Credit: wallgiv.com

More Troubles with Sitting – and What Won’t Help

Written by Dr. Ralph E. Carson on . Posted in Blog, Exercise, From the Desk of Dr. Carson

In his first of two articles, Dr. Carson presented evidence showing that sitting for long, uninterrupted periods has serious health risks. And he followed that with some techniques for mitigating or avoiding those risks. Here is a brief addendum to underscore both the risks and the ways to counteract too much sitting.

 Troubles with Sitting – Orthopedic Health Problems attributed to too much sitting

(Mathews ’12; Ford ’12; Berkowitz; Hamilton ’07; George ‘13)

Muscle degeneration (Back problems)too-much-sitting-back-pain

  • Slumped muscles go unused — tight back and weak abdominal muscles combined to cause serious back pain due to extreme lower curvature (lordosis)
  • Sore back: inflexible spine movement causes soft disc dehydrated and brittle. This can lead to a herniated disc. Typically the disc between vertebrae expand and contract like a sponge soaking up fresh blood and nutrients with activity.
  • Collagen hardens around supporting tendons and ligaments with extended inactivity

Tight hips: decreased hip mobility due to tight hip flexors (short and tight) limit range of motion and produce falls

Limp gluts (buttocks): hurt stability and stride

Strained neck: Craning neck forward over key board or tilting head to cradle phone

Sore Shoulders

Soft bones: Weight bearing exercises cause bone to grow thicker and lack thereof causes osteoporosis

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Sitting can reduce life expectancy

Standing could increase your life span. The more time on your feet strengthens the bits of DNA called telomeres (Sjogren ’14). Telomeres protect the ends of chromosomes (like the tips that keep shoelaces from fraying). Telomeres tend to get shorter and shorter until they can shorten anymore and cause cell death.

Women who spend too much time sitting around (>11 hours/d) had a 12% risk of premature death (13% more cardiovascular disease; 21% more cancer; 27% more coronary artery disease) than those who were inactive for <4 hours (Sequin ’14).

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Can scheduled exercise sessions offset the negative effects of sitting?

Adults spend 50% – 70% of their waking hours sitting or approximately 8 hours per day. Sitting for extended periods of time can harm even those that exercise (Craft ’12; Wilmot ’12). The increased risk of sitting is not offset by moderate to vigorous exercise or meeting the recommended physical guidelines. Regular exercise does not reduce the risk of an otherwise sedentary life style as one remains susceptible to just as great a risk of diabetes, cardiovascular disease, obesity and premature death. Short but frequent walks or alternative activity sparks (short term episodes of movement lasting 5 – 10 minutes) can counteract the harm caused by sitting long periods.

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References

Craft LL et al Evidence that women meeting physical activity guidelines do not sit less: An observational inclinometry study Int J Behav Nutr Phys Act (2012) 9: 122.

Ford ES and Caspersen CJ Sedentary behaviour and cardiovascular disease: a review of prospective studies Int J Epidemiol (2012) 41: 1338 – 1353.

George ES et al Chronic disease and sitting time in middle-aged Australian males: findings from the 45 and Up Study Int J Behav Nutr Phys Act (2013) 10:20.

Hamilton MT et al Role of Low Energy Expenditure and Sitting in Obesity, Metabolic Syndrome, Type 2 Diabetes, and Cardiovascular Disease Diabetes (2007) 56: 2655 – 2667.

Matthews CE et al Amount of time spent in sedentary behaviors and cause-specific mortality in US adults AJCN (2012) 95: 437 – 445.

Sjogren P et al Stand up for health–avoiding sedentary behaviour might lengthen your telomeres: secondary outcomes from a physical activity RCT in older people Br J Sports Med (2014) 48: 1407 – 1409.

Wilmot EG et al Sedentary time in adults and the association with diabetes, cardiovascular disease and death: systematic review and meta-analysis Dibaetologia (2012) 55: 2895 – 2905.

