Sugar Lobby vs Tobacco Lobby

Picture by Marlith

If you haven’t done so, Gary Taubes has a new article out on the history of the sugar industry that is worth a read. It is well written and the comparisons to the tobacco industry are eerily similar. Even more disturbing, according to the article, is how the sugar industry has been able to influence government policy and therefore public health policy during the past several decades. This influence extends to influential organizations such as the American Diabetes Association as well:

It is hard to overestimate Bierman’s role in shifting the diabetes conversation away from sugar. It was primarily Bierman who convinced the American Diabetes Association to liberalize the amount of carbohydrates (including sugar) it recommended in the diets of diabetics, and focus more on urging diabetics to lower their fat intake, since diabetics are particularly likely to die from heart disease. Bierman also presented industry-funded studies when he coauthored a section on potential causes for a National Commission on Diabetes report in 1976; the document influences the federal diabetes research agenda to this day. Some researchers, he acknowledged, had “argued eloquently” that consumption of refined carbohydrates (such as sugar) is a precipitating factor in diabetes.

If you go to the ADA’s website, they have a “Diabetes Myths” section to educate Americans on Diabetes “facts.” TheFatNurse finds this fact on the website about Type 2 Diabetes pretty interesting:

Pretty conventional stuff right? Being overweight is a risk factor and drinking sugared beverages is associated with Type 2 diabetes. Not too clear whether the ADA is trying to say the weight gain from consuming sugary drinks (which are high calories) is a risk factor for developing diabetes or if it’s the intake of high amounts of sugar in the drinks that leads to risk factors for diabetes. TheFatNurse is guessing it’s the former rather than the latter since the consumption of candies, ice cream, and other sugar added foods is not discussed. It seems the focus is only on sugared beverages. Does this mean a person can replace their sugar fix they get from coke with a bag of skittles instead to reduce their risk of diabetes!? Why all the focus on sugar added drinks and not the other sugar added junk foods!?

What you may find interesting is that the “Myth” fact on the ADA’s site was recently changed. In September 2012, TheFatNurse happened to take a screen shot of the previous statement on the myth that eating too much sugar causes diabetes:

This statement was as recent as September 2012 from the ADA!

So at least since September 2012, before the new changes mentioned earlier, the ADA was telling people that its ok to drink as much soda as you want provided you keep your weight under control? This was then changed to include warnings of sugar from sodas sometime between october and november 2012. This is strange considering a 2010 Meta-analysis from Diabetes Care, which is associated with the ADA, showed these links between sugared beverages and diabetes two years before the ADA decided to adjust their myths page. This meta-analysis also seems to hint that sugar’s damaging effects go beyond just causing obesity and a high amount of sugar by itself may lead to effects (SSB = sugar sweetened beverages):

Because of the high content of rapidly absorbable carbohydrates such as sucrose (50% glucose and 50% fructose) and high-fructose corn syrup (most often 45% glucose and 55% fructose), in conjunction with the large volumes consumed, SSBs may increase the risk of metabolic syndrome and type 2 diabetes not only through obesity but also by increasing dietary glycemic load, leading to insulin resistance, β-cell dysfunction, and inflammation

Although SSBs increase risk of metabolic syndrome and type 2 diabetes, in part because of their contribution to weight gain, an independent effect may also stem from the high levels of rapidly absorbable carbohydrates in the form of added sugars, which are used to flavor these beverages.

Exploring the links between sugar consumption and diabetes is nothing new. This debate started decades ago. From the Taubes article:

An international panel of experts—including Yudkin and Walter Mertz, head of the Human Nutrition Institute at the Department of Agriculture—testified that variations in sugar consumption were the best explanation for the differences in diabetes rates between populations, and that research by the USDA and others supported the notion that eating too much sugar promotes dramatic population-wide increases in the disease.

To be clear, one shouldn’t assume cause and effect with high sugar consumption and the development of diabetes. The statement from the ADA, “the answer is not so simple” is actually pretty accurate since the evidence isn’t quite conclusive yet, although there are some pretty strong associations. There are many factors and the significance of this subject deserves exploration of all its complexities. However, the “not so simple” response should have been the standard answer a long time ago rather than saying sugar has no role.

Additionally, Dr. Lustig (mentioned in the Taubes article) has been mentioning potential links between sugar consumption and metabolic syndrome (in which one of the criteria is impaired fasting glucose) for awhile. If you are not familiar with his name, I recommend watching his famous Sugar Lecture at UCSF which covers history, policy and biochemistry on sugar:

Things are changing tho and it seems TheFatNurse sees more and more public service campaigns advocating the reduction of sugars such as the “real bears” on youtube:

However, as mentioned previously, why such a focus on the sugar in sodas and not other sugar added foods like candy or kids breakfast cereals? Regardless, TheFatNurse is happy to see the conversation on the dangers of sugar progressing.

