Breast cancer and inflammation

Breast cancer is probably the greatest fear women have, even though they are 10 times more likely to die from heart disease. Yet both diseases are driven by cellular inflammation.

Cellular inflammation occurs when the most primitive part of your immune system (the innate immune system) is activated. The key player in the innate immune system is a gene transcription protein known as nuclear factor-kappaB (NF-κB). Once activated, NF-κB moves into the cell’s nucleus and causes the expression of a wide variety of pro-inflammatory mediators that accelerate the growth of the tumor. A recent publication in Cancer Research has demonstrated that complete inhibition of the NF-κB in the breast tissue prevents the development of breast cancer in animal models (1).

Of course, there is one slight problem with this approach. If you inhibit NF-κB too much, you make yourself a sitting target for microbial invasion. So the question is what activates the NF-κB in the first place? The answer is the diet, and specifically how the diet increases the levels of arachidonic acid, as I described in my most recent book, “Toxic Fat” (2). As the levels of arachidonic acid increase in the cell, there is an increased formation of inflammatory compounds (i.e. leukotrienes) that activate NF-κB (3).

So what might the best approach be for reducing the risk of breast cancer? The obvious answer is to decrease the levels of arachidonic acid in the breast tissue. The best way would be to follow a strict anti inflammatory diet to reduce the formation of arachidonic acid in the first place (4).

Unfortunately, most women (and men) are not willing to take that step. That being the case, then what other dietary approach can be used? I would suggest that supplementing the diet with high-purity omega-3 fatty acid concentrates rich in EPA and DHA is the one approach that everyone can follow. This is especially true since it takes only 15 seconds a day. The benefits of this approach was recently demonstrated in another article published last year in the American Journal of Clinical Nutrition that demonstrated supplementation with purified omega-3 concentrates can dramatically increase the levels of omega-3 fatty acids in the breast tissue of women who have a high-risk potential of developing breast cancer (5).

Of course, if you not only take high-purity omega-3 fatty acid concentrates, but also follow the anti inflammatory diet, then you will have done every possible dietary intervention to reduce the activation of NF-κB in the target tissue for breast cancer (not to mention also reducing the risk for heart disease). Of course, there are some side effects to this dietary approach: You become thinner, smarter and happier in the process.


  1. Liu M, Sakamaki T, Casimiro MC, Willmarth NE, Quong AA, Ju X, Ojeifo J, Jiao X, Yeow WS, Katiyar S, Shirley LA, Joyce D, Lisanti MP, Albanese C, and Pestell RG. “The canonical NF-kappaB pathway governs mammary tumorigenesis in transgenic mice and tumor stem cell expansion.” Cancer Res 24: 10464-10473 (2010)
  2. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN. (2008)
  3. Sanchez-Galan E, Gomez-Hernandez A, Vidal C, Martin-Ventura JL, Blanco-Colio LM, Munoz-Garcia B. Ortega L, Egido J, and Tunon J. “Leukotriene B4 enhances the activity of nuclear factor-kappaB pathway through BLT1 and BLT2 receptors in atherosclerosis.” Cardiovasc Res 81: 216-225 (2009)
  4. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  5. Yee LD, Lester JL, Cole RM, Richardson JR, Hsu JC, Li Y, Lehman A, Belury MA, and Clinton SK. “Omega-3 fatty acid supplements in women at high risk of breast cancer have dose-dependent effects on breast adipose tissue fatty acid composition.” Am J Clin Nutr 91:1185–1194 (2010)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Coffee and diabetes: What’s the connection?

One of the great controversies in nutrition is the role of coffee and human health. On the one hand, coffee is the primary source of polyphenols in the American diet because of the lack of consumption of fruits and vegetables. On the other hand, coffee is rich in caffeine, an alkaloid that acts as a stimulant on the central nervous system and is known to be an addictive agent (1). In fact, Roland Griffiths, professor of Behavioral Biology at the John Hopkins School of Medicine (and my old college roommate), says, “Caffeine is the world’s most widely used mood-altering drug.” So the question remains is caffeine good for you?

