Wednesday, August 20, 2014

INTESTINAL BUGS: the Good, the Bad, and the Ugly

Science is just beginning to study and understand the world of bacteria within our bodies. There are trillions of bugs inside each human, and these bugs can be “good” (beneficial) or “bad” (pathogenic, or disease-causing). Essentially, the human body is a donut, with a hole in the middle that goes from your mouth to your anus. The bacteria and food in the donut hole are not technically “in” our bodies, until they are actively absorbed by our bodies through the enterocytes (intestinal cells). With ten times more bugs than cells in our bodies, it’s almost more like they are the vehicle for humans rather than us being the vehicle for them.
Another, more harmful way that food and bacteria make it from the intestines into our blood stream is through tiny holes between the enterocytes. These tiny holes are called loose junctions, or “leaky gut”. Some researchers claim that up to 90% of people in the West have some amount of leaky gut, which is caused by a range of things like gluten (a protein found in grains like wheat), antibiotics, yeast overgrowth, eating a high-sugar diet, pharmaceutical medications, NSAIDS (ibuprofen or Advil), alcoholism, and drug use.
Two problems appear when our enterocytes are damaged and become leaky. First of all, food and bacteria from our gut leaks into the blood stream and the body responds with an immune attack. It not only attacks the invading bacteria, but also sees intact proteins (long strings of amino acids) from our food leaking into the blood stream, rather than the single amino acids that are normally absorbed through the intestinal cells. The body also “thinks” these are bacteria (especially gluten and casein from dairy) and attacks them as well. Over long periods of time, these heightened immune responses wreck havoc on the body and likely contribute or cause the development of autoimmune diseases like type I diabetes, rheumatoid arthritis, psoriasis, lupus, celiac, and multiple sclerosis.
The second way that damaged enterocytes further cause problems in the body is due to their inability to digest food properly. Instead of the food being broken up right away by enzymes (made by the enterocytes), the food sits in the gut and putrifies. This rotting food overwhelmingly feeds the pathogenic bacteria, especially the high carbohydrate, high sugar diets that are common in the West. When there is an imbalance in bacteria in the gut, it is referred to as “gut dysbiosis” and has been associated with inflammatory bowel disease, colitis, chronic fatigue syndrome, and cancer. For many people, the feeding of pathogenic bacteria also leads to bloating, belching, acid reflux, and constipation/diarrhea .
Not only are high numbers of pathogenic species thought to contribute to autoimmune disease and the diseases of gut dysbiosis, but they also cause inflammation and links are being made to chronic diseases as well like heart disease, type II diabetes, and obesity. The links to obesity are especially fascinating. A study from Washington University, published in the elite journal Science, showed that specific bacterial species are correlated with either obesity or thinness. Previous studies have found that obese people and thin people often have very different strains of intestinal bacteria. In this study, they inoculated germ-free mice (grown in a sterile environment) with bacteria from human twins, one of which was obese and one of which was thin. The mice receiving bugs from the obese twin gained statistically significant more weight than the mice given bugs from the thin twin, despite being fed the same chow. Although there is still much to be studied and learned about bacteria, studies like this show that it is a very promising topic in the field of obesity research.
Although much nutrition advice in this field has centered around adding probiotics like acidophilus to the diet, recent research has shown fermented foods (yogurt, kimchi, raw sauerkraut, and kombucha) and prebiotics to be even more effective at inoculating the digestive tract with beneficial species and healing disease. Feeding our existing beneficial bacteria with PREbiotics - like inulin, FOS (fructo-oligo saccharides), and resistant starch are thought by some to be even more effective than adding in new species. Coconut products and bone broth have also been found to be effective at healing leaky gut and helping beneficial species to thrive.
Another common gut problem that causes discomfort for many people is SIBO – small intestinal bacterial overgrowth. This is caused by an overgrowth of pathogenic species in the small intestine, rather than the beneficial bugs being concentrated in the large intestine, or colon, like they are in a healthy person. When numbers in the small intestine are closer to 104 rather than 103, which is normal, this can cause also symptoms like bloating, belching, acid reflux, stomach distention and pain.
There are a few different diets that are recommended for autoimmune diseases as well as other diseases associated with gut dysbiosis. One that has become very popular and effective for many is the SCD – specific carbohydrate diet. This diet recommends limiting carbohydrates that are made of two or more sugar molecules linked together (sucrose, maple syrup, and starches from things like potatoes and flour) based on the idea that damaged enterocytes are unable to produce the necessary enzymes to break them down and they feed the harmful bacteria. Carbohydrates made of single sugars like fruit and honey are allowed, since they don't require enzymes to be digested and so don’t feed the harmful bacteria but instead are absorbed quickly and used for energy by the body. People who suffer from bloating and gut-related discomfort like gas, belching, and constipation/diarrhea often find relief from this diet. Some believe that after a healing period, problematic foods can be added back into the diet without causing symptoms.
Another similar diet that is growing in popularity is the GAPS diet. This stands for Gut and Psychology Syndrome and was designed by Dr. Natasha Campbell-McBride. Her book by the same name details the relationship of high number of pathogenic bacteria and their relationship to issues of mental illness, including depression, anxiety, bi-polar disorder, the autism/Asperger's spectrum, and more. Her theory, which is fascinating and has shown correlation in a number of scientific studies, is that pathogenic bacteria emit neurotoxins which pass the blood-brain barrier and cause mental illness. This also explains the exponential increase in depression and mental illness we've seen in Western countries in the last century. She also discusses a phenomenon she calls "glue ear," which is the idea that reoccuring ear infections (otitis media) in children are caused by pathogenic bacteria making their way into the inner ear through the opening into the throat and causing mucus and infection in the middle ear. Her dietary advice is very similar to the SCD and excludes starch and double sugars as well as a gut-healing protocol including lots of bone broth. Many families report success treating depression and autism spectrum disorders in children using this approach.
There is variation of the SCD used in some circumstances is the low-FODMAP diet, which excludes foods containing even small amounts of short chain carbohydrates that are highly fermentable and poorly absorbed in the small intestine, including sugar alcohols, certain vegetables and fruits, grains, and some of the aforementioned prebiotics.
There are a number of supplements that are useful in removing the pathogenic bacteria and helping the beneficial bugs to take hold, as well as lowering the numbers of the harmful species present with SIBO. Often the harmful bugs include yeasts like Candida Albicans, which are able to take hold after the administration of antibiotics which kill off multiple species of good and bad bacteria and allow yeasts to take over. The yeasts and other harmful bugs create a home for themselves called a “biofilm” that makes it hard for beneficial bugs to kick them out. A commonly known biofilm is the plaque on our teeth, and one can think of biofilms as a plaque that covers the intestinal lining. There are a number of biofilm disruptors on the market that can be useful, as well as herbal versions like grapefruit seed extract and coconut oil.
Although definitely a strange concept at first, the medical treatment recently discovered that has shown the best results is the fecal transplant. Like it sounds, this involves taking the feces or isolated bacteria from the feces of a healthy person and injecting it or orally delivering it into the colon of the unhealthy person. For diseases with high mortality like Clostridium difficile, it has shown to be astonishingly effective. Although in its infancy, methods like this will likely be explored as a cure for a growing number of diseases and ailments.
Lastly, a group of researchers created the Human Food Project and are now conducting a study called American Gut, looking into the variety and specific species present in different Americans. For $99 (or less for 2 or more people’s samples) they send you a home kit to mail them a feces sample. They then send you a list of your bacteria species and their relative abundance in your gut, as well as on your skin and in your mouth, and compare this to other Americans (including famous author Michael Pollan) as well as a primitive tribe that they have been studying.
This very exciting field of science holds a lot of promise for people suffering from this long list of gut-related, auto-immune, and chronic diseases. There is much to learn but from what we already know, dietary changes and some simple supplements can be even more effective than any of the medications that western medicine now prescribes – which often only treat the symptoms and not the underlying reasons for the disease.
If you suffer from any of these digestive problems or diseases, I am a health coach and a nutritional consultant with an advanced degree in nutritional biochemistry. If you would like to schedule an appointment by Skype or in the person (in the Minneapolis area), please email me at We can tailor a diet and supplement schedule tailored to your individual symptoms and food preferences and create increased health and vitality in your body!