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National Cholesterol Awareness Month and Alcohol Policy to Solve Obesity?

Did you know that September is National Cholesterol Awareness Month? Via our US Department of Health and Human Services:

September may be “back to school month”, but it is also Cholesterol Awareness Month. Take a few moments to study up on this important health issue.

Yes sir! They were kind enough to even link a PDF pamphlet that you can give to all your friends and family. It has handy tips like:

Diet. Saturated fat and cholesterol in the food you eat make your blood cholesterol level go up. Saturated fat is the main culprit, but cholesterol in foods also matters. Reducing the amount of saturated fat and cholesterol in your diet helps lower your blood cholesterol levels

Err…wait a minute…story is a little more complex than that man!

Other tips include eating a:

a low- saturated-fat, low-cholesterol eating plan that calls for less than 7 percent of calories from saturated fat and less than 200 mg of dietary cholesterol per day…Foods low in saturated fat include fat-free or 1 percent dairy products, lean meats, fish, skinless poultry, whole grain foods, and fruits and vegetables. Look for soft margarines (liquid or tub vari- eties) that are low in saturated fat and contain little or no trans fat (another type of dietary fat that can raise your cholesterol level). Limit foods high in cholesterol such as liver and other organ meats, egg yolks, and full-fat dairy products.

Looks like it’s the same old story. If you’ve followed this blog or some of the other people in TheFatNurse’s links, you’ll know the story is way more complex and these diet guidelines may not work for everyone. Saturated fat’s relationship with heart disease is definitely debatable and cholesterol absorption from dietary factors may not have a significant effect on serum cholesterol. In addition, cholesterol as a predictive marker may not even be that accurate in predicting risk for certain people. Perhaps a better (and more informative yet light) way is to spread the cholesterol knowledge through TheFatNurse comics!

Another interesting report from last month that TheFatNurse didn’t see until now is from the CDC via RAND regarding the use of alcohol control policies in controlling obesity and it’s related diseases. They are proposing hypothetical solutions in controlling obesity through similar measures taken in regulating alcohol in the states. The report is aware of the potential controversy that such measures would face:

However, alcohol policies, especially those seen to infringe on individual choice (such as restrictions in outlet density) or to negatively affect moderate drinkers who do not cause harms (such as excise taxation) have been controversial. Over time, many of these measures have become widely accepted and do work in curbing problems related to alcohol use.

In otherwords, people will be upset at having their food choices regulated in order to control obesity…but its for their own good and they’ll get use to it! So what are some ideas? Below is a table from the report. The left column is the alcohol related control policy and how it could be translated to an obesity food regulation policy:

Wow…some of this stuff can look pretty extreme. You’ll see that “fat” foods are targeted. Perhaps before making all these regulatory theories one should question whether dietary fat is a cause of obesity in the first place?

Bottomline: It’s national cholesterol awareness month but the Dept of HHS seems to be putting out the same ol same ol on cholesterol and heart disease. Additionally, some reports are discussing potential ways to control obesity through hypothetical regulations derived from alcohol regulation. As seen with the knowledge on cholesterol, without a true consensus on what causes obesity and it’s related diseases, is food regulation really that wise of a choice? Let’s work on getting the message out on dietary fat and cholesterol beyond fat & LDL cholesterol = bad and HDL = good before working on policies that could potentially cause more harm than good.

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/

Fat Research During the MadMen Era

My friends keep obsessing over the new season of MadMen, so lets take a look at some of the landmarks of obesity related topics in this era. This era is well known for establishing Ancel Key’s Lipid hypothesis which states saturated fat increases cholesterol and increased cholesterol is a risk for heart disease therefore reduction of cholesterol and saturated fat reduced heart disease. This hypothesis is still widely accepted today. However, contradictory evidence was emerging around the same time. Two notable scientists providing an alternate hypothesis to heart disease at this time were Peter Ahrens and John Gofman.

John Gofman is famous for pioneering cholesterol research. While everyone was focusing on cholesterol as the circulating fat during the 50s, Gofman pointed out that the body circulated more lipid like substances than just cholesterol such as triglycerides. Additionally, there was also the lipoproteins that were involved in these lipids. This discovery naturally lead to the question: is there more to this story than just cholesterol? However, due to the technology at the time, it was only feasible to measure cholesterol (total).

