I know this information is already about a year out of date but I thought it might be worth republishing (as I just ran into this article and study this last weekend.) At the 2009 meeting of the American Heart Association, a study published in the New England Journal of Medicine showed that niacin (vitamin B3) treatments worked better than the Merck prescription drug Zetia at reducing the size of arterial blockages in the neck. Quoted from the New York Times who covered the story fairly well:
For patients taking a statin to control high cholesterol, adding an old standby drug, niacin, was superior in reducing buildup in the carotid artery to adding Zetia, a newer drug that reduces bad cholesterol, according to a new study.
The small study, with only 208 patients, has attracted outsize attention because the researchers did a head-to-head comparison of niacin and Zetia, which has been heavily marketed.
The Food and Drug Administration approved Zetia in 2002 to lower bad cholesterol, a risk factor for heart disease. But the drug has not yet proved to have a longer-term clinical benefit in reducing heart attacks and deaths. Merck, the maker of the drug, is conducting a clinical trial on that issue involving up to 18,000 patients.
The headline jumps out because a measly vitamin that has been available since humans existed appears to do more for the cardioprotection than Merck’s newest drug. But lets dig a little deeper here and keep a good head about you as we dig in here:
Carotid Artery (the big one shown)
1) The study showed that niacin was more effective solely at preventing plaques from forming in the carotid artery which runs up from the aorta into your neck. While blockages here matter, this artery is much larger than the the coronary arterials. Blockages in the coronaries cause heart attacks by depriving the heart’s ventricles of blood. It would logically follow that other arteries besides the carotid would remain less clogged based on the study but that was not proven here.
2) Zetia did lower LDL cholesterol a significant amount – about 20%. But this reduction has a very interesting side effect: it made the arterial plaque worse. From the NEJM study:
As compared with ezetimibe, niacin had greater efficacy regarding the change in mean carotid intima–media thickness over 14 months (P=0.003), leading to significant reduction of both mean (P=0.001) and maximal carotid intima–media thickness (P≤0.001 for all comparisons). Paradoxically, greater reductions in the LDL cholesterol level in association with ezetimibe were significantly associated with an increase in the carotid intima–media thickness (R=–0.31, P<0.001)
If we translate that bold part into english: Zetia lowered LDL but that made the artery plaque bigger. The scientists did not go into greater detail here and all the study participants had heart disease, so it is hard to draw conclusions here, but this finding may mean Zetia is doing more harm than good. Even more broadly, it brings into question the idea of blanket lowering LDL cholesterol dogma that is the foundation of most heart disease protocols.
3) This study is flawed because it did not use a placebo group and there was no mention of the study being double blinded (that is where neither the patients nor the scientists know whom is receiving which treatment).
4) The form of niacin used in this study was not the OTC Vitamin B3 Niacin but rather an extended release Rx version called Niaspan. So, of course, the kicker from the Times story hits hard:
Niaspan is made by Abbott Laboratories, which financed the study.
Some final thoughts:
The findings are significant but not terribly meaningful – this was a small study that did not have the proper rigor to demonstrably usher in a new paradigm, not to mention the findings conveniently coincide with the pharmaceutical company who funded the study. But it did show Abbott’s Niacin-based drug beats Merck’s Zetia. It would be interesting to see if, instead of using Abbott’s time release formula, there was a side-by-side comparison of what 2X/day niacin supplement, in all its $4.99/bottle-at-walmart-glory, might do next to the $100+/bottle of miracle drug Zetia, and even Abbott’s Niaspan. Some placebo controls would be nice as well.
The irony to this whole story is that regular old niacin can be found in the very products cardiologists tell you stay away from: beer, pork, fish and -above all – chicken. This situation seems just too convenient to be an accident. Just putting an idea out there – maybe the body evolved to use niacin as a natural cholesterol balance against cholesterol heavy foods like beef and chicken, considering the body would find niacin wherever it would find cholesterol in these meat products.
The latest examination of obesity rates by the CDC comes to some sobering conclusions about the state of public health in America. Their findings show a block of states, mostly concentrated in the South, now have obesity rates over 30%. Back in 1990, no states were over 20%, making the run-up in the last 20 years remarkable.
The Journal of the American Medical Association gave us the most recent update on obesity earlier this year from the highly respected NHANES data set about the 2007-2008 obesity timeframe. They came to slightly more upbeat conclusions, finding that the incidence of obesity in America was over 32% and still increasing but at a slightly slower rate. They had some other interesting tidbits, especially about how these trends date back to the civil war in the 1860s:
In the United States, a study of data from military recruits, veterans, and national surveys suggests mean BMI has increased over a long period since the Civil War up to recent times, with increases in the last several decades perhaps less steep than those observed earlier.25 Over the period 1960-1980 (covered by the earliest NHANES surveys and the National Health Examination Survey), obesity prevalence was relatively stable, but then it showed striking increases in the 1980s and 1990s. The data presented in our current study using 2007-2008 data suggest that the prevalence may have entered another period of relative stability, perhaps with small increases in obesity, although future large changes cannot be ruled out. Because relatively little is known about the causes of the trends previously observed, it is difficult to predict the future trends in obesity.
The CDC’s latest numbers update us for the 2009 calendar year, finding that the growth is accelerating again, possibly exacerbated by the dire financial situation many people found themselves in because of the recession. As we mentioned earlier, the rate of obesity is significantly over 30% for the entire nation now, and nearly 35% in the south. In certain ethnic groups, especially black and hispanic groups, the rate is bumping up near 40%. Remember, obesity is defined as being more than 30 pounds overweight in this survey – if we were also counting overweight people, which is generally considered more than 10 pounds overweight, we these numbers could be double what is being reported here.
Obesity Rates from 1990 to 2009, the growth is explosive
What is Causing this Surge?
While the usual suspects of diet and exercise are implicated in this rise, other research is coming to light on the subject. Just yesterday a new finding came out that suggests obesity may be related to a virus contracted during childhood. This virus, adenovirus 36, belongs to the larger class of adenoviruses that can cause a host of problems like eye infections, GI tract irritation and respiratory infections. What makes adenovirus 36 unique is that it infects fats, making it the only known virus to do so.
The study in the journal Pediatrics shows a correlation between having adenovirus 36 and being obese but it does NOT show adenovirus 36 causes obesity. This implies that the virus will may be able to attack an obese person due to a suppressed immune system or some other avenue; the researchers do not go into the causation subject in detail so it is hard to say. They emphasize this study is a starting point but it shows interesting promise in understanding childhood obesity.
Where does it go from here?
Given the gravity of this issue and the cost it is putting on the nation (and the world for that matter), major research dollars are being thrown at understanding the issue. I’m just not confident they will find very much here. This is a multifaceted issue – problems such as inactive work lives, the proliferation of car-culture and suburbia, fast food, bad diets and a lack of exercise are all playing a role. It is hard to tease out exactly which factors are the most important to pay attention to in the data sets because this situation is now so widespread. I think the research will get more specific moving forward, as we are seeing with the concentration on the adenovirus angle with children, the genetic dimension with minority groups and lifestyle choices with middle america. But obesity, at the end of the day, is an input/output issue – if you burn more calories than you consume, you will lose weight. Getting people to do that is a whole different story.
Tomorrow, we will reexamine high fructose corn syrup’s role in obesity in light of some new research.
Researchers at SMU are working with DARPA (the US hyper-advanced military research group that initially developed the internet) to create an artificial fiber optic signaling system that will directly interface with your body’s central nervous system. This technology, called neurophotonics, would allow bidirectional communication to and from the brain, giving amputees with prosthetic arms and legs the ability to feel heat, cold and pain in those artificial extremities. From the article:
The goal of the Neurophotonics Research Center is to develop a link compatible with living tissue that will connect powerful computer technologies to the human nervous system through hundreds or even thousands of sensors embedded in a single fiber.
Unlike experimental electronic nerve interfaces made of metal, fiber optic technology would not be rejected or destroyed by the body’s immune system.
“Enhancing human performance with modern digital technologies is one of the great frontiers in engineering,” said Christensen. “Providing this kind of port to the nervous system will enable not only realistic prosthetic limbs, but also can be applied to treat spinal cord injuries and an array of neurological disorders.”
This program follows in the footsteps of DARPA’s ‘Revolutionizing Prosthetics’ Program, whose goal was to have neuronal-controlled prosthetic arm to market before 2010. According to their website, those advanced prosthetics are already in testing but they are nowhere near as advanced as this project. A true fiber backbone for the body would act much like our spinal cords currently do, only faster.
