To spit or not to spit…


Candida albicans is a fungus which, along with thousands of other species of fungi and bacteria, lives symbiotically within the human body (1).  Proper Th1 (a type of lymphocyte) response of the immune system keeps its numbers in check as it goes about its daily business rendering it virtually incapable of producing infection or disease in the healthy host (1).  In immune suppressed persons, such as HIV patients or persons taking immunosuppressant medications, invasive growth may occur.

Candidal infections usually take over warm and moist areas of the body such as underarms, oral and genital areas.  Itching and irritation accompanied by rashes, blisters or painful cracks in the corners of the mouth (in the case of oral thrush), as well as discharge that resembles cottage cheese (in the case of vaginal infection) are the most common signs (2).  In rare cases, usually as a result of significantly depressed immune system function, the infection may spread to other areas of the body, and can affect the organs and blood (2). In such cases, symptoms are more severe, usually painful, with or without fever, and, if the infection is in the blood and spreads to the brain it can cause significant disruptions in mental function. Infections of this magnitude are usually life threatening (2).

Candidiasis affecting the skin, oral and/or genital cavities is treated with over the counter or prescription medications for a few days or a couple of weeks, whereas, infections affecting organs and the blood require hospitalization and intravenous medications as they can be fatal.

Infections affecting organs and the blood (aka “systemic infections”) occur primarily in hospital settings among patients undergoing immune system suppression (usually in the wake of transplant surgery or auto-immune disease/disorder treatment) (3).  The infection tends to recur several times during the first six months following surgery or immune system suppression treatment (4).  Its signs and symptoms are generally severe and require aggressive interventions.   Even so, death occurs in more than 1 out of 2 infected patients (3).  The good news is that infection rates hover around 2.9 per 100,000 people in Canada and anywhere between 6 and 10 per 100,000 people in the USA (depending on geographical region studied), making systemic candidiasis infections relatively rare (3).

ALTERNATIVE MEDICINE TAKE ON THIS

A surprising number of websites and their authors (who often also publish books on the subject or sell their own brands of remedies) may tell you that C. albicans is the leading cause of afflictions too many to list here, ranging from general fatigue and brain fog to asthma and obesity.  It takes over the body, organs, and blood, they claim, but keeps its population in check somehow, thus, remaining undetected by conventional methods, either because physicians do not (or pretend to not) have the necessary technology.  However, they tell us that if we spit in a glass of water and watch what the saliva does over the course of 20 minutes, we can detect the infection ourselves. Of course, everyone’s saliva is going to do something similar (or exactly the same) to what is described in this so-called “test”, rendering it less than useless.

Whatever your symptoms, C. albicans is generally considered to be the main culprit and changing your diet (which almost always includes taking whatever supplement the website author is peddling) is the remedy of choice.  Science based medicine is often seen as having an agenda that keeps it from diagnosing and treating the infection.  Assuming the diagnosis and treatment would involve trading money for services / tests / medications rendered, this agenda must involve something far more valuable than mere dollars.  Whatever it is, its value exceeds the potential windfall that treating nearly 90% of the population (the number of people afflicted by C. albicans systemic infection, according to the “treatment” promoting websites – a far cry from the less than 0.0003% actually documented by the Canadian Journal of Infectious Diseases) would provide (3).

REALITY CHECK

C. albicans, in the absence of a normal immune system response, will do what any pathogen will do:  it will spread relatively quickly until something stops it.  That something is usually medical intervention that restores immune system function and/or attacks the fungus itself.  When no intervention takes place, infection spreads unchecked and death soon occurs.  This process does not take years- or decades-worth of suffering from nebulous afflictions.  An out of control infection acts relatively quickly, its signs and symptoms don’t beat around the bush, and even with the best of care and prompt intervention, odds of survival are not good.

REFERENCES

  1. Kosonen J, Rantala A, Little CH, Lintu P, Harjamaki PR, Georgiou GM, Cone RE, Savolainen J.  Increased levels of Candida albicans Mannan-specific T-cell-derived antigen binding molecules in patients with invasive candidiasis. Clinical and Vaccine Immunology, 2006;13(4):467-474.
  2. Molero G, Diez-Orejas R, Navarro-Garcia F, Monteoliva L, Pla J, Gil C, Sanchez-Perez M, Nombela C.  Candida albicans: genetics, dimorphism and pathoginicity. Internatl Microbiol,  1998;1:95-106.
  3. Bow EJ, Evans G, Fuller J, et al.  Canadian clinical practice guidelines for invasive candidiasis in adults. Can J Infect Dis Med Microbiol, 2010;21(4):e122-e150.
  4. Danovich GM, Handbook of Kidney Transplantation, Philadelphia, PA: Lippincott Williams & Wilkins; 2010:269.
Posted in Woo

Protein powders and shakes


A few decades ago, protein powders used to lurk in gyms and so-called “health” food stores. They were stacked neatly on shelves amidst colourful ads that lured would-be buyers with images of famous bodybuilders and athletes whose physiques few of them would ever match. In those days, their primary targets were body builders. Claims varied, but most brands promised increased muscle gain that, according to the ads, run of the mill, food derived protein could not possibly provide.

Today, protein powders have escaped the confines of gyms and health food stores and have become ubiquitous on food market shelves, in pharmacies, and virtually anyplace else food, supplements, or pharmaceuticals are sold. Their user base has changed dramatically to include athletes (professional sports people who are not bodybuilders), recreational athletes (sport hobbyists and/or fitness enthusiasts), and lifestyle users (consumers who think protein powders are healthy snacks and/or will help them lose weight)(1). Vegetarian and vegan consumers of protein powders tend to fall in the last two categories and are likely to believe the powders, or other similar supplements, are necessary to meet their daily protein needs. Some users claim they “feel better” and have more energy when they consume protein powders, while others simply believe that without their daily dosage, their muscles would vanish into thin air.

ENERGY

“The extra protein gives me energy!” is a claim I hear surprisingly often. It is surprising because protein is a lousy source of energy. It is a last resort the body will tap when it runs out of its preferred fuel (particularly during exercise): glycogen (aka stored carbohydrate)(2). You may have heard of athletes engaging in something called “carb-loading” before events. This consists of consuming a higher ratio of carbohydrates to help the body handle the energy requirements of extended activity, particularly if the event involves increasing pace and effort to beat the competition (3). The more intense the exercise, the more carbohydrate the body burns. Consuming carbs before and during exercise helps athletes keep up the pace. In fact, a high carbohydrate diet increases endurance time three-fold when compared to a high protein diet (3). Once glycogen runs out, so does your energy and ability to keep going. Similarly, failing to replenish your glycogen stores after exercise, will impair your ability to recover and achieve your training goals.

During periods of extended low intensity exercise, such as walking, fat becomes an important source of energy, more so if you engage in regular exercise. The more you train, the more your body uses fat for energy when you are resting or performing less strenuous activities. As you pick up the pace, your body switches back to using glycogen.

Image source:  McArdle et al. – Sports and Exercise Nutrition, 3rd Ed., Chapter 5, Macronutrient Metabolism in Exercise and Training, page 157 (3).

In a nutshell, if you’re looking for extra energy, put away the protein powder and have some healthy carbs instead.

MORE MUSCLE

Muscle growth occurs as the result of training, not from the overconsumption of protein. There is only so much protein the body will use before it stores the excess away. Protein powders are digested faster than food derived protein, making protein available for muscle repair in a more expedited manner. “Aha!” you might say, “so, they ARE good for something!” Well, not really. In the long run, the end result is about the same – except, perhaps, for your wallet.

Studies looking at the effects of supplementation and strength training combined show insignificant or no difference between placebo and control groups (2,4).  In their 2009 joint position paper on nutrition and athletic performance, the American Dietetic Association, Dietitians of Canada, and the American College of Sports Medicine concluded the following (5):

“Current evidence indicates that protein and amino acid supplements are no more or no less effective than food when energy is adequate for gaining lean body mass. Although widely used, protein powders and amino acid supplements are a potential source for illegal substances such as nandrolone, which may not be listed on the ingredient label.”

In other words, as long as you meet your body’s protein requirements, it doesn’t make much difference if you’re getting the protein fast, from a powder, or slower, from food. What matters most is timing (6). Consumption of protein and carbohydrate containing foods immediately after training is far more important if you want to see results. The sooner you eat, the better. Letting as little as two hours pass after a workout without eating will lead to a lot of disappointment on your part if you’re looking to build muscle mass (7).

PRE-, DURING and POST-EXERCISE NUTRITION

For best results in terms of performance and overall health (the latter is sometimes overlooked when people consider a plan of action in the short term), remember that supplements are not a replacement for healthy food choices.