Recommended reading:

Thursday, June 6, 2013


It’s just the newest fad diet these days to go gluten-free, right? What is this stuff, “gluten,” anyway? Turns out this newest “fad” actually makes a lot of sense when we look into it. Gluten is the protein found in wheat and most other grains. Although grains (the seeds of grass plants) are mostly carbohydrate, there is a little fat and protein thrown in there too.
So let’s talk about grains. Grains are the newest food to be added to the human diet, from an evolutionary perspective (besides red #6 and weird processed food ingredients like butylated hydroxytoluene, but that’s another story). We’ve only been eating grains for about 10,000 years, at most. And that’s only in certain areas of the world. When you look at the fact that homo sapiens have been on the planet for over 400,000 years, and our older ancestors dating back to homo habilis have been on the planet for 2.3 million years, this is only the blink of an eye. Actually, this means we’ve been eating grains for only the last 0.04% of the time our species has been on this planet.
Grains are not human food. We do not have a gizzard, which is the organ that grainivores have that grinds the grains into flour inside their bodies. This is why we have to grind grains and cook them in order to eat them. Grainivores also eat little sticks and rocks to help their gizzards grind up the grains. Have you ever seen a wheat berry? It’s like a small rock. We would never eat that in the wild, that’s why our ancestors did not consider it food for the first 99.96% of human history.
Grain-eating started with the agricultural revolution. Humans realized that they could stop following the herd they relied on for survival, and stay in one place, if they planted the fields and kept domesticated animals. Thus was born farming. We needed foods that could be stored when animal foods were scarce, and increasingly came to rely on grains and beans, in addition to root vegetables, squash, and other foods that could be stored. These were used to supplement the animal foods that were available at the time.
Humans began experiencing a great increase in sickness and disease with the adoption of this foreign food group. Although many of us think of ancient humans as living short difficult lives, this is the experience of more recent people, after the agricultural revolution (like the middle ages). Pre-agricultural humans, or hunter-gatherers, often lived long and healthy lives. There are mummies that date back to pre-agricultural times that have all of their teeth and are believed to be close to 100 years old. Our human body evolved over millennia to be an amazing machine, when fed the right foods. Grains cause disease in multiple ways. First of all, there are a plethora of “anti-nutrients” in grains that strip vitamins and minerals out of the human body. The primary anti-nutrients are phytates, which bind to minerals and results in rickets, slowed skeletal growth, iron-deficiency anemia, and leaky gut syndrome.
Leaky gut is a very real issue in our society today. The main diseases that result from grain eating, besides vitamin and mineral deficiencies, are autoimmune disorders. When we eat grains, especially whole grains - which are actually worse for our bodies, the bran part of the grain that makes it a “whole grain” rips tiny microscopic holes in our intenstinal lining. (By the way, the reason they tell us whole grains are better for us is because they cause a slightly slower raise in blood glucose. This is similar to saying that low-tar cigarettes are slightly better for you than high-tar cigarettes so you should smoke a lot of them.) When we have these holes in our intestinal walls, intact proteins from our diet can leak into our blood stream instead of being broken down into individual amino acids. When the body sees certain intact proteins from our diet (like gluten and casein  - milk protein) in our blood, it thinks this protein is a pathogen because many germs and pathogens are long protein strings. The body reacts with an immune response against the imagined invader. When this goes on for years, the immune system eventually turns on its host and causes auto-immune problems. These include: Type I Diabetes Mellitus, rheumatoid arthritis and joint problems, Crohn’s disease, colitis, celiac, lupus, chronic fatigue syndrome, psoriasis and eczema, hypo- and hyperthyroidism, depression, anxiety, Sjogren’s syndrome, and irritable bowel syndrome, among many others.
So why are grains the base of the food pyramid and why are we told to eat a diet high in “healthy” whole grains? Well, the most obvious explanation is because the grain industry likes it that way. They make a lot of money off of our grain-eating ways, and the health care industry makes a lot of money off of treating these diseases. The reason this misinformation has been perpetuated for so many years, especially in our country, is because nutrition research in America is almost exclusively industry-funded. There is no federally-funded nutrition research in the U.S., like there is in many other Westernized countries. This means that most of the nutrition research here is funded by groups like the grain and sugar industries. This obviously sways the results of the research, and which studies not only get funded, but which get published.
Many people are forced to eat a diet higher in grains and other cheap carbohydrates because animal foods are more expensive. There is also an incorrect belief that grains and plant foods are easier on the planet that growing animals. Ironically, these days we not only eat grains ourselves but feed it to our domesticated animals – like chickens, who are omnivores and eat worms, and cows who are supposed to be eating grass. But is it really cheaper when we look at the costs of health care, and living shorter lives? There is a quote I like that says something like, Pay for food now or doctor’s bills later. When the destruction of the soil and our bodies is taken into account, we find that grain eating is not actually cheaper or better for the planet.
But how can we possibly give up bread? The staff of life, give us this day… Crusty baguettes and cake and donuts and cookies. Well, gluten-free has been a “fad” long enough that wonderful alternative have been put on the market. I have been off of gluten grains for almost a decade, and don’t miss them at all. I eat sandwiches, cake, cookies, and pizza – mostly made out of rice, tapioca, and potato starch, all of which are “safe starches”. But mostly I eat healthy animal foods. And in addition to watching the pounds melt away, I got to watch numerous health problems melt away as well.
 Or you can make gluten-free alternatives yourself, at home! 

