, just against the stigma that fat has gotten in today’s society. Additionally, please don’t make the mistake of treating this study as a low fat vs low carb high fat diet (LCHF) fight because the inclusion of orlistat makes true comparisons difficult. Not to mention this is just one study. TheFatNurse used this study to show results can run contrary to what is taught about eating fat and changes inside the body.

Other News: Yes TheFatNurse is updating at a snails pace so far lol. Lots of changes going on right now with TheFatNurse, will hopefully start posting more regularly once things settle down

References:

1) William S. Yancy Jr, MD, MHS; Eric C. Westman, MD, MHS; Jennifer R. McDuffie, PhD, RD, MPH; Steven C. Grambow, PhD; Amy S. Jeffreys, MStat; Jamiyla Bolton, MS; Allison Chalecki, RD; Eugene Z. Oddone, MD, MHS (2010). A Randomized Trial of a Low-Carbohydrate Diet vs Orlistat Plus a Low-Fat Diet for Weight Loss. Arch of Intern Med. 170(2) 136-145

2) B. Grunfeld, M. Gimenez, M. Balzaretti, L. Rabinovich, M. Romo,  and R. Simsolo (1995) Insulin Effect on Renal Sodium Reabsorption in Adolescent Offspring of Essential Hypertensive Parents. Hypertension 26  1089-1092.

HDL for all ages!

HDL cholesterol is often touted as a super stud in heart disease prevention. As a result, common knowledge has continually stressed increasing one’s HDL cholesterol without really moving beyond the “HDL Good LDL Bad” message. This belief can target researchers as well, but some recent studies, as covered by Peter Attia, reveal HDL cholesterol and heart disease not being as clear cut as one might believe.

As a result, TheFatNurse thought it would be a good idea to go over some simple basics about what exactly HDL is and does in your body through a comic. This comic is based on a series of lectures by Dr. Thomas Dayspring and is only a simplified version of his more detailed analysis. See below if you’re itching to read Dr. Daysprings more detailed lectures!

TheFatNurse also wants to extend a personal thank you to Dr. Dayspring. TheFatNurse is still beginning his journey in exploring all things lipid and Dr. Dayspring your encouragement, feedback and information have made exploration exciting.

Before reading, TheFatNurse recommends you read the first two comics on cholesterol as it builds upon some knowledge needed for this third comic. Click here to read the HDL comic (semi-long read!) or the picture below.

***For the first two comics see: #1 Cholesterol For All Ages and #2 Cardiovascular Markers For All Ages. Interested in more? TheFatNurse highly recommends you look up Dr. Dayspring’s lectures on HDL which you can start with here and here.

The World’s Most Powerful Doctor

TheFatNurse loves looking through the literature when exploring dietary issues to build a case for fats. However, even when providing numerous studies and quoting important researchers like Dr. Dayspring or popular healthcare bloggers like Dr. Eenfeldt…there are some doctors who are just too powerful to beat…how does one get through!?

The quote on cutting out fat to save lives from Dr. Oz @5:03 from:

LDL Cholesterol = Bad? Not Quite That Simple

Continuing with this week’s HDL mainstream news, TheFatNurse thought you should be aware of a man named Dr. Ronald Krauss and his work on LDL cholesterol (you know, the “bad” one). In the 1980’s, Dr. Krauss was one of the prominent researchers to point out that many studies showed those with heart disease and those without had almost the same LDL levels.

“If you look in the literature and just look at the average coronary patients…their LDL-cholesterol levels are often barely discernibly elevated compared to patients who do not have coronary disease.” (1)

So how prominent a figure was he? He was once the chairman for the nutritional committee for the American Heart Association (AHA) – The same AHA that was recommending low fat intake resulting in more carbohydrate intake as a consequence in order to decrease heart disease. This is ironic, as mention by Gary Taubes in Good Calories Bad Calories, since Krauss had found associations between carbohydrate increase and the risk of Heart Disease.

Did Krauss’ research make him a socially awkward penguin in the AHA?

Additionally, Krauss also found substituting fat with carbohydrates increased small dense LDL particles which are associated with increased heart disease compared with the not as dense LDL particles from saturated fat which is not as bad. (2) In a NPR interview (2007):

“…recommendations are now pushing hard for lowering LDL cholesterol by reducing fat and saturated fat…based on the assumption that it would improve LDL related heart disease risk. Our evidence is it doesn’t effect the dense LDL at all. Substituting carbohydrate for fat, a natural consequence of those recommendations will actually increase levels of the small LDL”

“…processed and refined starches and sugars that are the most deleterious metabolically…food that contain a lot of fiber…have a lot of bulk but not as much carbohydrates…this recommendation [eating more carbs rich in fiber] is very difficult in practice…[agree with Taubes in] considering all carbohydrates as  potentially adverse.”