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15 Tricks to Avoid Sitting Risks

Written by Dr. Ralph E. Carson on . Posted in Blog, Exercise, From the Desk of Dr. Carson

Don’t just sit theretry these

(Ekblom-Bak ’12; Loprinzi ’13; Yancy ’10; Healy ’08)

Last week, we learned of many possible health risks caused by habitual, uninterrupted sitting over long periods. Since it’s not how much but how often you exercise that matters, you can counteract the harmful effects of sitting with small lifestyle adjustments. The following activities may do just as much good as formal exercise to reduce chronic disease such as heart attacks, stroke, cancer, and diabetes (Ekblom-Bak ‘13).

An active lifestyle is an effective way to provide health benefits such as preventing high blood pressure, high cholesterol, and metabolic syndrome. Despite not exercising according to the recommendations, as many as 40% of adults may be achieving the exercise guidelines by making movement part of their life (Loprinzi ’13).

If your lifestyle requires a lot of sitting, try breaking up the stasis with some of these healthy movement activities:

  1. Standing with computer on top of the filing cabinet
  2. Sitting on exercise (stability) ball instead of desk chair
  3. Dance about, wiggle around, take a few steps back and forth, fidget
  4. Standing during meetings
  5. Standing talking on the telephone
  6. Walking during lunch breaks
  7. Gardening and lawn care
  8. Housework (vacuuming and mopping floors)
  9. Stand folding laundry or ironing
  10. Do-it-yourself projects
  11. Marching in place during TV commercials
  12. Getting up from your desk and doing jumping jacks, knee lifts and bends
  13. Purchase an activity monitor
  14. Set a timer for to go off once per hour
  15. Move printer farther away
  16. Sit up straight
  17. Take water breaks
Photocredit: Cat York, from "Get up and Stretch"

Photocredit: Cat York, from “Get up and Stretch”

References

Ekblom-Bak E et al The importance of non-exercise physical activity for cardiovascular health and longevity Br J Sports Med (2013) 092038.

Healy GN et al Breaks in sedentary time: beneficial associations with metabolic risk Diabetes Care (2008) 31: 661 – 666.

Loprinzi PD and Cardinal BJ Association between biologic outcomes and objectively measured physical activity accumulated in ≥ 10-minute bouts and <10-minute bouts Am J Health Promotion (2013) 27: 143 – 151.

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Love at Three G’s

Written by Marianne Messina on . Posted in Blog, Etc

Three Tips to the Lovelorn from FitRx Therapist Jonathan Rios

“Envy is the art of counting the other fellow’s blessings instead of your own.” – Harold Coffin

For many, the month around Valentine’s Day is a reminder of lost loves, longing for love, or even love not yet experienced. We can all agree, ours is a culture obsessed with fairy tale lovers and happily ever afters.

When these expectations aren’t met, our hearts are easily wounded. Those of us who don’t have a current love often turn to thoughts of our “lack” and become intensely critical of love itself. In fact, we may even find ourselves bitter towards those around us who seem to have found that “true love.” Does this sound like you?

Photo Credit: Photolibrary.com

Photo Credit: Photolibrary.com

How about any of these:

  • Are you unable to be happy for the love others have found?
  • Is it hard to congratulate others on their relationships?
  • Do you secretly rejoice when others experience heartbreak?

If you found yourself answering even the tiniest “yes,” let these three g’s help you avoid the trap of becoming embittered:

Gratitude – Write down all the romantic and platonic relationships (past and current) that have been a blessing in your life. (What lessons did you learn about yourself?). Instead of meditating on all the “misfires” and “heartache,” flip your focus to that of thanksgiving.

Generosity – Realize there’s someone in your immediate community who is “heartbroken” this year and could use a dose of love themselves. (Get the focus off of you and onto others.) Bring them a gift. Offer to babysit. Write them a note. Take them out for dinner. Actually verbalize how important they are to you.

Grace – Give yourself an unmerited treat. See a movie that inspires you. Spend time with people who care about you. Watch YouTube clips of your favorite comedian.  Visit your favorite museum. Go hiking. Go on a road trip. Call out sick. Declare a “self-enrichment day.”

It’s virtually impossible to be both jealous and grateful at the same time. Our internal world is one of constant tensions and we must do the hard work of choosing which thoughts and emotions will steer the ship.

This month of Valentine’s, I implore you to choose love in the truest sense by loving yourself and giving yourself away to the people around you. Someone nearby needs what you have to offer.