No one knows for sure, but one interesting point has been made that it appears the more coffee you drink, the lower your risk for developing diabetes (2). In fact, if you drink more than four cups of coffee per day, you decrease your risk of diabetes by 50 percent. This new research demonstrates that coffee increases the levels of sex hormone-binding globlin (SHBG) in the blood. As I pointed out in my book “The Anti-Aging Zone,” SHBG plays an important role in sequestering the levels of estrogen and testosterone in the blood so that levels of these unbound sex hormones that can interact with their receptors are tightly regulated (3). Usually as insulin resistance increases, the levels of SHBG decrease in the blood (4). This can lead to an over-stimulation of the receptors by the unbound sex hormones resulting in increased risk for breast and prostate cancer development.

What in the coffee actually causes the increase in SHBG is unknown, but what is known is that once you decaffeinate the coffee, all its benefits on the elevation of SHBG levels and any reduction in risk for diabetes disappear.

It is highly unlikely that caffeine by itself is beneficial for reducing type 2 diabetes, since there were no benefits related to drinking tea or to total daily caffeine intake (2). Perhaps some other compound that was also extracted with the caffeine may play a role in the reduction of type 2 diabetes.

So what really happens when you decaffeinate coffee? First, you soak the beans in water to remove the caffeine and flavors as well as the polyphenols. Then you treat the water with organic solvents (methylene chloride or ethyl acetate) to remove the caffeine (as well as many of the polyphenols and much of the flavor). Then (assuming you have removed all of the organic solvent), you add back the treated water extract to the beans to hopefully reabsorb some of the flavors back into them. Obviously, not all the flavors or polyphenols return since the resulting taste is far less robust than the original coffee bean.

So it seems to me that exploring what else has been extracted in addition to the caffeine may lead to new dietary treatments for diabetes. Whether that will be done is highly unlikely. Instead of waiting for such experiments, you might as well follow the best treatment for preventing diabetes, which is following the anti inflammatory diet for a lifetime. That is how you control cellular inflammation, which is the driving force for development of type 2 diabetes (5,6).


1. Juliano LM and Griffiths RR. “A critical review of caffeine withdrawal: empirical validation of symptoms and signs, incidence, severity, and associated features.” Psychopharmacology 176: 1-29 (2004)

2. Goto A, Song Y, Chen BH, Manson JE, Buring JE, and Liu S. “Coffee and caffeine consumption in relation to sex hormone-binding globulin and risk of type 2 diabetes in postmenopausal women.” Diabetes 60: 269-275 (2011)

3. Sears B. “The Anti-Aging Zone.” Regan Books. New York, NY (1999)

4. Akin F, Bastemir M, and Alkis E. “Effect of insulin sensitivity on SHBG levels in premenopausal versus postmenopausal obese women.” Adv Ther 24: 1210-1220 (2007)

5. Sears B. “Anti-inflammatory diets for obesity and diabetes.” J Coll Amer Nutr 28: 482S-491S (2009)

6. Sears B. “The Anti-Inflammation Zone.” Regan Books. New York, NY (2005)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Try the team approach to nutrition

One of the problems with nutrition is that it is too complex for simple thinking. Unlike drugs, which are designed to inhibit a particular target enzyme, nutrients often work in combinations like a team operating at the genetic level. When you try to apply drug-like thinking (i.e. one compound has to do all the work) to nutrient research, then the results are often underwhelming. Nowhere is this clearer than when we look at how nutrients interact to control body weight.

Weight gain can be best understood as a defect in both metabolism (the conversion of dietary energy into chemical energy) and storage (the stockpiling of excess dietary intake). This involves a four-way conversation between the brain, the gut, the liver and the adipose tissue. The only way these various organs can communicate with each other is via hormones. The gut sends signals to the brain when to stop eating. If the brain receives those signals loud and clear, your desire for food decreases (i.e. satiety). Finally, the food that has been ingested is either converted by the liver into suitable metabolites that can either be used for generating chemical energy (i.e. ATP) or stored (primarily in the fat cells) for future use. When it all works together, it runs smoothly. When it doesn’t work well, you end up gaining more body fat accelerating the pathway toward chronic disease.

