The no "BS" FAT LOSS thread!!!
ninerbuff
Posts: 48,984 Member
I will post some of the latest studies on fat loss along with the sources just to keep people in the loop. Many of the articles are studies with sources by many different people and organizations. The point of this is to help people to understand that there is actual science on how the body does lose fat.
Most the articles will be long just so you know up front.
Sleep your way to fat loss
Weight-loss gurus on television advise “exercise more” and “eat less,” as though these statements should have been included in the original 10 Commandments. There is a principle in logic called ‘Ockham’s Razor,’ which tells us that the simplest solution is usually the correct one. Well, what could be simpler than exercise more, eat less? Unfortunately, even Ockham’s Razor is not that simple. Friar William of Ockham stated that when making a choice, any assumptions that do not make a difference should be excluded; however, it is vital to include assumptions that are relevant.
Step away from the high-tech world of liposuction, gastric bypass, appetite suppressants, thermogenic and lipolytic drugs; the human body adapts to its environment. At the most basic level, that includes the amount of food available, the amount of activity needed to acquire that food, and the amount of rest one can obtain before needing to forage again.
Sleep is an under-appreciated need in American society. In fact, society often rewards individuals who forego sleep in order to work longer hours, party harder, watch adult entertainment and enjoy the ‘night life.’ People go to great lengths to eradicate the need for sleep. It is not just post-adolescent ravers taking methamphetamines and ecstasy to prolong nights of hedonism; the ranks of the sleep-deprived are filled with students and professors using Adderall® to allow for academic all-nighters; physicians and nurses using Provigil® to stay sharp during careers of extended hours; policemen and power plant workers walk the health store aisles looking for energy supplements that will get them through rotating shifts; children guzzle Red Bull® to pwn [sic] friends and strangers through early morning online gaming; and mothers brew coffee every morning to meet the demands of family.1-5
Prior to the information age, most jobs were labor or service related; social norms were more conservative and people were praised for being practical, not outrageous or risk-taking. One popular axiom was “Early to bed, early to rise, makes a man healthy, wealthy and wise.” These observations would suggest that previous generations may have actually hibernated. In fact, sleep patterns were not overly different from today, on a day-to-day basis. Of course, leisure time has been extended and the introduction of electric lighting and varied forms of entertainment remove many of the cues that would normally send one to sleep. Most conventioneers can attest to the temporal (time) confusion experienced inside the casinos of Las Vegas where fluorescent lights and the absence of clocks mask the passage of time.
Nonetheless, there has been an overall trend toward sleep deficit. In comparison to several decades ago, Americans are sleeping, on average, 90 minutes less per night.6 An hour or two makes little difference in the short-term, but over time, a chronic sleep deficit dramatically affects one’s health. A number of studies have shown that sleep deprivation results in reduced cognitive function (thinking), hormonal changes, negative changes in blood pressure, worsened insulin sensitivity, etc.7-9
In fact, during the recent daylight savings time-related time change, news channels reported the findings of a 2008 Swedish study published in the New England Journal of Medicine, showing that the risk of a heart attack increases 5 percent during the three days immediately following the ‘spring forward’ change that results in the loss of an hour’s sleep for most. Conversely, there was a smaller reduction in risk during the three days following the ‘fall back’ that gifts an extra hour of sleep. The authors posited that the increase in heart attacks following the loss of an hour of sleep was due to an increase in sympathetic tone (adrenalin) and a pro-inflammatory state.10 These factors are already elevated in the obese, making the time change very risky in this group.11 Perhaps it is time for the FDA to review daylight savings time.
Sleep Deprivation and Obesity
Sleep deprivation does not just increase risks associated with obesity, but it also increases the risk of obesity. Several studies have associated sleep deprivation with obesity, as well as the Metabolic Syndrome, which includes negative changes to cardiovascular health and insulin sensitivity, and changes in hormones that promote fat storage.12 Even as this article is being written, new studies are linking sleep deprivation with poor health. Research is being presented at the American Heart Association, reporting an increase in the risk of developing type II diabetes in people who sleep less than 6 hours per night, compared to those who sleep 6 to 8 hours.13
Is there more to the inverse association between sleep loss and weight loss than metabolic and hormonal changes? Could the increased number of waking hours somehow relate to foraging behavior as well? After all, except for the rare case of somnambulist bingers (those who sleepwalk to the refrigerator to eat), people don’t break their diet while they are asleep.14
Researchers investigated the effect of shorter daily sleep with food intake, confirming what many suspected— people who stay awake longer tend to be sedentary during those additional waking hours and increase their food intake by snacking. Look at the question from a personal perspective— late-night study sessions require pizza and Mountain Dew®; Left 4 Dead gamers down energy drinks and chips while waiting to be re-spawn; dates and parties take place over dinner, drinks and hors d’oeuvres; movie marathons require popcorn and Good & Plenty candy.
Anecdotal rumors of culture-wide, dark-dependent gluttony do not constitute scientific evidence; thus, Dr. Nedeltcheva and colleagues at the University of Chicago recruited 11 non-obese subjects who agreed to be followed in a controlled environment for 14 days on two separate occasions, in a study published in the American Journal of Clinical Nutrition.15 These five women and six men were healthy, normal individuals who were not actively trying to lose weight and did not exercise. During the study periods, they were allowed to follow a normal routine, including normal leisure activities such as watching television, reading, using the Internet, etc; access to food was unlimited. They were not allowed to leave the observation area for more than 30 minutes a day. Prior to each two-week ‘vacation,’ scientists measured 24-hour energy expenditure, total calories consumed (divided into meals and snacks), and the appetite-regulating hormones leptin and ghrelin.
