Basal metabolic rate

Basal metabolic rate (BMR) is the rate of energy expenditure per unit time by endothermic animals at rest.[1] It is reported in energy units per unit time ranging from watt (joule/second) to ml O2/min or joule per hour per kg body mass J/(h·kg). Proper measurement requires a strict set of criteria be met. These criteria include being in a physically and psychologically undisturbed state, in a thermally neutral environment, while in the post-absorptive state (i.e., not actively digesting food).[1] In bradymetabolic animals, such as fish and reptiles, the equivalent term standard metabolic rate (SMR) is used. It follows the same criteria as BMR, but requires the documentation of the temperature at which the metabolic rate was measured. This makes BMR a variant of standard metabolic rate measurement that excludes the temperature data, a practice that has led to problems in defining "standard" rates of metabolism for many mammals.[1]

Metabolism comprises the processes that the body needs to function.[2] Basal metabolic rate is the amount of energy per unit time that a person needs to keep the body functioning at rest. Some of those processes are breathing, blood circulation, controlling body temperature, cell growth, brain and nerve function, and contraction of muscles. Basal metabolic rate (BMR) affects the rate that a person burns calories and ultimately whether that individual maintains, gains, or loses weight. The basal metabolic rate accounts for about 60 to 75% of the daily calorie expenditure by individuals. It is influenced by several factors. BMR typically declines by 1–2% per decade after age 20, mostly due to loss of fat-free mass,[3] although the variability between individuals is high.[4]

Description

The body's generation of heat is known as thermogenesis and it can be measured to determine the amount of energy expended. BMR generally decreases with age, and with the decrease in lean body mass (as may happen with aging). Increasing muscle mass has the effect of increasing BMR. Aerobic (resistance) fitness level, a product of cardiovascular exercise, while previously thought to have effect on BMR, has been shown in the 1990s not to correlate with BMR when adjusted for fat-free body mass. But anaerobic exercise does increase resting energy consumption (see "aerobic vs. anaerobic exercise").[5] Illness, previously consumed food and beverages, environmental temperature, and stress levels can affect one's overall energy expenditure as well as one's BMR.

Indirect calorimetry laboratory with canopy hood
Indirect calorimetry laboratory with canopy hood (dilution technique)

BMR is measured under very restrictive circumstances when a person is awake. An accurate BMR measurement requires that the person's sympathetic nervous system not be stimulated, a condition which requires complete rest. A more common measurement, which uses less strict criteria, is resting metabolic rate (RMR).[6]

BMR may be measured by gas analysis through either direct or indirect calorimetry, though a rough estimation can be acquired through an equation using age, sex, height, and weight. Studies of energy metabolism using both methods provide convincing evidence for the validity of the respiratory quotient (RQ), which measures the inherent composition and utilization of carbohydrates, fats and proteins as they are converted to energy substrate units that can be used by the body as energy.

Phenotypic flexibility

BMR is a flexible trait (it can be reversibly adjusted within individuals), with, for example, lower temperatures generally resulting in higher basal metabolic rates for both birds[7] and rodents.[8] There are two models to explain how BMR changes in response to temperature: the variable maximum model (VMM) and variable fraction model (VFM). The VMM states that the summit metabolism (or the maximum metabolic rate in response to the cold) increases during the winter, and that the sustained metabolism (or themetabolic rate that can be indefinitely sustained) remains a constant fraction of the former. The VFM says that the summit metabolism does not change, but that the sustained metabolism is a larger fraction of it. The VMM is supported in mammals, and, when using whole-body rates, passerine birds. The VFM is supported in studies of passerine birds using mass-specific metabolic rates (or metabolic rates per unit of mass). This latter measurement has been criticized by Eric Liknes, Sarah Scott, and David Swanson, who say that mass-specific metabolic rates are inconsistent seasonally.[9]

In addition to adjusting to temperature, BMR also may adjust before annual migration cycles.[7] The red knot (ssp. islandica) increases its BMR by about 40% before migrating northward. This is because of the energetic demand of long-distance flights. The increase is likely primarily due to increased mass in organs related to flight.[10] The end destination of migrants affects their BMR: yellow-rumped warblers migrating northward were found to have a 31% higher BMR than those migrating southward.[7]

Physiology

The early work of the scientists J. Arthur Harris and Francis G. Benedict showed that approximate values for BMR could be derived using body surface area (computed from height and weight), age, and sex, along with the oxygen and carbon dioxide measures taken from calorimetry. Studies also showed that by eliminating the sex differences that occur with the accumulation of adipose tissue by expressing metabolic rate per unit of "fat-free" or lean body mass, the values between sexes for basal metabolism are essentially the same. Exercise physiology textbooks have tables to show the conversion of height and body surface area as they relate to weight and basal metabolic values.

