Just Read: Always Hungry, by David Ludwig, MD

I actually didn’t just read this book, I read it awhile ago, but haven’t posted on it, until now (thanks for the nudge @ePatientDave).

I recommend this book as a companion to the others I have reviewed here (Why We Get Fat, Big Fat Surprise, The Case Against Sugar) because it’s more practical, written for a non-clinician audience by an experienced physician expert in the field, David Ludwig, MD (@davidludwig).

(Editorial comment, unlike other heath-oriented movements I have interacted with, I am pleased to see so many in the nutrition movement to be using social media to communicate their ideas. This is not the case among other physician-involved health movements I have seen, and it’s a loss for them, because there’s nowhere to go to ask questions.)

The Science

David covers just enough of the science to be useful for someone to understand the why of this approach:

So, in the 1970s, prominent nutrition experts began recommending that everyone follow a low-fat diet, in the belief that eating less fat would automatically help lower calorie intake and prevent obesity. Thus began the biggest public health experiment in history. Over the next few decades, the U.S. government spent many millions of dollars in a campaign to convince Americans to cut back on fat, culminating in the creation of the original Food Guide Pyramid…

Ludwig, David. Always Hungry?: Conquer Cravings, Retrain Your Fat Cells, and Lose Weight Permanently (p. 18). Grand Central Publishing. Kindle Edition.

And one example of the answer to whether this approach worked (the Look Ahead Study):

The study, conducted in sixteen clinical centers in the United States, assigned about five thousand adults with type 2 diabetes to either a low-fat diet with intensive lifestyle modification or to usual care. The study, published in the New England Journal of Medicine in 2013,33 was terminated prematurely for “futility.” Analysis by independent statisticians found no reduction of heart disease among participants assigned to the intensive low-fat diet, and no prospect of ever seeing such a benefit emerge.

Ludwig, David. Always Hungry?: Conquer Cravings, Retrain Your Fat Cells, and Lose Weight Permanently (p. 59). Grand Central Publishing. Kindle Edition.

There’s tons of published information about these findings, though, this book is more directed at successful behaviors.

The Behavior

The book is really designed as a plan to change dietary habits to ones that are more consistent with maintaining a healthy weight. Ludwig appropriately diminishes the argument that being overweight is about lack of self-control or too-large portion sizes or calories-in vs calories-out.

Although the focus on calorie balance rarely produces weight loss, it regularly causes suffering. If all calories are alike, then there are no “bad foods,” and the onus is on us to exert self-control. This view blames people with excess weight (who are presumed to lack knowledge, discipline, or willpower)—absolving the food industry of responsibility for aggressively marketing junk food and the government for ineffective dietary guidance.

Ludwig, David. Always Hungry?: Conquer Cravings, Retrain Your Fat Cells, and Lose Weight Permanently. Grand Central Publishing. Kindle Edition.

As I have mentioned previously, I am a former-fat person, and even before I went to medical school, I felt the medicalization of obesity had serious shortcomings from my own personal experience – it appeared to me that the creators of this approach had never experienced being overweight, like so many other things in medicine that have been designed TO people and not WITH people.

One of the challenges of moving away from a low-fat diet, though, is that there are extreme versions of the opposite, such as ketogenic diets. These may be successful for some, however, they require a level of commitment and medical supervision that’s not feasible for everyone.

From my read, Ludwig takes a very reasonable patient-centered approach (since he’s a physician, after all :)), and steers away from extremes into a slow modification approach that a person could follow if they were thusly motivated (and that’s the caveat, see below). He does not permanently forbid foods and the book is obviously written with enough guardrails (he is a physician after all…) that it appears safe relative to other guides I have seen.

The Motivation

The book is great for those who are motivated and want to make a change. At the same time, it’s also very well known from studies that giving people information is not sufficient for them to change their behavior (see this review from the American Heart Association – the smartphone app graveyard continues to grow in size: Just Read: Current Science on Consumer Use of Mobile Health for Cardiovascular Disease Prevention).

I have recommended this book to some people, and my assessment of the uptake is “marginal,” not because of the book, because of where people are in their journey. Which is fine, that’s where information fits in, for the times that support is there and people are ready.

As Ludwig states, we’re in the middle (maybe the end?) of a 40-year failed experiment in changing the nutrition habits of the world. The data shows that people did in fact listen to the advice given and changed their habits (yet another perpetuated myth – “if people would just do as they were told”). It’s going to be an exciting next 40 years….