The study periods differed only in the number of hours of sleep allowed to the subjects; no naps were allowed at any time. During one session, subjects slept 8½ hours daily for the 14 days; during the second, they only slept 5½ hours per day. Surprisingly, there was not much difference in the total energy expenditure when these subjects were awake 3 hours more. Considering that the activity options were limited to normal, couch-potato activities, this shows that there is not a lot of difference metabolically between sitting on the couch versus sleeping. The appetite-regulating hormones, leptin and ghrelin, were similar between the groups as well. Of course, there was no calorie-restriction, so the subjects never experienced periods of hunger or starvation during this time.
The subjects were not provided with diet guidelines; they ate what they wanted and were provided with snacks of their choice throughout the study. As might be expected, with no restrictions and little to focus on, the subjects ate plenty. On average, the amount consumed during the three meals (breakfast, lunch and dinner) was similar during the two study periods. The macronutrient profile of the meals was typical American fare, with an approximate 52:34:14 ratio of carbohydrate:protein:fat by calories. The primary difference seen between the sleep-deprived state and sleep-aplenty state was in calories consumed as snacks. When restricted to 5½ hours of sleep daily, subjects consumed significantly more calories during snack time and tended to increase carbohydrate content of these snacks. Most importantly, the biggest difference was seen in snacking occurred between 7 p.m. and 7 a.m.15 It is believed that access to and temptation of snacks is a deciding factor in dieting success.
All subjects consumed in excess of the number of calories expended, eating more than 1,000 calories in excess every day when rested (1,012 calories during the 8½ sleep daily period). When sleep was restricted to 5½ hours for 14 days, 1,173 calories were consumed in excess. Those numbers (calories in excess) were calculated by measuring the food intake and subtracting the measured daily energy expenditure, so the number is as accurate as possible. Thus, when 2-3 hours of sleep deficit occurred, subjects consumed more food that resulted in an additional 161 calories per day; 161 calories above a baseline that was already over 1,000 calories in excess.
Lost Sleep is Lost Muscle
The question that logically follows is: did the additional calorie burden result in weight gain, or more importantly, fat gain? The subjects underwent both regular weigh-ins and DXA scans to measure body composition. Not surprisingly, subjects gained a similar amount of weight during both periods, approximately 2 kg; this follows the study design of sedentary conditions supplemented with freely available food.
Though the results were not significant, there was a noticeable trend in the character of that weight gained. During the 8½ hour sleep period, subjects gained (on average) 2.1 kg with 1.5 kg being fat— 71 percent. When restricted to 5½ hours of sleep, 1.9 kg weight gain was recorded, with 1.7 kg arising from fat gain— almost 90 percent. The authors did not comment on this observation, but it appears to suggest that the ‘stress’ of losing sleep is catabolic to lean mass (muscle). Given that the subjects consumed a similar amount of protein, the sleep-deprived conditions included a greater amount of calories, and the consumption of more carbohydrates would maintain a higher insulin concentration, one would expect that muscle would be better preserved and the sleep-deprived conditions would lead to equivalent changes in body composition, if not a preference to lean mass gains. Instead, the opposite was seen. Another explanation may be that adequate sleep promotes anabolic processes, allowing muscle to be maintained or increased when adequate rest is obtained.
It is likely no coincidence that as sleep hours have decreased society-wide, Americans have become fat and are developing metabolic conditions that are threatening the stability of the national health system. An impressive body of evidence is being reported, associating the loss of sleep with a number of health risks. Yet, people still burn the midnight oil, determined to squeeze the last bit of productivity or enjoyment out of each day if it kills them. Guess what? It might.16 Don’t sleep in though— too much sleep can be just as bad for you. For all the people who are attempting to lose weight to attract Mr. Right or Ms. Sweetheart, those late nights are taking a toll, not just on one’s health and lifespan, but also on the ability to be a hard body. Grabbing a good night’s sleep regularly is vital to promoting optimal weight management. Perhaps more relevant to the man or woman working to improve his/her physique is the negative impact those extra hours have on fat gain. Slip between the sheets for your daily eight and if conditions require you to stay awake longer, put away the snacks.
References:
1. DeSantis AD, Webb EM, et al. Illicit use of prescription ADHD medications on a college campus: a multimethodological approach. J Am Coll Health, 2008 Nov-Dec;57(3):315-24.
2. Kumar R. Approved and investigational uses of modafinil : an evidence-based review. Drugs, 2008;68(13):1803-39.
3. Jay SM, Petrilli RM, et al. The suitability of a caffeinated energy drink for night-shift workers. Physiol Behav, 2006 May 30;87(5):925-31.
4. Dworak M, Schierl T, et al. Impact of singular excessive computer game and television exposure on sleep patterns and memory performance of school-aged children. Pediatrics, 2007 Nov;120(5):978-85.
5. Hunter LP, Rychnovsky JD, et al. A selective review of maternal sleep characteristics in the postpartum period. J Obstet Gynecol Neonatal Nurs, 2009 Jan-Feb;38(1):60-8.