Eat breakfast, consume the appropriate amount of calories for your body (don’t forget to eat healthy fats), stay hydrated and be sure to eat before and after exercise. If you like coffee or tea, you may be surprised to know that caffeine is an effective ergogenic aid, particularly in racing events, but also in short term, high intensity events, if consumed one hour before exercise (8,9). If you’ve given up coffee and tea because you think it will hinder your performance, dehydrate you, or interfere with electrolyte balance, you may want to reconsider your choice (8,9,10).

While studies on the effects of protein restriction on performance have yielded inconclusive results, the same is not true when it comes to carbohydrate restriction which has been shown to be detrimental (11,12). The importance of carbohydrate consumption after workouts can not be overemphasized. The aforementioned position paper on nutrition and athletic performance provides the following guidelines for performance athletes (5):

  • Carbohydrate recommendations for athletes range from 6-10 g/kg (2.7-4.5 g/lb) body weight per day depending on extent and duration of exertion (5).
  • Protein recommendations for endurance and strength trained athletes range from 1.2-1.7 g/kg (0.5-0.8 g/lb) body weight per day. The authors stress that food sources can easily meet requirements and supplementation is not necessary (5).
  • Fat intake should range from 20%-35% of total energy intake. Note that consuming less than this will not improve performance (5).
  • Before exercise, a meal or snack “should provide sufficient fluid to maintain hydration, be relatively low in fat and fiber to facilitate gastric emptying and minimize gastrointestinal distress, be relatively high in carbohydrate to maximize maintenance of blood glucose, be moderate in protein, be composed of familiar foods, and be well tolerated by the athlete.”(5)
  • During exercise, it is important to replace fluid losses and “provide carbohydrates (approximately 30-60 g per hour) for maintenance of blood glucose levels.”(5)
  • After exercise, “a carbohydrate intake of ~1.0-1.5 g/kg (0.5-0.7 g/lb) body weight during the first 30 minutes and again every 2 hours for 4 to 6 hours will be adequate to replace glycogen stores. Protein consumed after exercise will provide amino acids for building and repair of muscle tissue.”(5)

To put things in perspective, let’s consider the nutritional requirements of a 160 pound male professional soccer player:

Calories: approx. 4,000 per day
Protein: approx. 110 grams per day, or 11% of daily calories
Carbs: approx. 640 grams per day, or 64% of daily calories
Healthy Fats: approx. 111 grams per day, or 25% of daily calories

Notice that although 110 grams of protein per day represents quite a bit more than the amount of protein recommended for weekend athletes or sedentary persons, this amount does not represent a higher percentage of daily calories. In other words, it is not added (or supplemented) protein.

BOTTOM LINE

If the only way you are meeting your protein requirements is by supplementing with protein powders, there is something wrong with your diet. It should not be difficult to meet the recommended 10% to 15% of your daily calories in the form of protein. In fact, I would be very surprised if this is the case, given the abundance of food varieties available in North America. In the unlikely event you are not getting enough protein or the necessary ratios of essential amino acids, tweaking your diet will be better for your health (and for your wallet) in the long run than starting a protein supplementation habit.

REFERENCES

  1. Overview of the Sports Nutrition Market—Food, Beverages and Supplements, 2010; ISSN 1920-6593 Market Analysis Report, AAFC No. 10745E.
  2. Maughan RJ. Nutrition in Sport – Volume VII of the Encyclopedia of Sports Medicine. MA: Blackwell Science, Inc.; 2000.
  3. McArdle WD, Katch FI, Katch VL. Sports and Exercise Nutrition, 3rd Ed. MD: Lippincott Williams & Wilkins; 2009.
  4. Williams AG, van den Oord M, Sharma A, Jones DA. Is glucose/amino acid supplementation after exercise an aid to strength training? Br J Sports Med, 2001;35:109-113.
  5. Nutrition and athletic performance. Journal of the American Dietetic Association, 2009; 109(3):509-527.
  6. Poole C, Wilborn C, Taylor L, Kerksick C. The role of post-exercise nutrient administration on muscle protein synthesis and glycogen synthesis. Journal of Sports Science and Medicine, 2010;9:354-363.
  7. van Essen M, Gibala MJ. Failure of protein to improve time trial performance when added to a sports drink. Med Sci Sports Exerc. 2006;38:1476-1483.
  8. Cox GR, Desbrow B, Montgomery PG, Anderson ME, Bruce CR, Macrides TA, Martin DT, Moquin A, Roberts A, Hawley JA, Burke LM. Effect of different protocols of caffeine intake on metabolism and endurance performance. Journal of Applied Physiology, 2002:93:990-999.
  9. Paluska SA. Caffeine and exercise. Current Sports Medicine Reports, 2003;2:213-219.
  10. Bell DG, McLellan TM. Effect of repeated caffeine ingestion on repeated exhaustive exercise endurance.  Medicine & Science in Sports & Exercise, 2003; DOI: 10.1249/01.MSS.0000079071.92647.F2
  11. Knechtle B, Knechtle P, Mrazek C, Senn O, Rosemann T, Imoberdorf R, Ballmer P. No effect of short-term amino acid supplementation on variables related to skeletal muscle damage in 100 km ultra-runners – a randomized controlled trial. Journal of the International Society of Sports Nutrition, 2011;8:6.
  12. Ivy JL, Res PT, Sprague RC, Widzer MO. Effect of a carbohydrate-protein supple- ment on endurance performance during ex- ercise of varying intensity. Int J Sport Nutr Exerc Metab. 2003;13:382-395.

Do detox plans work?


Short answer? No.

“But I feel better after a detox!” you might say.

Of course you do. You’ve avoided junk food and other unhealthy foods for several days or weeks. Your body is thrilled. This does not mean you’ve rid yourself of unwanted substances.

Detox claims

Various so-called “detox” products and diets claim to accomplish many different things (sometimes all at once), the most common of which tend to revolve around boosting the immune system, increasing energy, and/or promoting weight loss. The one claim they all have in common, as evidenced by the presence of the words “detox” and/or “cleanse” in their selected names, is that such diets or products will rid your body of some (or all) toxins that have accumulated in various tissues over the years.

The product being touted, be it a pill, shake, drink, diet, skin pad, or electronic contraption, is supposed to locate the silent killers in your body and escort them out via urine, faeces, or sweat. Together, these products and services amount to a multibillion dollar industry worldwide that dupes people into spending money that would be better spent on learning how to eat healthy, well rounded diets and engaging in more physical activities on a regular basis.

Dosage

We inhale, ingest, and absorb (through the skin) hundreds of different chemicals every day. Whether or not these chemicals are toxic to us depends on dosage, either at the time of exposure, or after years of accumulation in the body. I can’t stress this point enough: dosage is everything and any chemical, natural or man made, from ascorbic acid to zinc, can be toxic if enough of it is absorbed or accumulated. Heck, water can kill you if you drink too much at once.

It is very unlikely that any food item purchased in industrialized nations such as the US and Canada contains toxic doses of any chemical given that our food supply is fairly well controlled. Sure, there may be a mishap now and then, but this is the exception, not the rule. Thus, it is the slow accumulation of small amounts of unwanted chemicals in the body that detox and cleansing programs usually target, but fail to actually remove. These generally include substances that are purposely consumed (such as food) and substances which are involuntarily consumed (such as polluted air – we have to breathe and can’t generally hold our breaths until we can escape to the mountainside for some fresh air).

What happens to all the unwanted stuff we take in?

Except in cases of overdose (poisoning), harmful chemicals are usually blocked from harming the body by natural barriers such as the gastrointestinal (GI) system, lungs, and skin (1). Those which sometimes break through these barriers are excreted with the help of the liver, kidneys, and lymphatic system (more than half the tissue of which surrounds the digestive tract)(1). These systems work together to eliminate threats to the body and do a great job of it in the absence of disease – if cirrhosis is present, for example, the liver will have a hard time doing its job. Thus, unless you have been diagnosed with something which directly involves these systems, most substances that pose a threat to your health will be eliminated with or without any added help (1).

Although some of the chemicals commonly used to control pests in our food supply stick around the body for a while, they generally do so in insignificant doses, or for less time than it is necessary for them to cause significant harm. One exception involves persistent organic pollutants (POPs). You may have heard of POPs as the “dirty dozen”. These include DDT and other chemicals that were predominantly used in manufacturing of various items, as well as in food production (particularly as pesticides), a few decades ago when we didn’t know any better. Their use has been outlawed in most countries, with some limited use (such as the use of DDT to fight malaria) still allowed in certain circumstances. Although they are no longer in use today, they are still around in our environment, left over from their heyday. If present in your body, no diet, shake, pill, foot pad, foot bath, colon irrigation, or any other means of so-called “detoxification” method is going to help you rid yourself of them. You simply have to wait them out and hope they aren’t doing too much damage while they’re camping out in your body. Most will, eventually, surpass their respective points of half-life and begin to slowly disappear on their own before you do.