Credit: wallgiv.com

The Trouble with Sitting

Written by Dr. Ralph E. Carson on . Posted in Blog, Exercise, From the Desk of Dr. Carson

Are you doing too much sitting?
Metabolic Health problems attributed to “too much sitting”

 The last few years have seen a good bit of research showing health risks associated with “too much sitting,” where “too much” suggests periods of more than an hour at a time. For better or worse, here’s a list of the bodily systems found to be compromised by “too much sitting.”

Heart Disease:

  • Blood pools in legs because muscles are not contracting and pumping blood effectively
    • Impairment of endothelia function (inability of arteries to expand). Endothelia function is reduced by over 50% with just one hour of sitting (Thosar ’14).
    • Men who walked 5 minutes per hour had no reduction in function of arteries during a 3-hour period
  • Blood flows more sluggishly during a long period of sitting allowing fatty acids to more easily clog the heart
  • Linked to high blood pressure
  • Linked to high cholesterol
  • Twice as likely to have cardiovascular disease
  • Older men who spend a great deal of time sitting are more than twice as likely to face heart failure even for those who exercise regularly (Young ’14)
  • Men reporting 24 hours per week of sedentary activity have a 64% greater risk of dying from heart disease than those who were inactive < 11 hours per week (Blair ’11)

Metabolic Syndrome (Bey ’03)

  • Decrease in lipoprotein lipase (LPL) in skeletal muscle explains poor lipid metabolism and metabolic syndrome
  • Riding in cars and watching TV are significant predictors of metabolic syndrome (High BP, high triglycerides, High cholesterol, high blood sugar and excess belly fat) (Warren ’10)

Diabetes (Over productive pancreas)

credit: wellbeingmagazine.co.uk

credit: wellbeingmagazine.co.uk

  • Most consistent association of sitting and diabetes (Wilmot ’12)
  • Three (15 minute) bouts of moderate post meal (30 minutes after meal) walking significantly improved 24 hour blood sugar control in older people at risk of impaired glucose tolerance (DiPietro ’13)
  • Interrupting sitting time by walking lowers post prandial (after meal) glucose and insulin levels in overweight and obese (Dunstan ’12)
  • Cells in sedentary muscles do not respond readily to insulin – pancreas as a result has to produce more insulin
  • Decreases in insulin response were seen just one day of prolonged sitting (Stephens ’11)

Cancer (Schmid ‘14b; Zhang ’14)

  • Colon cancer (Schmid ‘14a)
  • Breast cancer
  • Endometrial cancer
  • Excess insulin encourages cell growth
  • Movement boosts natural anti-oxidants that scavenge and destroy cell damaging free radicals

Poor circulation in legs

  • Fluid pools, swollen ankles, varicose veins, and deep vein thrombosis (DVT)

Larger waistline

  • Burn 6x fewer calories
  • Risk of inflammation (due to visceral abdominal fat) which can result in heart disease, diabetes and metabolic syndrome
  • Each hour of daily sitting was associated with 2.39 cm of pericardial fat (fat collecting around the heart) and explains the high incidence of coronary heart disease. This pericardial fat stayed in place even when undertaking exercise (Larsen ’14)

Foggy brain

  • Circulation triggers release of cognitive and mood enhancing chemicals

Next: 15 Ways to Counteract Too Much Sitting


References

Bey L and Hamilton MT Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity: a molecular reason to maintain daily low-intensity activity J Physiology (2003) 551: 673 – 682.

Blair S Sitting All Day Is Worse For You Than You Might Think: NPR (April 25, 2011).

DiPietro L et al Three 15-min bouts of moderate post-meal walking significantly improves 24-h glycemic control in older people at risk for impaired glucose tolerance Diabetes Care (2013) 36: 3262 – 3268.

Dunstan DW et al Breaking up prolonged sitting reduces postprandial glucose and insulin responses Diabetes Care (2012) 35: 976 – 983.

Ford ES and Caspersen CJ Sedentary behaviour and cardiovascular disease: a review of prospective studies Int J Epidemiol (2012) 41: 1338 – 1353.

George ES et al Chronic disease and sitting time in middle-aged Australian males: findings from the 45 and Up Study Int J Behav Nutr Phys Act (2013) 10:20.