With time, scientists eventually discovered three important Lipoproteins involved with cholesterol: HDL (the so called good one), LDL (what we commonly think of as the bad one) and VLDL (which carries most of the triglycerides). While everyone else was concerned about total cholesterol, Gofman realized that LDL seemed to be in larger amounts in patients with atherosclerosis independent of their total cholesterol. Therefore, Gofman pointed out that measuring total cholesterol was useless. However, even more compelling, was Gofman’s research on VLDL.

Gofman discovered that eating saturated fats could raise LDL which would fall in line with our current way of thinking. However, he also discovered that eating more carbohydrates would raise VLDL levels! The implications of this finding showed the potential dangers of using a low fat – high carbohydrate diet. For example, Gofman pointed out that the substitution of saturated fats for carbohydrates (the “carbohydrate factor” as he put it) could potentially cause more harm for individuals if it elevated their VLDL levels too high. This was of particular concern since cholesterol levels during this era was measured as total cholesterol and not into more specific subsets.

John W. Gofman

“If LDL was abnormally elevated, then this low-fat diet might help, but what Gofman called the ‘carbohydrate factor’ in these low-fat diets might raise VLDL so much that the diet would do more harm than good.”

– Gary Taubes, Good Calories Bad Calories

Another prominent scientist at this time was Peter Ahrens who is associated with terming the phenomenon of carbohydrate-induced lipemia. Simply put, this is circulation of fatty triglycerides in the blood (carried by VLDLs as shown from Gofman’s research) which is a risk for heart disease. The question is: was a person more likely to have this circulating systemically on a high carb or a high fat diet?

Since VLDLs were more likely to increase under carbohydrates consumption, you would be right if you said a diet focused more on carbohydrates. Ahrens demonstrated this by showing blood serum from the same patient following a high fat or high carbohydrate meal. The test tube was cloudy with triglycerides if they had eaten the carbohydrate diet but clear if they had eaten the high fat diet. However, during this period, having a high triglyceride level was still being questioned whether or not to play a role in heart disease. Ahrens warned the lipid hypothesis needed more questioning before low-fat diets (which would mean an increase of calories from carbohydrates) should be recommended since they did not know whether carbohydrates, fats or some other factor played a role in heart disease.
***Of note, Ahrens showed that a high carbohydrate diet would have less triglyceride levels if the total caloric intake was very low. A point he used to argue certain Asian countries having lower heart disease despite having a high carbohydrate diet at the time.

Margaret Albrink, at the metabolic division of Yale Medical School would provide some observations on the importance of triglycerides. Her findings showed high triglycerides were more common than elevation of cholesterol in patients with cerebral, coronary and aortic atherosclerosis. And that potential accumulation of triglycerides may be the most common lipid derangement in coronary artery disease.

Albrink presented her results to the association of the American Physicians but was met with anger and disbelief. This occurred only recently after the American Heart Association decided to accept and endorse Ancel Key’s idea of saturated fat and cholesterol (Lipid hypothesis) being the culprit. Albrink would continually be attacked by proponent’s of the lipid hypothesis. However, she would receive more support from other scientists later such as Nobel laureate Joseph Goldstein who found elevated triglyerides just as common if not more so than cholesterol in over 500 patients with heart disease. Even more interesting was a study done by Peter Kuo which showed:

More than 90% of the 286 patients were found to have hyperglyceridemia derived from increased endogenous lipogenesis from carbohydrate. This abnormal carbohydrate sensitivity was revealed with an ad libitum carbohydrate (35% to 40%) diet. Since lipoproteins synthesized from carbohydrates were shown to be rich in both triglyceride and cholesterol, carbohydrate-sensitive hyperglyceridemia was frequently found in association with hypercholesteremia. The abnormal metabolism was controlled by a sugar-free diet, with a carbohydrate allowance of 125 to 150 gm supplied as starches.

So 90% of the subjects had elevated triglycerides related to carbohydrate consumption. Additionally, since VLDLs carry triglycerides and cholesterol (majority triglycerides), that could potentially mean increases in cholesterol levels could be related to carbohydrate consumption as well. Interestingly enough, the elevated triglycerides and cholesterol were controlled when patients were put on limited carbohydrates…

Even more interesting was an editorial put out by the Journal of the American Medical Association about these new discoveries:

“Research,like therapeutics, experiences cyclic fads. These are characterized by a rush of investigators towards an avenue of research initiated by publication of a few promising studies. For nearly fifteen years, an almost embarrassingly high number of researchers boarded the “cholesterol bandwagon” in pursuit of understanding of atherosclerosis. This fervent embrace of cholesterol to the exclusion of other biochemical alterations resulted in a narrow scope of study of a disease which is probably multifaceted in causation. Fortunately, other fruitful approaches have been made possible in the past few years by identification of the fundamental role of such factors as triglycerides and carbohydrate metabolism in atherogenesis.”