My favorite gluten-free flour blend (use this instead of wheat flour in any recipe)
6 Cups white rice flour
2 Cups potato starch
1 Cup tapioca flour or starch
xantham gum, guar gum, or agar agar as a binding agent – amounts vary depending on whether the recipe is for bread, cake, or cookies and will be given on the package.

Monday, February 25, 2013

Excerpts from my Masters Thesis

The Effect of Fructose on Triglyceride Levels in Humans: A Systematic Review and Research Proposal

Background: The monosaccharide fructose is being investigated as a potential risk factor for cardiovascular disease, based on the premise that it causes serum triglycerides (TAG) to increase to a greater extent than glucose.
Objective: A systematic review was conducted of clinical trials comparing fructose and glucose in order to determine their respective effects on TAG levels in adults.
Design: Utilizing a literature search on MEDLINE (through May 2012), relevant controlled trials of pure fructose in comparison to glucose were examined. All such studies included a dietary fructose exposure that can be achieved through normal dietary intake.
Results: Nine of the twelve studies in this review found some evidence of a difference in the effect of fructose on TAGs, compared to the effect produced by glucose.  One of the nine trials found this result among men and not women, and one trial found that only postprandial TAGs (not fasting TAGs) were significantly increased with fructose. The remaining three studies did not find any evidence of a difference in the effect produced by fructose on TAG concentrations, compared to the effects from glucose.
Conclusions: The data in this systematic review suggest that the consumption of fructose may cause a larger increase in TAGs than the consumption of glucose. However, more research is needed on this topic due to shortcomings of studies conducted to date.

            Cardiovascular disease (CVD) is the leading cause of death in the developed world, and despite the advances in therapeutic approaches like statin drugs, rates are continuing to climb(1). Currently, 36.9% of U.S. adults have some form of CVD, which includes cardiac disease, peripheral arterial disease, vascular diseases of the kidney and brain, hypertension, heart failure, stroke, and coronary heart disease. This percentage is expected to rise to 40.5% by 2030(1).
            Atherosclerosis and hypertension have both been identified as factors that lead to the development of CVD. Meta-analyses and systematic reviews of CVD have established elevated serum triacylglyceride (TAG) levels as one of the independent risk factors for this collection of diseases(2).
            There are a variety of factors that are believed to contribute to raised TAG levels, including weight gain/obesity, a lack of physical activity, the use of tobacco, excessive amounts of alcohol, the excessive consumption of carbohydrates, diseases like type 2 diabetes and renal disorders, the use of certain drugs, and a genetic predisposition toward dyslipidemia(2).
TAGs are usually measured as part of a lipid profile, which also includes total cholesterol levels, high-density lipoproteins (HDL), and low-density lipoproteins (LDL). Occasionally an extended lipid profile may be taken which includes very-low density lipoproteins (VLDL) as well. High levels of LDL and VLDL, both of which contain large amounts of TAGs, indicate the presence of hyperlipidemia and are well established as risk factors for not only CVD but also pancreatitis and stroke(3).
Hypertriglyceridemia is a very common form of dyslipidemia in our population today(4). Generally, normal levels are considered less than 150 mg/dL, borderline high is 150-199 mg/dL, high is 200-499 mg/dL, and very high levels are considered to be greater than or equal to 500 mg/dL(5). In the 1999-2004 National Health and Nutrition Examination Survey it was found (measuring fasting TAG levels) that 33% of American adults have borderline high TAGs, 18% have high levels of TAGs, and 1.7% have very high TAG concentrations(5).  
Because of the presence of large concentrations of TAGs following a meal, fasting TAG concentrations may not be the best indicator of coronary risk. Many studies have attempted to determine whether postprandial or fasting TAG concentrations are the better predictor of atherosclerosis. Recently, several studies(6, 7), as well as several reviews(8-10) indicate that postprandial triglyceride measurements, compared to fasting values, are a better indicator of risk for coronary disease.
Carbohydrates have been found to raise TAG levels more than other dietary substances. Recent studies have attempted to determine if fructose raises TAG levels more than the consumption of other monosaccharides. Fructose is a component of a variety of commonly consumed sweeteners including sucrose (table sugar), high-fructose corn syrup (HFCS), maple syrup, and honey, among others. A potential mechanism for this physiological effect may be an increase in de novo lipogenesis (DNL), whereby the synthesis of the saturated fatty acid palmitate is activated in the liver by excess fructose consumption. The resulting hepatic metabolism may culminate in an increased flow of TAGs, high in palmitate, which are packaged in very low-density lipoproteins (VLDLs)(11). Some researchers have found that the monosaccharide fructose is unique, compared to glucose, in its tendency to cause DNL(11-13), while other researchers have failed to find this differential effect(14, 15).
Fructose consumption in the US is significant, with mean consumption estimated by The National Health and Nutrition Examination Survey (NHANES) to be 54.7 g/day, which accounts for 10.2% of total energy intake(16). Approximately 41% of the total sugars in the American diet come from fructose(16). Hence, if fructose has a more adverse effect on TAG than glucose (the other primary monosaccharide in the diet) there may be significant public health implications. The purpose of this paper is to review human studies that have evaluated whether fructose increases TAG levels to a greater extent than glucose. 