6. Spiegel K, Leproult R, et al. Impact of sleep debt on metabolic and endocrine function. Lancet, 1999;354:1435-9.
7. Kahol K, Leyba MJ, et al. Effect of fatigue on psychomotor and cognitive skills. Am J Surg, 2008 Feb;195(2):195-204.
8. Samuels C. Sleep, recovery, and performance: the new frontier in high-performance athletics. Neurol Clin, 2008 Feb;26(1):169-80; ix-x.
9. Mullington JM, Haack M, et al. Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Prog Cardiovasc Dis, 2009 Jan-Feb;51(4):294-302.
10. Janszky I, Ljung R. Shifts to and from Daylight Saving Time and Incidence of Myocardial Infarction. N Engl J Med, 2008;359(18):1966-68.
11. Good D, Morse SA, et al. Obesity, hypertension, and the heart. J Cardiometab Syndr, 2008 Summer;3(3):168-72.
12. Miller MA, Cappuccio FP. Inflammation, sleep, obesity and cardiovascular disease. Curr Vasc Pharmacol, 2007 Apr;5(2):93-102.
13. Wilbert C. Sleep Deprivation Linked to Prediabetes. WebMD 2009 March 12. Available at http://diabetes.webmd.com/news/20090312/sleep-deprivation-linked-to-prediabetes, accessed March 15, 2009.
14. Schenck CH, Mahowald MW. Review of nocturnal sleep-related eating disorders. Int J Eat Disord, 1994 May;15(4):343-56.
15. Nedeltcheva AV, Kilkus JM, et al. Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr, 2009 Jan;89(1):126-33.
16. Ferrie JE, Shipley MJ, et al. A prospective study of change in sleep duration: associations with mortality in the Whitehall II cohort. Sleep, 2007 Dec 1;30(12):1659-66.
A.C.E. Certified Personal Trainer
IDEA Fitness member
Kickboxing Certified Instructor
Been in fitness for 28+ years and have studied kinesiology and nutrition
Most the articles will be long just so you know up front.
Sleep your way to fat loss
Weight-loss gurus on television advise “exercise more” and “eat less,” as though these statements should have been included in the original 10 Commandments. There is a principle in logic called ‘Ockham’s Razor,’ which tells us that the simplest solution is usually the correct one. Well, what could be simpler than exercise more, eat less? Unfortunately, even Ockham’s Razor is not that simple. Friar William of Ockham stated that when making a choice, any assumptions that do not make a difference should be excluded; however, it is vital to include assumptions that are relevant.
Step away from the high-tech world of liposuction, gastric bypass, appetite suppressants, thermogenic and lipolytic drugs; the human body adapts to its environment. At the most basic level, that includes the amount of food available, the amount of activity needed to acquire that food, and the amount of rest one can obtain before needing to forage again.
Sleep is an under-appreciated need in American society. In fact, society often rewards individuals who forego sleep in order to work longer hours, party harder, watch adult entertainment and enjoy the ‘night life.’ People go to great lengths to eradicate the need for sleep. It is not just post-adolescent ravers taking methamphetamines and ecstasy to prolong nights of hedonism; the ranks of the sleep-deprived are filled with students and professors using Adderall® to allow for academic all-nighters; physicians and nurses using Provigil® to stay sharp during careers of extended hours; policemen and power plant workers walk the health store aisles looking for energy supplements that will get them through rotating shifts; children guzzle Red Bull® to pwn [sic] friends and strangers through early morning online gaming; and mothers brew coffee every morning to meet the demands of family.1-5
Prior to the information age, most jobs were labor or service related; social norms were more conservative and people were praised for being practical, not outrageous or risk-taking. One popular axiom was “Early to bed, early to rise, makes a man healthy, wealthy and wise.” These observations would suggest that previous generations may have actually hibernated. In fact, sleep patterns were not overly different from today, on a day-to-day basis. Of course, leisure time has been extended and the introduction of electric lighting and varied forms of entertainment remove many of the cues that would normally send one to sleep. Most conventioneers can attest to the temporal (time) confusion experienced inside the casinos of Las Vegas where fluorescent lights and the absence of clocks mask the passage of time.
Nonetheless, there has been an overall trend toward sleep deficit. In comparison to several decades ago, Americans are sleeping, on average, 90 minutes less per night.6 An hour or two makes little difference in the short-term, but over time, a chronic sleep deficit dramatically affects one’s health. A number of studies have shown that sleep deprivation results in reduced cognitive function (thinking), hormonal changes, negative changes in blood pressure, worsened insulin sensitivity, etc.7-9
In fact, during the recent daylight savings time-related time change, news channels reported the findings of a 2008 Swedish study published in the New England Journal of Medicine, showing that the risk of a heart attack increases 5 percent during the three days immediately following the ‘spring forward’ change that results in the loss of an hour’s sleep for most. Conversely, there was a smaller reduction in risk during the three days following the ‘fall back’ that gifts an extra hour of sleep. The authors posited that the increase in heart attacks following the loss of an hour of sleep was due to an increase in sympathetic tone (adrenalin) and a pro-inflammatory state.10 These factors are already elevated in the obese, making the time change very risky in this group.11 Perhaps it is time for the FDA to review daylight savings time.
