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.