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Showing posts from March, 2010

Vitamin D and Crohn's disease

Vitamin D deficiency may actually contribute to Crohn's disease because the hormone modulates the immune system. According to endocrinologists at McGill University, vitamin D appears to turn on genes to encode antimicrobial peptides that fight against intestinal invaders (1). The immune support may help avoid inflammation associated with an autoimmune response in Cronh's disease. This may explain why Crohn's disease is more prevalent in Northern latitude countries. It also suggests that increased vitamin D could assist in avoiding Crohn's disease in the future. How do these findings affect what we know about ulcerative colitis? I hope we find out soon. Reference 1. McGill University Health Centre (2010, January 27). Vitamin D supplements could fight Crohn's disease. ScienceDaily. Retrieved March 31, 2010, from http://www.sciencedaily.com­ /releases/2010/01/100127104904.htm

Managing Diverticulitis After Treatment

It is well documented that a diet low in insoluble fiber is considered the main etiological factor in leading to diverticulitis. The intake of insoluble fiber speeds up transit of food and increases bulk reducing pressure on the intestine (1). On the other hand, intake of red meat appears to increase risk (1). Patients treated for diverticulits are often prescribed antibiotic therapy and recommended to stay on a low-fiber diet and reintroducing insoluble fiber gradually (2). In some cases, surgery is needed (2). Afterward, nutritionists would recommend gradual increases of fiber because a diet high in fiber can lead to high amounts of gas and forceful diarrhea (2-3). Because of possible damage in the intestine, nutritionists should also evaluate patients are at higher risk of malnutrition. Malnutrition can lead to slow healing and recovery as well as deterioration of muscle, respiratory and immune function (4). To receive adequate nutrients, higher protein intake as well as supplemen

Helping a Patient Manage IBS and Diarrhea

When IBS is diarrhea-predominant, a doctor may prescribe an antimotility agent to assist patients with symptoms (1). He or she may also prescribe an antibiotic if the IBS is a result of small intestinal bacterial overgrowth (1). As a dietary aid for patients, a nutritionist may suggest soluble fiber such as from oats because it can help act against symptoms such as diarrhea by helping bind fat and slow emptying of food from the stomach into the small intestine (2). The soluble fiber can include prebiotics such as fructo-oligosaccharides or resistant maltodextrin, which support growth of healthy intestinal bacteria. The prebiotics taken in conjunction with probiotics particularly after antibiotic therpay may help with promoting the growth of the good bacteria. This integrative therapy can help to alleviate symptoms by promoting competition against small intestinal bacterial growth (3). Nutrionists should recommend suspending intake of insoluble fiber such as from wheat and cereal grains

Adiponectin supplementation: Body fat loss

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Adiponectin is a hormone exclusively secreted by body fat. This hormone has been recently gaining attention from researchers because of some of its functions. Two important ones are the regulation of glucose and fat metabolism. Elevated levels of adiponectin are associated with increased insulin sensitivity, and increased fat catabolism (i.e., fat burning). And these associations appear to be causal. That is, adiponectin levels do not seem to be only markers, but causes of increased insulin sensitivity and fat catabolism. In other words, an increase in circulating adiponectin seems to lead to increased insulin sensitivity and increased fat catabolism. Insulin sensitivity is the opposite of insulin resistance. The latter is a precursor to diabetes type 2, and is associated with elevated fasting and postprandial (i.e., after a meal) glucose levels. Adiponectin also seems to work closely with leptin, another hormone implicated in a number of diseases of civilization. It appears that adipo

LDL, chylomicrons, HDL, and atherosclerosis: A lazy Sunday theory

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Notes:   - This post is a joke, admittedly a weird one, which is why it is labeled “humor” and is filed under “Abstract humor”.   - I apologize for this spoiler. Some people probably like humor posts better if they do not know what they are in advance, but several others may think that reading a post like this is a waste of their time. If you are in the latter category, move on to another post! If not, here it goes … *** Today I was spending some time under the sun, in one of the year’s 364 sunny days in Laredo, Texas. The goal was to see if I could obtain a precise count of the number of advanced glycation endproducts (a.k.a. AGEs) that would form as my skin was exposed to the sun’s damaging rays. Then I read a post by Peter at Hyperlipid, and inspiration consumed me. A new theory was born regarding the interplay of LDL, chylomicrons, HDL, and atherosclerosis. By the way, Peter is a fat genius, by which I mean a genius regarding all fat issues – who happens to be thin. A key observat

