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.