Just Read: “Why We Get Fat,” by Gary Taubes

I actually read this book some time ago and didn’t post on it until now.

This book would be a companion to 2017’s “The Case Against Sugar” also by Gary Taubes (see my review of that book here) (@GaryTaubes). Written in 2010, it explores the causes of obesity, and makes the case away from a “calories in-calories out” approach to an endocrine (hormonal) mediated one.

The reason I am interested in exploring this is because of the potential harm I see in blaming culture around obesity. What if the medical profession is telling people to do the wrong things, and then blaming them when their biology achieves the goals of their physician-directed behavior?

A recent (2012) study of medical students has shown that the explicit biases (ones they are willing to endorse) are:

  • Bias against lesbian, gay, bisexual, and transgender (LGBTQ) human beings
  • Bias against human beings who are obese

In fact, the bias against obese people is stronger than that against LGBTQ:

Explicit attitudes among medical students 54441
Explicit attitudes among medical students 54441 (View on Flickr.com)

Of all the dangerous ideas that health officials could have embraced while trying to understand why we get fat, they would have been hard-pressed to find one ultimately more damaging than calories-in/ calories-out. That it reinforces what appears to be so obvious— obesity as the penalty for gluttony and sloth— is what makes it so alluring. But it’s misleading and misconceived on so many levels that it’s hard to imagine how it survived unscathed and virtually unchallenged for the last fifty years. It has done incalculable harm.

Taubes, Gary (2010-12-28). Why We Get Fat: And What to Do About It (Kindle Locations 1187-1191). Knopf Doubleday Publishing Group. Kindle Edition.

This book is clearly not intended to guide a person on how to alter their diet in a step by step method – it is aimed more at a scientific explanation around the causes of obesity. There are other books to guide a person through a different dietary approach, most notably “Always Hungry,” by David Ludwig, MD (@DavidLudWigMD), which I’ll post on separately.

Just Watched: Low-Carb High Fat Diet in Type 1 Diabetes

The origin of this post is that I sent a tweet earlier this week regarding the current crisis in insulin pricing referring to the Banting Diet, which is the precursor of the low-carb high fat diet (or LCHF diet). I sometimes do this (sending unclear messages) assuming that people will figure them out, and usually, that’s not the outcome 🙂 . At least it starts conversation (maybe I do this subconsciously, I don’t know).

In any event, I have been interested in nutrition for a long time and more interested recently (see:Just Read: Why Eating Fat May Not Make You Fat (The Big Fat Surprise) ), as more data is being produced about where our dietary guidelines came from. In the case of diabetes, I have been curious about the ways the medical and other professions counsel patients on diets in ways that may actually increase their risk of diabetes and increase their insulin requirement.

My question, therefore, has been whether the need for insulin could be eliminated in some people and reduced in others, which would blunt the impact of pricing and make living with diabetes more affordable. The other question I have is about the whether reducing the use of specialized insulins for some population would have an added effect, making the pricing power, less powerful.

I’ve read a few papers about this. I don’t feel comfortable doing a literature review myself because these days it’s really hard to interpret papers if hidden biases aren’t known. That and I may be a physician, but I do not know what it is like to live with diabetes. I do know what it is like to live as a former fat person so there is some relevance here for me.

Through the magic of YouTube, Dr. Troy Stapleton (@drtroystapleton) explains his own journey as a person with type 1 diabetes and the LCHF diet. He’s going to to have much more credibility than I and this is a good science-based + authentic overview from a patient perspective. Watch:

A person who produces insulin on this diet is going to have an insulin production curve closer to a person with type 1 diabetes (flat) compared to a person without diabetes (insulin spikes), with the idea that insulin and specifically too much insulin is a requirement for obesity.

#ILN innovating in nutrition, too. #LCHF in Chicago. #ketogenic #ketogenicdiet #lessinsulin

A post shared by Ted Eytan (tedeytan) on

I’m planning to do some more study this summer. At the same time, there are far more experienced researchers, journalists, physicians and scientists engaged in this work, so I’m more interested in dialogue than leadership (they are doing just fine). I always say if there’s a better way to do something, I want to know about it.