If you are concerned about the presence of pesticides, herbicides, fungicides, fumigants, hormonal growth promoters, anthelmintics (used to control internal parasites in farm animals), and antibiotics in your food, then, a change in mind-set is needed: rather than looking for ways to “cleanse” yourself of these things, look, instead, for ways to consume less of them in the first place. If you smoke and agree that smoking is bad for your health, do you look for things that can help your lungs cope with your habit, or do you concentrate instead on ways to help yourself quit smoking?

Which foods contain the most unwanted substances?

Animal foods. If you’re veg*an, you have very little to worry about since the amount of unwanted chemicals you ingest by consuming non-organic plant foods pales in comparison to what you would be ingesting if you were eating animals. Even so, if you can afford to buy organic, great. The cleaner your food, the better. If not, don’t sweat it. Wash your veggies, soak your strawberries, be mindful of the worst offenders in the plant foods category, and don’t stress yourself out needlessly.

Animals are higher on the food chain than plants and their products. The higher up the food chain we go, the higher the concentrations of unwanted substances we find. For instance, predatory fish (i.e. tuna, salmon, sword fish) have higher concentrations of mercury in their flesh than plant eaters (i.e. sardines). Such harmful substances accumulate primarily in muscle tissue and organs (some set up camp in fatty tissues). The less animals you eat, the less likely it is you will ingest and accumulate questionable chemicals in meaningful amounts. Of course, regardless of dietary choices, we must still breathe and live surrounded by plastics and other man made materials, so, resistance to exposure is… well… futile.

What about the sludge sticking to the inside of my intestines? Will diet or colonic irrigation get rid of that?

There is no sludge. I will happily state otherwise (and eat my husband’s hat) if anyone can show me footage from a colonoscopy that shows this sludge hanging out inside the colon or anywhere else in the GI tract for that matter.

How can I boost or stimulate my liver, kidneys, lymphatic system?

You can’t. You can avoid taxing them unnecessarily (for instance, don’t drink alcohol to excess), but you can’t “boost” them into performing beyond their limitations. If their performance is diminished, medical intervention is very likely needed, since this implies something is wrong (kidney disease, liver disease).

Bottom line

Don’t waste your money and don’t torture yourself with bad tasting concoctions or invasive and uncomfortable procedures. Your body “detoxes” itself just fine and the stuff it can’t get rid of on its own is not going to be removed by special diets, products, or visits to the local colonic irrigation shop. Avoid exposure within reason, eat less, or no animal products, and save the stress for things that truly are worth worrying about… like healthcare reform.

References

  1. Mahan LK, Escott-Stump S. Krause’s Food and Nutrition Therapy. MO: Saunders-Elsevier; 2008.

  2. Lasky T, Sun W, Kadry A, Hoffman MK. Mean total arsenic concentrations in chicken 1989 – 2000 and estimated exposures for consumers of chicken. Environmental Health Perspectives, 2004:112(1):18-21.
  3. Leeman WR, Van Den Berg KJ, Houben GF. Transfer of chemicals from feed to animal products: the use of transfer factors in risk assessment. Food Additives and Contaminants, 2007:24(1):1-13.

Physician nutrition training – throwing the baby out with the bathwater


It is a little known fact that most medical doctors (MD’s) in the United States (and probably Canada) know little more about nutrition than the average person, regardless of the latter’s occupation.  During the 70's – 80's, a handful of medical schools provided some semblance of nutrition training.  In the 90's, as the roles of diet and lifestyle in the development and treatment of disease became more known, the number of medical schools providing nutrition education to would-be physicians went up slightly.  Today, that number is back down to pre-1980 levels, with most schools failing to provide the recommended 25 hours of nutrition training (which is comparable to a three day workshop on the subject (1,2,3).

From:  Nutrition education in US medical schools: latest update of a national survey. Academic Medicine (5).

This would be a non-issue if family physicians, pediatricians, and a host of other specialists would refrain from giving nutrition advice and, instead, refer their patients to registered dieticians.  However, a survey of primary care practitioners reveals that over two thirds of respondents provide dietary counseling to patients, in spite of glaring gaps in knowledge and training of the practitioners themselves (4).

In February 2011, in California, a handful of physicians gave testimony to support the introduction of a senate bill which would require that medical doctors complete seven continuing education credits (CEC’s), on nutrition and lifestyle behavior, by the year 2016.  In May of the same year, the bill passed, but not before the required seven credits were crossed off (what is left of the bill can be viewed here).  A shame, one might say, given the astronomical amount of tax and insurance dollars spent every year on lifestyle diseases (e.g. heart disease, stroke, type 2 diabetes, and a number of cancers).


But is increasing nutrition education of future and/or practicing physicians an appropriate solution? At a time when med student and/or physician burnout rates are at an all time high, probably not.  They have enough on their collective plate as it is.

BECOMING A PHYSICIAN

Requirements:

  • 4 years of university to earn a BS or BA with emphasis on basic science +
  • 4 years of medical school to earn a medical degree (MD) +
  • 3 – 7 years of graduate medical education which involves entering a residency program (e.g. 3 years for family practice, 5 years for general surgery, etc.) +
  • 1 – 3 years in a fellowship program should the new MD desire to become highly specialized in a particular field such as oncology or gastroenterlogy +
  • Passing the licensure exam and recertification exams on a regular basis after that +
  • Ongoing CECs from various medical arenas.

All of this amounts to barely enough time to cover the required material.

IS THE ADDITION OF NUTRITION TRAINING REALISTIC?

When and how, in scaling that mountain of education and clinical practice, is a future physician supposed to include the amount of nutrition education that would place him/her on par with a registered dietitian or, harder still, a CNS?  The first requires a four year bachelor’s degree in dietetics, of which 2.5 years concentrate on nutrition topics alone, and six months of clinical practice.  Adding nearly three years of nutrition education to an already extended MD program is absurd.  More so if trying to achieve a CNS level of education in this field, which requires a graduate degree in nutrition and 2,000 hours of practice.  It can be done, as some MDs sporting CNS credentials will attest, but how necessary is it to go to such great lengths, when registered/certified nutrition professionals are but a referral away?

On the other hand, simply taking basic nutrition courses over the course of those 11+ years of schooling (which, some medical schools do provide) or earning the recommended CECs in this domain after becoming a physician, doesn’t even begin to cover the tip of the nutrition information iceberg that might be of some use in terms of chronic disease or developmental nutrition (e.g. paediatrics, gerontology) management. Moreover, given that most physicians are spread too thin and can only spend a short amount of time on individual patient visits, how much quality nutrition advice can they provide under such circumstances? My guess is not much beyond that of which most patients are already aware. Nutrition advice is joined at the hip with behavioral modification counseling, both of which take time – and time is a luxury most physicians can not afford these days.

REFERRALS TO NUTRITION PROFESSIONALS

There isn’t enough time, or money, for that matter, to properly educate physicians about nutrition to the extent that they may counsel patients beyond what the patients already know.  That’s why the medical community saw fit to train nutrition professionals, such as RDs and CNSs, instead.  Most, however, rarely see a referral outside hospital walls.

The answer is not additional nutrition coursework for physicians. Instead, let’s introduce mandatory medical school courses and CECs for practicing physicians on how to recognize those instances in which referrals to nutrition specialists are necessary.  Furthermore, regulations should be in place requiring physicians to make dietician or CNS referrals instead of offering what amounts to sub-par, and often times erroneous, nutrition advice.

BABY, BATHWATER

This lack of initiative in terms of recognizing the need for, and providing, referrals has led some people (particularly those who tend to mistrust the medical community as a whole) to discount science based medicine altogether and jump ship to the alternative medicine side, in some cases with disastrous results.

In doing so, they are throwing the baby out with the bathwater.  Ditching one’s family physician over something s/he is not supposed to know about in the first place does not make a whole lot of sense, but to some patients it seems like the right thing to do when faced with a physician who is handing out incorrect information about nutrition.  They assume the doc may advise them poorly even when dealing in his/her own area of expertise.  Sometimes, this line of thought evolves into conspiracy theories about the medical profession that are well into tin hat territory.

BOTTOM LINE

Let physicians do what they are trained to do, but require they complete coursework on how to recognize those instances in which nutrition referrals are necessary, as well as any psychological factors that may keep referrals from happening in the first place.