Hamilton MT et al Role of Low Energy Expenditure and Sitting in Obesity, Metabolic Syndrome, Type 2 Diabetes, and Cardiovascular Disease Diabetes (2007) 56: 2655 – 2667.

Hamilton MT et al Too Little Exercise and Too Much Sitting: Inactivity Physiology and the Need for New Recommendations on Sedentary Behavior Curr Cardiovasc Risk Rep (2008) 2: 292 – 298.

Larsen BA et al Associations of Physical Activity and Sedentary Behavior with Regional Fat Deposition Med Sc Sports Exerc (2014) 46: 520 – 528.

Matthews CE et al Amount of time spent in sedentary behaviors and cause-specific mortality in US adults AJCN (2012) 95: 437 – 445.

Schmid D and Colditz G Sedentary behavior increases the risk of certain cancers J Natl Cancer Inst (2014b) 106 (7): dju206.

Stephens BR et al Effects of 1 day of inactivity on insulin action in healthy men and women: interaction with energy intake Metabolism (2011) 60: 941 – 949.

Thosar SS et al Effect of Prolonged Sitting and Breaks in Sitting Time on Endothelial Function Med Sci Sports Exerc (2014, Aug 18).

Warren TY et al Sedentary behavior increase risk of cardiovascular disease mortality in men Med Sci Sports Exerc (2010) 42: 879 – 885.

Wilmot EG et al Sedentary time in adults and the association with diabetes, cardiovascular disease and death: systematic review and meta-analysis Dibaetologia (2012) 55: 2895 – 2905.

Young DR et al Effects of physical activity and sedentary time on the risk of heart failure Circulation: Heart Failure (2014) 7: 21 – 27.

Orbital frontal cortex (OFC)

FDA-approved “Gastric Pacemaker” – What do the studies say?

Written by Dr. Ralph E. Carson on . Posted in Blog, From the Desk of Dr. Carson

For many years, gastric electrical stimulation (GES) has been under investigation as a treatment for obesity and overeating, but until last week, it has only been experimental. After 12 years, the FDA finally approved EnteroMedics device for treatment of obesity, making it the first “gastric pacemaker” to be approved for obesity treatment.

About the size of a pacemaker and implanted into the person’s abdomen, the EnteroMedics’ Maestro™ device is intended to offer potential weight loss for those struggling with obesity. Called VBLOC™ for vagal blocking therapy, its electrode touches the vagus nerve at a point between the esophagus and the stomach, and it works by intermittently down-regulating or blocking input from the stomach’s vagal nerve to part of the brain linked to appetite in people who have issues with obesity and metabolism.

Historically, the independent research of such devices has not been earth shattering. Both SBU (’04) and Buchwald (’02) felt that the results were not conclusive and that EGS did not provide satisfactory results. This discouraged them from carrying on with the study (Salvi ’09).

In a 2009 study, Shikora et al compared implantable gastric stimulation therapy to a standard diet and therapy regimen. Within their group of obese subjects, the team evaluated differences in weight loss and found that the control group lost 11.7% and the IGS group also lost 17.6% of excess body weight. The difference in results between the two groups was less than a high recommendation of the treatment.

In a more recent study, after 12 months with the EnteroMedics device, those with the device fitted lost an average of 24 per cent of their excess weight, while those in the control group without the device fitted lost only 16 per cent. The device produced an overall difference in total body weight of only 3% over the sham device, which did nothing (Ikamuddin’14). Therefore, though there was certainly clinically significant weight loss with this device, the procedure fell short of being as effective as the researchers had hoped.

Repeated evidenced-based failures to support the “stomach fullness theory” suggest seeking alternative signals to relay cessation of eating. This adds credibility to the idea that the primary feedback may be dictated by satisfaction rather than fullness. This suggests placing more emphasis on hedonic (pleasure) messages in research and potential therapy.

While this FDA approval may show some promise, who will it work for, what will it work with?