In this systematic review of RCCTs and crossover trials, data suggest that the consumption of fructose may cause a larger increase in TAG concentrations than the consumption of glucose, however, the quantity of quality studies are insufficient to draw concrete conclusions about this relationship and indicates that more research is needed on this topic.
Nine of the twelve studies in this review found some evidence of a difference in effect from fructose, compared to glucose, on TAG concentrations. In general, studies that measured postprandial TAGs; used a hypercaloric diet; and were short in duration (one day exposure) more often reported a difference in effect. Other systematic reviews on the effects of fructose on TAGs in humans have come to mixed conclusions(9, 27, 28), although only one of these reviews examined the isocaloric exchange of fructose for other dietary carbohydrates(28) and none of them compared the results of fructose exposure to equal glucose exposure on TAGs.
In this review, there were only seven studies that were rated as high quality, measured postprandial TAGs, and compared the exposure of pure fructose to an equal exposure of pure glucose(11, 20-25), six of which found some evidence of a difference in effect on TAGs for fructose, compared to glucose(11, 20-22, 24, 25).
There is a proposed biologic mechanism of action whereby fructose may increase TAG levels to a greater extent than glucose (see Figure 1). The metabolisms of the monosaccharides fructose and glucose have a number of major differences. Whereas virtually every cell in the body can metabolize glucose, fructose is largely shunted to the liver by the hepatic portal vein for metabolism. The liver responds to fructose consumption by engaging in lipogenesis, manufacturing triglycerides and packaging them in lipoproteins. Of relevance to this review is that whereas glucose metabolism is inhibited by excess energy intake, through cytosolic ATP and citrate levels(11), as well as the production of leptin and insulin, fructose consumption doesn’t affect these hormones, and the metabolism of fructose isn’t believed to be regulated by levels of intake(24). Because of these distinctions between metabolism of fructose and glucose, it is important to examine the relative effect of fructose and glucose on TAG levels at different levels of intake and in the context of both isocaloric and hypercaloric diets to evaluate whether meaningful differences in effect on TAG exist. 
The research on fructose and its relative effects on TAGs, compared to glucose, has a number of shortcomings. These include relatively small sample sizes used (the largest sample in this review had only 34 subjects); doses that are on average larger than those consumed by the general population; the limited duration of exposure in the studies conducted so far, which prevents long-term effects to be known (7 of the 12 trials in this review lasted for < 1 day); the low amount of human studies on this topic; and the fact that some of the existing studies do not compare fructose with a comparable form of glucose but use starch or another glucose source instead.
Three studies in this review had design flaws that were significant enough to question their findings regarding the effect that fructose has on TAGs compared to glucose. Two studies used starch or maltodextrose as the source of glucose rather than liquid monosaccharides in identical form for both the fructose and glucose interventions. Consequently, the validity of findings from these studies may be called into question(14, 19). The study that used starch (delivered in bread) as the source of glucose found evidence of a greater effect of fructose on TAG compared to glucose(19). The study that used maltodextrose (provided as part of a liquid diet) did not find a difference in the effect of fructose and glucose on TAG(14). Since starch, as well as maltodextrins (a lightly hydrolyzed starch product) are both made up of longer chains of glucose molecules that must be lysed during digestion, it is possible that these products may take significantly longer to digest than pure glucose. This is especially true for starch, which may be only partially digested. Adding to concern with the study that used starch as the source of glucose is the use of a food matrix (bread) for delivery of the starch, whereas the fructose was delivered in liquid from. It could be speculated that the difference of effect found between fructose (delivered in liquid form) and glucose (delivered as starch in bread) in this study is attributable to this design flaw(19). The other study in this review with a major design flaw, Hudgins, et al., compared liquid fructose to liquid glucose, but the researchers failed to compare equal doses of the two monosaccharides(13). After undergoing an OGTT (75 grams glucose in liquid form), subjects were given a single bolus dose of either fructose alone, or two different ratios of both glucose and fructose together in a randomized crossover design. The fructose dose was 0.5 g/kg body weight (BW), a second dose was 0.5 g/kg BW of both glucose and fructose (F:G), and the third dose was 1.0 g/kg BW of both glucose and fructose (2X F:G). The OGTT was a similar dose of glucose as the total amount of sugar in the F:G dose for an average subject’s body weight, so that is the dose of most interest for this review. Unfortunately, no statistical data was given for the F:G dose but the researchers stated that all three doses of fructose or fructose/glucose had significant increases in total TAG. Despite these increases in TAGs, without a direct comparison of equal doses of glucose and fructose, serious limitations exist in the ability to interpret the results of this study on the difference of effect between fructose and glucose. An order effect is also of concern in this study because the OGTT (glucose dose) was always administered first.
Another important shortcoming in the literature on this topic is the lack of consensus on whether fasting or postprandial TAG measurements are a stronger risk factor for CVD. Although recent research has shown postprandial measurements to be a better indicator of atherosclerosis, historically, fasting TAG measurements were considered to be a better indicator and therefore were used more commonly as an outcome measure. This has resulted in many older studies neglecting to take postprandial measurements, and consequently there is a lack of postprandial TAG data in three of the 12 studies included in this review. A larger percentage of studies in this review measuring postprandial TAGs, compared to studies that measured fasting TAGs, found evidence of an effect of the fructose intervention on increased TAG levels compared to the glucose intervention. Since postprandial TAG measurements have been found by many reviews(8-10) to be more reliable at predicting CVD than fasting measurements, these studies may be more indicative of the effect of fructose feeding on increases in TAG levels. Of the five studies in this review that were longer term, only two of these studies measured postprandial TAGs, and both found that fructose raised postprandial TAG levels more than glucose(11, 20), although one of them, Bantle et al., with a trial lasting 6 weeks, only found this result among men and not women(20). Stanhope et al., in 2009, with an intervention period of 10 weeks, conducted the longest study in this review. They also measured fasting and postprandial TAG levels, and found a significant increase for both men and women for postprandial TAG levels, although, interestingly, this result was not observed for fasting TAGs(11).
There are two additional shortcomings in the research conducted on this topic to date. Many studies on the effect of fructose on TAGs were of very short duration. For example, 7 of the 12 studies in this review lasted for < 1 day. Since fructose exposure is usually chronic, it is necessary that future research consists of longer trials, examining the effect that fructose has compared to glucose, over longer time periods. Also, 10 of the 12 studies here used relatively high doses, comparing fructose and glucose exposures of  > 100 g/day, or up to 30% of daily energy intake. This makes it challenging to evaluate the effect that fructose has on TAG levels, compared to glucose, at more typical intake levels, like those present in average American diets. Because of this, it is important that future research examines the effects of fructose at more realistic doses and for longer durations.
In order to accumulate an adequate amount of evidence to determine whether fructose has a greater effect on TAG levels than glucose, more high-quality research is needed. It will be necessary to conduct this research with RCCTs or randomized crossover trials lasting four weeks or more, containing large enough sample sizes in order to have the necessary statistical power, measuring postprandial TAGs, and using dosages of fructose and glucose that are more typical in the standard American diet in order to determine if fructose is the primary monosaccharide contributing to hypertriglyceridemia. Additional studies are also necessary in order to determine whether hypertriglyceridemia is the primary biomarker for atherosclerosis. If future studies provide conclusive evidence that fructose increases TAG concentrations more than glucose, both public policies and dietary recommendations may need to be adjusted. By altering these guidelines, the progression of dyslipidemia and cardiovascular disease could potentially be reduced.