REFERENCES

  1. Bruer RA, Schmidt RE, Davis H. Nutrition counselling – should physicians guide their patients? Am J Prev Med. 1994;10(5):308-11.
  2. Adams KM, Linderll KC, Kohlmeier M, Zeisel SH. Status of nutrition education in medical schools. Am J Clin Nutr, 2006;83(4):941S-944S.
  3. Flynn M, Sciamanna C, Vigilante K. Inadequate physician knowledge of the effects of diet on blood lipids and lipoproteins. Nutrition Journal, 2003;2:19.
  4. Kushner, R.F., Barriers to providing nutrition counselling by physicians: a survey of primary care practitioners, Preventive Medicine, 1995 Nov;24(6):546-52.
  5. Adams KM, Kohlmeier M, Zeisel SH.  Nutrition education in US medical schools: latest update of a national survey. Academic Medicine, 2010;85(9):1537-1542.

Lab meat – a healthier alternative?


Over the last decade, news stories featuring the advent of lab meat technology and its pink and pasty results have been peppering the virtual landscape, showing up in places like NBC, Forbes and a number of other news outlets.  It seems the lab grown burger is now ready for production, and, at some point in the future, for sale in your local stores and restaurants.  It has been touted as a way to improve diets in emerging economies by introducing cheaply produced meat on their markets, but is it any healthier than its traditionally produced counterpart?

WHAT’S IN IT?

Lab grown meat is cultivated from animal cells, so, in the case of hamburger, the cells come from a cow.  Unlike conventional meat, lab meat can be produced with far less fat, but not without the use of growth hormones, seeing how it has to grow quickly in order to be profitable (1).  Since lab meat is real animal flesh, haem iron is present, as is the increased risk for cardiovascular disease and bowel cancer it represents (see my earlier post on iron).  Producers are going out of their way to make sure this type of iron is included in the final product since they see any deviation from the real thing as a downside in terms of marketing (1).

No mention has been made regarding the presence of neu5gc in non-human mammals, nor of any possibility that lab meat can be produced without it (2). This is unfortunate given this molecule’s effects on the human body include a chronic state of low grade inflammation (for as long as meat and dairy are consumed),   involvement in arteriosclerosis, cancer progression, and the facilitation of hemolytic ureic syndrome, among other things (3,4,5). “Neu5Gc is present both in endothelium overlying plaques and in subendothelial regions, providing multiple pathways for accelerating inflammation” in arteriosclerosis (3).

Neu5gc is a sialic acid present on cell surfaces of all mammals with the exception of humans. We do not produce it, but we have antibodies which, to the surprise of its discoverers, are unable to fight it off completely (4).  When found setting up camp in our bodies it is there because we ingested it (5).  It is the only known non-human dietary molecule that becomes incorporated onto human cell surfaces  even after the immune system responds against it.  The immune response to the ever-present molecule sets off a repeating cycle wherein the resulting chronic inflammation helps tumours grow even as antibody response is boosted.  But it isn’t all bad news. All this research into what is now known as the “meat eater’s molecule” has yielded one surprising result:  aggressively boosting antibody response against it may help fight the tumours it helps produce in the first place (4).  Of course, staying away from eating the meat of four legged creatures, natural or lab made, would be the easiest way to avoid this whole cycle.

Lastly, animal protein is animal protein regardless of whether it comes from a slaughtered animal or artificially maintained animal cells.  Recent evidence suggests animal protein may increase cardiovascular disease risk in healthy men after controlling for confounders such as saturated fat (7).  Potential manufacturers have considered introducing plant protein into their final product but canned the idea as fears this may raise allergy issues for consumers prevailed (1).

BOTTOM LINE

Lab meat will give the environment and farm animals a break, to be sure, but, aside from containing less fat than conventional animal products, daily consumption will yield many of the same risk factors as conventional, organic, or wild caught meats.

REFERENCES

  1. Datar I, Betti M. Possibilities for an in vitro meat production system.  Innovative Food Science and Emerging Technologies, 2010;11:13-22.
  2. Varki A. Uniquely human evolution of silica acid genetics and biology. PNAS, 2010;107(2):8939-8946.
  3. Pham T, Gregg CJ, Karp F, Chow R, Padler-Karavani V, Cao H, Chen X, Witzum JL, Varki N, Varki A.  Evidence for a novel human-specific xeno-auto-antibody response against vascular endothelium. Blood, 2009;114(25):5225-35.
  4. Hedlund M, Padler-Karavani V, Varki N, Varki A. Evidence for a human-specific mechanism for diet and antibody-mediated inflammation in carcinoma progression.  PNAS, 2008;105(48):18936-41.
  5. Lofling JC, Paton AW, Varki NM, Paton JC, Varki A.  A dietary non-human silica acid may facilitate hemolytic-uremic syndrome.  Kidney Int., 2009;76(2):140-144.
  6. Varki N, Varki A. Diversity in cell surface silica acid presentations: implications for biology and disease.  Laboratory Investigation, 2007;87:851-7.
  7. Preis SR, Stampfer MJ, Spiegelman D, Willett WC, Rimm EB.  Dietary protein and risk of ischemic heart disease in middle-aged men. Am J Clin Nutr, 2010;92:1265-72.

The protein myth


There are a number of food myths currently in circulation, some of which have been around for decades.  They generally revolve around particular micro- and macro-nutrients, their sources, and/or their imaginary abilities to cure us of all sorts of ailments ranging from the common cold to cancer.  Among these, we find the “protein myth” which, in a nutshell, states that protein from animal foods is superior because it contains all essential amino acids.

WHAT ARE PROTEINS?

Proteins are the most complex of the three macro-nutrients. They are composed of long chains of amino acids and, in some cases, include other components that are strung together in complicated formations consisting of carbon, hydrogen, oxygen, and nitrogen.  Every cell in the human body contains protein. It is a major part of the skin, muscles, organs, glands and all body fluids, except bile and urine.  Proteins in the body act as enzymes (catalysts), messengers (hormones), structural elements, immunoprotectors (immunoglobulins or antibodies), transporters, buffers, fluid balancers, or receptors on cell surfaces.  They also play a role in cell adhesion, storage of minerals in the body, and as conjugated proteins (glycoproteins) (1).

Three types of amino acids fold into acid chains to form proteins.  They are:

Essential or indispensable amino acids

  • Essential amino acids cannot be made by the body. As a result, they must come from the foods we eat.
  • They are: histidine (infants only), isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine.

Nonessential amino acids

  • “Nonessential” means that our bodies produce an amino acid, even if we don’t get it from the foods we eat.
  • They include: alanine, asparagine, aspartic acid, and glutamic acid.

Conditional amino acids

  • Conditional amino acids are usually not essential, except in times of illness and stress, and are made in the body.
  • They include: arginine, cysteine, glutamine, tyrosine, glycine, ornithine, proline, and serine.

The chains are held together by hydrogen bonds, and, sometimes, by ionic bonds, depending on how the chain is folded (i.e. positive and negative ions face each other), by van deer Waals dispersion forces, or by sulphur bridges.

HOW MUCH PROTEIN DO WE NEED?

Although the human body contains a large amount of protein, it does not need to consume large amounts to maintain itself.  According to the World Health Organization (WHO), the average adult needs to consume approximately 60 grams of protein per day (0.8 grams per kilogram of body weight or 10 to 15% of total calories (assuming daily caloric needs are met) (2). As far as amino acids are concerned, we do not need to consume all of the essential amino acids at every meal, but getting a balance of them over the course of a 24 to 48 hour period is important.

PLANT vs ANIMAL PROTEIN

Plants produce/contain all of the essential amino acids because they can not get them from their environment by consuming other living organisms (the exception being carnivorous plants such as the Venus Fly plant which “eats” insects).  The amino acid profile of each plant varies – for instance, beans are high in lysine, while grains are low in it, but both contain it.  There is no such thing as a plant that lacks one or more amino acids (3). It is surprising, and disappointing, to see that, in spite of all we have learned about nutrition in the past couple of decades, the notion that plants lack certain amino acids persists (often in places one would least expect to find such false assumptions).

It is not necessary to consume animal products to meet essential amino acid needs, as long as the diet includes plant foods from all the food groups and caloric needs are met. Keep in mind, there is enough protein in plants to grow elephants and Panda bears. Contrary to popular belief, animals don’t make the essential amino acids we require. They ingest them by consuming plants (or one another).