The Future
Neurophotonics is an interesting field just in its infancy and it is going head to head with genetic engineering. It will be interesting to see if this neurophotonic method, where structures we engineer are grafted into humans, takes hold or if genetic engineering, where genes are manipulated to bring similar results, will win out. Another research company called Neuralstem is attempting to reconnect spinal cords damaged spinal cords from Lou Gerhig’s Disease with genetically engineered stem cells.
Stem cells have come under intense pressure as they are harvested from fetuses (sometimes). Using them for research purposes was outright banned earlier this year in the US by a court ruling but the ban has since been lifted. This neurophotonic method may win out because it is less controversial but first, both methods have to prove successful in further clinical trials.
The New York Times has a really good piece on the coming rules regarding the amount of antibiotics that can be given to confinement livestock.
Now, after decades of debate, the Food and Drug Administration appears poised to issue its strongest guidelines on animal antibiotics yet, intended to reduce what it calls a clear risk to human health. They would end farm uses of the drugs simply to promote faster animal growth and call for tighter oversight by veterinarians.
The agency’s final version is expected within months, and comes at a time when animal confinement methods, safety monitoring and other aspects of so-called factory farming are also under sharp attack. The federal proposal has struck a nerve among major livestock producers, who argue that a direct link between farms and human illness has not been proved. The producers are vigorously opposing it even as many medical and health experts call it too timid.
Scores of scientific groups, including the American Medical Association and the Infectious Diseases Society of America, are calling for even stronger action that would bar most uses of key antibiotics in healthy animals, including use for disease prevention, as with Mr. Rowles’s piglets. Such a bill is gaining traction in Congress.
What a CAFO looks like
In case you are not familiar with the situation, often pigs, chickens and even cows are put into caged areas much to small for any living creature move around freely. These confinement animal feeding operations (CAFOs) result in large amounts of animal waste that creates an ideal breeding ground for bacterial infection among the animals. Farmers are aware of this and supplement their animal feeds with a range of antibiotics.
But the point here is more nuanced. The battle over the line for antibiotic use on the farm center around their use as a growth promotion agent in animals. Many CAFO farmers have learned that antibiotic cocktails cause their chicken to grow faster, their pigs to grow larger, etc. Ag-centric scholarly journals have dubbed these agents ‘antibiotic growth promoters’ (AGPs) and they are subject of the FDA’s scrutiny. Here is a good review of how they have been used:
Public health officials note that antibiotic resistance has grown by this abundant use of antibiotics. The use is so abundant that is far outpaces the amount of antibiotics used by human beings. According the Union of Concerned Scientists – a reputable NGO – non-therapeutic use of antibiotics in livestock represents over 70% of the total amount of antibiotics created in the US. The FDA is listening to those worries, which have been ignored up until now, with new ears.
Imagine if you had to live your life in a subway car with 300 of your closest friends. It wouldn’t take long before somebody got the sniffles and, pretty soon, the whole car would be sick. That’s the basic scenario at the CAFO that farmers are worried about. Public health officials are worried about what happens if those resistant strains of bacteria get out of the CAFO and jump into humans.
This new FDA rule will not be an easy sell. The agriculture and public health industries are extremely well connected on Capitol Hill and I’m not sure who’s dollar bills will look better to elected officials. I see major resistance shaping the end product here.
ost of us already know that we should be eating fiber – according to the Institute of Medicine, adults should be eating 20-35 grams of it per day. But why? What’s so important about fiber anyway? What does it do for us physiologically? And does it matter what kind of fiber we eat?
I can hear some of you now – wait, there’s more than one kind of fiber? Yes, there is, though you won’t see it detailed on any nutritional label. Most of the time, we’re told to simply focus on total fiber , no matter where it comes from. While getting enough total fiber is key, getting enough of each kind of fiber may be just as important in having a healthy, happy digestive system.
What is Fiber? And what does it do?
Peas, an excellent source of fiber – thanks to Sami Taipale flickr
Fiber is similar to starches and sugars in that it’s mostly made of carbohydrates . The difference is that fiber refers to the carbohydrates that your body can’t digest, while starches and sugars are carbohydrates that humans easily digest. Why would we want to eat something our bodies don’t digest? As it turns out, even though we can’t digest it, fiber helps us digest other things and keeps our digestive system running smoothly. Of course, the kind of fiber matters.
There are two main categories of fiber: soluble and insoluble. Soluble fiber dissolves in water, while insoluble fiber, as the name suggests, doesn’t. The average American fiber intake contains 75% insoluble fiber and 25% soluble fiber, each having its own special physiological impacts on digestion.
Insoluble fiber, like the fiber in whole wheat foods, bran, nuts, and seeds, mostly helps by simply being there. It’s what forms the mass that moves through your bowels, and while that might sound a little gross, it’s key to preventing conditions like diarrhea and constipation. Because it stays in a solid form, it helps compact the forming stool, which allows it to move more easily through the intestines. Some health professionals also believe that insoluble fiber acts like a sponge or scrub brush, cleaning the digestive tract as it goes along by gently scraping the walls and snowballing with stray particles so they are removed from the body.
Soluble fiber, found in fruits, vegetable and flax seed, acts differently because it becomes gel-like in water, actually incorporating with liquids. Soluble fiber helps hydrate stool, allowing it to slip though the intestines smoothly, a key in preventing digestive disorders. But soluble fiber does so much more – often called “viscous fiber“, soluble fiber makes your digestive contents into a thick slurry, which slows down your digestive system, slowing the process of absorption in the small intestine.
The effect of this is that you feel fuller, longer, because of slower, steadier increases in blood glucose levels, and your body requires less food to attain the same absorption of energy and nutrients. One study found that adding one kind of soluble fiber to their subject’s diets reduced the their food intake by 11%!
But soluble fiber also helps regulate the levels of glucose in our blood more directly. Soluble fiber is often fermented during our digestive processes, producing compounds called short-chain fatty acids and gasses (FYI, this is where increases in flatulence can come from when eating beans – legumes are high in soluble fiber and fructo-oligo-saccharides).
Short-chain fatty acids have a number of physiological roles. These small fat molecules have been shown to directly influence insulin release from the pancreas and glycogen breakdown in the liver, leading to stable and healthy glucose levels. Short-chain fatty acids also influence the liver’s production of cholesterol. The effect of this is that increased fiber consumption lowers the circulating bad cholesterol in the blood. They’ve been found to promote the production of immune cells and antibodies, potentially boosting immune function. Furthermore, these little acids help regulate the pH (acidity) of the intestines and the colon, keeping it in the right range to promote nutrient absorption and discourage microbes from producing toxins and carcinogenic substances.
A good video review of this information can be found here:
Fiber and Disease
Mega Burgers, not so hot on fiber – credit, marshall astor
The old adage “an apple a day keeps the doctor away” may be more true than we thought. Apples are great sources of fiber, and both soluble and insoluble fibers help reduce the risk of a variety of diseases. One of the most well understood is fiber’s connection to diabetes. Because fiber slows down your digestive system, glucose enters your bloodstream at slower, more stable rate, and this helps with managing Type 1 diabetes. But fiber can help prevent Type 2 diabetes, too.
Type 2 diabetes can be induced by our diets when our bodies are exposed to high blood glucose levels for a long period of time. This can happen because of consistent over-intake of sugars and carbohydrates, but it can also occur because our bodies are unable to produce enough insulin to lower rising blood sugar levels, or we become desensitized to insulin activity. By creating a slow, steady stream of glucose uptake, fiber helps our bodies avoid the sudden spikes glucose and insulin that, over time, can lead to Type 2 diabetes.
Studies have shown that diets high in fiber reduce the risk of Type 2 diabetes significantly. For example, a meta-analysis of several large studies (totaling to over 700,000 people) found that eating an additional 2 servings of whole grains a day decreased the risk of Type 2 diabetes by 21%. Both soluble and insoluble fiber intake are correlated with reduced diabetes risk, though how the insoluble fiber is involved is less understood.
Fiber is also strongly linked to reducing risk of heart disease. This is likely due to its positive influence on blood cholesterol levels. A number of large, long-term studies have found that people with high-fiber diets have up to a 40% lower risk of coronary heart disease.