A trip to Europe: Some health-related routines and observations

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Every year I travel to Europe on business, normally once or twice a year. These trips usually involve meetings with engineers, researchers, and project managers from various European countries; often 5 to 10 countries are represented. Here are some of my notes on a recent trip to Europe. In this trip I spent time in two cities: Amsterdam, Netherlands and Antwerp, Belgium. Below is a set of the photos I took in Antwerp, of a statue depicting the roman soldier Silvius Brabo holding the severed hand of the giant Druon Antigoon. According to legend Druon Antigoon had terrorized and extorted the people of Antwerp, cutting off the hands of several people and throwing them in the nearby Scheldt River, until the brave Silvius Brabo came into the scene and not only cut off the giant’s hand but also killed him. This legend has probably been concocted toward the end of the Roman Empire, largely by the Romans, who first established Antwerp as a Roman outpost. After this small digression, here are

Low-carb diets and dehydration

It is well known that dehydration is a potential adverse effect of a ketogenic diet, which is one higher in fat with adequate protein and lower in carbohydrates. Nutritionists should be watchful, in particular, of those who use ketogenic diets as therapy for certain conditions such as epilepsy and type 2 diabetes. A study in epileptic children on ketogenic diets, for example, found dehydration to be the "most common early-onset compllication"and higher in those who fasted (1-2). The dehydration could be partly blamed on the incidence of GI tract adverse effects (1). When treating those with type 2 diabetes with a ketogenic diet, it is advisable to instruct drinking up to eight 8 oz. glasses of water daily. There may also be need for adjusting those recommendations if certain medications were used such as diuretics. According to the researchers who performed an intervention trial on those with type 2 diabetes and a ketogenic diet that resulted in a few adverse effects, the f

Kidneys: Animal vs Veggie Protein

I was curious to know what it is about animal protein in general that would affect kidneys more than vegetable protein. So I went searching for a study. There was a human intervention trial from the Dept of Internal Medicine in Texas that I found, which had evaluated animal protein-rich diet on kidney stones and calcium. The study took 15 subjects and fed them either vegetable protein, vegetable and egg protein or animal protein for 12 days in three different periods (1). What the study found was that the animal protein diet "conferred an increased risk for uric acid stones" but a lesser risk than the vegetarian diet for "calcium oxalate or calcium phosphate stones" (1). Because my question really wasn't sufficiently answered by this study, I decided to pursue what National Kidney Foundation had to say. Finally, I found a publication they put out referencing nutrition and speaking to vegetarian diets in which they basically state that the veggie diets aren't

Why Evidence-based Nutrition

As a result of my profession in science communications, it is a fact of life that I come in to work to find 1-2 papers to read every morning on my desk. I must read an average of between 10 new scientific papers weekly. They can range from culture studies, animal studies, human clinical trials, epidemiological studies, meta-analyses or simply review articles. As a writer who specializes in topics of nutrition, I am continually faced with the labor of assessing just how “big” the news coming from the study really is, whether or not it merits more attention by our research and sciences team, and whether or not we should communicate it to the public. If I had any special talent for pointing out flaws or problems in studies, I would be thrilled. I don’t. Not at all. Lucky for me, however, I work with a few knowledgeable scientists with a keen awareness for what’s hot and what’s definitely not. I doubt that many of my own colleagues share the same luxury that I have for being able to pass a

How much water do I drink?