The terms “complete” and “incomplete” proteins, when referring to protein foods, are no longer considered accurate or useful, and educators are encouraged to abstain from using them in the classroom (4).  Such terms are misleading and can create confusion since “incomplete” proteins are often described as “lacking” one or more essential amino acids.  This, of course, is not true and can be easily verified by looking up the amino acid content of plant foods using the USDA National Agricultural Library Nutrient Database.

From Young and Pellet’s review on plant proteins in relation to human protein and amino acid nutrition – click on image for larger version (5).

Should you, for whatever reason, want to include so-called “complete” proteins in one single meal, you may consume any of the following:

  • Soy, or
  • Eggs, or
  • Dairy, or
  • Legumes + Grains (e.g. peanut butter sandwich, burrito), or
  • Legumes + Nuts  (e.g. lentils and cashews), or
  • Legumes + Seeds (e.g. hummus)

In a review of plant based diets and their adequacy in meeting amino acid needs, Millward concludes:  “it is clear that meat-free, largely plant-based diets available in developed countries can supply protein in the amount and quality adequate for all ages” (6).  Similarly, the American Dietetic Association (ADA), in its position paper on vegetarian diets, states the following:  “Plant protein can meet protein requirements when a variety of plant foods is consumed and energy needs are met. Research indicates that an assortment of plant foods eaten over the course of a day can provide all essential amino acids and ensure adequate nitrogen retention and use in healthy adults; thus, complementary proteins do not need to be consumed at the same meal(7).

In the same paper, the ADA further adds:  “Vegetarian diets are often associated with a number of health advantages, including lower blood cholesterol levels, lower risk of heart disease, lower blood pressure levels, and lower risk of hypertension and type 2 diabetes. Vegetarians tend to have a lower body mass index (BMI) and lower overall cancer rates. Vegetarian diets tend to be lower in saturated fat and cholesterol, and have higher levels of dietary fiber, magnesium and potassium, vitamins C and E, folate, carotenoids, flavonoids, and other phytochemicals. These nutritional differences may explain some of the health advantages of those following a varied, balanced vegetarian diet” (7).

Animal protein, on the other hand, has been associated with cardiovascular disease and cancer, even after confounders such as saturated fat have been taken into account (8,9).

A VEGETARIAN MENU

To illustrate the ease with which amino acid requirements are met on a meat-free diet, let’s look at a modest sample menu for a 170 lbs man in his 30′s.  The selection is modest on purpose, and not representative of the wide variety of plant based foods consumed by the average vegetarian or vegan.

Breakfast:

2 scrambled eggs (or, for vegans an equivalent amount of tofu scramble)
2 pieces of toast with margarine
1 glass of orange juice

Snack:

1 avocado

Lunch:

1 Frozen bean burrito, microwaved
1 Small salad (1 cup of shredded lettuce, 1 sliced tomato, with dressing)
6 oz. soy milk

Snack:

1/2 cup pistachio nuts

Dinner:

1 bowl vegetarian stew (peas, tomatoes, green beans, carrots, onions, parsnip, olive oil, seasonings)
1 cup mashed potatoes
1 tomato
2 slices of bread
1 small slice of cherry pie

Amino acid requirements for our subject:          Amino acid content of selected  menu:In this example, the vegetarian menu meets and surpasses the amino acid requirements of our hypothetical man.

Evidence that plant based diets can meet all of our essential amino acid needs abounds (1,3,4,5,6,7,9,10).  Yet, the myth persists.  Education, particularly in the medical community, is key to putting this silliness to rest.

REFERENCES

  1. Gropper SS, Smith JL, Groff JL. Advanced Human Nutrition, 5th Ed. 2009;179-182.
  2. World Health Organization. Nutrition Health Topics – Population nutrient intake goals for preventing diet-related chronic diseases. Available at: http://www.who.int/nutrition/topics/5_population_nutrient/en/index.html  Accessed February 21, 2012.
  3. Mangels R, Messina V, Messina M. The Dietitians’s Guide to Vegetarian Diets, 3rd Ed. 2011;65-83.
  4. Millward DJ.  The nutritional value of plant-based diets in relation to human amino acid and protein requirements. Proc Nutr Soc, 1999;58:249-260.
  5. Young VR, Pellett PL.  Plant proteins in relation to human protein and amino acid nutrition.  Am J Clin Nutr, 1994;59:1203S-12S.
  6. U.S. National Library of Medicine National Institutes of Health – Medline Plus Fact Sheets.  Protein in the diet. Available at:  http://www.nlm.nih.gov/medlineplus/ency/article/002467.htm  Accessed February 21, 2012.
  7. Position of the American Dietetics Association:  Vegetarian Diets. Journal of the ADA, 2009;109(7):1266-82.
  8. Preis SR, Stampfer MJ, Spiegelman D, Willett WC, Rimm EB.  Dietary protein and risk of ischemic heart disease in middle-aged men. Am J Clin Nutr, 2010;92:1265-72.
  9. Fontana L, Klein S, Holloszy JO. Long-term low-protein, low-calorie diet and endurance exercise modulate metabolic factors associated with cancer risk. Am J Clin Nutr, 2006;84:1456-62.
  10. Millward DJ, Fereday A, Gibson NR, Pacy PJ.  Human adult amino acid requirements: leucine balance evaluation of the efficiency of utilization and apparent requirements for wheat protein and lysine compared with those of milk protein in healthy adults. Am J Clin Nutr, 2000;72:112-21.

Caloric restriction


In 1935, a study on caloric restriction in mice provided evidence, for the first time, that such an undertaking can promote longevity and disease fighting ability in mammals1.  Until then, only studies on yeast and lower animals had been completed in this area of research.  The novelty of the mouse study soon wore off, however, and the findings were not revisited until some time in the late 1980’s / early 1990’s, when interest in caloric restriction was renewed.  At that time, scientists wondered if the effects would be similar in primates, and, as a result, in humans.

Longitudinal studies using primates were soon underway, and now, nearly three decades later, the results look promising.  The primates of choice, for most undertakings, were (are) Rhesus monkeys.  Rhesus monkeys have a lifespan of approximately 35 to 40 years, making them easier to study, in terms of longevity and disease development, than higher primates such as chimpanzees or humans, whose lifespans are generally twice as long.

Research using mice, and a host of other species, continued alongside primate studies in an effort to accumulate as much comparable data as possible.  Yeast research has also continued, in most part due to striking working mechanism similarities that seem to span across all species studied thus far.

The question on everyone’s mind was “will caloric restriction have the same effect on all species studied?”.   An affirmative answer would strongly suggest the same to be true of humans.  Indeed, this is precisely what research to date has determined:  all species studied thus far have reacted in much the same way to caloric restriction.  Human studies following these findings have also yielded promising results.

CALORIC RESTRICTION DEFINED

Caloric restriction should not be confused with, or lead to, malnutrition.  Two types of caloric restriction have been identified to have an effect on aging and disease:  transient and sustained caloric restrictions.   Moderate and pronounced caloric restrictions have been found to improve health and longevity.

Transient caloric restriction refers to short-term restrictions that occur once, or several times, over the course of the lifespan.   Sustained caloric restriction involves a drop in daily caloric intake from the onset of the study through the end of the subject’s life.  Of these, sustained, pronounced caloric restriction has been found to have the greatest positive impact on disease prevention and longevity.

Moderate caloric restriction entails a reduction of daily caloric intake by 15% to 17%, whereas, pronounced caloric restriction involves a reduction of approximately 30%.  In terms of human caloric needs, 30% less calories would translate into a reduction of approximately 700 calories per day for a healthy adult whose BMI is in the recommended range and who normally consumes 2,500 calories daily, leading to a total caloric intake of 1,800 per day. 

TRANSIENT CALORIC RESTRICTION AND CANCER RISK

Transient caloric restriction studies are scarce, yet, they are as important as sustained restriction studies because the former is the most likely to be implemented by people over the course of their lives.  While most people have difficulty maintaining sustained caloric restriction for the entirety of their lifespans, many have dieted over the courses of their lives, and some have repeatedly engaged in “yo-yo dieting”, the latter having been shown by recent studies to be most likely to have detrimental effects on overall health.

The Dutch famine of 1944 – 1945 has been the subject of a number of studies on transient caloric restriction and its long term effects, in most part because the subjects were human. The first studies of the Dutch famine had surprising results (which more recent studies have since replicated).  Unlike sustained moderate or pronounced caloric restriction, transient restriction emerged as a risk factor for breast cancer later in life.  In addition, women who were exposed to the famine as children experienced subsequent reproductive difficulties.