Wednesday, July 25, 2012

Excerpt from a systematic review I wrote on Fructose and Insulin Resistance

The Effects of Fructose on Insulin Resistance in Humans: A Systematic Review

Sugar consumption has been steadily increasing in the U.S. and across the world, and has been implicated as a potential causal agent in the development of obesity and other metabolic diseases. Dietary sugars usually come in the form of cane sugar or high-fructose corn syrup, both of which are made of roughly equal parts of the monosaccharides fructose and glucose. Fructose, as opposed to glucose, has been linked in a number of studies to biomarkers for metabolic disease, such as insulin resistance and dyslipidemia. Since the presence of insulin resistance predisposes individuals to an increased risk of most chronic diseases, this review attempts to elucidate the relationship between fructose and impaired insulin sensitivity among studies published in peer-reviewed journals in the last decade. Ten studies were included in this review, the majority of which display a statistical relationship between fructose consumption and biomarkers of increased insulin resistance. An adequate number of studies with sufficient statistical power do not yet exist to determine whether fructose is the nutrient primarily responsible for the formation of insulin resistance but these preliminary study results indicate the need for additional research in this field.

            Chronic diseases, including obesity, diabetes, and heart disease, are quickly spreading across the world. The World Health Organization estimates that these diseases will cause twice as many deaths in the next decade as malnutrition, infectious disease, and childbirth combined, killing 388 million people (1). Type 2 diabetes mellitus rates alone are expected to double within the next generation, from 190 million to a projected 335 million by 2025(2).  Many health professionals are beginning to understand these chronic metabolic diseases are linked, and possibly have common causes. This is based on the presence of a few shared characteristics, one of which is insulin resistance.
These chronic diseases are grouped together into a condition called “metabolic syndrome”, or “insulin resistance syndrome”, as it is sometimes referred. There are a variety of disease criteria an individual must display in order to be diagnosed with metabolic syndrome. Usually these must include the presence of diabetes or some marker of insulin resistance (like impaired glucose tolerance or impaired fasting glucose levels) along with high blood pressure, dyslipidemia, or visceral adiposity. Once diagnosed with metabolic syndrome, an individual is at a greatly increased risk for any number of these metabolic diseases, which include diabetes, hypertension, non-alcoholic fatty liver disease (NAFLD), cardiovascular disease (CVD), stroke, obesity, and even cancer(3). Nutrition scientists often link the development of these Western diseases to a range of potential dietary causes, one of which is the increasing consumption of fructose - primarily from sugar and high-fructose corn syrup. This systematic review evaluates recent studies published in scientific journals regarding high dietary fructose consumption in adults (compared to controls consuming low fructose diets) as well as measures of insulin sensitivity to determine the extent to which fructose consumption is associated with insulin resistance.

MEDLINE was searched with PubMed through March 7, 2012, using the MeSH headings “Insulin Resistance” AND “Fructose” with the limits of “Human,” “English,” and “Adults.”  This review excludes animal studies and pediatric studies, as well as reviews, commentaries, and editorials. These limits were created in order to ascertain the effects that a diet high in fructose has on the human body and on biomarkers for disease. The primary biomarker investigated here was insulin resistance because it is a primary precursor for the diseases associated with metabolic syndrome. 
A majority of studies, most of which are randomized controlled clinical trials, found a correlation between fructose intake in adults and insulin resistance, including hepatic insulin resistance, adipose tissue insulin resistance, increases in fasting glucose and fasting insulin, and decreases in EGP(8-10,12,13,15-17). Many of these studies found increases in whole-body insulin resistance, measured by HOMA indices, the HEC clamp, and ISI, which was the focus of this review(8,12,13,15-17). Much of the clinical research on this topic has only been conducted in the last decade. Since insulin resistance is considered a causal factor in the development of metabolic syndrome, it is imperative that additional studies on fructose and its effects on disease biomarkers in humans are conducted in RCCTs with sufficient statistical power to determine the exact nature of the relationship between fructose and insulin resistance.
Of the ten studies reviewed, nine are clinical intervention trials, only one of which failed to find an increase in insulin resistance in the group fed additional fructose compared to the group fed additional glucose(14). The authors of this study admit to the fact that they carried out multiple analyses, which requires a more conservative level of statistical significance. The researchers also acknowledged that their subjects “were younger and had lower BMI and therefore less metabolic risk,” their study contained a shorter fructose feeding intervention than many other studies on this topic, and that the small number of participants greatly reduced this study’s power(14).
This review has a few shortcomings, primarily the lack of human studies on this topic, as well as a lack of studies on fructose and insulin resistance published in English. The fact that this topic has only been studied in humans largely in the last decade or two, means that RCCT studies in humans with fructose consumption lasting longer than 10 weeks have not yet happened. The longest RCCT studies to date to be undertaken on fructose and insulin resistance are by Stanhope, et al. from UC Davis, because these studies have been of longer duration and with a larger dosage, evaluating the effects fructose has on the human body over a ten-week period(15-17).  Many of the studies in this review are from countries outside the U.S. that have conducted studies with a larger dosage, longer duration, and larger sample sizes than the studies from the U.S., allowing them to potentially make more reliable correlations between fructose and its effects on insulin sensitivity(8,12,13). Studies that have not been reported in English may contain necessary information to better understand the association between fructose intake and insulin resistance.
Also, a larger number of human studies in the U.S. have been conducted with fructose and biomarkers for heart disease such as the creation of VLDL in the liver as well as the effects of fructose metabolism on uric acid levels and hypertension. Less research exists describing the association between fructose and impairment in insulin and glucose regulatory systems, as well as obesity. Animal studies have been convincing as to the development of disease indicators for metabolic syndrome from high-fructose feeding(19-21), but sufficient data from human studies needed to conclusively answer the question of whether fructose intake contributes to insulin resistance is not yet available.
            Another shortcoming of this review is the lack of a clear metabolic pathway for the development of insulin resistance from the consumption of dietary fructose. Although nutritional biologists recognize that fructose is metabolized much differently than glucose, the potential pathway linking fructose intake to whole-body insulin resistance is unclear. Glucose can be used as energy by every living cell, including every organ and tissue in the human body, and also releases insulin (which is responsible for upregulating glucose receptors in peripheral tissues) but only the liver can metabolize fructose. Once the fructose reaches the liver, it is metabolized by fructokinase, which is not regulated by levels of ATP like glucose enzymes(22). When fructose levels build up in the hepatocytes, they activate de novo lipogenesis, which is linked to increases in NAFLD as well as hepatic insulin resistance(22). Whereas only 0.5% of glucose enters hepatic de novo lipogenesis pathways, up to 30% of fructose is converted into fat, leading to large increases in VLDL(23). This increased hepatic lipid accumulation leads to activation of protein kinase C (PKC), which interrupts normal insulin responses, and the increased liver fat also impairs insulin receptor substrate (IRS)-1, which decreases hepatic glycogenesis(22). It is not well understood if and how this hepatic insulin resistance leads to decreased insulin sensitivity in the peripheral tissues, especially in muscle and other organs, but it has been suggested as a causal factor in the development of whole-body insulin resistance(22,23).
Further complicating the connection between fructose, insulin resistance, and the establishment of these disease pathways is the fact that postprandial plasma insulin levels generally show decreased values following high-fructose feeding, but when researchers began to measure fasting insulin and fasting glucose after long-term high-fructose diets, they noticed that fructose feeding had detrimental effects on these biomarkers of insulin resistance(compared to glucose or another control)(23).
            Until more adequate research is conducted, with RCCTs lasting ten weeks or more, containing large enough sample sizes, and using sufficient dosages (at least the NHANES average, if not three times more to mimic upper intake ranges), these preliminary findings are not decisive enough to change current dietary recommendations. If future studies do provide conclusive evidence linking fructose to insulin resistance, both public policies and dietary recommendations should be altered in order to potentially slow the progression of insulin resistance and the numerous chronic diseases to which it is linked.