There are still several important under-researched questions to consider coming out of the trials to date:

  • How useful is it to rely solely on stomach hunger and fullness to create eating cessation? (Ikamuddin’14)
  • How will gastric stimulation stack up in more comprehensive comparisons to other treatments – such as diet, behavioral therapy, exercise? (Ikamuddin ’14; Dixon ’11).
  • We should be looking at response systems other than fullness, such as hedonic (pleasure) messages, for which treatment would be entirely different, less invasive, and possibly more long-lasting.
  • Cross-study between the medical mechanisms of obesity and the psychological/behavioral components is needed for optimum diagnoses – that is, which patients will benefit from which treatments – surgical, pharmaceutical, psychotherapeutic, and implant – or treatment combinations.

References:

Buchwald H and Buchwald JN Evolution of operative procedures for the management of morbid obesity 1950-2000 Obes Surg (2002) 12: 705 – 717.

Salvi PF et al Gastric pacing to treat morbid obesity: Two years’ experience in four patients Ann Ital Chir (2009) 80: 25 – 28.

Shikora SA et al Implantable gastric stimulation for the treatment of clinically severe obesity: Results of the SHAPE trial Surg Obes Relat Dis (2009) 5: 31 – 37.

Swedish Council on Technology Assessment in Healthcare (SBU)n Gastric pacing (gastric electrical stimulation) for the treatment of obesity — early assessment briefs (Alert) Stockholm, Sweden: SBU (2004).

Yao S et al Retrograde gastric pacing reduces food intake and delays gastric emptying in humans: A potential therapy for obesity? Dig Dis Sci (2005) 50: 1569 – 1575.

Dixon JB et al Surgical approaches to the treatment of obesity Nature Reviews Gastroenterology and Hepatology (2011) : 429 – 437.

Ikamuddin S et al Effect of reversible intermittent intra-abdominal vagal nerve blockade on morbid obesity: the ReCharge randomized clinical trial JAMA (2014) 312: 915 – 922 [VBLOC-DM2 ENABLE Trial].

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Why stress can make you fatter around the middle

Written by Dr. Ralph E. Carson on . Posted in Blog, Etc, From the Desk of Dr. Carson

As we have been seeing, those struggling with obesity are beset by many vicious cycles of fat begets fat. This self-fueling problem explains why only a slow, steady approach, accompanied by lifestyle changes that carry through the long haul, is the best solution. Another way that fat begets fat occurs in the area of belly fat. Studies paint an interesting picture on the nature of belly fat – its composition, and how it responds to stress, alcohol, fried foods, and processed foods, and how it increases. These studies shed light on why certain behaviors add to belly fat.

There are two different types of fat stores, the fat that forms a layer beneath the skin (called subcutaneous adipose tissue – SCAT), and fat that forms an apron around the belly, visceral belly fat. Within the body, and as a response to what you do on the outside (eat, exercise, undergo stress), these two types of fats act in very different ways. Subcutaneous fat can be exercised away much more easily than belly fat. This visceral belly fat receives more blood flow and is more responsive to cortisol than the subcutaneous fat deposited around the waist (beneath the skin).

The abdominal fat cell environment contains more nerves, more inflammatory and immune cells, has more testosterone (androgen) receptors, and produces a greater percentage of large fat cells (as opposed to greater numbers). It’s a lively, responsive cauldron of activity. As a consequence, intra-abdominal fat cells are more metabolically active, absorb and store more dietary fatty acids from circulation, and are less inclined to release fat during dieting (Ibrahim ’10).

The absorptive nature of belly fat is quite significant because these absorptive properties make belly fat more responsive to cortisol – the stress hormone. Stress increases the enzyme (11beta-HSD-1) that regulates cortisol in the belly.

What this means to the dieter, the average person watching his or her waist, is that when you add stress to excess belly fat, you get a chain reaction in which the 11beta-HSD-1 enzyme speeds up the conversion of inactive cortisone to active cortisol. And enough studies have shown that the over-expression of 11beta-HSD-1 in belly fat tissue results in a host of problems, not the least of which is more fat. The problems include an amazing fourfold cortisol receptor increase (greater sensitivity to cortisol), insulin resistance (glucose intolerance or the inability to utilize sugar appropriately) and central obesity (Kannisto ’04; Anderson ’02; Morris ’05).

Since the enzyme activity is higher in belly fat than subcutaneous fat, it explains how stress significantly increases girth (Tomlinson ’02).