This discovery prompted researchers to attempt replicating the findings using animal models.  They were not disappointed.  Studies in mice have repeatedly shown that while sustained caloric restriction works wonders against cancer onset and development, transient restriction has the opposite effect.  A study on the influence of underfeeding during the “critical period”, or thereafter, on carcinogen-induced mammary tumors in rats, concluded that transient restriction followed by ad libitum feeding could lead to increased cancer risk.  Another similar study by Kritchevsky on the promotion phase of cancer development found that not only was the risk of cancer increased in the wake of transient caloric restriction (“yo-yo dieting”), but that the study subjects gained a disproportionate amount of weight, very quickly, once the restriction was lifted3.

SUSTAINED CALORIC RESTRICTION AND CANCER RISK

Another 2002 study on the effects of sustained caloric restriction in mice found a 60% reduction in the number of precancerous intestinal polyps in mice at high risk for gastrointestinal cancers4.  The same study found that mice consuming a diet high in fruits and vegetables had 33% fewer polyps that the control mice, suggesting that even moderate caloric restrictions have a positive effect on the reduction of tumor formation.

A longitudinal study on Rhesus monkeys which began in 1989 at the Wisconsin National Primate Research Center (WNPRC) is perhaps one of the most telling in that it documented not only the effects of sustained caloric restriction on cancer, but on longevity and overall health of the subjects.  The photographic account/evidence of physiological changes is most striking1.

The Rhesus monkeys who participated in the WNPRC study generally have a lifespan of about 27 years.  All animals were adults when the study began (the results of which are a testament that it is never too late to impact the outcome of one’s life), ranging in ages from 7 years to 14 years.  Over the course of a six month period, the caloric restriction group (CR group) was slowly acclimated to a 30% decrease in daily caloric intake.  The CR animals maintained this level of caloric intake for the remainder of their lives.

Age related diseases in Rhesus monkeys had been well documented at the WNPRC and are very similar to those of humans’.  They include cancer, cardiovascular disease, and diabetes.  Over the course of the study, the CR animals experienced a decrease in body weight while maintaining a healthy BMI, thus, reducing their risk for obesity, which, in turn, is a risk factor for cancer.  Furthermore, they consistently experienced improved metabolic function, specifically, insulin sensitivity.  The incidence of cancer, which normally increases with age in Rhesus monkeys, was reduced by 50% in the CR group (as was the incidence of cardiovascular disease, also by 50%).  The biological age of the CR group monkeys became significantly younger than that of their cohorts in the control group.  A similar effect has been found in studies of people on long term CR1.

MECHANISM OF ACTION

Restriction of calories stresses the organism resulting in a response by DNA repair enzymes and apoptosis (programmed cell death) which protect the body from environmental insults.  “[The] proliferation of cells is reduced with both increased rates of apoptosis together with decreased DNA synthesis and increased DNA repair, limiting the number of preneoplastic lesions. Oxidative stress is reduced, resulting in decreased reactive oxygen species that can damage DNA. Furthermore, of interest to hormone associated tumours, levels of a number of hormones and growth factors are altered during caloric restriction: glucocor- ticoids are increased whereas concentrations of IGF-I (and to a lesser extent IGFBP-3 resulting in decreased bioavailability of IGF-I), insulin, prolactin, estrogens and leptin are decreased.”3.

A DNA transcription factor called heat shock factor 1 (HSF1), which is regulated by the enzyme sirtuin 1 (SIRT1), exists as a monomer in unstressed mammalian cells.  It responds to stresses such as the free radicals that play a role in carcinogenesis by resolving damaged, misfolded, and aggregated proteins.  As we age, the amount of SIRT1 protein decreases and HSF1 concentration increases.  Sustained caloric restrictions has been found to cause overexpression of SIRT1, which, in turn, enhances the ability of cells to survive prolonged exposure to heat shock temperatures.  SIRT1, therefore, functions as a positive cofactor of HSF1 and enhances the heat shock response5.

The discovery that caloric restriction is beneficial has been publicized in the main stream media for many years, albeit not as heavily as it deserves to be. Public reaction has generally been positive, yet, as expected, no sustained efforts to adopt lower calorie lifestyles have been observed in the general population.

In the West, where high calorie foods are stocked in great proportions on supermarket shelves and fast food restaurants pepper the landscape in astronomical numbers, temptation is unavoidable.  It is around every corner, invading our homes, workplaces, and cars via the airways, with corporate advertisements designed to entice and titillate, all of which are backed by significant market research into what people like and what works best to get them pining for the goods on display.  Few people stand a chance, and fewer yet are aware of the impact such advertisements and supermarket food displays have on us. Most of us are convinced that such things do not sway us, yet our collective Western girth seems to indicate otherwise.

Complicating matters is the average person’s upbringing and dietary habits that follow and impact our lives since before we are born.  According to recent studies, an expectant mother’s dietary choices can influence her unborn child’s future eating habits and overall health2.  High fat, high calorie food exposure in the womb can adversely affect the development of normal leptin balance in the fetus and can predispose the child to calorie rich food cravings that eventually result in life long weight and related health problems.  Adding insult to injury, most parents will feed their children the same kind of unhealthy diets that they themselves consume, further ensuring that poor dietary habits become engrained and more difficult to break later on.  Many still believe that being plump and cherub-like are desirable qualities in small children and often insist that children finish everything on their plates.

A reduction in caloric intake generally requires a significant change in food choices.  A person accustomed to eating a diet heavy in processed foods, meats, and dairy would have a fair amount of difficulty reducing caloric intake while at the same time continuing to enjoy these foods and not be left feeling hungry.  Reduced caloric intake without a life-long struggle against hunger can only be achieved by adopting a Mediterranean, vegetarian, or vegan life style.  Since most people are unfamiliar with these kinds of eating styles, they often assume they would feel hungry or deprived and opt not to try.  Some who attempt to make significant changes are ill prepared to do so and usually revert to their old, familiar ways.

BOTTOM LINE

That caloric restriction has a positive effect in the prevention of cancer, degenerative diseases in general, and on the extension of lifespan is difficult to dispute.  The overwhelming evidence suggests it is a plausible tool for prevention and, as is the case for diabetes and heart disease, an effective tool in the treatment of a number of illnesses.  Implementation of sustained, pronounced caloric restriction, however, is difficult because most people do not have the tools (psychological and practical) to make such a lifestyle change a permanent one.  Sustained, moderate caloric restriction stands a better chance of implementation and sustainability, however, it is a viable option only when coupled with education (i.e. cooking methods, shopping habits, family support).

Transient caloric restriction is perhaps the most likely to be adopted by most people, however, there are risks involved in choosing this path that may outweigh the benefits.  Transient caloric restriction followed by a return to “normal” feeding habits has been shown to be detrimental to health and to be a risk factor for cancer.  This kind of dietary restriction, commonly known as “yo-yo dieting” is not recommended, and is particularly dangerous for persons who already have cancer.

REFERENCES

  1. Colman RJ, Anderson RM, Johnson SC, Kastman EK, Kosmatka KJ, Beasley TM, Allison DB, Cruzen C, Simmons HA, Kemnitz JW, Weindruch R.  Caloric restriction delays disease onset and mortality in Rhesus monkeys.  Science 2009;  325:201-204.
  2. Wellcome Trust (2008, July 1). Poor Diet During Pregnancy May Have Long Term Impact On Child’s Health, Study Suggests. ScienceDaily. Retrieved November 23, 2009, from http://www.sciencedaily.com­ /releases/2008/06/080630200951.htm
  3. Elias SG, Peeters PHM, Grobbee DE, van Noord PAH.  Transient caloric restriction and cancer risk (The Netherlands).  Cancer Causes Control 2007; 18:1-5.
  4. Federation Of American Societies For Experimental Biology (2002, April 25). Even Moderate Caloric Restriction Lowers Cancer Risk In Mice. ScienceDaily. Retrieved November 24, 2009, from http://www.sciencedaily.com­ /releases/2002/04/020424073022.htm
  5. Saunders L, Verdin E.  Stress response and aging. Science 2009; 323:1021-1022

Coffee may protect against cardiovascular disease


Image

Coffee drinking was first recorded in the Middle East over 500 years ago.  Today, coffee is one of the most popular beverages in the world, with over 70 countries supplying it and nearly every country in the world consuming it.  Thanks to its popularity, it is not surprising that coffee and its components have been the subjects of a wide range of studies that assess the risks and benefits of consumption.

Findings on the association of coffee consumption and cardiovascular disease (CVD) risk have been contradictory, with some studies revealing an increased risk for CVD, others showing no risk, and some finding benefits against it (1,2,3). Gender differences, types and amounts of coffee consumed, genetic factors, a tendency to focus on caffeine alone, lengths of studies, and a host of other confounders can make findings appear contradictory. Yet, in spite of these somewhat conflicting results, recent findings appear to offer some support to the hypothesis that low to moderate consumption of coffee may offer protection against some of the risk factors for CVD over the long term.