Furthermore, a meta-analysis of seven large studies found that the risk of developing cardiovascular disease was 21% lower in people who ate 2.5 or more servings of whole grain foods a day compared with those who ate much less. Mostly, these studies suggest that soluble fiber is the key player in preventing cardiovascular problems. Because of the extensive, strong correlation between soluble fiber intake and lowered risk, soluble fiber is one of the very few things that the FDA officially recognizes as reducing the risk of heart disease.
Furthermore, a recent study has found that increasing soluble fiber intake, but not insoluble fiber intake, actually helps boost our immune systems. Mice were fed low-fat diets that either contained regular amounts of soluble or insoluble fiber for six weeks before being subjected to an agent that mimics a bacterial infection. When the two groups were compared, the soluble-fiber eating mice were only half as sick as their insoluble-eating counterparts, and they recovered 50% sooner. What made the soluble fiber so much better for the mice?
Scientists discovered that the soluble fiber-eating mice were producing higher levels of anti-inflammatory compounds, perhaps due to short-chain fatty acids. Immune cells in our bodies have to deal with both invaders like infections and self-caused problems like inflammation. The researchers believe that by reducing the inflammation response, ingesting soluble fiber altered the mice’s immune cells, making them switch from problematic inflammatory cells to anti-inflammatory cells that can deal with other problems, like the faked infection. While this research is preliminary, it’s impressive that the mice immune systems were altered by manageable amounts of fiber that could easily be eaten by people.
The one thing fiber intake doesn’t help much with, though, is the one disease it’s most often touted as a way of preventing: colon cancer. The truth is that the connection between dietary fiber and reduced risk of developing colon cancer is weak at best. While some smaller studies have linked high-fiber diets to lowered risk of colon cancer, larger ones, like a 16-year Harvard study of more than 80,000 nurses, have found no connection.
Take Home Message: EAT MORE FIBER!
The scientific evidence is unmistakable – fiber is vital for a healthy digestive system. More often than not, you’ll be told to simply eat more fiber, but from the evidence I’ve seen, you should be particularly eating more soluble fiber. And that isn’t the kind of fiber normally touted – often, you hear people push for whole grains, which are good sources of insoluble fiber, even though it’s soluble fiber that is much more strongly linked to fiber’s various health benefits. There’s another problem, too – according to nutrition labels, fiber is fiber. There is no distinction between soluble and insoluble fiber in packaged foods. Instead, you have to be your own nutrition expert, and know which fiber-filled foods are naturally high in soluble fiber. Here are a few good ones:
Foodstuff
Serving Size
Total Fiber (g)
Soluble Fiber
Insoluble Fiber (g)
Grapefruit
1/2 fruit
1.3
0.9
0.4
Squash, summer
1/2 cup
2.3
1.1
1.2
Zucchini
1/2 cup
2.5
1.1
1.4
Brown rice
1/2 cup
1.3
1.3
0
Rolled Oats
3/4 cup
3
1.3
1.7
Orange
1 medium
2
1.3
0.7
Plums
2 medium
2.3
1.3
1
Broccoli
1 stalk
2.7
1.3
1.4
Carrots
1 large
2.9
1.3
1.6
Tangerine
1 medium
1.6
1.4
0.4
Peas
1/2 cup
5.2
2
3.2
Pinto beans
1/2 cup
3
2.2
0.7
Potatoes
1 small
3.8
2.2
1.6
Apple
1 small
3.9
2.3
1.6
Psyllium husk
10g
8
7.1
0.9
Of course, no matter what you should probably be eating more fiber. Studies have found that Americans eat 50% or less than the recommended intake every day! So while soluble fiber may be the best option, any fiber is a start!
What are the downsides to eating fiber? After all, it sounds so wonderful – there must be something bad about it, right? Well… there is the gas produced by soluble fiber fermentation, but that seems a small price to pay compared to the many benefits that fiber intake can have. Sorry to sound unbelievable, but no, in my opinion, there aren’t any real downsides. Actually, I’ll rephrase – there aren’t any downsides to eating the amount of fiber you get from the kinds of foods people eat, so long as you still get the necessary amounts of protein and other nutrients, too. Switch to eating entirely fiber-rich grasses instead of the normal grains, fruits and veggies and you might not fare so well. The only thing I will recommend, though, is that if you plan on dramatically increasing your dietary fiber intake, do it somewhat slowly to allow your body to adjust to the rise in non-digestible material in your diet. This will help you prevent the only known clinical side effects of sudden, high-fiber intake – tummy trouble.
Previous posts in the Understanding Our Bodies series:
Leathwood P, & Pollet P (1988). Effects of slow release carbohydrates in the form of bean flakes on the evolution of hunger and satiety in man. Appetite, 10 (1), 1-11 PMID: 3355122
Ruottinen S, Lagström HK, Niinikoski H, Rönnemaa T, Saarinen M, Pahkala KA, Hakanen M, Viikari JS, & Simell O (2010). Dietary fiber does not displace energy but is associated with decreased serum cholesterol concentrations in healthy children. The American journal of clinical nutrition, 91 (3), 651-61 PMID: 20071642
de Mello VD, & Laaksonen DE (2009). [Dietary fibers: current trends and health benefits in the metabolic syndrome and type 2 diabetes] Arquivos brasileiros de endocrinologia e metabologia, 53 (5), 509-18 PMID: 19768242
de Munter, J., Hu, F., Spiegelman, D., Franz, M., & van Dam, R. (2007). Whole Grain, Bran, and Germ Intake and Risk of Type 2 Diabetes: A Prospective Cohort Study and Systematic Review PLoS Medicine, 4 (8) DOI: 10.1371/journal.pmed.0040261
Pereira, M. (2004). Dietary Fiber and Risk of Coronary Heart Disease: A Pooled Analysis of Cohort Studies Archives of Internal Medicine, 164 (4), 370-376 DOI: 10.1001/archinte.164.4.370
Rimm, E. (1996). Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men JAMA: The Journal of the American Medical Association, 275 (6), 447-451 DOI: 10.1001/jama.275.6.447
Brown L, Rosner B, Willett WW, & Sacks FM (1999). Cholesterol-lowering effects of dietary fiber: a meta-analysis. The American journal of clinical nutrition, 69 (1), 30-42 PMID: 9925120
MELLEN, P., WALSH, T., & HERRINGTON, D. (2008). Whole grain intake and cardiovascular disease: A meta-analysis Nutrition, Metabolism and Cardiovascular Diseases, 18 (4), 283-290 DOI: 10.1016/j.numecd.2006.12.008
Fuchs, C. (1999). Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women New England Journal of Medicine, 340 (3), 169-176 DOI: 10.1056/NEJM199901213400301
Almost everyone has heard of Insulin. You probably know that people with type 1 diabetes need to inject themselves with insulin to survive, and must constantly monitor the amount of sugar they eat. But what do you really know about insulin? What is its purpose in the body, and why do we need it? How does it relate to our diets? What happens when things go wrong with it? And why should anyone who doesn’t have diabetes give a hoot?
Insulin is one of the most important hormones in the human body, and yet most people don’t really understand why our bodies make it or how what we eat affects the levels of insulin we produce. More so than any other hormone, our diet is key in regulating insulin levels, and thus a number of biological processes. As you’ll soon see, everyone should think about how what they eat impacts their body’s insulin release to be at their happiest and healthiest.
Why We Need Insulin
Every living thing requires energy to survive. In cells, energy is stored and shuttled around using a molecule called Adenosine Tri-Phosphate, or ATP. Whenever the cell then has an energy-requiring reaction, enzymes can use the energy stored in ATP’s phosphate bonds to fuel it. Cells rely on ATP to survive, and to create ATP, they rely on glucose.
ATP – the fuel for life
All cells, from bacteria and fungi to us, take glucose and use it to generate ATP by a process called Oxidative Phosphorylation. First, glucose is converted to an intermediate molecule called pyruvate via a process called glycolosis. As long as there is oxygen around, this pyruvate is further converted to Acetyl CoA, which enters a cycle of reactions called the Citric Acid Cycle. This takes the carbon to carbon bonds and uses them to create high energy electrons, which are then passed down a chain of enzymes which use the electron’s energy to create a proton gradient, the force of which fuels ATP synthase, the enzyme which creates ATP from ADP. Without glucose, cells cannot create ATP, and eventually die.