Somehow tho, saturated fats and cholesterol being the culprit behind heart disease has still become unquestionable medical facts to many practitioners and thus society. Just how sure are we of this?

Peter Ahrens

“Some thought him to be obtuse or stubborn, as he refused to endorse claims that changing our diets by lowering cholesterol intake would be the sole and most effective weapon to win the battle against heart disease. He was indefatigable in pointing out the necessity of additional clinical research in human subjects to delineate individual differences in response to diet. Unpopular as these views may have been, time has revealed the correctness of his views.
http://www.jlr.org/content/42/6/891.full

Serum Lipids and Cerebral Vascular Disease
ROBERT G. FELDMAN, MD; NEW HAVEN; MARGARET J. ALBRINK, MD
Arch Neurol. 1964;10(1):91-100.

Hyperlipidemia in Coronary Heart Disease I. Lipid levels in 500 survivors of  Myocardial InfarctionJOSEPHL.GOLDSTEIN,WILLIAMR.HAzzmm, HELMUTG.ScinoTT, EDWINL.BIERMAN,andARNoG.MOTULSKYwiththeassistanceof MARYJoLEVINSKIandELLEND.CAMPBELL

Hyperglyceridemia in Coronary Artery Disease and Its Management
Peter T. Kuo, MD JAMA.1967;201(2):87-94. doi: 10.1001/jama.1967.03130020033007

CORONARY HEART DISEASE AND CARBOHYDRATE METABOLISM JAMA.1967;201(13):1040-1041. doi:10.1001/jama.1967.03130130066017CORONARY HEART DISEASE AND CARBOHYDRATE METABOLISM JAMA.1967;201(13):1040-1041. doi:10.1001/jama.1967.03130130066017

How Much Longer Can We Expect To Live By Cutting Out the Saturated Fat?

Interesting tidbit I found in Good Calories Bad Calories from page 65:

“Between 1987 and 1994, independent research groups from Harvard Medical School, the University of California, San Francisco, and McGill University in Montreal addressed the question of how much longer we might expect to live if no more than 30 per cent of our calories came from fat, and no more than 10 percent from saturated fat, as recommended by the various government agencies…

“The Harvard study, led by William Taylor, concluded that men with a high risk of heart disease, such as smokers with high blood pressure, might gain one extra year of life by shunning saturated fat. Healthy nonsmokers, however, might expect to gain only three days to three months …

“The UCSF study, led by Warren Browner, was initiated and funded by the Surgeon General’s Office. This study concluded that cutting fat consumption in America would delay 42,000 deaths each year, but the average life expectancy would increase by only three to four months. To be precise, a man who might otherwise die at 65 could expect to live an extra month if he avoided saturated fat for his entire adult life. If he lived to be 90, he could expect an extra four months. The McGill study, published in 1994, concluded that reducing saturated fat in the diet would result in an average life expectancy of four days to two months.”

“Michael McGinnis, the deputy secretary for health, then wrote to JAMA trying to prevent publication of Browner’s article, or at least to convince the editors to run an accompanying editorial that would explain why BRowner’s analysis should not be considered relevant to the benefits of eating less fat.”

Now if these studies are true (and to be honest I haven’t gone through them personally), they were not the only ones at the time down playing the dangers of saturated fat. However, the fact that the McGovern report chose to test a low fat hypothesis without conclusive evidence as recommendations for the US people…and only for the government to try and silence research that downplayed their own recommendations decades later….sounds fishy. More importantly, the rage I feel for denying myself bacon and eggs for breakfast all these years cannot be understated!

Looking at refined carbohydrates and not fat is so……..1986?

While I’m anxiously waiting for Dr. Lustig’s UCSF series on obesity to come out, I came upon a video that echoes exactly what he’s talking about…more than 25 years ago. While the video is more focused on refined sugar instead of carbohydrates as a whole, the basic arguments are all there. Additionally, Nobel laureate Dr. Linus Pauling is found in the video stating he has never seen any correlation with saturated fat intake and heart disease in the studies he has seen, but has seen some correlation of sugar consumption and heart disease.