Sleep Deprivation and Obesity
Sleep deprivation does not just increase risks associated with obesity, but it also increases the risk of obesity. Several studies have associated sleep deprivation with obesity, as well as the Metabolic Syndrome, which includes negative changes to cardiovascular health and insulin sensitivity, and changes in hormones that promote fat storage.12 Even as this article is being written, new studies are linking sleep deprivation with poor health. Research is being presented at the American Heart Association, reporting an increase in the risk of developing type II diabetes in people who sleep less than 6 hours per night, compared to those who sleep 6 to 8 hours.13
Is there more to the inverse association between sleep loss and weight loss than metabolic and hormonal changes? Could the increased number of waking hours somehow relate to foraging behavior as well? After all, except for the rare case of somnambulist bingers (those who sleepwalk to the refrigerator to eat), people don’t break their diet while they are asleep.14
Researchers investigated the effect of shorter daily sleep with food intake, confirming what many suspected— people who stay awake longer tend to be sedentary during those additional waking hours and increase their food intake by snacking. Look at the question from a personal perspective— late-night study sessions require pizza and Mountain Dew®; Left 4 Dead gamers down energy drinks and chips while waiting to be re-spawn; dates and parties take place over dinner, drinks and hors d’oeuvres; movie marathons require popcorn and Good & Plenty candy.
Anecdotal rumors of culture-wide, dark-dependent gluttony do not constitute scientific evidence; thus, Dr. Nedeltcheva and colleagues at the University of Chicago recruited 11 non-obese subjects who agreed to be followed in a controlled environment for 14 days on two separate occasions, in a study published in the American Journal of Clinical Nutrition.15 These five women and six men were healthy, normal individuals who were not actively trying to lose weight and did not exercise. During the study periods, they were allowed to follow a normal routine, including normal leisure activities such as watching television, reading, using the Internet, etc; access to food was unlimited. They were not allowed to leave the observation area for more than 30 minutes a day. Prior to each two-week ‘vacation,’ scientists measured 24-hour energy expenditure, total calories consumed (divided into meals and snacks), and the appetite-regulating hormones leptin and ghrelin.
The study periods differed only in the number of hours of sleep allowed to the subjects; no naps were allowed at any time. During one session, subjects slept 8½ hours daily for the 14 days; during the second, they only slept 5½ hours per day. Surprisingly, there was not much difference in the total energy expenditure when these subjects were awake 3 hours more. Considering that the activity options were limited to normal, couch-potato activities, this shows that there is not a lot of difference metabolically between sitting on the couch versus sleeping. The appetite-regulating hormones, leptin and ghrelin, were similar between the groups as well. Of course, there was no calorie-restriction, so the subjects never experienced periods of hunger or starvation during this time.
The subjects were not provided with diet guidelines; they ate what they wanted and were provided with snacks of their choice throughout the study. As might be expected, with no restrictions and little to focus on, the subjects ate plenty. On average, the amount consumed during the three meals (breakfast, lunch and dinner) was similar during the two study periods. The macronutrient profile of the meals was typical American fare, with an approximate 52:34:14 ratio of carbohydrate:protein:fat by calories. The primary difference seen between the sleep-deprived state and sleep-aplenty state was in calories consumed as snacks. When restricted to 5½ hours of sleep daily, subjects consumed significantly more calories during snack time and tended to increase carbohydrate content of these snacks. Most importantly, the biggest difference was seen in snacking occurred between 7 p.m. and 7 a.m.15 It is believed that access to and temptation of snacks is a deciding factor in dieting success.
All subjects consumed in excess of the number of calories expended, eating more than 1,000 calories in excess every day when rested (1,012 calories during the 8½ sleep daily period). When sleep was restricted to 5½ hours for 14 days, 1,173 calories were consumed in excess. Those numbers (calories in excess) were calculated by measuring the food intake and subtracting the measured daily energy expenditure, so the number is as accurate as possible. Thus, when 2-3 hours of sleep deficit occurred, subjects consumed more food that resulted in an additional 161 calories per day; 161 calories above a baseline that was already over 1,000 calories in excess.
Lost Sleep is Lost Muscle
The question that logically follows is: did the additional calorie burden result in weight gain, or more importantly, fat gain? The subjects underwent both regular weigh-ins and DXA scans to measure body composition. Not surprisingly, subjects gained a similar amount of weight during both periods, approximately 2 kg; this follows the study design of sedentary conditions supplemented with freely available food.
Though the results were not significant, there was a noticeable trend in the character of that weight gained. During the 8½ hour sleep period, subjects gained (on average) 2.1 kg with 1.5 kg being fat— 71 percent. When restricted to 5½ hours of sleep, 1.9 kg weight gain was recorded, with 1.7 kg arising from fat gain— almost 90 percent. The authors did not comment on this observation, but it appears to suggest that the ‘stress’ of losing sleep is catabolic to lean mass (muscle). Given that the subjects consumed a similar amount of protein, the sleep-deprived conditions included a greater amount of calories, and the consumption of more carbohydrates would maintain a higher insulin concentration, one would expect that muscle would be better preserved and the sleep-deprived conditions would lead to equivalent changes in body composition, if not a preference to lean mass gains. Instead, the opposite was seen. Another explanation may be that adequate sleep promotes anabolic processes, allowing muscle to be maintained or increased when adequate rest is obtained.