In plants, a process called photosynthesis takes light energy from the sun and uses it to combine carbon dioxide (CO2) and water (H2O) to create glucose (C6H12O6). This means that to survive, all they need is light, air and water. Unlike plants, though, we cannot create our own glucose, so we rely on our diets to provide it for us.
Just about everything we eat is able to be used to create glucose. Carbohydrates, by definition, are sugars, and all sugars are readily converted to glucose. The amino acids that make up proteins can be converted to glucose via an enzymatic process called gluconeogenesis. Fats, too, are converted to glucose or its derivatives; glycerol, for example, can be converted to glucose via gluconeogenesis, and fatty acids can be converted to Acetyl CoA via beta oxidation. No matter where it comes from, the glucose from our meals then ends up in our blood to travel around our bodies to the tissues that need it.
Obviously, having a blood glucose level that is too low would be bad – not enough glucose will get to our various tissues, and our cells won’t be able to generate enough ATP to function. This is a condition known as hypoglycemia, and the effects can range from mildly ‘feeling bad’ to seizures, unconsciousness, permanent brain damage or even death, all of which are due to a lack of ATP. But you can tip the scale too far in the other direction, too. You would think that since it’s so important, we would want a ton of glucose in our blood, but too much causes our blood to thicken, slowing it down and drawing fluid from our tissues to try and make it thin again. Too high of a blood glucose level, called hyperglycemia, can result in blurred vision, fatigue, dry mouth and heart problems that can sometimes be fatal. So our bodies work very hard to maintain our blood glucose levels between 3.6 and 5.8 mM (mmols/liter). This is about enough glucose to provide energy to the body for 20-30 minutes, so as we use up the glucose in our blood, our bodies constantly release more (hopefully) without overdoing it.
It’s particularly important for our bodies to maintain glucose levels every time we eat. Whenever we ingest food, our bodies have to quickly adjust to the sudden flood of glucose entering our systems as our meals are digested. Take something as small as a roll of Smarties, for example. One roll of Smarties contains 6 grams of sugar. At around 125 lbs, my body contains an average of 4 liters of blood. This means that if all the sugar from a single roll of those delicious candies were to enter my bloodstream at once and remain unchecked, it would raise by blood sugar by 8 mM! Four smarties packs, and my blood sugar levels would be fatal. So why, then, when I enjoy a sugary treat, do I not go into severe hyperglycemia?
The answer is insulin. Our bodies release insulin right before and during eating, and that insulin tells our bodies to start taking glucose out of the blood, thus lowering our blood glucose levels. It does this by both promoting uptake of glucose by cells and the storage of glucose within our cells. Without insulin, we would all go into hyperglycemic shock and die from something as common as a hamburger.
What is Insulin?
Insulin is a relatively small peptide hormone produced by β-cells in the pancreas. It’s main job is to signal the liver, muscle and fat tissues to take up glucose from the blood and store it as glycogen. As the glucose level in the blood drops to normal, insulin release slows or stops. If it drops too low, an antagonistic hormone, called glucagon, is released which does the opposite of insulin, stimulating cells to break down glycogen and release glucose.
The insulin and glucose process illustrated
But insulin does much more than just control blood glucose levels. Its effects depend on the cell type that receives its signal. Fat cells, for example, don’t take up or store glucose. Instead, they respond to insulin by taking the fats that enter the blood stream and turning them into fatty acids, which they store in large vacuoles. Thus insulin promotes the uptake and storage of fat in our adipose tissues. While insulin levels are high, our bodies don’t digest or use fats for fuel. Instead, we rely on the glucose in our blood and tissues. This is key to keep in mind when trying to lose weight – you body simply won’t break down and use your fat reserves with insulin around.
Furthermore, insulin stimulates the body to absorb most amino acids. However, it doesn’t lead to intake of tryptophan by cells. This creates an effective rise in tryptophan concentration in the blood, allowing it to pass through the blood brain barrier. In the brain, tryptophan is converted to serotonin, a neurotransmitter whose primary purpose, in this case, is to reduce appetite. But serotonin has a lot of other effects, as those of you who have read the previous Understanding Our Bodies on Serotonin know well. In general, increased serotonin leads to a feeling of happiness and calm, which is why we get such satisfaction when we eat. Thus insulin is important not just when it comes to dealing with fats and sugars but in regulating our emotions, too!
It turns out insulin in the brain has a lot of functions, very few of which we understand well. Mice that lack insulin and leptin receptors in their brains, however, exhibit insulin resistance that is characteristic of diabetes. Strangely, though, they have a lot of reproductive deficiencies, too – the females have poor fertility, high testosterone levels and deformed ovaries, for example. Why insulin has these effects on reproduction is unknown, but it just goes to show that insulin does a lot more than regulate blood sugar levels, and is far more important in our bodies than we once thought.
Regulating Insulin
While insulin levels are mostly regulated by the amount of glucose in our blood, other things can stimulate its release. Other molecules from digestion, like certain amino acids, proteins and lipids, can similarly stimulate insulin release. But most incredibly, our bodies begin releasing insulin before we even take a single bite of food. When we think about, smell, or slightly taste foods, our brains trigger what is called Cephalic Phase Insulin Release. A food’s color, appearance, flavor, aroma, and texture can all impact how our brains respond to the idea of eating it. The goal is to prepare the body for what the brain thinks will be a sudden flood of glucose. The sweeter and sugarier the brain thinks the meal will be, the more insulin it stimulates the pancreas to release before the food even enters the mouth.
Merely waiting in line for food can ramp up the body’s insulin system – credit, flickr -Eleets121
Once we start to eat, our bodies ramp up insulin secretion, in what is often called first phase insulin release. Insulin that was kept in storage while our blood glucose levels were normal is released all at once, leading to a dramatic increase in insulin levels. The amount of insulin secreted in the first phase response to a meal is determined by the amount of glucose encountered in the previous meal – the more you needed last time, the more is released in this first phase. In a healthy person, this first phase response peaks a few minutes after you’ve started your a meal.
The β-cells then take a quick pause. If the first pulse was enough, then they slowly take up the insulin they released, and store it for the next meal. If the blood glucose levels stay high, though, the β-cells begin producing and releasing insulin in pulses every ten to twenty minutes. They continue this until the body’s blood glucose gets back to normal levels. The blood sugar rise caused by the meal peaks about half an hour after eating, and this, in turn, leads to a decrease in insulin production and release.
There are other regulators of release of insulin, too. Stress hormones like noradrenaline inhibit insulin release. This makes sense when you think about it evolutionarily. The purpose of stress hormones is to prepare our bodies for a sudden need to act. If we see a tiger, for example, our stress hormones spike so we can be prepared to fight if it attacks or run like hell to get away. Either way, we’ll need extra energy on hand to deal with the stressful situation, so stress hormones stop insulin from being released to ensure that a little extra glucose is in the bloodstream and able to reach whatever body parts need it most.
Not all insulin is produced in the pancreas, though. The brain also produces its own supply of insulin. The brain is a complex organ and needs lots of fuel to run properly. Insulin in the brain enhances learning and memory. Meanwhile, reduced levels of insulin and its related proteins are linked to Alzheimer’s disease and other degenerative disorders.
Insulin and Disease
Insulin is at the heart of many diseases. As I just explained, insulin in the brain is particularly key, and can lead to neurological disorders. But too much or too little insulin in the body is a big problem, too. There is a special name for the series of diseases caused by impaired insulin signaling in the body. You might have heard of it: Diabetes Mellitus.
When your body stops producing insulin, injections are all that is left – credit, i5a, flickr
Diabetes occurs when the body does not have the insulin signaling it should. There are two major types: type 1 and type 2. People with type 1 diabetes tend to realize their condition early in life, and must deal with it throughout their lifetime, while those with type 2 tend to develop symptoms later on. What’s the difference? While both conditions involve problems with the insulin pathway, type 1 diabetes is caused by a lack of insulin, while type 2 is caused by chronically high levels. People with type 1 diabetes have innately low levels of insulin due to genetic mutations. Without the ability to produce enough of this vital hormone, they usually have consistently high blood glucose levels. While this is a problem, there are many forms of treatment, including insulin injections. By carefully controlling their sugar intake and taking insulin when they need it, people with type 1 diabetes can regulate their blood glucose levels to being almost normal.