One of the key hormones in this complex communication process is adiponectin. Apidonectin is an anti-inflammatory hormone made by the fat cells that is essential for reducing insulin resistance and preventing lipotoxicity (1). In other words, it is at the center of this complex hormonal communication system to help keep body weight in check and slow the development of chronic disease. Great, but how do you increase adiponectin?

First, there is no drug that can do it, but there are nutrients that can. One approach is to consume more omega-3 fatty acids (1). High levels of omega-3 fatty acids activate a genetic transcription factor that causes the increased production of adiponectin. But it takes a lot of high purity omega-3 oil to turn on that gene transcription factor. Now there appears to be another way: Taking polyphenols (2). The polyphenols don’t increase the activity of the genetic transcription factor, but they do facilitate the assembly of adiponectin into its most active form. Of course, if you don’t have enough omega-3 fatty acids in the diet, you can’t produce the necessary adiponectin building blocks to be assembled. When you combine the two (high purity omega-3 oil and polyphenols), then you don’t need to use as much of either one for the desired end result (3).

That’s how nutrition really works. You have to use a team nutrient approach to alter genetic expression. A lot more complicated than giving a single drug, but of course without the inherent side effects.


  1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  2. Neschen S, Morino K, Rossbacher JC, Pongratz RL, Cline GW, Sono S, Gillum M, and Shulman GI. “Fish oil regulates adiponectin secretion by a peroxisome proliferator-activated receptor-gamma-dependent mechanism in mice.” Diabetes 55: 924-928 (2006)
  3. Wang Q, Liu M, Liu X, Dong LQ, Glickman RD, Slage TJ, Zhou Z, and Liu F. “Up-regulation of adiponectin by resveratrol.” J Biol Chem 286: 60-66 (2011)
  4. Shirai N and Suzuki H. “Effects of simultaneous intakes of fish oil and green tea extracts on plasma, glucose, insulin, C-peptide, and adiponectin and on liver lipid concentrations in mice fed low- and high-fat diets.” Ann Nutr Metab 52: 241-249 (2008)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Does living longer mean living poorly?

America has the highest health-care costs in the world. But are we really living better as a consequence of this massive cost? The January 2011 issue of the Journals of Gerontology says maybe not (1). There is no question that Americans are living longer, but our years of disease-free and functional living are declining faster. In particular, the chances of someone age 65 reaching age 85 have doubled from (from 20 percent to 40 percent), but a longer life is coming with more chronic disease and an increasing inability to function normally. In other words, the number of healthy years we can expect to have has actually decreased over the last decade.

So where are all our health-care dollars going? They appear to be keeping us alive. We are delaying death at the price of decreased quality of life as we age. As the lead author stated, “Longer life is what we want. But we’re going to have to pay for it with more treatment of diseases and accommodations for disability.” Since 40 percent of our health-care costs come after age 65, we can expect that Medicare costs will rise even faster than expected as an increasingly sicker baby-boomer population begins to enter Medicare starting this year.

But what about all the news we hear about “anti-aging” research where we can just inject “youth hormones,” like growth hormone, to reverse the aging process? It turns out that there may be trouble brewing in that area also. These hormones are growth factors. This means they turn on DNA synthesis that leads to a shortening of telomeres at the end of a DNA strand. When these telomeres become short enough, any future DNA turnover stops, and the cell dies. This has been demonstrated to occur in mice in which you can increase the levels of growth hormone. When you do so, the animals die prematurely, and there appears to be an acceleration of aging in many organs, including the brain (2).