It is likely no coincidence that as sleep hours have decreased society-wide, Americans have become fat and are developing metabolic conditions that are threatening the stability of the national health system. An impressive body of evidence is being reported, associating the loss of sleep with a number of health risks. Yet, people still burn the midnight oil, determined to squeeze the last bit of productivity or enjoyment out of each day if it kills them. Guess what? It might.16 Don’t sleep in though— too much sleep can be just as bad for you. For all the people who are attempting to lose weight to attract Mr. Right or Ms. Sweetheart, those late nights are taking a toll, not just on one’s health and lifespan, but also on the ability to be a hard body. Grabbing a good night’s sleep regularly is vital to promoting optimal weight management. Perhaps more relevant to the man or woman working to improve his/her physique is the negative impact those extra hours have on fat gain. Slip between the sheets for your daily eight and if conditions require you to stay awake longer, put away the snacks.
References:
1. DeSantis AD, Webb EM, et al. Illicit use of prescription ADHD medications on a college campus: a multimethodological approach. J Am Coll Health, 2008 Nov-Dec;57(3):315-24.
2. Kumar R. Approved and investigational uses of modafinil : an evidence-based review. Drugs, 2008;68(13):1803-39.
3. Jay SM, Petrilli RM, et al. The suitability of a caffeinated energy drink for night-shift workers. Physiol Behav, 2006 May 30;87(5):925-31.
4. Dworak M, Schierl T, et al. Impact of singular excessive computer game and television exposure on sleep patterns and memory performance of school-aged children. Pediatrics, 2007 Nov;120(5):978-85.
5. Hunter LP, Rychnovsky JD, et al. A selective review of maternal sleep characteristics in the postpartum period. J Obstet Gynecol Neonatal Nurs, 2009 Jan-Feb;38(1):60-8.
6. Spiegel K, Leproult R, et al. Impact of sleep debt on metabolic and endocrine function. Lancet, 1999;354:1435-9.
7. Kahol K, Leyba MJ, et al. Effect of fatigue on psychomotor and cognitive skills. Am J Surg, 2008 Feb;195(2):195-204.
8. Samuels C. Sleep, recovery, and performance: the new frontier in high-performance athletics. Neurol Clin, 2008 Feb;26(1):169-80; ix-x.
9. Mullington JM, Haack M, et al. Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Prog Cardiovasc Dis, 2009 Jan-Feb;51(4):294-302.
10. Janszky I, Ljung R. Shifts to and from Daylight Saving Time and Incidence of Myocardial Infarction. N Engl J Med, 2008;359(18):1966-68.
11. Good D, Morse SA, et al. Obesity, hypertension, and the heart. J Cardiometab Syndr, 2008 Summer;3(3):168-72.
12. Miller MA, Cappuccio FP. Inflammation, sleep, obesity and cardiovascular disease. Curr Vasc Pharmacol, 2007 Apr;5(2):93-102.
13. Wilbert C. Sleep Deprivation Linked to Prediabetes. WebMD 2009 March 12. Available at http://diabetes.webmd.com/news/20090312/sleep-deprivation-linked-to-prediabetes, accessed March 15, 2009.
14. Schenck CH, Mahowald MW. Review of nocturnal sleep-related eating disorders. Int J Eat Disord, 1994 May;15(4):343-56.
15. Nedeltcheva AV, Kilkus JM, et al. Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr, 2009 Jan;89(1):126-33.
16. Ferrie JE, Shipley MJ, et al. A prospective study of change in sleep duration: associations with mortality in the Whitehall II cohort. Sleep, 2007 Dec 1;30(12):1659-66.
A.C.E. Certified Personal Trainer
IDEA Fitness member
Kickboxing Certified Instructor
Been in fitness for 28+ years and have studied kinesiology and nutrition
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Replies
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I should probably go to bed then.0
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Wow, thank you so much for posting!! (I've gotten about 10 hours of sleep this WHOLE WEEK due to schoolwork....<___< whoops lol)0
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Good thread, I will be following this.0
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bump0
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bump0
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have sleep monitor app. avg 8hrs here
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Where is that "Like" button...?0
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I stayed awake to read this.0
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love it
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That was a really fantastic article. . Thank you so much for posting it. . Will look forward to further postings.0
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I wonder what happens when you oversleep, and how much longer it would have to be for it to be harmful. I normally sleep 8 to 12 hours a night.0
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Getting a good 7-8 hours of straight sleep is one thing I need to improve on (among others)0
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Does this suggest I should skip the gym to go to bed earlier? :-p0
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The Science on Fat Loss: Lipolysis and Fat Burning
It is peak time for making New Year’s resolutions. As it has been every year, losing weight sits on or near the top of the list for the majority of people. Given the economic conditions, it may have taken a back seat to financial goals (save more, pay off debt, eat at home, etc.)— but it remains a perennial favorite.
Of course, health clubs and weight loss centers depend upon this annual parade of lemming-like couch potatoes, with the month of January accounting for nearly 50 percent of new membership enrollments in established clubs.1 Invariably, the advice of eat fewer calories, perform cardiovascular exercise to burn fat, and lift weights to build muscle (and bone if you are a woman) is given in an office furnished with a Steelcase® desk, flat screen monitor, and those blue fabric chairs.
The charming early-20s trainer, upbeat music, as well as the digital flashiness and iPod® compatibility of the machines are designed to motivate and inspire members to meet their goals. Unfortunately, fat loss does not occur because one wishes it will. Fat loss is the result of a series of chemical reactions.