INFLAMMATION

Inflammation is a normal response to injury and plays an important role in tissue repair and restoration of tissue function.  However, prolonged inflammation can be too much of a good thing, in no small part due to its involvement in oxidative stress – chronic inflammation is a major contributor to a host of degenerative diseases, including CVD (2,3).  A 2008 study of 459 Japanese women revealed a significant, independent, inverse correlation between coffee consumption and serum C-reactive protein (CRP) levels (2).  This is an important finding because CRP has been recognized as a marker for systemic inflammation and has been shown to have predictive value for CVD, stroke, and death (4). Similarly, the Iowa Women’s Health Study provides additional support through its finding of an inverse association of coffee consumption with death attributed to inflammatory diseases (3).

LDL AND OXIDATIVE STRESS

Oxidized LDL plays a key role in the pathogenesis of atherosclerosis (5).  It has a number of atherogenic properties, so, the body uses a complex defense system to rapidly remove it from circulation.  Dietary and genetic factors can aid or overwhelm this system. The susceptibility of LDL to oxidation is dependent upon serum concentrations of conjugated dienes, lipid hydroperoxides, and antioxidant species (5). Diets high in fruits and vegetables confer protection against this susceptibility, in part, by providing a consistent, dependable source of antioxidants.  Data from a study on the effects of caffeic acid on LDL indicates that the consumption of just one cup of coffee (200 ml) per day significantly improves oxidative resistance in humans (5).

Several studies have shown a J-shaped association between coffee consumption and CVD risk (5). This is similar to the association seen with wine consumption – drinking a small amount each day improves your odds of avoiding CVD, but overdoing it swiftly swings those odds against you and adds a number of other health and social problems to your tab.

The correlation with lowered CVD risk may be a result of protection conferred by polyphenols, volatile aroma compounds, and eterocyclic compounds found in coffee, all of which contribute to its antioxidant capacity (3).  Since plasma antioxidants increase after its consumption, coffee has been associated with reduced oxidative stress (3).   The consumption of coffee for a period of just seven days has been shown to significantly decrease LDL serum concentrations and LDL susceptibility to oxidation (5).

INSTANT, FILTERED AND UNFILTERED COFFEE

The above mentioned anti-oxidative effect of coffee consumption on LDL has not been replicated in filtered coffee studies (5).  This may be due, in part, to the ability of paper filters to keep some of coffee’s antioxidants from passing through, and, thus, from being consumed.  However, paper filtered and instant coffee do not raise LDL levels after consumption, whereas, LDL serum concentrations have been shown to increase in the wake of drinking unfiltered coffee (6). Consumption of 6 cups of boiled coffee (i.e. French press, espresso) per day was estimated to increase serum LDL levels by 17.8 mg/dL (6).  Diterpene cafestol is the likely cause of this increase. So, on one hand unfiltered coffee improves LDL oxidative resistance (which is good), but raises LDL levels (which is bad).

BLOOD PRESSURE

Caffeine has been shown to increase blood pressure in people who are not habitual caffeine consumers (6).  The key word here is “habitual”.  Partial tolerance to caffeine’s effects on blood pressure takes place in as little as one week in most people (6).  Thus, it is difficult to extrapolate the findings on increased blood pressure to long term use of coffee.  In addition, trials comparing the effects of caffeine capsules vs. placebo capsules have shown much stronger effects than trials looking at caffeinated coffee vs decaffeinated coffee consumption (6).  This is likely due to the fact that coffee is not comprised of caffeine alone.  Instead, coffee, whether caffeinated or decaffeinated, contains a number of antioxidants and other compounds which confer protection against the detrimental effects of its caffeine component (6).

Perhaps most telling of the importance of these other components in coffee was the finding that caffeinated cola consumption is associated with a higher incidence of hypertension than caffeinated coffee consumption (6).  Something to keep in mind the next time you feel like frowning when you see a teenager, or even a child, sipping a Cafe Misto. Furthermore, chlorogenic acid, a component of coffee, has been shown to reduce blood pressure in hypertensive rats (6).  And, in humans, green coffee bean extracts, which are low in caffeine, were shown to reduce hypertension in a randomized, Japanese trial (6).

BOTTOM LINE

Instant coffee and filtered coffee can protect against CVD if consumed in quantities of up to 4 cups (not mugs!) per day.  Unfiltered coffee does not and can have detrimental effects in the long run if it is consumed on a regular basis.  All caffeinated coffee, regardless of how it is prepared, is contraindicated for persons who already have CVD and/or high blood pressure.

So, put away the soda, espresso, and espresso mixed drinks (i.e. latte, cappuccino) and reach for instant or filtered coffee instead.  Your heart will thank you.  I’m not suggesting you must swear off the aforementioned concoctions for the rest of your days. I certainly haven’t.  But if you are drinking unfiltered coffee on a daily basis, you may want to reconsider and train your palate to enjoy the many other varieties of roasts available that are prepared with paper filters.  Or you can rig your espresso machine to brew using paper.

Let me know how that works out.  :)

REFERENCES

1)    Balk L, Hockstra T, Twisk J.  Relationship between long-term coffee consumption and components of the metabolic syndrome:  the Amsterdam Growth and Health Longitudinal Study.  Eur J Epidimiol 2009; 24: 203-209.

2)    Kotani K, Tsuzaki K, Sano Y, Maekawa M, Fujiwara S, Hamada T, Sakane N.   The relationship between usual coffee consumption and serum C-reactive protein level in a Japanese female population.  Clin Chem Lab Med 2008; 46(10): 1434-1437.

3)    Andersen L, Jacobs D, Carlsen M, Blomhoff R.  Consumption of coffee is associated with reduced risk of death attributed to inflammatory and cardiovascular diseases in the Iowa Women’s Health Study.  Am J Clin Nutr 2006; 83: 1039-1046.

4)    American Heart Association.  Inflammation, heart disease and stroke:  the role of C-reactive protein.  2010.  Available at: http://www.americanheart.org/presenter.jhtml?identifier=4648.  Accessed May 9, 2010.

5)    Natella F, Nardini M, Belelli F, Scaccini C.  Coffee drinking induces incorporation of phenolic acids into LDL and increases the resistance of LDL to ex vivo oxidation in humans.  Am J Clin Nutr 2007; 86: 604-609.

6)    Van Dam R M.  Coffee consumption and risk of type 2 diabetes, cardiovascular diseases, and cancer.   Appl Physiol Nutr Metab 2008; 33: 1269-1283.

A word on iron


The most abundant metal in the body and an essential component of red blood cells, iron is primarily responsible for oxygen binding/transport and electron transport.  It’s important.  But too much of a good thing can have devastating effects and, iron, unlike other nutrients, can’t always be denied entry into the body or be ushered unceremoniously out the door when too much of its ilk has overstayed their welcome.  So, how much is too little or too much?  What can happen?  How do we make sure we meet our requirements without going overboard?

First, it is important to understand how and why our bodies manage dietary iron as they do.  At a time when Homo sapiens were at a significantly higher risk of losing their contents, in no small part due to being mauled by cave lions and the occasional prehistoric hyena, or by simply stepping off a cliff while trying to escape neighbouring tribes, we developed an iron storage mechanism to ensure rapid recovery should sudden loss of blood take place.  And it was great.  Particularly since the human body can synthesize blood cells by more than 20 times the rate at which it can incorporate dietary iron.  In the absence of existing iron stores, scarfing down copious amounts of red meat in such instances would have resulted in a well fed corpse and not much else.

The ability to store iron, however, came at a cost.  As the risk of sudden blood loss decreased with time, our bodies retained the pesky habit of storing excess iron with no mechanism in place to get rid of it should it exceed our needs.  Today, iron stores are obsolete, thanks to blood banks and modern medical interventions should accidents occur, but the liability of iron stores indefinitely hanging around remains.

SO, WHAT CAN HAPPEN?

In the healthy, young body, not a whole lot, and this is true for a number of other excesses such as the occasional alcohol overload after a night out on the town.  A healthy body in its prime disposes of over-consumed substances by excreting or incorporating them for later use.  Iron can’t be disposed of once absorbed, so, it gets packed away in bio-storage “bins” throughout the body, which would be great, except we don’t stay young and in perfect health all of our lives.  We age, and as our years grow in number, so do our iron stores, unless we start paying more attention to our dietary choices early on.