Tuesday, October 25, 2011

Insulin Resistance

 Why are so many of us overweight, and what links does obesity have to diabetes and other major disease of our time, like heart disease and cancer? Even the "experts" agree that these diseases are all linked - its called the "Metabolic Syndrome," and that insulin plays a major role.

The part that is unclear to most nutritionist and doctors is the cause and effect. Most health care professionals believe that obesity is caused by simply eating too many calories and that its the obesity itself that causes insulin problems in the body. I believe they have it backwards.

Insulin is a hormone in the body that plays many roles. Its primary job is to enable us to use glucose as fuel for our cells. It is, in fact, the only hormone that causes fat to be stored. We have insulin receptors on our cells - all cells. Heart, liver, adipose (fat), muscle, and brain all have insulin receptors that sense the presence of glucose in our blood stream, and allow the addition of GLUT4 receptors on the cell membrane to uptake the glucose into our cells.

When the body is overwhelmed by the presence of carbohydrate, the insulin receptors begin to stop being as productive. They become resistance to the presence of glucose. (Fructose as well, which is a major cause of the problem, and I'll get to that in a little bit.) Sometimes the receptors work properly, but they are unable to signal the introduction of the GLUT4 receptors that actually absorb the glucose into the cell. Either way, the body responds by releasing additional insulin from the "islets of Langerhans" cells in the pancreas. This additional release of insulin has tragic consequences.

Frequently, the first cells to become resistance to insulin, and thus become unable to use the glucose as fuel, are the muscle cells. Usually adipose tissue is less insulin resistant. So the body responds to this additional insulin by dumping fat and protein into the fat cells. See, its not even the glucose that gets stored. Many in the field of nutrition talk about glucose as being the "preferred fuel" but that doesn't make sense, as glucose is simply empty calories. The body is poisoned by the glucose because it raised blood sugar levels, which have to be kept within strict limits - between 4-6 mM. Because the body wants to be rid of the glucose, it stores the fat and protein in the blood stream for energy use after the glucose is burned off. And any excess glucose is stored as well.

Fructose is even more poisonous to the body. It only exists in the wild in very small amounts in fruit. Most fruit grows in the summer, or in tropical climates, when there is ample sunlight available to also produce large amount of vitamin D in the body. Vitamin D plays a big role in the digestions of carbohydrates and the release of insulin, although this relationship is not well understood. Fructose is digested exclusively by the liver, and has to be packaged into very-low-density-lipoproteins (VLDLs) to be carried through the blood stream. These VLDLs have strong links to heart disease. Also, the fructose often get stored in the liver, and has strong links to fatty liver and liver cirrhosis, also known as "non-alcoholic fatty liver disease." Fructose makes up half of the sugar molecule, as well as about half of high-fructose corn syrup (HFCS), and has never been present in the human diet in the amounts seen today. Mainly this consumption comes from soda (which I call the "cigarette of the future"). There is a growing body of evidence that the fructose itself is what causes the insulin resistance in the first place, and creates the situation where the body can't effectively digest glucose.

So how do we improve our insulin sensitivity, especially in the muscle cells? How do we get our bodies to begin to use the glucose in our blood streams as fuel, rather than storing it as fat, along with the dietary fat and protein? How do we lose weight?

There are a number of things we can do. The first and most obvious, which I have written about extensively, is to cut our carbohydrates, especially sugar and other forms of fructose like HFCS and excessive fruit. A little fruit is not the problem, but it's also not the health food it's made out to be. It's meant to be eaten in the fall at harvest time, in order to store fat for winter, or eaten in tropical climates with 8 hours a day of sunlight on the skin.

In addition to vitamin D (which is needed in much larger amounts in places like Minnesota -I take 10,000 IUs a day), the other less obvious solutions include supplements of magnesium and fish oil. The long chain fatty acids in fish oil improve our cell membrane structure, and allow the body to heal from insulin resistance.

And most importantly, we can engage in a type of exercise called "interval training". This includes small periods of high heartrate-inducing exercise, followed by periods of rest. Usually about 60 seconds on, and then 75 seconds off. This is more effective than long periods of cardio, which is suspected to be hard on the heart and nervous system. It's not so much the "calories" burned by the exercise, as it is the increased insulin receptors that the exercise creates on the muscle cells. When we have additional insulin receptors on our muscle cells, our body is able to use the (small) amount of glucose that we consume as fuel, rather than only storing it and the food we eat with it, as fat.

This not only enables us to continue to safely eat a little carbohydrate, but it helps us lose weight and improves our resistance against metabolic diseases, which are the number one killer in our society!

Thursday, January 27, 2011

What Should We Eat?

So once we realize that the food pyramid has been upside-down our whole lives, what do we eat? We pretty much have to re-think everything that goes in our mouths. They have literally turned the truth completely upside-down on us! They tell us that sugar is innocent and that animal fat is killing us, and the exact opposite is true. Sugar and grains are killing us and animal fat is the healthiest food we can eat. Saturated fat is absolute health food! The Inuit (Eskimos) are the healthiest people we've ever found and they eat 80% animal fat. There is an amazing researcher responsible for this discovery, Vilhjalmer Steffansson. You can read his book, My Life With the Eskimo, on google books.

Basically this man went to live with the Inuit mulitple times for months or years at a time, spending more than 5 years of his life living with them. He adopted their diet and then studied himself and brought Inuit people into the lab as well, taking blood samples and measuring all kinds of disease parameters and nutrient levels. Off the chart healthy. They eat nothing but animal foods for almost 9 months of the year, and show no deficiencies, no disease. They do have some health problems, like high infection rates, which is attributed to their close living conditions and the unsanitary nature of living in a small ice house with many people.

The question people most often ask me is, What should I eat? So here is a list of meal and snack ideas.