Dissecting Heart Disease Like a Boss

Much of Krauss’ work points to how much of the advice that is considered fact may instead be harmful to us. In an interview just last month (3):

“…we fed these low fat diets and reduced the fats by substituting carbohydrates, which was at that time and still remains the current paradigm, we really didn’t achieve what we had wanted to achieve…some improvement in the overall amount of cholesterol in the very small percentage of individuals who had very high amounts of small LDL particles in their blood already… the majority of people we studied, the high percentage of people who had the normal metabolic profile, with more of the safer, Pattern A, larger particle LDL, shifted into the riskier, pattern B mode when we reduced their saturated fat intake.”

Because of his work, Krauss is well known in the low carb community when they need supporting claims from a well established nationally recognized physician and researcher:

“…we were certainly concerned about increasing heart disease risk, so we turned our attention ultimately away from feeding higher carbohydrate, lower fat diets, to doing the reverse, to lowering carbohydrate and raising fats, and that’s where we intersected with the world of people very interested in very low carbohydrate diets.”

“[Interviewer] You’re saying that in people who ate more fat and less carbohydrate, and in fact, who ate more saturated fat, they had a little more total cholesterol fat in their blood, but it was mainly being transported in big, fluffy LDL particles, which are the kind that scientists who study heart disease consider pretty safe.

[Krauss] Yes. When people ate more fat and less carbohydrate, the number of small particle LDLs remained low, and switching from monounsaturated to saturated fat didn’t increase their number at all.  In fact, when people switched from mono- to saturated fat in this study, the large particle LDLs might have gone up a little bit…the small particles went down.  So by anybody’s current criteria about whats’s important for heart disease risk, saturated fat caused no increase in risk.”

What is interesting about the LDL particle theory is the debate on whether or not the size and density of the particles matter. Krauss seems to believe the smaller denser particles are more of a concern, whereas others believe it doesn’t matter such as Dr. Dayspring from last week’s post. As Krauss states:

“I and many of my colleagues would argue that the biggest concern is warranted when the number of smaller particles is high, not the larger ones.”

However, both viewpoints can be compatible based on numbers and the ability of the larger LDLs to carry more cholesterol:

“It’s definitely associated with lower heart disease risk if the cholesterol is carried in larger particles, and that’s because there are fewer of them”

Confused? Here’s a lecture from Dr. Tara Dall that might clarify things better:

So does Krauss’ work offers more support that you can eat all the saturated fat you want? After all in the same interview last month:

“…in our 2006 study, the blood work was better when feeding people higher fat diets, than…feeding them lower fat and more carbohydrates…keep in mind, this was in the setting of lower carb and a mixed protein diet, proteins from various sources from white meat and dark meat and chicken and fish and beef.”

However, you may recall TheFatNurse posting last month about another Krauss study that showed saturated fat could be associated with increased CHD risk if it came from high amount of red meat (all beef in that study). Krauss touches upon that study in this interview:

“…keep in mind, this was a very high beef diet.  People were eating beef breakfast lunch and dinner.  So this is really way outside of what we would ever consider to be a usual health practice.  Maybe some people do it.  But not many.”

Cause you’re in the low beef study group dude

Currently, Krauss is using these latest results to try and isolate the reason for excessive red meat being associated with heart disease. Whereas before someone might easily blame it on the saturated fat, Krauss believes it could be other dietary consumptions with the saturated fat in red meat. Is it the iron? That’s one idea from Krauss and TheFatNurse looks forward to seeing more from Dr. Krauss in the future.

Bottom Line: Dr. Ronald Krauss has been a pioneer in the field of dietary consumption and heart disease. His work throughout the years shows how science and nutrition are constantly evolving and we must never accept anything as fact until it’s been fully tested. When long held facts such as “HDL = good LDL = bad” or “saturated fats can cause heart disease” are no longer that clear cut, we as a society need to be open to reexamining these long held beliefs and begin research on new ones.

1) Taubes, Good Calories Bad Calories, page 170

2) http://www.npr.org/templates/story/story.php?storyId=15886898

3) http://www.meandmydiabetes.com/2012/04/17/ron-krauss-saturated-fat-red-meat-it-depends/