Type 2 diabetes is different. Type 2 diabetes results from the body having high insulin levels for too long. Insulin is meant to be a fast acting hormone – you release it when glucose levels are high, so that they drop. Then the signal stops. If you constantly eat too much or have a very sugary diet, you can end up with high insulin levels all the time. This leads to the body becoming desensitized to insulin. It’s kind of like trying to listen to a radio with static. If you only get a little static every once in a while, you can hear the song fine, and understand what the artist is saying. But start having high static all the time and you can’t tell what song is playing anymore. Your body, in effect, can’t tell what signal it’s supposed to be getting, and instead stops listening all together. Type 2 diabetes is that much more dangerous because the body will rarely respond to insulin treatment, meaning that drastic diet changes and exercise are the only ways to fight back.
Sadly, more than 90% of diabetes cases are type 2. Prevalence rates of type 2 diabetes doubled between 1990 and 2005, causing the CDC to declare it an epidemic.
Insulin is also a key player in Metabolic Syndrome. Metabolic syndrome, often called prediabetes, is poorly characterized, and even more poorly understood. Symptoms include elevated blood pressure, high blood cholesterol, and increased waist circumference. The main cause appears to be decreased response to insulin in certain tissues, specifically muscle and fat. The thing is, we’re not sure if it’s treatable or an irreversible first step in Type 2 diabetes. Often, people with metabolic syndrome are overweight, and at higher risk for other, even more life threatening conditions like heart disease. While some drugs can be prescribed to treat the symptoms like high blood pressure, the only long-term solution is to lower chronic blood glucose levels and restore insulin sensitivity, if, indeed, it can be restored at that point.
Nutrition and Insulin: Glycemic Indexes, Glycemic Loads and Beyond
Everyone should think about insulin and blood glucose levels, not just people with diabetes or metabolic syndrome. What we eat, how much of it, and when can impact our insulin release, which in turn can have a big impact on our bodies and how we feel.
Refined carbohydrates like spaghetti can exacerbate blood sugar issues – credit, flickr, Bxl06
The major dietary players in insulin regulation are carbohydrates. While fats, proteins and everything else can increase blood glucose levels, carbohydrates do it much faster for two simple reasons: firstly, they’re one of the first things we break down in digestion. There are enzymes in our saliva that begin carbohydrate breakdown before the foods even reach our stomachs! But more importantly, carbohydrates lead to immediate rises in blood glucose because theycontain glucose. Other molecules must first be converted to glucose, but carbohydrates, which include sugars, just need to be hacked into pieces by our digestive enzymes. Different carbohydrates contain different amounts of the monosaccharides, like glucose or fructose. Thus they each have different impacts on immediate rises in blood glucose levels.
This difference in effect on blood sugar level is the basis of the Glycemic Index, or GI. The glycemic index rates foods based on how much of an immediate impact they have on blood glucose per 50 grams of carbohydrate. If you picture the rise in blood glucose levels in response to a food on a graph over time, the glycemic index is a number that is related directly the area under a two-hour curve. The higher the spike in blood glucose levels, the larger the area under the curve is, and thus the higher the glycemic index, which is somewhere on a scale of 1 (low) to 100 (high). Most foods that have a low GI induce lower spikes in insulin, but not all of them. There is another index, called the Insulin Index, that looks directly at rises in insulin levels. While the glucose and insulin scores of most foods are related, high-protein foods and baked goods that are rich in fat and refined carbohydrates usually elicit much higher insulin responses than their glycemic index values would suggest.
Research into the glycemic index have found strong support of the idea that low GI foods are better for us. People who eat less high GI foods have lower risks of developing both type 2 diabetes and heart disease. It’s uncertain if this is due to overall lower blood sugar levels or reduced glycemic “spikes.” When glucose levels increase dramatically, our bodies ramp up the release of insulin and the processing of glucose from the blood, including ATP generation. While ATP is great, the process by which we make it – oxidative phosphorylation – has side effects. Mainly, the faster it’s churning, the more likely the machinery is to leak reactive oxygen species (ROS). These oxygen radicals are highly reactive and tend to transform whatever they come in contact with, which can cause damage to proteins, membranes, or even our DNA. By eating foods that increase glucose levels more slowly, we limit ROS bursts that can damage our cells.
The glycemic impact of foods can be strikingly different for your body
However, the glycemic index isn’t perfect. Glycemic indices aren’t the whole story since they are based on a per-carbohydrate basis. Two foods that have the same GI can have dramatically different effects on blood glucose per serving if one has significantly higher carbohydrate content than the other. The affect a serving of food has on blood glucose is referred instead to its Glycemic Load. Glycemic load is calculated by multiplying the weight (in grams) of carboydrate in a serving by the food’s overall GI and divided by 100. A GL of 10 or less is considered low, while 20 or more is considered high. Let’s say you want to eat a baguette, for example. Both whole gain and French baguettes have similar GIs (roughly 73). But there’s a lot less carbohydrates per serving in the whole gain loaf, and thus its GL is only 9 while the GL of the french baguette is 27!
The GI or GL of a food isn’t the only thing you should consider when it comes to insulin and your diet. When you eat matters a lot, too. Our bodies react to the same foods differently at different times of day. Morning is a special time for your body because you’ve just spent a while in a comatose state. The changes your body undergoes while you sleep can have a dramatic impact on how it responds to food. Insulin levels tend to be low in the early morning, for example, because your body releases stress hormones just before you wake up. Once you’re awake, though, your body ramps up insulin secretion to metabolize the high glucose levels and give your cells a little fuel to start the day with.
These alterations have a big impact on how our diets affect us. When different foods were tested for their GI values at different times of the day, for example, researchers found that the same food eaten for lunch instead of breakfast induced a lower glucose response. This is why it may be particularly important to eat a protein-rich breakfast, like eggs, instead of high glycemic foods like white bread toast. Time of day has been found to have a larger effect on insulin responses in women than in men, though no one understands why. Furthermore, studies have shown that the quality of sleep you get affects how strongly your body reacts to food. A restless night can lead to higher glucose responses and larger spikes in insulin in response to food in the morning. So getting a good night’s sleep is also important in preventing the kinds of spikes which may be a major factor in type 2 diabetes.
Also, foods can interact with each other to lower or raise the GI values of a meal. For example, foods that contain fiber, protein, or fat will generally reduce the GI of the meal as a whole. Recent studies have even shown that having a small volume of alcohol (one drink) prior to a meal reduces the GI of the meal by 16-37% – which, as far as I’m concerned, is fantastic news. Furthermore, many cultures eat high GI foods like potatoes or rices but have low occurrences of diabetes and obesity. The truth is we have yet to tease out all the factors that lead to these conditions, and the GI level of our diets is likely only one of many related factors.
The Even Bigger Picture
Clearly, what we eat, with what and when matters a lot when it comes to insulin levels. This is important in keeping healthy and reducing the risk of metabolic syndrome and type 2 diabetes. But insulin affects so many other things in our bodies, from amino acid uptake to fat storage. We need to consider insulin whether we’re worried about type 2 diabetes or not!
Thinking about how our diet affects insulin is especially key when trying to lose weight or maintain a healthy weight. Insulin actually triggers the storage of fats in adipose tissues, so sustained high levels of insulin promote weight gain! Furthermore, recall that our bodies don’t break down fat while insulin is circulating. This means that if we eat foods with high GIs that produce sustained insulin levels, we’re shooting ourselves in the foot, even if we eat less calories overall.
Understanding how our bodies regulate insulin release also explains why certain foods are worse for us than we’d expect. Sugary drinks are particularly bad for us, for example, even when we take into account their calorie and sugar content. This is because our brains don’t judge their sugar content well in advance. Thousands of years of evolution led our brains to believe that drinks, overall, were low-cal things that mostly contain water. Our brains aren’t wired to think that fluids contain a lot of sugar. Thus when we look at a soda or even begin to sip one, we don’t have the same level of cephalic phase insulin release or first phase insulin release that we would for a solid treat. The end result of this is that our bodies are unprepared for the sudden sugar rush, and have to instead release a massive amount of insulin all at once to deal with what it considers an inexplicable rise in blood glucose.
High spikes in insulin lead to dramatic drops in blood glucose, which can cause your body to feel hungry sooner. Eating low GI and GL foods can help you lose weight by making you feeling fuller longer. Low GI foods don’t cause dramatic drops in glucose levels, thus you tend eat less throughout the day. It’s thought that this effect, on top of the high-sensitivity of our bodies to high GI foods in the AM, is why eating eggs, a low GI food, instead of cereal or toast in the morning has been found to reduce overall food intake for the day by as much as 18%. You can create lower spikes in insulin not only by avoiding sugary drinks and eating lower GL foods but also by eating smaller meals. This is because the amount of first phase insulin release is dependent on the amount of insulin needed for the previous meal. The bigger meals are, the larger the spike at the beginning of every meal, and the bigger the drop in glucose afterward.