I've been perusing through Dr. Batmanghelidj's book Your Body's Many Cries for Water . Yes, I'm well aware that it does not entirely scientific and does have a few claims that could be regarded as sensationalism for water (excess cholesterol is a result of too little water intake, really?). I was intrigued, however, at some of the references to the possibility of chronic dehydration as an influence on disease and the beginnings of cellular aging, which can fuel chronic disease. Plus, anyway, I needed to write a paper on water. So, of course, I had to ask myself, "How much water do you drink?" So here goes my diet for today: 8am: 1 cup of green tea (with 1 yogurt/protein shake/fruit) 10am: 1 cup of yerba maté (a habit passed from Argentine mom) 12pm: 1 cup iced tea (with chicken salad lunch) 2pm: 1 shot espresso 4pm: 1 cup yerba maté 6pm: 1 glass red wine (with 1 cup lentil-asparagus soup dinner) 9pm: 1 cup green tea (Plenty of liquid, but no straight glasses

More on the Harvard study on saturated versus polyunsaturated fats

This is a follow up on this post , which addressed the main argument put forth in a recent BBC article. The BBC article argued that people should replace saturated with polyunsaturated fats to reduce their risk of heart disease. Let us take a look at the actual Harvard study itself (i.e., the study discussed in the BBC article). The Harvard study is linked here . This post , by Stephan Guyenet, already pointed out several problems with the study. Stephan actually reviewed the studies used in the meta-analysis, and also some that were excluded in the meta-analysis and that he believes should have been included. Here are a few other problems, in addition to the ones already pointed out by Stephan: One thing that looks suspicious about this Harvard meta-analysis study is that they say that: “Statistical evidence for substantial between-study heterogeneity was not present (Q-statistic p = 0.13; I2 = 37%).” A meta-analysis is a study that essentially summarizes, in a statistically sophistic

BBC article's advice: Replace saturated with polyunsaturated fats

The BBC article is here . It is based on meta-analysis of eight previous studies conducted by Harvard researchers, which the article states cover more than 13,000 people. The article also says that: “… [saturated] fats raise the levels of bad cholesterol that block the arteries to the heart.” They are of course referring to LDL cholesterol as the "bad cholesterol". Sourcing bias is a notorious problem with meta-analyses (i.e., the choice of studies to use in a meta-analysis). Another problem is that you cannot tell what the studies sourced controlled for. Consider a study that compares health markers for smokers and non-smokers, where the smokers eat more saturated fat than the non-smokers. This study may confuse the effect of smoking with that of saturated fat consumption. To be reliable, the study must analyze the effect of saturated fat consumption, controlling for smoking habits. There are other statistical issues to be considered in meta-analyses. For example, some of th

PepsiCo to reduce sugar and fat in products

I guess PepsiCo is moving ahead of the competition, but in a snail pace and in a very, very politically correct way. Will this help in any way? I doubt. It is just too little, too late. See article here . The article states that: The company also set two goals for the next 10 years: to cut the average added sugar per serving by 25 percent and saturated fat per serving by 15 percent, in addition to adding more whole grains, fruits, vegetables and low-fat dairy into its array of products. While it is nice to see more of a focus on sugar than on saturated fat, I would have preferred to see something like this: The company also set two goals for the next 5 years: to cut the average added sugar per serving by 95 percent and increase saturated fat per serving by 50 percent, in addition to adding more vegetables and full-fat dairy into its array of products. What would happen? Well, Indra Nooyi is a very smart CEO, and the company has many competent people. They know that they would probably

Online calculators to assess cardiovascular disease risk: No LDL needed

Researchers can build mathematical equations (sometimes referred to as structural equations) that predict health outcomes based on health factors. Those mathematical equations can then be used in online calculators. This link takes you to a government-sponsored calculator based on the Framingham Heart Study. It estimates 10-year risk for “hard” coronary heart disease outcomes (myocardial infarction and coronary death). As you will notice, the link above does not take family history of disease into consideration. A different risk calculator, linked here , estimates a risk score called the Reynold Risk Score. It takes hsCRP (high sensitivity C-reactive protein, an inflammation marker) and family history in addition to the Framingham parameters in its risk score calculation. Neither calculator asks for LDL cholesterol levels. I wonder why .