Fat Storage
Before talking about fat loss, it may help to understand fat storage. Ask most people where fat is stored and they will grab the skin around the navel as though there is a Tupperware® container of Crisco® belted around the belly. In part, this is true at the cellular level. Body fat is thought of by many as being unsightly lumps and bumps; in the U.S., this often lowers one’s social standing. To the body, fat is wealth, as it represents energy reserves that will allow a person to withstand days to months of famine; it also allows for long periods of low-to-moderate activity between meals. To the mitochondria (the power factories of living tissue), stored fat is like cash in the bank.
Unlike wealth, the display of a fortune in body fat is neither envied nor advantageous as is the opulence of financial wealth. Let’s face reality; people turn green with envy when they see a multi-millionaire being chauffeured in a Maybach 62 S. Conversely, very few in the U.S. demonstrated the same response when they see the body of a person with a 10-year savings account of adipose (fat). A million calories of stored fat is not as wonderful as a million dollars.
Of course, millionaires don’t carry their cash on them in bundles of $10 bills. Ironically, one gram of fat has nine calories and a million calories of fat would weigh 244 pounds. A million dollars in $10 bills (as close as one can get to a $9 bill) would weigh a little more than 220; coincidentally, a $10 bill also weighs a gram.
Despite the abhorrence most have towards morbid obesity, and the epidemic of increased deaths and disease that accompany this degree of fat accumulation, the human body is still designed to absorb and store as many calories as possible. This seems inappropriate in today’s society here in the U.S., but traveling to many parts of the world will confirm that starvation and famine remain common. Even in the venerable U.S., food rationing and soup kitchens were a national way of life 60-80 years ago. Global genetic adaptation (evolution) to discourage rather than promote the storage of fat is unlikely to occur for many, many generations, if ever.
Body fat is primarily stored in specialized cells called white adipose tissue (WAT).2 Folklore suggested that people are born with a set number of fat cells and individuals are stuck with those cells for life; the same was also said of brain cells. Medical science has proven this is not true. Fat cells arise from a self-replenishing pool of precursor stem cells— the same precursor cells that can also turn into skeletal muscle.3 Contrary to another folktale, even though muscle and fat arise from the same pre-cursor, muscle does not and cannot turn into fat when a person stops exercising. Instead, muscle atrophies (shrinks or wastes away) if a person stops training and fat stores increase due to the decrease in physical activity, often in the setting of overeating.
Calories are consumed in the diet. The focus used to be on dietary fat as being the source of body fat. It made sense to the general public and marketing agencies across the nation; if fat is being stored, then it must come from fat that is being consumed. Then the Atkins Diet diverted blame onto carbohydrates and their wicked habit of raising insulin, which in turn promoted fat storage. Now, the public is back to not knowing what to think.
Breaking it Down
Fat is a generic term— it can be a relative comparison; refer to either tri-acyl-glycerides or specific fatty acids; or if spelled P-H-A-T describe a particularly attractive woman. For the purposes of this article, the term fat refers to tri-acyl-glycerides (TAG), a chemical class of molecules defined as three fatty acids bonded to a common glycerol atom. To make it an easy visual, hold your hand out and extend only three fingers (pointer, middle, and ring fingers). The hand is glycerol and each finger represents a fatty acid. There are many different fatty acids in the diet and in stored fat. Many are familiar with the terms saturated and unsaturated fat (fatty acids). Omega-3 fatty acids are a subset of unsaturated fatty acids, as is oleic acid— a monounsaturated fat rich in olive oil. The differentiation between saturated and unsaturated is not important for the purposes of this discussion.
When dietary fat is consumed in a meal, it is commonly in the form of a TAG. TAG will form big globules in the watery environment of the stomach and intestines; drop some cooking oil into a bowl of water for a demonstration. To break up these globules, the gallbladder secretes bile acids, which make the TAG form smaller globules so that enzymes can attack. Lipases are enzymes that break down TAG to 2-monoglycerol and fatty acids.4 These digested fragments are taken up or absorbed in the small intestine and re-formed into TAG, packaged with cholesterol in lipoproteins, and transported through lymphatic ducts before entering the bloodstream. Some free fatty acids and TAG directly enter the bloodstream and can be taken up by exercising muscle and other active tissue (e.g., heart) for energy or to be stored in those tissues as an immediate source of long-term energy.5,6
TAG are packaged in the liver for transport to adipocytes (fat cells), where they are again broken down into fatty acids by a fat-cell bound enzyme called lipoprotein lipase (LPL).6 High concentrations of insulin increase the number of LPL in fat cells, increasing fat uptake for storage rather than as energy for muscle, heart, etc.6,7 The fatty acids released by LPL can circulate in the blood or be taken up by the fat cell and converted once again into TAG which is stored in a fat globule in the fat cell. If a person eats a calorie-appropriate diet, the process is well-balanced, providing for immediate and long-term energy needs while avoiding excess body fat accumulation.
That may be everything and more than most wish to know about how fat gets from the lips to the hips. What is the primary concern for most is how to shed the saddlebags.
Losing It
Fat loss occurs when the fat cells are stimulated by certain hormones (growth hormone, glucagon, ACTH, etc).8 A common pathway stimulates the activation of several enzymes, as well as “opening doors” in the fat globule so the enzymes can deconstruct the TAG into glycerol and free fatty acids.