This potential side effect of increased growth hormone is further confirmed in another recent study (3). This particular study demonstrated that giving mice inhibitors of the release of growth hormone increased their longevity. What was unique in this study was that they used specially bred mice that age prematurely. So if you want to speed up the aging process by taking growth hormone injections, you might look great in the process, but don’t count on an extended lifetime.

Of course, there is another way of looking better and living a longer, healthier life: Calorie restriction without hunger or deprivation. This is the foundation of the anti inflammatory diet. By maintaining the appropriate balance of protein to carbohydrate at every meal and snack, you are able to maintain satiety (i.e. absence of hunger). If you aren’t hungry, then you don’t eat as many calories. This automatically slows down the aging process as long as you are getting adequate protein and supplying necessary micronutrients (4). Not surprisingly, this is also how you squeeze out more quality years as you age.

1. Crimmins EM and Beltran-Sanchez H. “Mortality and morbidity trends: Is there a compression of morbidity?” Journals of Gerontology Series B 66B: 75-86 (2011)
2. Bartke A. “Can growth hormone accelerate aging?” Neuroendocrinology 78: 210-216 (2003)
3. Banks WA, Morely JE, Farr SA, Price TO, Ercal N, Vidaurre I, and Schally AV. “Effect of a growth hormone-releasing hormone antagonist on teleomerase activity, oxidative, stress, longevity, and aging in mice.” Proc Nat Acad Sci USA 107: 22272-22277 (2010)
4. Sears B. “The Anti-Aging Zone.” Regan Books. New York, NY (1999)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

The secret of blueberries: It’s the dephinidins

We continually hear about the benefits of fruits and vegetables for better health. There are a number of them. One is obviously their lower glycemic load that reduces insulin secretion. Another is their polyphenol content that gives fruits and vegetables their colors. Although virtually no research was conducted on polyphenols before 1995, since that time there has been a explosion of animal studies that have indicated their remarkable benefits as anti-oxidants and anti-inflammatory agents.

Upon deeper inspection, there is one group of polyphenols that seems to generate the most consistent health benefits. These are the delphinidins. Delphinidins are a subgroup of a family of polyphenols known as anthocyanidins. To make the story about delphinidins more intriguing, they are primarily found in blueberries. More specifically, the primary sources of delphinidins are the American blueberry, the Russian blueberry (i.e. bilberry), and the Patagonian blueberry (i.e. maqui berry). This is why the published clinical studies in humans seem to consistently involve blueberries. And the clinical data is impressive. Whether it is about reducing oxidized cholesterol or improving insulin resistance in patients with metabolic syndrome (1,2) or improving memory in patients with early dementia (3), the human data on the use of blueberries simply jumps out at you.

Since the active ingredient in each of these varieties of blueberries appears to be the delphinidins, then it is reasonable that the higher the levels of this particular polyphenol, the better the potential results. The Russian blueberry contains six times more delphinidins than American blueberries, and the Patagonia blueberry contains 14 times more delphinidins than the American blueberry. This probably reflects the harsher growing climates that other forms of blueberries are exposed to when compared to the American blueberry, which has become overly domesticated (making it richer in fructose and lower in delphinidins).

However, as with all natural products you have to take a therapeutic dose to get a therapeutic effect. You could measure this therapeutic threshold in terms of their anti-oxidative potential (measured in ORAC units) or the actual amounts of delphinidins themselves. It appears that for a blueberry extract to be effective requires that it provides at least 16,000 ORAC units per day. To put this in perspective, this level of ORAC units is equivalent to eating greater than 20-30 servings of vegetables on a daily basis.

But if the delphinidins are so important for the benefits of blueberries, isn’t it possible that the smaller amounts of the maqui berry might be even more beneficial because of its higher delphinidin concentration? That’s why we have several ongoing clinical trials to explore that potential. I will keep you informed as the results start coming in. Yet in the meantime, keep eating lots of those colorful carbohydrates just like your grandmother told you to eat.