The average 70 kg adult man has approximately 2,800 mg of iron in his body.  Contrast this to the amount of dietary iron intake recommended for the same:  about 8 mg per day.  Compared to the amount of iron our bodies recycle on a daily basis, the amount we need to eat seems minuscule, and, as such, harmless should we overindulge a little bit.  But is it harmless?  Not exactly.  One or more extra mg per day, every day, month, year, and decade build up to become a risk factor for heart disease and colon cancer.

While a risk factor is just that, and not necessarily an assurance that disease will develop, it is, none the less, wise to make an effort and eliminate as many risk factors as we can, within reason.  To do so, we must understand which type of iron is most likely to be of benefit and why, and we need to identify a number of sources from where to get it.

TYPES OF IRON

There are two types of dietary iron. Haem iron is found in hemoglobin (the protein in red blood cells responsible for carrying oxygen) in most animal based foods.  It can not be regulated by humans, thus, regardless of actual need, approximately 20% to 30% of haem iron present in food is absorbed.  The rest ends up in our lower intestine stirring up trouble. Needless to say, you want to consume very little, if any, of this type of iron, particularly if you are male or post-menopausal.

Non-haem iron is found in plant foods, eggs, insects and any other animals who do not carry hemoglobin (i.e. red blood).  Uptake, transport, and storage is tightly regulated to prevent both iron deficiency and toxicity.  Absorption rates increase up to ten fold when iron stores are depleted.  This is the good stuff!

ROLE IN DISEASE

In men and in postmenopausal women the iron stores increase almost linearly with age, generating an additional risk for oxidative stress-related diseases like arteriosclerosis, chronic inflammatory diseases or cancer.

Cancer – regular consumption of heme-iron has been shown to increase the production of N-nitroso compounds (NOC’s) in the colon – NOC’s are carcinogenic and are usually involved in gastro-intestinal cancers.

Diabetes – low iron stores, such as those found among vegetarian populations, are inversely related to insulin sensitivity (low iron stores = high insulin sensitivity = lowered risk for diabetes). Conversely, the more stored iron a person has, the more insulin resistant s/he is, thus, increasing risk of developing diabetes.

DEFICIENCY, ANEMIAS

Iron deficiency takes months to years to develop depending on dietary intake, gender, and age. Symptoms include: chronic fatigue, weakness, dizziness, headaches, difficulty thinking. Incidentally, some symptoms of iron overload overlap, so, it is best to leave the diagnosis to your family physician.

As iron is slowly depleted from stores, iron in hemoglobin remains normal. It is only once hemoglobin levels start to become affected that a deficiency is declared and when the body can no longer meet daily functional needs dependent on iron, the diagnosis becomes iron deficiency anemia. Low iron stores, however, do not necessarily lead to anemia.  This explains the lack of difference in anemia rates between vegetarian and non-vegetarian populations (vegetarians and vegans usually have lower iron stores than the rest of the population). In fact, there is no conclusive evidence that an absence of iron stores has any negative consequences in otherwise healthy individuals.  It is only when we are in negative balance that unpleasant things begin to happen.  Should this occur, it is better to reach for a good quality iron supplement and include more leafy greens in your diet until the problem is corrected, rather than make a run for the local steak house.

RISK FACTORS FOR ANEMIA

Obesity – hepcidin, a peptide produced by the liver and adipose tissue is a key regulator of iron homeostasis. Obesity increases hepcidin expression which, in turn, increases iron deficiency risk by decreasing iron absorption and increasing chronic inflammation in the body.

Vitamin A deficiency – can also lead to anemia. Vitamin A plays a role in releasing iron from ferritin stores for use by the body. Approximately 50 carotenoids (i.e. alpha-, beta-, and gamma-carotene) are converted by the body into vitamin A. Sources include: eggs, fortified cereals, dark orange or green vegetables.

Diet – very low intake or lack of dietary sources of iron may eventually result in a negative balance of iron in the body, primarily in premenopausal women.

Menstruation – premenopausal women require higher intakes of iron to counteract monthly losses.

HOW MUCH DO YOU NEED?

  • Adult men: 8 mg
  • Pre-menopausal women: 18 mg
  • Post-menopausal: 8 mg
  • Pregnant women: 27 mg
  • Athletes: depends on level of activity

SOURCES OF NON-HEME IRON

In plants, leaves are the major site for iron accumulation. The amount of iron in leaves increases with leaf development, with mature leaves containing the highest amounts. The exception is legumes – iron is found in higher concentrations in the beans themselves.

Dietary iron in plant foods varies depending on crop growing conditions, the specific food type, and the part of the plant consumed. In soybeans, for example, much of the ferritin is found in the hulls. Thus, foods made from whole soy such as soymilk or soy nuts contain more ferritin than foods from dehulled soy beans or processed foods such as tofu.

The best vegetarian sources of iron include:

  • Legumes (lima, soy, peas, kidney beans)
  • Dried fruits (prunes, raisins, apricots)
  • Iron-fortified cereals (depending on type of iron used for fortification)
  • Whole grains (wheat, millet, oats, brown rice)
  • Vegetables (broccoli, spinach, kale, collards, asparagus, dandelion greens)

INHIBITORS

Phytate – antioxidant found in plant foods that, when consumed in excessive amounts, interferes with iron absorption. Soaking, fermentation, germination or cooking significantly decrease this effect.

Polyphenols – found in a variety of plant foods, but only significantly inhibitory in tea (both herbal and black), beans, and chili powder. Most common are tannins.

Calcium – inhibits non-heme iron absorption, so, try to abstain from drowning your veggies in cheese.

Although phytates, polyphenols and calcium inhibit absorption in single meals, consuming a varied diet provides a fair amount of protection against these effects.

PROMOTERS

Ascorbic acid – aka vitamin C, chelates iron and reduces it from ferric to ferrous form so that it can be absorbed more easily. When consumed along with polyphenols, the inhibiting effect of these is cancelled out and vice versa. The trick is not to cook the vitamin C when using it to enhance iron absorption (i.e. use lemon juice on your spinach, after the spinach has been cooked).

Ascorbyl palimate – is a derivative of ascorbic acid that is commonly found in processed foods. It has the same beneficiary effect and is not affected by high cooking temperatures (as in baking).

FORTIFIED FOODS

The World Health Organization (WHO) recommends fortifying foods (particularly flour) with ferrous sulfate, ferrous fumarate, ferric pyrophosphate, and electrolytic iron powder. Most food manufacturers, however, use low cost elemental iron powders that are contra-indicated by WHO. Thus, unless manufacturers start to follow WHO recommendations, the fortification you see on food labels doesn’t usually amount to a hill of beans.

SUPPLEMENTS

Supplements are useful in replenishing iron stores, but should not be used indefinitely because they usually interfere with zinc absorption.

REFERENCES

  • Emerit J, Beaumont C, Trivin F. Iron metabolism, free radicals and oxidative injury. Biomed Pharmacother, 2001; 55: 333-9.
  • Hua N, Stoohs RA, Facchini FS. Low iron status and enhanced insulin sensitivity in lacto-ovo vegetarians. British Journal of Nutrition, 2001; 86: 515-9.
  • Hurrell R, Egli I. Iron bioavailability and reference values. Am J Clin Nutr, 2010; 91(suppl): 1461S-7S.
  • Loh Y, Jakszyn P, Luben R, Mulligan A, Mitrou P, Khaw K. N-nitroso compounds and cancer incidence: the European Prospective Investigation into Cancer and Nutrition (EPIC) – Norfolk Study. Am J Clin Nutr, 2011; 93: 1053-61.
  • Lonnerdal B. Soybean ferritin implications for iron status of vegetarians. Am J Clin Nutr, 2009;89(suppl): 1680S-5S.
  • McCord JM. Iron, free radicals and oxidative injury. J. Nutr., 2004;134:3171S-3172S.
  • Sesink ALA, Termont DSML, Kleibeuker JH, Van der Meer R.  Red meat and colon cancer: the cytotoxic and hyper proliferative effects of dietary heme. Cancer Research, 1999;59:5704-9.
  • Theil EC, Briat JF. Plant ferritin and non-heme iron nutrition in humans. HarvestPlus Technical Monograph 1. Washington, DC and Cali: International Food Policy Research Institute and International Center for Tropical Agriculture (CIAT); 2004.
  • Tsai CJ, Leitzmann MF, Willett WC, Giovannucci EL.  Heme and non-heme iron consumption and risk of gallstone in men. Am J Clin Nutr, 2007;85(2):518-22.
  • Van der A D, Peeters PHM, Grobbee DE, Marx JJM, van der Schouw YT.  Dietary haem iron and coronary heart disease in women.  European Heart Journal, 2004;26(3):257-62.