For some time, the scientific model held that a single enzyme was primarily responsible for most of fat breakdown and release. Further, the thought was that the freed fatty acids either fled the bondages of TAG incarceration or were re-incorporated into TAG that was confined behind the prison-like membrane of the intracellular fat globule (possibly charged with additional time for a failed escape attempt).
However— and this will probably only thrill the biology geeks for the most part— a fuller understanding of the processes relating to the release and breakdown of TAG stored in the intracellular fat globule of the adipocyte (fat cell) has recently been gained through ultra-fine research.9 Scientists have determined that stored fat is brought to the surface of the fat globule inside the cell when gateway proteins are phosphorylated (turned on).10 There, a newly-discovered/understood enzyme call desnutrin/ATGL breaks off one of the three glycerol-bonded fatty acids.11
Think back to holding three fingers from your hand to demonstrate what a TAG looks like; desnutrin/ATGL just breaks off the pointer finger. The TAG becomes DAG when it loses one fatty acid. DAG is attacked by a second enzyme called hormone-sensitive lipase (HSL) that only breaks off the ring finger; after that there is another enzyme that takes care of the remaining fat fragment called a MAG— tearing off the “middle finger” fatty acid.9
The three free fatty acids and the glycerol molecule that have been created by breaking apart TAG can either enter the circulating bloodstream or be converted back into fat. Yet, researchers have now found that the free fatty acids can also be used by the fat cell itself for energy. In fact, when lipolysis (fat breakdown) is turned on, the fat cell’s energy factories appear to be pushed into high gear, burning fat for energy at a higher rate.12,13
It was long believed that fat cells were metabolically quiet, but the last decade has shown that they produce hormones that affect the metabolism and appetite, as well as being a place where calorie burning occurs. This agrees with recent observations that it is healthier to have a large number of small fat cells rather than relatively few fat cells that are large.14 After all, it takes more to feed a hundred hungry children (small fat cells) than a couple of sumo-wrestlers (large fat cells).
Not surprisingly, fat cells of obese people absorb fatty acids more readily than lean people and do not burn fatty acids for calories, preferring to store the energy as fat.15 It is beneficial to the body that the fat cells do use up fatty acids as they are being released to some degree as an overload of free fatty acids in the system causes a condition known as insulin resistance, sometimes called pre-diabetes.16,17
There are two relative states that directly affect the fat cell’s willingness to release and break down fat. When the body is fasted (has not eaten for many hours), certain hormones are elevated, promoting a lipolytic (fat breakdown) response to the fat-losing hormones and neurotransmitters, the most important being norepinephrine— an adrenalin-like chemical released from nerve endings.18 When the body is fasted, the concentration of glucocorticoids is elevated, which upregulates (similar to stimulating or promoting) the production of desnutrin/ATGL.19 In the fed state, insulin concentrations are high, which activates the enzyme that turns off the fat-loss signal generated by the adrenaline-like biochemicals and drugs.18 There are a number of other hormones and signaling molecules that affect the fat cell’s preference to store or break down stored fat.
Prostaglandins
One other recent discovery (biology geek time again) that revealed another way fat cells regulate fat storage/breakdown was reported. Prostaglandins are signaling molecules that communicate only with surrounding cells, or sometimes even just the originating cell itself. They are the biochemical equivalent to a whisper, and as all know, the most interesting information is usually told in whispers.
The fat cell has a relatively unique enzyme that generates a prostaglandin called PGE2. In the fat cell, PGE2 slows down fat loss by degrading cAMP, a chemical messenger signal that is produced when fat loss hormones/chemicals attach onto receptors located on the fat cell.12 These fat loss hormones and drugs that circulate through the bloodstream cannot enter or turn on the fat loss mechanisms of the fat cell. That happens when cAMP is generated, carrying the fat loss message to various enzymes and proteins like an office gofer passing out memos. If the gofer is fired (or cAMP degraded), the office (or fat cell) has no direction and just sits there biding its time. If there is a cell-level version of solitaire, this is when the fat cell would be playing. PGE2 degrades cAMP (fires the gofer), slowing down fat loss.12 The enzyme that produces PGE2 (called AdPLA) is turned on by insulin which is highest in the fed state.12
Pretty amazing— the interaction between so many regulating processes. When one considers all the various hormones, drugs, enzymes, etc., involved in fat storage/breakdown, it becomes clear why one drug could never circumvent all the regulatory pathways.
This article presents a lot of science and describes (only superficially) how complex fat storage/breakdown is within fat cells. However, as the Chinese philosopher Sun Tzu wrote, “If you know the enemy and know yourself, you need not fear the result of a hundred battles.” [paraphrased] People know how much they eat, drink, exercise, and sleep; knowing how the body responds, especially a part of the body that many struggle to control, will help win the fat loss battle.
References:
2009 Jan 6. Available at http://archives.chicagotribune.com/2009/jan/06/business/chi-tue-consumerland-0106-jan06, accessed Nov 15, 2009.
2. Voshol PJ, Rensen PC, et al. Effect of plasma triglyceride metabolism on lipid storage in adipose tissue: studies using genetically engineered mouse models. Biochim Biophys Acta, 2009 Jun;1791(6):479-85.