1. Stull AJ, Cash KC, Johnson WD, Champagne CM, and Cefalu WT. “Bioactives in blueberries improve insulin sensitivity in obese, insulin-resistant men and women.” J Nutr 140: 1764-1768 (2010)
2. Basu A, Du M, Leyva MJ, Sanchez K, Betts NM, Wu M, Aston CE, and Lyons TJ. “Blueberries decrease cardiovascular risk factors in obese men and women with metabolic syndrome.” J Nutr 140: 1582 1588 (2010)
3. Krikorian R, Shidler MD, Nash TA, Kalt W, Vinqivst-Tymchuk R, Shukitt-Hale R, and Joseph JA. “Blueberry supplementation improves memory in older adults.” J Agric Food Chem 58: 3996-4000 (2010)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

A cash cow based on bad science

There has been no more profitable class of drugs than the cholesterol-lowering statins. Their success is based on a very simple premise: High cholesterol levels mean certain cardiovascular death. While there has always been questioning of the cholesterol story at the fringes of academic research (1), now the cries are rising within the highest reaches of the academic research community that something is just not right.

Since no one wants to die, you would think that measurement of mortality would be the primary clinical end-point for any clinical trial of a statin drug. There is no question that for people who have already had a heart attack, taking a statin prolongs their life by reducing all-cause mortality. But what about the people who have never had a heart attack but have high cholesterol levels? There the answer is much more open.

One recent article has studied all the published studies with some 65,000 patients who had high cholesterol but no evidence of heart disease to see the effect that statin drugs have on their mortality (2). The answer was virtually none. In fact, in all the statin trials published since 2005, there has been a striking lack of benefits in populations that simply had high cholesterol levels but no evidence of any cardiovascular disease (3). This is true except for one trial that was funded by a drug company that makes a new powerful, statin and run by the individual who has the patent for measuring C-reactive protein as a marker for cardiovascular risk (3).

Here was a new premise: People who had normal levels of cholesterol and no heart disease but high levels of C-reactive protein also need even more powerful statins. The fact that C-reactive protein is an unreliable marker in cardiovascular patients because it changes so quickly was conveniently ignored (4). Nonetheless a successful trial would generate more sales for the drug company and more testing of C-reactive protein for everyone going to see a physician.

So when a careful analysis of this “highly-successful” trial was published this year, it was found that there were no benefits in reducing cardiovascular mortality between the active and placebo groups (3). As the cholesterol story appears to have a growing number of flaws in it, I predict it will become more commonplace to have drug companies and medical researchers continue to use sleight-of-hand statistical dodges to make it appear their “wonder” drugs are actually doing wonderful things, like reducing death from heart disease in those who have no evidence of heart disease.

Maybe it’s time to return to a better working hypothesis of what really drives heart disease—inflammation and to use anti-inflammatory diets to prevent the occurrence of cardiovascular disease (5,6).


1. Ravnshov U. The Cholesterol Myths. New Trends Publishing. Warsaw, IN (2002)
2. Ray KK, Seshasai SRK, Erqou, S, Sever P, Jukema JW, Ford I, and Sattar N. “Statins and all-cause mortality in high-risk primary prevention.” Arch Intern Med 170: 1-024-1031 (2010)
3. De Lorgeril M, Salen P, Abramson J, Dodin S, Hamazaki T, Kotucki W, Okuyama H, Pavy B, and Rabaeus M. “Cholesterol lowering, cardiovascular diseases, and the rosuvastatin-JUPITER controversy.” Arch Intern Med 170 1032-1036 (2010)
4. Bogaty P, Brophy JM, Boyer L, Simard S, Joseph L, Bertrand F, and Dagenais GR. “Fluctuating inflammatory markers in patients with stable ischemic heart disease. Arch Intern Med 165: 221-226 (2005)

5. Sears B. “The Zone.” Regan Books. New York, NY (1995)
6. Sears B. “The Anti-Inflammation Zone.” Regan Books. New York, NY (2005)

Nothing contained in this blog is intend to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Aspirin…not just for heart disease

As I pointed in my first book, “The Zone,” more than 15 years ago, aspirin remains a wonder drug because of its ability to reduce inflammation (1). The medical community now uses aspirin for the prevention of strokes and heart attacks, but a recent study may extend its anti-inflammatory benefits to cancer survivors.