It’s important to know what behaviors tend towards the creation of belly fat. And not just from the perspective of a waist watcher. We’ve also seen studies that connect belly fat to learning, memory, and decision-making.

For more (graphic view):


References

Andrews RC et al Abnormal cortisol metabolism and tissue sensitivity to cortisol in patients with glucose intolerance The Journal of Clinical Endocrinology (2002) 87: 5587 – 5593.

Ibrahim MM Subcutaneous and visceral adipose tissue: Structural and functional differences Obesity Reviews (2010) 11: 11 – 18.

Johnstone AM et al Influence of short-term dietary weight loss on cortisol secretion and metabolism in obese men Eur J Endocrinol (2004) 150: 185 – 194.

Kannisto K et al Overexpression of 11 beta-hydroxysteroid dehydrogenase-1 in adipose tissue is associated with acquired obesity and features of insulin resistance: studies in young adult monozygotic twins J Clin Encocrinol Metab (2004) 89: 4414 – 1421.

Morris KL and MB Zemel ,25-dihydroxyvitamin D3 modulation of adipocyte glucocorticoid function Obesity Research (2005) 13: 670 – 677.

Tomlinson JW and PM Stewart The functional consequences of 11-beta hydroxysteroid dehydrogenase expression in adipose tissue Hormone and Metabolism Research (2002) 34: 746 – 751.

White PC et al 11 beta hydroxysteroid dehydrogenase and its role in syndrome of apparent mineralcocoricoid excess Pediatri Res (1997) 41: 25 – 29.

Diet is not the solution!

Written by Dr. Ralph E. Carson on . Posted in Blog, From the Desk of Dr. Carson

48 clinical trials attest; diet is not the solution.

For the umpteenth time, researchers have published proof that no matter what diet a person chooses (Paleo, Wheat Belly, Atkins, Weight Watchers, Jenny Craig, NutraSystem, etc.), the chances for success are the same. Whether the plan focuses on low fat or low carbohydrate, the study, involving 48 clinical trials and 7000 patients, resulted in an average weight loss of 18 pounds over 6 months. From one diet program to another, the differences were minimal. Basically, the difference between Jenny Craig, Atkins, NutraSystem, and you name it, was not enough to matter. Among scientists, the study was confirming, leading scientists to conclude that there is nothing magical about cutting carbohydrates or fat or adding protein.

These findings are not particularly new, but with every new fad diet that bursts on the scene, there’s an implicit challenge to the conclusion. The more interesting and persistent question is why test subjects in the reviewed studies had begun to gain weight back by the one-year mark – to wit, in all 48 trials, the participants started gaining weight back by one year. This caused the authors of the study to call out the true challenge for diet research: the need to understand how people can maintain their initial weight losses.

A total mind-body-spirit solution

A total mind-body-spirit solution

The authors reached an obvious conclusion, that the best dietary plan is one you can live with for a long time (i.e. the rest of your life).

The long view should be considered when comparing ways to lose weight and gain health. Considering the long view means choosing an approach that gives you the fewest challenges. And though the medical community often focuses on shedding pounds as a goal-oriented metric for improving health among the the obese, the root of the problem is rarely found in weight loss and weight control. FitRx focuses on health and well-being rather than the number of pounds. We consider the gold standard for longevity is an approach that offers encouragement and insight on attuned eating, healthy choices, image empowerment, physical wellness, joyful movement, mindfulness, and stress reduction.


References:

Johnston BC et al Comparison of weight loss among named diet programs in overweight and obese adults: a meta-analysis JAMA (2014) 312: 923 – 933.
Van Horn L et al Diet by any other name is still about energy JAMA (2014) 312: 900 -901.

Am I hungry or just not full?

Pleasure Overrides “Fullness”

Written by Dr. Ralph E. Carson on . Posted in Blog, From the Desk of Dr. Carson

Hedonics trump homeostasis

There is a belief that tuning into physical and mental “fullness” signals, when eating, will decrease the likelihood of mindless over-consumption. However, “research is continually finding that regardless of how full a person may feel, the body is hard wired to chemically reward itself by overeating” when faced with highly palatable foods (*Monteleone ’12).  Two gut compounds are credited with causing us to indulge in goodies well beyond the point of caloric need. One of these is a stomach hormone called ghrelin, which helps regulate the motivation and drive to eat as well as the capacity to experience reward or pleasure.