Breakfast: easy peasy, as long as you love eggs and bacon. If you don't, it's time to learn. After a couple days of eggs for breakfast, you will start to crave them right when you wake up. Eggs have an amino acid profile of 100. They essentially set the standard for all other proteins. Plus they are full of extremely healthy cholesterol (doesn't cause heart disease, that is a huge myth), other healthy fats, and vitamins. For some reason, I just love pork products in the morning. Beef, chicken, or fish for breakfast just seems gross, but bring on the bacon, sausage, and ham for breakfast! Then eat beef and fish for lunch and dinner, since they are healthier than pork. I also have a quarter or half of a grapefruit most mornings, or some berries with yogurt, or maybe a piece of grain-free toast (the gluten-free bread from the Wedge makes better toast than any wheat bread) if I want a carb serving in the morning, which lately I usually don't.

Frittata: 8 eggs, 1 cup of cheddar cheese, half cup cream, 10 pieces of bacon or sausage or both, any other ingredients you want like mushrooms, scallions, tomato, garlic, onion, spinach. Fry up the meat and veggies in some butter or bacon fat, then stir in the beaten eggs, cream, and cheese, then bake in the oven for 20-30 mins at 350 degrees until cooked through. Delish.

Another amazing breakfast recipe that can be premade and frozen to have something quick to grab in the morning: Bacon Muffins! These are fabulous.

Lunch or dinner ideas:
Wild caught salmon burger (frozen), on a bed of greens with melted cheese, dill, and lemon

Pizza toast - Gluten free bread with pizza sauce, pepperoni, sausage, and mozzarella in the oven for 10 minutes. Great for kids.

Brats with kim chi or sauerkraut and mustard, with cheese melted on top

Grilled summer sausage and cheese sandwich on GF bread.

Coconut curry -  soup or stirfry with any veggies or meat you want, fish sauce, ginger, garlic

Shepard's Pie, heavy on the meat and non-root vegetables and light on the potatoes

No pasta lasagna - julienned zucchini, artichoke hearts, olives, diced tomatoes and spinach instead of pasta with the usual meat sauce, ricotta, parmesan and mozzarella layers

Spaghetti with meat sauce and spaghetti squash instead of noodles - just cut the spag squash in half, rub with olive oil and bake cut-side down for 20 mins in the oven at 350 or so. Then scrape with a fork and instant spaghetti noodles!

Any big piece of meat like a steak or some oven baked chicken, with a green vegetable side like asparagus, broccoli, brussel sprouts, swiss chard, kale, etc. My favorite new way to cook green veggies is sprinkled with o.o. and salt/pepper, then baked in the oven. They get all crispy, like green potato chips. Yum. Baked chicken is really good with herbs, garlic, and butter smeared on it before you bake it.

Pot roast. So easy and so good. Brown the roast in a hot pan with some bacon fat or o.o. in it, then pour broth over the top, add celery, onion, garlic, and a couple carrots and cook on low heat for many hours. Maybe add some baby portobellos toward the end for the last half hour or so.

Three awesome dessert ideas:
These first two can be made with stevia, and hardly anyone could tell it wasn't made with sugar. I especially like the Sweetleaf Stevia, although it has inulin in it, so don't eat it if you struggle with candida.
Panna Cotta. The best recipe is Giada's, just use 1/4 of the sugar she calls for (a good rule of thumb for any dessert recipe, if you get your tolerance down, you won't even notice after a short adjustment time) or a little stevia. No, honey, maple syrup, and agave are not better for you than sugar. Just the same, or even higher in fructose, which is worse for you than glucose.

Egg Custard. So good and so easy, I could make it in my sleep. I eat this constantly. You can use 4 cups of cream instead of the cream and milk if you are trying to lose weight. Milk has lactose - milk sugar which is half glucose and will cause a insulin release, which causes fat storage.
8 eggs, 2 cups cream, 2 cups whole milk, a little bit of some sweetener (or better yet, a teaspoon of stevia), 1 t vanilla, couple dashes of nutmeg (I like to add some before mixing and also dust some on top) and a dash of fine salt. Wisk or hand-mix, then set your custard cups or large glass bowl in a slightly larger cake pan and pour an inch of hot water in the bottom, and place the whole thing in the oven at 325 degrees (not above 350 so the water doesn't boil much) for about 35-40 mins.

Best cookies ever, and they are gluten-free. No one will ever know. So yummy. Just skip the weird grapeseed oil and use room temp butter, and you can go easy on the raisins, or even better, use dark chocolate chips instead! And you don't even need the full quarter cup of sugar - I usually aim for less than 5 grams of sugar per cookie. Stevia doesn't work so well with chocolate, almond flour, or other flours. Stevia is best with dairy and eggs. Best to just use a little sugar here and skip your fruit or other carbs for today.

Hope that gives you some good ideas to get you started! Remember calories don't exist, they only truly measure carbohydrates. Keep your carbohydrates below 50-80 grams/day for weight loss - about 2 or 3 small servings, spaced throughout the day. Then eat all the beef, bacon, sausage, chicken, cream, yogurt, eggs, and fish that you desire and watch the pounds fall away! Happy eating!