This is life in the family medicine revolution (#FMrevolution), where unlimited curiosity reigns in the interest of a person, family, community’s long healthy life. Feel fee to let me know your thoughts in the comments.

Just Read: The Case Against Sugar

One of my earliest memories was the rush to the grocery store by my family to stock up on saccharin sweetened beverages when it was feared they would be pulled off the market, in 1977. The shelves were bare (it was as much an emergency as any I remember in the household)…

This was the headline (behind paywal, if you have library access):

By, Tom Shales. 1977. “Tears & Fears: Threat to Saccharin Spurs New Hoarding! Diet-Rite Dementia, Tab Teetotaling in the Offing?” The Washington Post (1974-Current File), Mar 15, 2..

I looked this piece of history up online after I read Gary Taubes’ The Case Against Sugar, and amazingly, in this piece from March, 1977, they seemed to express some of the wisdom that’s now being discussed 40 years later (almost to the day):

From Pending FDA Saccharin Ban A Bitter Dose for Many in U.S. – The Washington Post, April 4, 1977

There are various problems with the high current levels of consomption, according to food experts. Measured in calories, sugar and other sweeteners – the main other sweetener is corn syrup – now provide about a fifth of the average American’s daily diet. But sweeteners contain none of the protein, vitamins and minerals the average person needs. These things must come from the other four-fifths of the diet: in this sense, the sugar fifth is wasted.

A second problem is the more familiar and simpler one, that sweetened foods are fattening. A third, related problem is the pervasiveness of sweeteners. A high percentage of our food today is processed, as opposed to fresh, and a high percentage of processed food is sweetened.

More than two-thirds of our daily sugar and other sweeteners comes to us in processed foods, including soft drinks and other processed beverages.

The wisdom they may have not had, at least in popular thought, was that sugar is more than wasted calories. There’s evidence that it is a metabolically active distinct subtance that changes the chemistry of our bodies in ways other forms of calories do not.

And actually, many scientists already knew that, however that science wasn’t promoted or supported by various interests….

Exonerating Fat, Arguing Against Sugar

This book continues a series of works by Taubes and others calling into question a 40 year experiment (see: Just Read: Why Eating Fat May Not Make You Fat (The Big Fat Surprise) in changing American (and global) eating habits to banish fat, which by definition means promoting carbohydrates (you have to eat something).

And promote they did, according to the record –

et tu, Consumer reports? American Heart Association?

In our lifetimes…

The magazine Consumer Reports may have captured this logic perfectly (of creating sugar sweetened cereals) in 1986 when it claimed, “Eating any of the cereals would certainly provide better nutrition than eating no breakfast at all.”

(By the mid-1990s, even the American Heart Association was recommending we have sugar candies for snacks, rather than foods that contained saturated fat.)

Bringing Occam’s Razor

The book adopts a philosophy that is used in medicine widely – Among competing hypotheses, the one with the fewest assumptions should be selected. Otherwise quoted as “if it swims like a duck, sounds like a horse, etc etc.”

In doing so, the possible causes of what are known as “Western Diseases” (read location 3729 on kindle to see the list) are reviewed through a lens that involves insulin metabolism, and specifically insulin resistance, which is known to be central to diabetes and probably a requirement for obesity. The counter-discussion is that obesity is a cause of insulin resistance, this is what we were taught in medical school, and this is extensively reviewed in the book.

In any event, everything from gout to hypertension is recast in an Occam’s mindset, in that the things we’ve been taught about what causes these diseases (purines for gout, salt for hypertension) may actually link back to insulin resistance as causing the causes we were taught about.

Which happens to track the increase in consumption of sugar in society.

In fact, a review of my own postings from social media in 2012 reveals that I was unsure about the causes of hypertension, based on my own medical training and extensive review of the literature. That says something: (7) Ted Eytan’s answer to Does weight loss cause blood pressure to go down, or are both the result of something else (like more physical activity)? – Quora

The People and the Science

As with Nina Teicholz’ book, there’s a discussion of the people and personalities involved in the science and sociology of our diet, and like most humans, they are fallible, imperfect beings. It is true now that when I read a paper involving nutrition, I now have to study who the authors are and which institution they are from so that I can track back to the potential conflicts they may have. We always have done that with medical literature (review the science and relate it to the person doing the science), this book just gives a roadmap (along with Teicholz’) to the nutritional science community.