But you shouldn’t just cut out everything that leads to insulin release! Insulin is important, and too little is just as bad as too much. Even small drops in daily insulin levels can affect us negatively. For example, dieters often experience depression around 2 weeks after they begin cutting high-glycemic foods like carbohydrates out of their diet. Why? Because they have much lower levels of insulin than they did before. Decreased insulin means decreased amino acid uptake, and because the level of other amino acids affects how well tryptophan crosses the blood brain barrier, decreased insulin means less serotonin which leads to, in layman’s terms, feeling like crap. While you should monitor the GI of your meals to reduce insulin spikes, you shouldn’t go for rock bottom either. At least you shouldn’t if you want to be happy about it!
Previous posts in the Understanding Our Bodies series:
Van Cauter E, Polonsky KS, & Scheen AJ (1997). Roles of circadian rhythmicity and sleep in human glucose regulation. Endocrine reviews, 18 (5), 716-38 PMID: 9331550
Hill, J., Elias, C., Fukuda, M., Williams, K., Berglund, E., Holland, W., Cho, Y., Chuang, J., Xu, Y., & Choi, M. (2010). Direct Insulin and Leptin Action on Pro-opiomelanocortin Neurons Is Required for Normal Glucose Homeostasis and Fertility Cell Metabolism, 11 (4), 286-297 DOI: 10.1016/j.cmet.2010.03.002
Spiegel K, Knutson K, Leproult R, Tasali E, & Van Cauter E (2005). Sleep loss: a novel risk factor for insulin resistance and Type 2 diabetes. Journal of applied physiology (Bethesda, Md. : 1985), 99 (5), 2008-19 PMID: 16227462
Brand-Miller JC, Fatema K, Middlemiss C, Bare M, Liu V, Atkinson F, & Petocz P (2007). Effect of alcoholic beverages on postprandial glycemia and insulinemia in lean, young, healthy adults. The American journal of clinical nutrition, 85 (6), 1545-51 PMID: 17556691
Ratliff J, Leite JO, de Ogburn R, Puglisi MJ, VanHeest J, & Fernandez ML (2010). Consuming eggs for breakfast influences plasma glucose and ghrelin, while reducing energy intake during the next 24 hours in adult men. Nutrition research (New York, N.Y.), 30 (2), 96-103 PMID: 20226994
The most common advice as to how to lose weight given my doctors to people that are overweight or obese is to cut calories. Reduced caloric intake has been lined to all kinds of health benefits, from extended life span to reduced risk of heart disease. But the primary goal of people who slice their caloric budget is to lose weight.
Empty Plate, by iamchanelle, flickr
In principle, this makes perfect sense. Your body uses the calories you eat to fuel its metabolism. Eat less food, and the body must make up for the lack of fuel somehow, ideally, by beginning to digest stored fats that were deposited in specialized cells when the you were eating more food than your body needed.
But as anyone who has tried to diet knows, it never seems that simple. Even when you are as loyal to your diet as you can be, you never seem to lose the kind of weight you want. Now, new research out of the Oregon Health and Science University may explain the discrepancy between theory and reality. They found that, at least in some of our closest relatives, cutting calories isn’t enough because the body compensates for the reduced intake by lowering activity levels.
The Study
Because controlling diet in people is notoriously difficult, the OHSU research team used a primate model to determine how well reducing calorie intake in adults works as a weight loss strategy. They took 18 female macaques and fed them a high-fat diet for several years, allowing the monkeys to pack on the pounds. They then cut their dietary fat intake dramatically, leading to a 30% reduction in calories. They monitored the monkeys’ weight and activity levels over time to see if the change in diet caused the animals to lose weight.
The Results
Instead of losing weight, the calorie-restricted macaques got lazier. Indeed, despite cutting almost a third of the calories from their diet, the macaques didn’t lose any weight at all in the first month. When researchers cut their calorie intake even more, down another 30% for the second month, the same thing happened. There was a little weight loss during the extreme calorie cutting, but not much, and instead there was much less activity. Meanwhile, a control group that was forced to run on a treadmill for an hour every day lost plenty of weight, even though the treadmill had no effect when they were on the high-fat diet.
What It Means For Us
Everyone wants to believe that if they just cut back a little, they’ll lose weight. Yet time and time again we’re reminded that diets almost never work. Perhaps part of the problem is that while we focus on cutting things out, we forget that we need to keep up our body’s energy utilization for the lack of calories to have any effect. The body has many natural mechanisms to conserve energy during times of food shortage. Decreasing activity levels are likely just one way in which our bodies compensate for perceived starvation. While this was great for the chaotic and troubled paleolithic man, it gets in out way when we try to slim down in a fat-filled, food-plentiful modern society. So if you’re trying to lose weight, instead of just changing your diet, be sure to keep up an exercise regimen that will force you to keep active. You don’t have to work out four hours a day or anything – just do something that ensures that you use up some energy and don’t just sit around. That way your body feels the need to use your fat stores for fuel, and you see what you expect from being faithful to your diet.
Citation: Sullivan, E., & Cameron, J. (2010). A rapidly occurring compensatory decrease in physical activity counteracts diet-induced weight loss in female monkeys AJP: Regulatory, Integrative and Comparative Physiology, 298 (4) DOI: 10.1152/ajpregu.00617.2009
Once you start to understand the science behind a lot of diet, nutrition and health science publications, you realize that it’s rare for the recaps of science in the newspaper to accurately depict a scientist’s results or a study’s real-world implications. I’m not trying to take a shot at all health journalists – just a large number of them. I think they need to be called out for their shoddy reporting and exaggeration techniques. Take, for example, a recent study published in the Journal of Physiology. From the headlines it made, you’d think that scientists have stumbled upon a miracle workout regime:
Marathon or sprint? (credit, Frederic de Villamil, flickr)
Read a few paragraphs into each and you’ll be told that science has revolutionized how people should work out. “Alternating short bursts of intense activity with brief rest periods delivers more benefit for less exercise, research shows.” “A set of ten one-minute sprints on an exercise bike three times a week holds the same benefits as ten hours of ‘conventional’ distance cycling.”
Indeed, the articles even tell you that: “Tests afterward showed that their muscles had improved as much as if they had been involved in endurance training.”
The bottom line: research has reportedly shown that by working out for just ten minutes three times a week, you can be as in shape, if not more so, than quadrupling the standard thirty minutes a day five days a week.
Here’s a hint: if it sounds too good to be true, it probably is.
The Research: What They Did
All of these articles center around a recent paper in The Journal of Physiology titled, “A practical model of low-volume high-intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms.” It centers around a recent fashion in workouts called High-Intensity Interval Training, or HIT. HIT is a method of exercise which involves working as hard as you can for brief intervals followed by brief rest intervals. For example, you might sprint for a minute and then jog for thirty seconds, and repeat this for a half and hour. The idea is that by doing higher intensity workouts for shorter time intervals, you can work out “less” but get the same, or even more, benefit.
Of course, that’s not what this study showed. The study at hand followed seven men with an average age of 21 through a two-week, lower-intensity HIT training regimen where volunteers rode a stationary exercise bike for 12 cycles of 60 seconds of peddling above their comfort zone followed by 75 seconds of rest. The researchers tested the volunteers’ levels of a number of fitness variables, including cycling time trials and the activity of exercise-related enzymes like citrate synthase and cyctochrome c oxidase. They also tested for increases in muscle glyocgen, GLUT4, and PGC-1α, which is a transcription factor that is proposed to be upregulated during muscle creation.
In a vast sweep, they found that the training increased everything that could be associated with increasing muscle and being more fit. They state that:
“this study demonstrates that a practical model of low volume HIT is a potent stimulus for increasing skeletal muscle mitochondrial capacity and improving exercise performance.”
The Research: What They Didn’t Do
You might have noticed that there’s no mention of what happened to the group that did 10 hours of moderate exercise instead of the HIT training regimen: that’s because it didn’t exist. The study did not, in any way shape or form, compare HIT to regular training techniques. Where did the headlines get the idea that this somehow beat 10 hours of conventional exercise? That’s a good question, because it isn’t in the paper. The paper’s last remarks are that future studies need to look into this type of exercise in further depth, “to determine whether this type of training is an effective health-enhancing exercise strategy.”