Tuesday, November 30, 2010

A Day in the Life of a Nutrition Student

My professor started out our first day of Advanced Human Nutrition this semester with the baffling statement: “Its very hard to find a study that shows that soda is bad for you.” She laid this whammy on us while introducing our first assignment. We had to design a scientific study on a nutritional topic of our choosing. I immediately weighed my options - definitely something related to a low- or no-carb diet. We didn’t actually have to conduct the hypothetical experiments, obviously, but just come up with a design.
Since a single soda can has 12 teaspoons of sugar in it, I knew there were scores of studies linking sugar consumption to a host of problems: type II diabetes, ADHD, obesity, high blood pressure, and heart disease, to mention a few. Amazingly enough, not a single student raised a hand, including me, to question this inane comment. What is it about the science of nutrition that turns us all into mind-numb zombies? We are weary after decades of contradicting information, unable to sort out the conflicting advice and filter out any remaining truths. Here we sit at a Big Ten University, and no one has the confidence to argue with a professor with the gall to state that there is no scientific proof that 12 teaspoons of pure sugar is bad for you.
And then, just when I thought it couldn’t get worse. To further aid us in generating topic ideas for the assignment, she put up a powerpoint slide with the steps of the scientific method displayed. Underneath the first step, Hypothesis, was the question: “Is the Atkins diet more effective at weight loss than a calorie-restricted diet?” Here we go, I thought.  “Has anyone here tried the Atkins diet?” The question hung in the air a few seconds, and slowly I and an athletic guy a few rows down raised our hands. She turned to us. “How did it work?” She asked with a slight smirk.
“Good,” I said, and Beefcake College Boy agreed, "Awesome."
“Does anyone have an idea as to why there are so many testimonials of people losing weight on the Atkins diet?”
A girl across the room raised her hand. “Because fat has more calories than carbs or protein, so you get full quicker and eat less calories.” Prof nodded approvingly.
“Anyone else?” I felt my hand go up before I could stop it. 
“Well, a low-carb diet utilizes little or no insulin for digestion, and insulin is the primary hormone that promotes fat storage in adipose tissue.” I could have gone on about triglyceride formation, but I left it at that.
Her smirk turned into a puzzled stare. “Hmm,” she turned away and flipped to the next slide without responding to my statement.
Second step, Design a scientific study to attempt to answer the question. This slide says: “Put half the study participants on a reduced calorie diet, and half on the high-fat, low-carb Atkins diet.” And in the bubble below: “Study shows no difference between weight loss at one year amongst the two groups.” I shake my head. Unbelievable. The only thing that causes weight gain is carbohydrates. I scribble down the journal and article number in small print below the proclamation. “Lastly, see if follow-up studies agree with your finding, and develop the hypothesis into a theory.” Underneath was an additional study that found no increased weight loss with the Atkins diet. I scribbled it down, too, vowing to look up the studies when I get home, knowing the real story won’t be quite so simple.
And my prediction was right. I found the first study right away at home, and it turns out that the half on the Atkins’ plan lost significantly more weight at 3 months, 6 months, and still an average of over 9 pounds more at a year. Then, in complete contradiction, the study also claims, “Participants had no significant difference in weight lost at 12 months” in the next paragraph. I suppose the margin of error could be large enough for that claim, but I suspect that my professor isn’t the only professional who twists the results of studies when they don’t show what is predicted by mainstream nutritional advice.
Reading further, I discovered that the researchers used a “self-help” style of nutritional advice, simply handing half of the participants a copy of Atkin’s diet book and leaving them to forge through an introduction to a low-carb diet on their own, while trudging through this maze of nutrition misinformation in our carb- and sugar-obsessed culture. As if large group of study participants could adhere to the Atkins diet without any counseling or support! Obviously this was a ridiculous assumption on the part of the researchers, as they admit that ”attrition was high” and that “during the first three months, the percentage of patients who tested positive for urinary ketones was significantly greater in the group on the low-carbohydrate diet than in the group on the conventional diet, but there were no significant differences between the groups after three months,” which of course means that no one was on a low-carb diet and the results of this study at one year are meaningless if your purpose is to study the effects of a low-carbohydrate diet.
The next sentence of this study is very confusing: “There was no significant relation between weight loss and ketosis at any time during the study.” What? This is completely inaccurate. They are completely contradicting themselves. After telling us that the low-carb group had “significantly” more ketones in the beginning of the study, and that “subjects on the low-carbohydrate diet lost significantly more weight than the subjects on the conventional diet at 3 months (P=0.002) and 6 months (P=0.03),” now we’re being informed that there was no “significant relation” between the presence of ketones and weight loss.  
I printed out the study, wondering what to do with the information. I wanted to raise my hand at the beginning of the next lecture and confront her with the accurate facts, if only to educate my classmates – all future doctors, nurses, and dieticians. A room full of people about to spend entire careers spreading this mininformation and furthering the development of chronic disease, all while attempting to heal people.  The irony fell on me like dead weight.
Later in the lecture, she told us that the studies say that the higher a person’s total carb intake is, the thinner they are – and does anyone know why this would be? A student raised a hand and postulated that it must be because they get more exercise. Prof nodded and shrugged, telling us that it was also discovered in the Nurse’s Health Study in the 80’s that those who eat the most are the leanest. She then completely flaked out of any sensical conversation about these facts by stating, and I quote: “In the field of nutrition, it would be nice if we had real rules.”
As if science doesn’t exist. I would have loved to raise my hand and explain most of this. First of all, as for the study that supposedly tells us that eating carbs makes us skinny, obviously there is more at play here than simply calories in, calories out. Different people's bodies have differing abilities to digest carbohydrates as fuel rather than storing them as fat. People with a highly evolved ability to digest carbs can eat more of them, and still have enough insulin and insulin-responsiveness in the cells to use the glucose as fuel and burn it off. People who eat "less carbs" and weigh more are really probably eating less food overall, not just carbohydrates because THEY HAVE A SLOWER METABOLISM and a reduced ability to digest carbohydrates so their bodies are STORING the food they are eating.
And then we get to the Nurse’s Health Study. I love this study. You just can’t argue with a solid, well-executed study involving thousands of reliable participants, even if the findings aren’t at all what would be predicted by modern nutritional theories. Despite the fact that the nurses demonstrated that it is not simply caloric intake that causes weight loss and gain, researchers and professors alike simply brushed aside this inconvenient finding with the explanation that the thin participants must also get the most exercise. This is so ridiculous. Do you have any idea how much more exercise one would have to get to be able to eat an additional 1000 calories a day and still be thinner? You would need to run 10 miles a day or do 60 minutes of heated power yoga with weights EVERY DAY. Not likely. 
Here once again, the cause and effect have been reversed because of a correlation, which does not infer causation. One cannot assume cause and effect just because two concepts are found to be related. In this case, researchers assume that some people are overweight because they consume too many calories. But there is ample evidence that obesity is a hormonal disease, and that people are overweight because their bodies are storing the food they eat as fat because of a metabolic defect. This defect is likely caused by the excessive insulin that is produced by the insanely high amounts of carbohydrates being eaten in our society, as well as many other countries across the globe.
There are a few more random comments that my professor made in the first couple lectures that I just shouldn’t finish this post without mentioning. On the second day of class, she professed while introducing the carbohydrate lecture: “Carbohydrates are my life!” I had to stifle a snort and duck behind the girl in front of me. Later she told us that she is so well known for her tolerant attitude toward sugar and sweets, that recently someone asked her, “Aren’t you the pro-sugar nutritionist?” Now this really blows my mind. As if someone could actually call themselves a nutritionist and be pro-sugar! This is a tenured professor at a major university. Obviously the brainwashing of of academia by the grain and sugar industries is a resounding success! And to then announce it to her college class with a guilty laugh and a breezy attitude was almost more than I could bear. Glancing around the room filled with future nurses and dieticians, I imagined them sprouting this dogma of nutritional bullshit to overweight, disease-ridden Americans for decades. I wanted to get up and storm out of the room, muttering profanities as I slammed the door behind me.
There was one last off-hand comment toward the end of the carbohydrate lecture that pretty much sums it all up: “When you’re working with carbs, you run into problems!”