A study pre-published online from The Lancet examined various clinical trials comparing the long-term mortality of those individuals who used aspirin or didn’t (2). This meta-analysis study indicated that relatively low-dose aspirin (about 75 mg or a baby aspirin a day) reduced cancer deaths in various long-term cancer survivors by about 20 percent. So should all of us be taking a baby aspirin daily? Possibly, but aspirin does have side effects, especially in terms of bleeding.

But one thing you can do with total safety is to boost your intake of fruits and vegetables. It turns out that fruits and vegetables contain salicylates, the group of compounds that represents the major active ingredient in aspirin. In addition, fruits and vegetables also contain other anti-inflammatory polyphenols (the chemicals that give plants their color). Since plants don’t have access to the local pharmacy to protect themselves from microbial invasion, they have to synthesize their own “drugs”. By consuming fruits and vegetables, we are constantly visiting our “food” pharmacy. Their defense mechanisms now become our nutritional allies in silencing inflammatory gene expression that is turned on when certain food components (such as omega-6 and saturated fats) fool the most primitive part of the immune system (the innate immune system) to think it is under microbial attack.

Most of the inflammation that drives cardiovascular disease and cancer starts with this type of cellular inflammation induced by our diet (3). It’s taken new breakthroughs in molecular biology to finally understand that what’s good for the plant is also going to be great for us if we want to live a longer and better life.

1. Sears B. “The Zone.” Regan Books. New York, NY (1995)
2. Rothwell PM, Fowkes FG, Belch JF, Ogawa H, Warlow CP, and Meade TW. “Effects of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomized trials.” Lancet, Early Online Publication, 7 December (2010)
3. Sears B. “The Anti-Inflammation Zone.” Regan Books. New York, NY (2005)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Is there a link between inflammation, intelligence and death?

According to a recent study in Brain, Behavior, and Immunity, there appears to be a connection.  The study was based on data from a two-day nationwide survey conducted on 50,000 Swedish males 18-20 years of age in 1969-70 before they went into military service.  Blood samples were taken at that time to test for a general marker of inflammation known as ESR (erythrocyte sedimentation rate).  Although ESR is a very crude marker of inflammation, it was one of only a few available in the late ‘60s.  Then the blood samples were taken again 35 years later.  In their statistical analyses, the authors took into account a wide number of other variables, which may have influenced the results (socio-economic status, height, weight, blood pressure, smoking, etc.) and concluded that as inflammation (as measured by ESR) increased, there was a decline in IQ.  In addition, a higher level of inflammation at age 18–20 was significantly associated with an increased risk of mortality during a 35-year follow-up (1).  The results of the study show that even at an early age low-grade inflammation can significantly impact intelligence and premature death.

The underlying cause of chronic disease (and therefore early mortality) is increased cellular inflammation.  Likewise a drop in intelligence is usually an indication of an increase in dementia at an earlier age.  Dementia is also driven by cellular inflammation in the brain.   The most sensitive marker of cellular inflammation is the AA/EPA ratio in the blood.  Therefore it is not surprising that five years ago it was demonstrated the higher the AA/EPA ratio in the blood of elderly age-matched individuals, the greater their degree of their cognitive deficits (2).

The anti inflammatory diet was developed to reduce cellular inflammation and has been clinically validated to do exactly that (3,4).  So if you have a wish to live a longer and better life, then life-long control of cellular inflammation through the anti inflammatory diet makes perfect sense.  That’s why the anti inflammatory diet is not a diet but a way of life.