Where we came from

I have always believed that we have to know where we came from to know where we’re going, and there’s a ton of history in here. It’s a marvel to think about what was going on in Washington, DC, and even my home state of Arizona, when I was growing up, that would shape our country’s health destiny.

(side story: while I was an undergrad in Tucson, Arizona, I did some data entry on a nutritional study to get research experience, and I remember that the software that we were using didn’t have entries for the new “fat free” foods being marketed. My faculty sponsor told me, “Fat free salad dressing is really just sugar and water, so code it like that”)

The question of whether artificial sweeteners are healthy or not is not fully addressed in the book, because it’s not fully addressed in the science. What they (sweeteners) did, though, was raise the cry for a healthier life and a freedom from obesity and diabetes. Just read the quotes from the above Washington Post article:

“Please . . .” a woman from Dallas implores. “I don’t know what we would do for grandma if saccharin is banned.”

“I am . . . a former fat person!” another woman, from Huntington Beach, Calif., exclaim. “I use saccharin every day in cooking.”

“As the mother of a 12-year-old diabetic child, I appeal to you . . .” writes a third petitioner, from Dunwoody, Ga.

And this commercial from 1979, when a calorie was a calorie, and people were so…thin*.

*As a former fat person, the intent of sharing this bit of history is not to fat shame, it’s to explore the history of obesity and causes that might be reversible or preventable in the interest of health, with the recognition that health is multi-dimensional and factorial 🙂

Just Read: Triglycerides and Cardiovascular Disease – American Heart Association Scientific Statement

Yes, all 40+ pages of the American Heart Association’s scientific statement, published in 2011 (the most recent one – citation below), for leisure.

Why?

Triglycerides are that lipid component in our blood that we (or let’s say I) are trained not to pay that much attention to, especially relative to cholesterol (LDL, HDL, etc), and yet its story unlocks a lot of mysteries around nutrition and health (again, for me).

Jumping right in.

  • “It is especially disconcerting that in the United States, mean triglyceride levels have risen since 1976, in concert with the growing epidemic of obesity, insulin resistance (IR), and type 2 diabetes mellitus (T2DM).”
    • As much as we’re fighting LDL, we don’t seem to be winning on this one. Why? And does it matter? (several reasons, and yes)

The dyslipidemic triad and diabetes

High triglyceride levels that accompany either normal or impaired fasting glucose predict the development of Type 2 Diabetes,1and therefore, hypertriglyceridemic states should prompt surveillance to rule out T2DM. In addition, 35% of T2DM adults have fasting triglyceride levels > 200 mg/dL associated with decreased HDL-C and small, dense LDL particles.

Size matters – of LDL particles, that is

LDL particles in patients with DM may be atherogenic even at normal LDL-C concentrations..In addition, hypertriglyceridemia is associated with small, dense, and CE-depleted LDL particles. Thus, individuals with T2DM and mild to moderate hypertriglyceridemia exhibit the pattern B profile of LDL (smaller, denser particles) described by Austin and Krauss; these particles be more susceptible to oxidative modification and catabolism via macrophage scavenger receptors

That’s the not good thing that happens inside blood vessels that causes disease and it’s connected to triglycerides.

In other words (my interpretation), it’s not what triglycerides mean by themselves, it’s the pattern that they are connected to. And therefore, looking at just one number (LDL) has limitations to predict disease. On the other hand, focusing on LDL is easy to do and simple to understand…hence the need for this scientific statement to understand the biology better than most people probably do.

Continuing on.

How we got here. The low-fat diet aka SnackWells USA

The relationship between percent of total fat intake and change in triglyceride and HDL-C concentrations was reported in a meta-analysis of 19 studies published by the Institute of Medicine. In this analysis comparing low-fat, high-CHO diets versus higher-fat diets, for every 5% decrease in total fat, triglyceride level was predicted to increase by 6% and HDL-C to decrease by 2.2%

Overall, optimization of nutrition-related practices can result in a marked triglyceride-lowering effect that ranges between 20% and 50%. These practices include weight loss, reducing simple CHO at the expense of increasing dietary fiber, eliminating industrial-produced trans fatty acids, restricting fructose and SFA, implementing a Mediterranean-style diet, and consuming marine-derived omega-3 PUFA (Table 11). Dietary practices or factors that are associated with elevated triglyceride levels include excess body weight, especially visceral adiposity; simple CHOs, including added sugars and fructose; a high glycemic load; and alcohol.