Standard deviation is not the same as range of variation

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Often research results are expressed in means and standard deviations. For example, in the study reviewed in this post , it is stated that the weight of participants in a 12-week weight loss study varied from: 87.9 plus or minus 15.4 kg (at baseline, or before the 12-week intervention) to 81.7 plus or minus 16.2 kg (after the 12-week intervention). The 87.9 and 81.7 are the average weights (a.k.a. “mean” weights), in kilograms, before and after the 12-week intervention. However, the 15.4 and 16.2 are NOT the range of variation in weights around the means before and after 12-week intervention. They are actually the ranges around the means encompassing approximately 68 percent of all of the values measured (see figure below, from www.electrical-res.com). In the figure above, the minus and plus 15.4 and 16.2 values would be the “mean(x) – s” and “mean(x) + s” points on the horizontal axis of histograms of weights plotted before and after the 12-week intervention. This assumes that the dis

What's the most dangerous item on a fast food menu?

When I first saw the movie Super Size Me I was first pretty shocked that someone would actually risk his own body this way. Then, I was shocked at how quickly this guy was able to gain weight. This may simply be because I don't tend to gain any weight even after stuffing myself day after day. Of course, I've never tried to stuff myself with McDonald's day after day. Maybe that would do it. It did for this guy. And it does for our children. Sure opened my eyes. What's the most dangerous item on the fast food menu? I remember a time when I was younger I would go off with my grandpa to Burger King. He'd say, "Let's get you a Whopper. They're only a buck." I'd gush with enthusiasm. He'd buy me one. He'd buy himself too. My grandpa died of heart disease. I blame it on those Whoppers. I blame them because they're cheap and because the name itself, like the Big Mac, suggest that you're getting a lot of meat for your money. What you

Why Statins May Require You Take Extra CoQ10 and Vitamin E

Statins are drugs used to lower cholesterol by blocking cholesterol synthesis in the liver (1). By lowering total and LDL cholesterol, in effect, they help lower risk of heart disease and death (1). The most commonly known statin drugs are simvastatin (Zocor), lovastatin (Mevacor), pravastatin (Pravachol), and rosuvastatin (Crestor). Currently, it is theorized that as statins block cholesterol synthesis, they also block synthesis of coenzyme Q10 (2). This is unfortunate because coenzyme Q10 plays a key role in the mitochondria in the electron transport chain, as an antioxidant and as a regenerator of vitamin E (3). Statin therapy, then, could potentially lead to deficiencies of both coenzyme Q10 and, possibly, increase the need for vitamin E in cells (4). It has been theorized that deficiencies in both coenzyme Q10 and vitamin E are why statins cause statin-related muscle pain and statin-related myopathy (3-4). References 1. LaRosa JC, He J, Vupputuri S. Effect of statins on risk of co

What are blood thinners and how do they work?

Blood thinners, or anticoagulants and antiplatelet agents, are drugs to thwart blood clotting of which could block flow of blood to your heart causing a heart attack or your brain causing a stroke. Common anticoagulants are Coumadin, Warfarin and Heparin. It controls the rate in which clotting can occur and prevents them from forming inside blood vessels and the heart. It can also help prevent existing clots from enlarging. Common antiplatelet agents are Aspirin, Plavix (clopidogrel bisulfate) and Ticlid (ticlopidene hydrochloride). As the name suggests, they keep platelets from aggregation to prevent possible clotting, specifically where an injury to a blood vessel may have occurred. Blood thinners aren't associated with any specific nutrient deficiency, but are contraindicated taken with foods and supplements high in vitamin K1 (a clotting factor) or large amounts of vitamins E and C. They are also contraindicated with alcohol, certain herbs and teas, and other dietary agents tha

Ketosis, methylglyoxal, and accelerated aging: Probably more fiction than fact

This is a follow up on this post . Just to recap, an interesting hypothesis has been around for quite some time about a possible negative effect of ketosis. This hypothesis argues that ketosis leads to the production of an organic compound called methylglyoxal, which is believed to be a powerful agent in the formation of advanced glycation endproducts (AGEs). In vitro research, and research with animals (e.g., mice and cows), indeed suggests negative short-term effects of increased ketosis-induced methylglyoxal production. These studies typically deal with what appears to be severe ketosis, not the mild type induced in healthy people by very low carbohydrate diets. However, the bulk of methylglyoxal is produced via glycolysis, a multi-step metabolic process that uses sugar to produce the body’s main energy currency – adenosine triphosphate (ATP). Ketosis is a state whereby ketones are used as a source of energy instead of glucose. (Ketones also provide an energy source that is distinct

Ketosis, methylglyoxal, and accelerated aging: Fact or fiction?