The other is the endocannabinoid 2-AG (2-arachidonoylglycerol) which is involved also with appetite and drive to eat. When a person wants a particular kind of food, these chemicals team up to override the sense of fullness. In other words, we are programmed to stuff ourselves for a rainy day. In one study, individuals originally planned to eat significantly more of their favorite food, than they planned to eat of a bland or unappetizing selection, despite the feeling of being satiated. When participants ate their favorite food, their blood levels of ghrelin increased significantly and stayed high for as much as two hours post-ingestion. (*Monteleone ’12)

BrainFix-DrRalphCarson

“The plasma levels of ghrelin and 2-AG increased during hedonic eating, with the favorite foods, but not with non-hedonic eating,” Science Daily said of Monteleone’s work.

After eating an unappetizing nutritionally equivalent item, the ghrelin levels went progressively down. Levels of the compound 2-AG decreased after eating both the favorite and the unappetizing food. However, exposure to and consumption of a favorite food allowed 2-AG levels to remain higher for up to two hours compared to the non-favorite food.

Many treatments for obesity attempt to curb eating by recreating the feeling of fullness, either mechanically or surgically. But the work of Monteleone and Mozes suggests that in dealing with binge eating behavior, a focus on the hedonic (pleasure-center driven) response will be more efficacious than a focus on “fullness.” (Monteleone ’12; Mozes ’12)

At FitRx, we use the technique of “attuned eating,” which approaches the problem from the angle of meal satisfaction rather than fullness. The distinction between these two hypotheses is important when looking at treatment facilities because they result in different treatment approaches.

Next time: Highly palatable foods trigger continuation of eating whether or not one is full or recently finished a meal.


References:

*Monteleone P et al Mozes A Why You Overeat Even When You’re Full: Small study explores how body reacts when aroused by tempting treats HealthDay: A Pilot Study Journal of Clinical Endocrinology and Metabolism (2012) 97(6):E917-24.

Mozes A Why You Overeat Even When You’re Full: Small study explores how body reacts when aroused by tempting treats HealthDay (May 3, 2012).

obesity begets obesity

Obesity Begets Obesity

Written by Dr. Ralph E. Carson on . Posted in Blog, From the Desk of Dr. Carson

Caught in a Vicious Cycle

People who struggle with size have high levels of leptin, the “satiety hormone.” But at the same time, they are leptin resistant. When functioning correctly, leptin will promote production of the appetite suppressant α-MSH after a meal. This is how the average person knows they are full and stops eating. In those struggling with obesity, there’s an abundance of leptin, which originates from large fat cells. And yet it has been found, counterintuitively, that this over-abundance of leptin does not produce an abundance of the α-MSH needed to increase metabolism and lower appetite. Essentially, these obese individuals lack a proper leptin response after a meal. There is no suppression of food-seeking behavior and no increase in TSH, which increases metabolism and therefore spurs caloric burning.

In a sense, there are so many leptin signals the brain shuts down to them. But for the more accurate picture of this disruption of healthy processing, we begin by looking at PC2, an enzyme necessary for making POMC, which eventually converts into α-MSH (to increase metabolism and lower hunger). The leptin overload in people of size stresses the POMC’s nucleic endoplasmic reticulum serving as the assembly line for making PC2. By mishandling PC2, the POMC protein leaves the POMC nucleus unfolded (useless and needing to be discarded) and impairs α-MSH production. Some people of size are 53% lower in PC2 and have 50% less α-MSH.

Vicious cycle of obesity

Vicious cycle of obesity

Any way you look at it, the normal feedback system is impaired in people of size, and it disrupts the body’s mechanism for maintaining one’s natural weight. What this means for obesity programs: Leptin should work to keep us at our natural weight. With leptin resistance that often occurs in people of size, the leptin is unable to tell the brain to eat less and burn more calories. As a result, the buildup of excess leptin stresses the manufacturing of the messenger that tells u, s to eat less and produces one that is useless. There is then no message to tell us to stop eating and/or increase activity. The result is that excess fat continues to accumulate as a consequence of gaining weight. To put it simply: “obesity begets obesity.”