The Tortoise or the Hare? This study did nothing to clear up the debate.
The news coverage would have you think that this training method is somehow better than how you might normally work out, and yet the study doesn’t compare it to any kind of normal workout regime. They don’t even try to compare their results to other studies. They simply state that working out this way can be good, too. And are you surprised that adding an additional 15-30 minutes of high-intensity workouts a few times a week improves your health? After all, shouldn’t adding any kind of exercise improve something?
That’s not to say that high-intensity training isn’t potentially better than longer, low-intensity training. Studies have shown that improvements in many exercise variables are directly related to intensity, duration, and frequency of training. In short, the harder you work, the better it is for you, and you don’t have to work as long to achieve the same results. In principle, this makes sense: a half hour run is going to do more for you than an hour walk. The question is how hard do you have to work for how long and how often to get the kind of results you want – and the answer to that isn’t anywhere in this paper.
The point is that this study didn’t test how long moderate training took to equal the interval training results, or compare the interval training to a given, conventional training regimen. It didn’t show that HIT improved fitness more or less than any other method, nor more or less quickly. For that matter, it worked with young, fairly in shape men, so its application to the masses is very limited. Is it better for a 60 year old, overweight woman to undergo a HIT workout than power walk around her neighborhood every morning? No one knows – it hasn’t been studied.
Don’t Judge A Study By Its News Coverage
The take home message is that you can’t believe everything you read in a newspaper. Scientific studies are, more often than not, couched in a way that the journalists will think is eye-catching, even if it distorts the actual study’s findings. The goal of these journalists isn’t to pass on vital information. It’s to gain as many readers as they can without being so false as to get in trouble. Indeed, sensationalized headlines get attention, but they do so in the wrong way. They make the science unimportant and diluted, and lead to a mistrust of scientific research. After all, if every day you’re told that scientists are a day away from curing cancer, but a cure still isn’t there, you start to think that the scientists are full of crap. But it’s not the scientists that are full of it – it’s the journalists that blow findings out of proportion and skew results in whatever way they think will sell articles. Even worse, the mainstream journalists do so without linking to the actual studies – meaning you can’t even click on a link and read the paper’s abstract to see if the article written about it is doing it justice. That’s simply unacceptable.
Little, J., Safdar, A., Wilkin, G., Tarnopolsky, M., & Gibala, M. (2010). A practical model of low-volume high-intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms The Journal of Physiology, 588 (6), 1011-1022 DOI: 10.1113/jphysiol.2009.181743
“Pain in the abdomen. Splitting Headache. Nausea and vomiting. Choking and couldn’t get their breath. Coughing up blood.” Phone calls like these broke the dawn of a fall day in the mill town of Donora, Pennsylvania back in October, 1948. Already two had died and another 18 were soon to follow. The death toll would have been far higher if not for a couple brave firemen filling oxygen tents as quickly as they could. Still, no one was quite sure what was going on. Only later would it be discovered that the thick smog covering this Appalachian valley was due to a severe temperature inversion. Its killer characteristic? Fluoride.
The Fluoride Deception’s Cover
Few public health issues in American history have riled people quite like fluoride. Its story is replete with famous figures in American history, dramatic tales from the Manhattan Project, corporate cover-ups, redacted research, shattered careers of those that spoke against it’s use and the tragedy at Donora in 1948. The tide that binds all these accounts together is a fascinating book called, “The Fluoride Deception” by Christopher Bryson. His work paints a picture with enough intrigue to be nominated for an Oscar but remains deftly aware of itself long enough to stay away from hyperbole – most of the time at least.
Fluoride, The Way Low Down
The Fluoride Deception by Christopher Bryson
Bryson takes his readers on an exhaustive journey of the molecule through the eyes of those that have known it first hand. We learn the perils of researching the subject from carefully placed protagonists like scientist Dr. Phyllis Mullenix, whose entire career was derailed by publishing information about fluoride’s neurotoxic effect at disturbingly low concentrations [1], and Kah Eli Roholm, a Danish pioneer in the research of fluoride’s effects and publisher of the groundbreaking work, Fluorine Intoxication [2], back in 1937. Shady, villain-like characters named Dr. Harold Carpenter Hodge and Dr. Robert A. Kehoe act as provocateurs in the background, silently pushing a pro-fluoride agenda with their work – at the behest of the Department of Defense’s Manhattan Project and major fluoride users like US Steel and Alcoa.
Intrigue is definitely a current running through the text – and it helps readability. Bryson works hard at establishing the links between the industrial uses of fluoride and its eventual role in water fluoridation. His case is circumstantially strong as the middle of the book describes the legal wrangling mill workers would endure to get compensation from corporations using fluorides industrially in the workplace. But what comes away as the most surprising aspect of his account is how the type of fluoride used in water fluoridation is actually just fluosilicic acid, a toxic byproduct of aluminum smelting and other heavy industrial processes. It becomes clear here that the waste is being dumped into the water supply in lieu of having to dispose of it in some other way.
Given most people’s proclivity for considering fluoride as a beneficial tooth decay reducer, his evidence is both striking and damning. You can reserve judgment temporarily against toothpaste, as it uses sodium fluoride as its preferred molecular combination – not fluosilicic acid, but still take a moment with the thought of people using the water supply as a dumping ground. For just for this insight alone, you would be remiss not to pick up the title. However, for those of you with a scientific nose, it is the moment just after you make the connection between water fluoridation and fluoride’s industrial uses that will both haunt and fascinate you as the book continues. It will also be the moment after which this book’s value to the discussion notably decreases.
Crying for More, Crying for Less
Once you wrap your head around the arguments Bryson is making in the book, it starts to fit the vicious battle some people wage against water fluoridation. For the most part, the battle against fluoride is mostly a cold war, although the occasional community, like Southampton in the UK recently, will organize itself in protest of water fluoridation. Frankly, it’s amazing more hasn’t been said here in the US about its use, although there is certainly an underground resistance to its use, spearheaded by the Fluoride Action Network.
Dr. Frederick McKay, the first person to make the connection between fluoride and cavities
This evolved agency view comes from a series of observations by Dr. Frederick McKay throughout the early 1900s that showed areas in the Western US, where calcium fluoride levels in the water are naturally higher, exhibited stained teeth with far less decay than areas with less fluoride in the water [3]. Landmark studies corroborated these views, especially the 1945 study involving the first test case in Grand Rapids, Michigan that showed adding sodium fluoride to water resulted in up to 54% fewer cavities [4].
All of this early science on the subject was an issue Bryson mostly avoids, to the book’s detriment. In fact, the way the science is presented is confusing. Fluorides are brought up haphazardly and never fully explained. What are chemical differences between fluoride (the ionized molecule), fluorine (the element), fluoride salts (the compound found in toothpaste), calcium fluoride (naturally found in water) and fluosilicic acid (the waste product often added to fluoridate water)? Given the science we have on fluoride’s neurotoxic effects, could it play a role in the autism epidemic? How does this relate to ADHD, Alzheimer’s, MS – or any neurological disorder for that matter? Fluoride ions have an affinity for calcium in bones, how does fluoridation relate to osteoporosis? The audience desperately needs these type of answers but we never get them.
What we need is a more nuanced dialogue about the role of fluoride in the body, not less. Bryson should have embraced the controversy a bit more here and explained these different avenues of thinking instead of simply leaving the science of his opposition out of the text. It severely detracts from what this book could be.
Fluoride science has evolved further since this work was published back in 2006. There are now epidemiological studies examining the role of fluoride and bone fractures, with mixed results in low exposures (like the 1ppm rates CDC aims for in US public water system fluoridation) but more conclusive, damaging results in slightly high 2-4ppm window [5]. It’s still unknown which ethic groups could be most at risk from bone fractures though. More disturbing has been the development of studies that confirm fluoride (along with arsenic) has serious effects on the brain [6, 7, 8], lowering IQ in SE asian children. Again, these effects are seen in the higher 2-4ppm samples of fluoride, rather than the 1ppm exposures most Americans are seeing, but any time a substance causes neurological damage further study should be considered mandatory.