Ketosis is a state typically associated with very low carbohydrate diets, such as the Atkins diet. In this state, the liver produces ketones based on fat (body fat or dietary fat). Unlike fats, ketones are water soluble and used by many tissues (including brain tissues) as a source of energy. Unlike glucose and lipoprotein-bound fats (in VLDL, for example), unused ketones cannot be converted back to substances that can be stored by the body. Thus excess ketones are eliminated in the urine; leading to their detection by various tests, e.g., Ketostix tests. This elimination of unused ketones in the urine is one of the reasons why very low carbohydrate diets are believed to lead to enhanced body fat loss. From an evolutionary perspective, one could argue that a ketosis state that involves the elimination of ketones in the urine is an inefficient and unnatural emergency mechanism. For our Paleolithic ancestors, dying of starvation was a much bigger problem than dying of obesity complicatio

Steamed gulf shrimp with vegetables

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Few would argue against eating seafood several times a week, except in the case of seafood allergy. Shrimp is a very good option, especially if it is not farm raised. 100 g of shrimp will typically have 20 g of protein, and about 152 mg of cholesterol (this is good for your health ). It will also have about 0.6 g of omega-3 fats, and 0.03 g of omega-6; an omega-3 to omega-6 ratio of about 20. My wife prepared this steamed gulf shrimp with vegetables dish. And it was very, very delicious. Here is her recipe: - Add a small amount of olive oil and water to a frying pan. - Add 1 lb of wild-caught peeled gulf shrimp, cabbage, onion, and asparagus (or green beans, as in the photo). - Cook in low heat for 15 minutes. - Add spinach and cook in low heat for another 10 minutes. - Turn off heat, season to taste while mixing; I suggest using garlic powder, cumin powder, and parsley flakes. Peeled shrimp is usually farm raised, which does not have the same amount of omega-3, or the same ratio of om

Adiponectin and tumor necrosis factor-alpha levels after a high saturated fat meal

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This is one of those interesting studies where the authors start with some pre-conceived assumptions and end up concluding something else, some way toward the opposite of what they assumed. My final interpretation of the study results is a bit different though. It suggests that the results are actually the opposite of what the authors originally assumed. The authors of the study (Poppitt et al., 2008; full reference at the end of this post) start by stating that since “… dietary fat is associated with increased lipid storage, weight gain, and obesity …” it is important to study the effect of dietary fat intake on the blood levels of certain substances that are associated with lipid disorders, weight gain and obesity. In short, the authors start from the assumption that dietary fat is bad. By the way, this type of indictment of all fats is not very common these days. Usually saturated fat is the target. Since dietary fat is assumed to be bad for us, that justifies the authors’ goal of s

Adiponectin, inflammation, diabetes, and heart disease

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Humans, like many animals, evolved to be episodic eaters and spend most of their time fasting. Body fat is the main store of energy in the human body. Excess dietary carbohydrates and fat are stored as body fat, in specialized cells known as adipocytes. Excess dietary protein is not normally stored as body fat . Adipocytes can be seen as being part of a very important and distributed endocrine organ, being responsible for the release of many different hormones into the bloodstream. One of these hormones is adiponectin. Other important hormones secreted by body fat tissue are leptin and tumor necrosis factor-alpha. Among hormones, adiponectin is particularly interesting because it is negatively correlated with body fat mass. That is, unlike other hormones such as leptin and tumor necrosis factor-alpha, a decrease in body fat mass (a well known health marker) is associated with an increase in adiponectin. This has led some researchers to speculate that adiponectin is a causative factor t