At some point a simple solution to the leptin issue was sought in TUDCA (Tauroursodeoxycholic Acid), a chemical that eliminates ER stress and increases α-MSH in obese mice, but not normal mice. However, TUDCA is not readily applicable in treating excess fat in people of size. So while the leptin issue can be addressed, the most workable solution to date is programmatic and diet-related as opposed to organ or site-specific and treatable with a pill or procedure.

A total dietary program would include things like cutting out the fructose, the processed foods, the refined and simple starches, and adding things like oily fish, whole grains, etc. Once again, the evidence supports a whole-system or global approach to obesity. It also suggests the need to address complex dietary interactions, rather than narrowing in on simplistic solutions such as “portion control” or “calorie control.”

Next Week: Pleasure Overrides Fullness; Hedonics Trump Homeostasis


References:

Cakir I et al Obesity induces hypothalamic endoplasmic reticulum stress and impairs proopiomelanocortin (POMC) post-translational processing J Biol Chem (2013) 288: 17675 – 17688.

How Diet & Hygiene Alter Gut Microbiota, Influence Our Health

The “Healthy Choice” Food Plan

Written by Dr. Ralph E. Carson on . Posted in Blog, From the Desk of Dr. Carson

Retrain the brain to stop craving food

As humans, we do not start out loving French fries, potato chips and Oreos and hating whole wheat pasta, raw vegetables, and grilled salmon. It took years of consuming highly palatable recipes (high fat, high sugar, and high salt) to establish these unhealthy brain circuits. The good news is, the brain is mutable, and you can retrain it to stop craving calorically dense, unhealthy impulse foods. The even better news is that you can do this in a matter of months. By making healthy choices, even the brain with years of bad food training can be rewired in six months. In fact, studies report seeing some changes in as early as 2 weeks.

In a Tufts University study, scientists imaged (fMRI) obese individuals’ brains at the beginning of the study and again six months later. While the subjects observed pictures of healthy and unhealthy foods, the researchers noted activity in the reward centers of their brains. On initial screening, the reward center sparked activity only after highly palatable foods were viewed. This was true for all participants. In the ensuing months, the group was divided in half, with the control group eating whatever it wanted and the Healthy Food Choice group working with brain retraining.

Six months later, brain images of the group in the Healthy Food Choice program demonstrated activity in the reward center when they saw healthy, low calorie foods. The brain circuitry had changed. Conversely, that same area now also showed decreased sensitivity to unhealthy, high caloric foods.

This is excellent news for those who, due to long-standing habits of sugar or fat consumption, may feel daunted by the idea of retraining their food choices.

The Tufts study showed a clear delineation all around between those who received the Healthy Choice retraining and those who didn’t. Over the six-month period, people on the Healthy Choice plan lost 14 pounds, and those who continued to eat solely what they desired gained 5 pounds.

This study lays the groundwork for comprehensive programs in the treatment of obesity (such as the FitRx program) that include brain retraining along with exercise and the other components. Healthy Choice brain retraining could turn out to be simpler and more long-lasting than many of today’s popular, but desperate, measures.

For example, the healthy choice group outperforms those on restrictive diets because deprivation sets the restricted individuals up to feel hungry and miss eating their favorite foods. Unconsciously, the fat-sugar-salt-trained brain tells the individual not to continue restriction. Eventually, the individual gives in to these messages and returns to old ways.

Another drastic measure, gastric bypass surgery, generally decreases the amount of enjoyment the person derives from food. While this invasive procedure works, it works by a sort of forced deprivation. Taking away food enjoyment becomes pretty hard to justify when you can make healthier food more appealing through brain retraining, leave intact the individual’s ability to savor food, and avoid an invasive (and costly) procedure all at the same time.

Next week: Caught in a Vicious Cycle: Obesity Begets Obesity


References:

Deckersbach T et al Pilot randomized trial demonstrating reversal of obesity-related abnormalities in reward system responsivity to food cues with a behavioral intervention Nutr Diabetes (2013) 4:e129.