And the American Heart Association recommended high carbohydrate diets and even candy in the prevention of cardiovascular disease. Oops.

For the biologists/scientists – how carbohydrates may result in higher triglycleride levels and unhealthy lipid profiles

Mechanistically, high CHO intake triggers pancreatic insulin release in response to increased blood glucose. Insulin, in turn, activates sterol regulatory element–binding protein, (SREBP-1c), a transcription factor that regulates fatty acid and triglyceride synthesis. Recently, 2 additional transcription factors, X-box binding protein 1 (XBP1) and CHO response element–binding protein (ChREBP), have been identified as inducers of hepatic lipogenesis in response to ingested CHOs (eg, fructose and glucose) that is independent of insulin.431,432 In contrast, unsaturated fatty acids reduce or inhibit SREBP-1c transcription, thereby reducing hepatic fatty acid synthesis430 and plasma triglycerides.

Using drugs to treat

However, in LIPID, although baseline triglyceride level was not signifi- cantly associated with CVD risk in patients given placebo, each 89-mg/dL decrease in on-treatment triglyceride level in patients given pravastatin significantly decreased CVD risk by 11%, as well as by 14% after adjustment for nonlipid risk factors. However, the lipid-related parameters most strongly associated with CVD risk in LIPID were apo B, LDL-C, and the ratio of TC to HDL-C

Again, the dyslipidemic triad.

Taken together, reductions of 50% or more in triglyceride levels may be attained through intensive therapeutic lifestyle change.

A low fat, high carbohydrate diet increases triglycerides and decreases HDL, the opposite, a higher fat, lower carbohydrate diet reduces triglycerides and increases HDL. For me this explains the non-sequitir of my pathology textbook in medical school stating that high carbohydrate diets are a risk factor for heart disease at the same time high carbohydrate diets were being recommended to prevent heart disease.

A discussion of statins is out of scope here – many many many, many many, articles already cover this.

Andrew Weil, MD’s advice to us in medical school – understand what you’re prescribing to your patients

…I think he may have said that we should try every drug we prescribe to understand its effects (with rationality of course) but human memory can be semi-faulty after so many years…either way it was something of a gift for him to be on faculty at my medical school (University of Arizona) because it promoted an embrace of curiosity that persists to this day, every day.

In any event, I’ve switched to a low carbohydrate diet over the past year. I’m not ready to share my personal health information here, but I will eventually. And my biology is tracking science, as expected, because, well, that’s how science works :).

More to come. In the meantime, here’s a helpful piece on the low-fat diet and what it has done for our health.

Citation: Miller M, Stone NJ, Ballantyne C, Bittner V, Criqui MH, Ginsberg HN, et al. Triglycerides and Cardiovascular Disease. Circulation [Internet]. 2011 [cited 2016 Dec 25];123(20).

Just Read: What should people with diabetics eat? Study of a low-calorie ketogenic diet

Just catching up on my blogging and continuing a closer look at nutrition and health.

This paper discusses a different and emerging approach about diet in people with diabetes, beginning with the declaration that we really don’t know what the optimal diet for people with diabetic is:

The optimal degree of caloric restriction and macronutrient distribution of medical nutritional therapy in T2DM is not well defined.

Traditionally, a low-fat diet has been prescribed, which really is a high-carbohydrate diet that brings with it questions about why feeding carbohydrates to people who are intolerant of them makes sense.

In this intervention, subjects were divided and some were feed a ketogenic (higher fat, lower carbohydrate) diet. In medical school, we’re taught that ketones are a bad thing because of their association with a life-threatening condition known as keto-acidosis. However, in people who have some insulin left, ketones become an alternate fuel from the breakdown of fat.

The diet used here appears to be a little “engineered” compared to what I have read is also done, which is little to no calorie restriction.

And…the results show significant weight loss, glucose control, and as seen in other studies, a significant drop in triglycerides, that other under-emphasized lipid in our training (I’ll post on that later).

Interestingly, I ran across this medical practice based in San Francisco (@VirtaHealth) using this approach to achieve better outcomes in Diabetes. So, I suppose this is becoming a thing. With science attached to it, including its own published intervention trial.

Maybe we are set to really change the way we think about healthy eating….