1.    Karlsson H, Ahlborg B, Dalman C, and Hemmingsson T.   “Association between erythrocyte sedimentation rate and IQ in Swedish males aged 18–20.” Brain, Behavior, and Immunity 24: 868–873 (2010)
2.    Conquer JA, Tierney MC, Zecevic J, Bettger WJ, and Fisher RH. “Fatty acid analysis of blood plasma of patients with Alzheimer’s disease, other types of dementia, and cognitive impairment.” Lipids 35:1305-1312 (2005)
3.    Pereira MA, Swain J, Goldfine AB, Rifai N, and Ludwig DS.  “Effects of a low glycemic-load diet on resting energy expenditure and heart disease risk factors during weight loss.” JAMA 292: 2482-2490 (2004)
4.    Johnston CS, Tjonn SL, Swan PD, White A, Hutchins H, and Sears B.  “Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.” Am J Clin Nutr 83: 1055-1061 (2006)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Ward off the common cold with exercise

There is nothing like fall in New England — the crisp air on your face, the changes in foliage and all the fun activities like apple and pumpkin picking.  Even though the calendar says the season lasts three months, the end of daylight savings in my mind signals the beginning of winter.  I think it’s the combination of the cold air and driving home in the dark that makes me feel this way.  With the change in season comes the rise in sniffles, sneezes and coughs; but before you run out for your supply of Vitamin C or the newest remedy to ward off a cold, you may want to look no further than your activity level.

According to the British Journal of Sports Medicine, individuals who reported five days or more of aerobic exercise per week compared to those who were sedentary (less than 1 day/week of activity) were 43 percent less likely to have an upper respiratory tract infection (URTI) (1).  The investigators studied 1,002 adults aged 18-85 over 12 weeks during the autumn and winter of 2008.  Individuals reported their aerobic level and used a 10-point scale to assess the level of physical fitness.

The authors took into account other factors that may have confounded the results (e.g., lifestyle, diet and stress) in their analyses.  In addition, they found that people’s perception of how fit they felt and the amount of activity performed lessened the severity of URTI and symptoms by 32-41 percent.

More intriguing is another recent paper (2) in which rats that like to exercise, were bred with similar exercise-loving rats for 11 generations.  These were compared to rats that didn’t like to run who were bred with other exercise-hating rats for 11 generations.  The super rats could not only run more distance than their coach potato cousins, but several groups of genes were up-regulated.

1).   D.C. Nieman, Henson D.A., Austin M.D et al. Upper respiratory tract infection is reduced in physically fit and active adults. Brit J Sports Med doi:10.1136/bjsm.2010.077875.

2)  R. Kivela, M. Silvennoinen, M. Lehit et al.  Gene expression centroids that link with low intrinsic exercise capacity and complex disease risk.  FESEB J 24: 4565-4574 (2010)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Don’t let those treats play tricks on your body

For those of you who celebrate Halloween, you know that the holiday isn’t contained to just one day. After the trick-or-treaters are gone and the costume parades are over, now you are have to deal with the leftover candy. Even though it’s tempting to just consume all of it and start fresh when it’s gone, this doesn’t fare well for your waist line. On the other hand, moderation may not work either. The thinking might be that it won’t hurt due to the treat’s small size and fewer calories. That sounds good until you consume four or five pieces in one sitting and feel the effects.

So what should you do? For those of you who know you can moderate your intake, try to limit your consumption to just a one or two pieces per day and after a few days or a week throw away the rest. I know this sounds wasteful, but your body will thank you. Try to have the candy at the end of a meal after you’ve consumed protein so that you can blunt the rise in blood sugar as much as possible and be less apt to go back for more.

To avoid temptation, put the candy in the freezer or on a very high shelf out of reach. The bigger issue is having to deal with your kids. Put a couple pieces in their healthful lunch and pack their lunch in the morning when you are less prone to start off your day with candy. If moderation is not your style, then simply throw it all away after Halloween passes or consider giving out healthy treats.

This is the time of year when people start the slippery slope of weight gain toward the New Year; so don’t let Halloween trick you into sabotaging your efforts before the holidays even begin.

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.