Advancing from this epidemiological base, one Chinese study group has recently isolated fluoride’s neurotoxic target as the hippocampus in the brain [9, 10], giving future researchers a tangible ‘fluoride pathogenesis’ to work with here. The hippocampus governs many of the higher cerebral functions of humans like memory storage and spatial orientation; any damage to it could cause a number of different, severe neurological issues – similar to the epidemiological observations showing impacts to IQ from SE Asia.
Even before this new evidence was published, the EPA and the National Academy of Sciences have been reexamining the data surrounding water fluoridation since 2006 . The EPA sets a maximum contaminant level (MCL) and a secondary maximum contaminant level (SMCL) for all water contaminants; effectively the MCL is the ceiling and SMCL is the least amount allowed. For fluoride that range has long been 2-4 mg/L in drinking water but the National Academy agreed that skeletal issues were found from fluoride exposures at levels as low as 1.5 mg/L, nearing the CDC’s water fluoridation targets of 1ppm.
*We would like to note that 1ppm is equivalent to 1mg/L and they are often used interchangeably in the research. It should also be noted the National Academy mentioned they choose not to examine fluoridation’s effects at .7 – 1.2 mg/L – the CDC’s target range – for reasons that go unmentioned but could easily be implied. Further, all figures here are per liter fluoride exposures that downplay the actual fluoride exposures many people will be exposed if they follow the Institute of Medicine’s (IOM) 3.7L/day water intake recommendation. Taken together, the average CDC fluoridated water range exposure (.95mg/L) multiplied by IOM’s average daily water intake (3.7L) would give the average American 3.515 mg worth of daily fluoride exposure – a figure that falls in the National Academy’s range for concern for skeletal problems and the recent IQ-reducing fluoride exposures from the Chinese study group mentioned above.
Moving Through the Fog
We gave you an overview of science surrounding fluoride here because it is complex – and evolving – but the fact Bryson remained silent on the matter, only pounding the conspiratorial angles of this drama, strikes us as foolish. While that makes for a juicy read, storming Alcoa for reparations will not help well-meaning scientists establish fluoride’s true toxicity. Echoing Bryson’s sentiments, we do agree that the industry connections are important to understanding the depths of this story. The fact CDC, FDA and ADA all remain in lockstep behind water fluoridation, even in the face of this new science, is disturbing. And for all we know, the avoidance of fluoride science could have been an editorial decision on his part or his publishing company but, with such charged subject matter, that was an exceedingly poor choice. We just wish he had done more to further the conversation, just as we wished Food Inc. had extended the sustainable agriculture dialogue in a meaningful way (it did not).
You could easily question Bryson’s objectivity when you read the book but you shouldn’t. Large passages pull from Bryson’s muckraking journalism background and you can almost feel the resentment he has towards those that have fluoridated our water. But he keeps himself in check very well. This stance creates a tone that is both a strength and weakness for Bryson. If you gravitate towards social justice issues, you will soak up this book’s charged approach; the more scientifically minded amongst you might find his angles off putting and his lack of science infuriating. We were somewhere in the middle, we found ourselves enjoying his style but longing for a more exhaustive scientific review somewhere in the text.
In general, Bryson does a masterful job of weaving political intrigue into an exceedingly readable text considering the subject matter. He creates a story with genuine heroes and villains you may find yourself thinking about long after you put the title down. Experts will surely find fault with Bryson’s work, especially on the scientific front, but if your only exposure to fluoride is the cursory knowledge of its presence in your toothpaste or water, you would be wise to visit this text. We recommend it.
Additional Resources:
CDC’s List of New Fluoridated Water Supply Communities (aiming for 75% coverage by 2010):
Childhood obesity is becoming a hot topic in health circles, even to the point of being called an epidemic. Experts estimate that 20% of children between the ages of 6 and 17 are overweight, predisposing them to terrible diseases like diabetes and heart disease. Why have the world’s children ballooned over the past hundred years?
Ice Cream Adds Up! (thanks to flickr user lepiaf.geo)
Part of the problem is the popularity of fast food restaurants and cheap, fattening foods readily available at the grocery store. Policy makers have tried to tackle the problem at a variety of angles, promoting better package labeling and restriction or outlawing of the worst offending foods. Reformers have even targeted the meals provided by schools (efforts which have vastly improved the quality and nutrition of school meals), but the problem extends much deeper. Any nutritionist will tell you that healthy eating starts at home, and that is exactly where the problem now lies for the world’s children.
It turns out that the vast majority of parents are failing their kids, at least when packing them lunch. When Dr. Charlotte Evans and colleagues form the University of Leeds surveyed children’s packed lunches in the UK, they found that only 1 in 100 met the standards for nutritional value set by government agencies. In the UK, 50% of students pack their own lunches, and the findings of this study might explain part of why 1 in 6 of them are obese.
The research was done at the request of the UK’s Food Standards Agency, whose School Meals Review Panel (SMRP) has dictated what’s good and what’s not for schoolchildren since 2005. The government, at the urging of the panel, has restricted schools from serving foods high in salt, fat and sugar or made with poor-quality meat, and established mandatory food items such as protein-rich options, low-fat starch choices, dairy products, fruit and vegetables in the daily diet of students fed by the schools. But the board does not control the meals of the kids who bring their own, so the FSA wanted to know how the meals of these students measured up to the SMRP’s standards.
Researchers randomly selected primary schools throughout England, Scotland, Wales and Northern Ireland, and selected one class of 8 to 9 year olds from each school. All and all, almost 1,300 lunches were examined by a trained administrator, who went through the lunch and had the child go through a lunch box questionnaire. The administrator also weighed the lunch before and after to determine how much the kid ate.
What They Found
Most lunches contained sandwiches, sweet treats, snacks and sweetened drinks, and the kids ate 76% of what they were given. Few contained vegetables, milk or fruit juice. Of the 1294 lunches examined, only 14 (1.1%) met all of the standards for school meals and 66 (5.1%) met five or more. Fewer than half met the standards for energy, saturated fat, non-milk extrinsic sugars, non-starch polysaccharides, sodium, vitamin A, folate, iron or zinc. Interestingly, the researchers found that girls consumed more vegetables than boys.
The results were sobering.
As the authors write, “since 2004, there may have been some improvements in the nutritional profile of packed lunches due to changes in the composition of some manufactured foods; however, there have been no improvements in children’s packed lunches in terms of the types of food provided.”
While it might save some cash to pack lunches instead of paying for cafeteria food, you’re not doing your family any favors if you don’t pack a healthy meal. Studies have shown that kids that grow up with bad nutritional habits have a hard time breaking them later in life, so how you feed your kids has a dramatic impact throughout their years.
Kids Going to School…with lunches! from flickr user photomequickbooth
To learn more about how to pack the right kinds of meals, check out the School Food Trust’s website or ask your doctor what your child needs nutritionally. Here’s some examples of the good and the bad as described by a parent pamphlet explaining the UK’s 2007 update of the school lunch standards (view pamphlet here):
Good Choices to Eat:
Filled sandwiches, rolls, baguettes, bagels, pittas and wraps
Toasted sandwiches and paninis
Breakfast cereals with lower fat milk
Jacket potatoes, pasta and rice salads
Salads and vegetable sticks with dips
Yogurts/fromage frais
Fruit – all types including tinned (in juice) and dried
Combination of nuts, seeds and dried fruit (with no added salt, sugar or fat)
Good Choices to Drink:
Plain water (fresh tap water, still or sparkling bottled water)
Skimmed or semi-skimmed milk
Pure fruit or vegetable juices
Soya drinks enriched with calcium
Yogurt or milk with artificial sweeteners or less than 5% added sugar
Bad Choices to Eat:
Sweets/chewing gum (including sugar free)
Chocolate bars
Bars/biscuits containing or covered in chocolate
Processed fruit bars
Cereal bars
Chips and related products, like tortilla chips, potato sticks, puffs, crackers, corn chips, pretzels, breadsticks
Rice crackers, bombay mix, salted popcorn
Cakes, pastries, sweets
Bad Choices to Drink:
Flavored waters
Squash/cordials
Sweetened fizzy drinks like sodas and lemonade
Sports drinks
Diet drinks
Reference: Evans CE, Greenwood DC, Thomas JD, & Cade JE (2010). A cross-sectional survey of children’s packed lunches in the UK: food- and nutrient-based results. Journal of epidemiology and community health PMID: 20089755
. His work paints a picture with enough intrigue to be nominated for an Oscar but remains deftly aware of itself long enough to stay away from hyperbole – most of the time at least.