3. Singh R, Artaza JN, et al. Androgens stimulate myogenic differentiation and inhibit adipogenesis in C3H 10T1/2 pluripotent cells through an androgen receptor-mediated pathway. Endocrinology, 2003 Nov;144(11):5081-8.
4. Armand M. Lipases and lipolysis in the human digestive tract: where do we stand? Curr Opin Clin Nutr Metab Care, 2007 Mar;10(2):156-64.
5. Koonen DP, Glatz JF, et al. Long-chain fatty acid uptake and FAT/CD36 translocation in heart and skeletal muscle. Biochim Biophys Acta, 2005 Oct 1;1736(3):163-80.
6. Fielding BA, Frayn KN. Lipoprotein lipase and the disposition of dietary fatty acids. Br J Nutr, 1998 Dec;80(6):495-502.
7. McTernan PG, Harte AL, et al. Insulin and rosiglitazone regulation of lipolysis and lipogenesis in human adipose tissue in vitro. Diabetes, 2002 May;51(5):1493-8.
8. Kastin AJ, Redding TW, et al. Lipid mobilizing hormones of the hypothalamus and pituitary. Pharmacol Biochem Behav, 1975;3(1 Suppl):121-6.
9. Ahmadian M, Duncan RE, et al. The skinny on fat: lipolysis and fatty acid utilization in adipocytes. Trends Endocrinol Metab, 2009 Nov;20(9):424-8.
10. Miyoshi H, Souza SC, et al. Perilipin promotes hormone-sensitive lipase-mediated adipocyte lipolysis via phosphorylation-dependent and -independent mechanisms. J Biol Chem, 2006 Jun 9;281(23):15837-44.
11. Lafontan M, Langin D. Lipolysis and lipid mobilization in human adipose tissue. Prog Lipid Res, 2009 Sep;48(5):275-97.
12. Jaworski K, Ahmadian M, et al. AdPLA ablation increases lipolysis and prevents obesity induced by high-fat feeding or leptin deficiency. Nat Med, 2009 Feb;15(2):159-68.
13. Ahmadian M, Duncan RE, et al. Adipose overexpression of desnutrin promotes fatty acid use and attenuates diet-induced obesity. Diabetes, 2009 Apr;58(4):855-66.
14. Bays HE. "Sick fat," metabolic disease, and atherosclerosis. Am J Med, 2009 Jan;122(1 Suppl):S26-37.
15. Walewski JL, Ge F, et al. Adipocyte Accumulation of Long-Chain Fatty Acids in Obesity is Multifactorial, Resulting from Increased Fatty Acid Uptake and Decreased Activity of Genes Involved in Fat Utilization. Obes Surg, 2009 Oct 29. [Epub ahead of print]
16. Guilherme A, Virbasius JV, et al. Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes. Nat Rev Mol Cell Biol, 2008 May;9(5):367-77.
17. Schenk S, Saberi M, et al. Insulin sensitivity: modulation by nutrients and inflammation. J Clin Invest, 2008 Sep;118(9):2992-3002.
18. Jaworski K, Sarkadi-Nagy E, et al. Regulation of triglyceride metabolism. IV. Hormonal regulation of lipolysis in adipose tissue. Am J Physiol Gastrointest Liver Physiol, 2007 Jul;293(1):G1-4.
19. Villena JA, Roy S, et al. Desnutrin, an adipocyte gene encoding a novel patatin domain-containing protein, is induced by fasting and glucocorticoids: ectopic expression of desnutrin increases triglyceride hydrolysis. J Biol Chem, 2004 Nov 5;279(45)
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Been in fitness for 28+ years and have studied kinesiology and nutrition0 -
definately bumping this for later.0
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bump for the morning crowd0
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I'm glad you posted about sleep and fat loss! It's so true, and many people don't realize those healthy little tweaks can make a big difference in their results. Also getting enough sleep decreases belly fat. 0
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bump0
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I wonder what happens when you oversleep, and how much longer it would have to be for it to be harmful. I normally sleep 8 to 12 hours a night.
Oversleeping isn't good either. Part of that depends on your age though. Teens actually need more sleep. I have read that more than 8 1/2 hours is to much. I don't have the awesome reference list of the original poster though. I just know I read it in a CNN article. 0 -
bump0
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Bump.0
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I need someone to explain the whole "sleep in important" thing to my children.0
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bump0
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Bump so I can keep it in my list :flowerforyou: Thanks!0
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Man, I cannot begin to tell you the difference I notice in my body/weightloss when I sleep enough. IT IS SO MUCH BETTER.0
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This is awesome!0
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bump0
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thank you!0
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Reminds me to get enough sleep! I work and go to school so sometimes I sleep during the day instead of at night, and it can get tricky to find time to sleep!0
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It is beneficial to the body that the fat cells do use up fatty acids as they are being released to some degree as an overload of free fatty acids in the system causes a condition known as insulin resistance, sometimes called pre-diabetes.16,17
16. Guilherme A, Virbasius JV, et al. Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes. Nat Rev Mol Cell Biol, 2008 May;9(5):367-77.
17. Schenk S, Saberi M, et al. Insulin sensitivity: modulation by nutrients and inflammation. J Clin Invest, 2008 Sep;118(9):2992-3002.
Just had to quote this, from the second study posted, and even quoted the citations. I think a lot of people need to read this part.0
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