The primary organ responsible for regulating metabolism is the hypothalamus. The hypothalamus is located on the diencephalon and forms the floor and part of the lateral walls of the third ventricle of the cerebrum. The chief functions of the hypothalamus are:

  1. control and integration of activities of the autonomic nervous system (ANS)
    • The ANS regulates contraction of smooth muscle and cardiac muscle, along with secretions of many endocrine organs such as the thyroid gland (associated with many metabolic disorders).
    • Through the ANS, the hypothalamus is the main regulator of visceral activities, such as heart rate, movement of food through the gastrointestinal tract, and contraction of the urinary bladder.
  2. production and regulation of feelings of rage and aggression
  3. regulation of body temperature
  4. regulation of food intake, through two centers:
    • The feeding center or hunger center is responsible for the sensations that cause us to seek food. When sufficient food or substrates have been received and leptin is high, then the satiety center is stimulated and sends impulses that inhibit the feeding center. When insufficient food is present in the stomach and ghrelin levels are high, receptors in the hypothalamus initiate the sense of hunger.
    • The thirst center operates similarly when certain cells in the hypothalamus are stimulated by the rising osmotic pressure of the extracellular fluid. If thirst is satisfied, osmotic pressure decreases.

All of these functions taken together form a survival mechanism that causes us to sustain the body processes that BMR measures.

BMR estimation formulas

Several equations to predict the number of calories required by humans have been published from the early 20th–21st centuries. In each of the formulas below:

  • P   is total heat production at complete rest,
  • m   is mass (kg),
  • h   is height (cm), and
  • a   is age (years),[11]
The original Harris-Benedict equation

Historically, the most notable formula was the Harris–Benedict equation, which was published in 1919.

  • for men,
  • for women, [11]

The difference in BMR for men and women is mainly due to differences in body weight. For example, a 55 year-old woman weighing 130 lb (59 kg) and 5 feet 6 inches (168 cm) tall would have a BMR of 1272 kcal per day.

The revised Harris-Benedict equation

In 1984, the original Harris-Benedict equations were revised[12] using new data. In comparisons with actual expenditure, the revised equations were found to be more accurate.[13]

  • for men,
  • for women,

It was the best prediction equation until 1990, when Mifflin et al.[14] introduced the equation:

The Mifflin St Jeor Equation
  • , where s is +5 for males and −161 for females.

According to this formula, the woman in the example above has a BMR of 1204 kcal per day. During the last 100 years, lifestyles have changed and Frankenfield et al.[15] showed it to be about 5% more accurate.

These formulas are based on body weight, which does not take into account the difference in metabolic activity between lean body mass and body fat. Other formulas exist which take into account lean body mass, two of which are the Katch-McArdle formula, and Cunningham formula.

The Katch-McArdle Formula (Resting Daily Energy Expenditure)

The Katch-McArdle formula is used to predict Resting Daily Energy Expenditure (RDEE).[16] The Cunningham formula is commonly attributed as being used to predict RMR instead of BMR, however the formulas provided by Katch-McArdle and Cunningham are the same.[17]

where is the lean body mass (LBM in kg)

where f is the body fat percentage. According to this formula, if the woman in the example has a body fat percentage of 30%, her Resting Daily Energy Expenditure (the authors use the term of basal and resting metabolism interchangeably) would be 1262 kcal per day.

Causes of individual differences in BMR

The basic metabolic rate varies between individuals. One study of 150 adults representative of the population in Scotland reported basal metabolic rates from as low as 1027 kcal per day (4301 kJ/day) to as high as 2499 kcal/day (10455 kJ/day); with a mean BMR of 1500 kcal/day (6279 kJ/day). Statistically, the researchers calculated that 62.3% of this variation was explained by differences in fat free mass. Other factors explaining the variation included fat mass (6.7%), age (1.7%), and experimental error including within-subject difference (2%). The rest of the variation (26.7%) was unexplained. This remaining difference was not explained by sex nor by differing tissue size of highly energetic organs such as the brain.[18]

Differences in BMR have been observed when comparing subjects with the same lean body mass. In one study, when comparing individuals with the same lean body mass, the top 5% of BMRs are 1.28–1.32 times the lowest 5% BMR.[19] Additionally, this study reports a case where two individuals with the same lean body mass of 43 kg had BMRs of 1075 kcal/day (4.5 MJ/day) and 1790 kcal/day (7.5 MJ/day). This difference of 715 kcal/day (67%) is equivalent to one of the individuals completing a 10 kilometer run every day.[19] However, this study did not account for the sex, height, fasting-state, or body fat percentage of the subjects.

Biochemistry

Energy expenditure breakdown[20]
Liver 27%
Brain 19%
Skeletal Muscle 18%
Kidneys 10%
Heart 7%
Other organs 19%
Postprandial thermogenesis
Postprandial thermogenesis increases in basal metabolic rate occur at different degrees depending on consumed food composition.

About 70% of a human's total energy expenditure is due to the basal life processes taking place in the organs of the body (see table). About 20% of one's energy expenditure comes from physical activity and another 10% from thermogenesis, or digestion of food (postprandial thermogenesis).[21] All of these processes require an intake of oxygen along with coenzymes to provide energy for survival (usually from macronutrients like carbohydrates, fats, and proteins) and expel carbon dioxide, due to processing by the Krebs cycle.

For the BMR, most of the energy is consumed in maintaining fluid levels in tissues through osmoregulation, and only about one-tenth is consumed for mechanical work, such as digestion, heartbeat, and breathing.[22]

What enables the Krebs cycle to perform metabolic changes to fats, carbohydrates, and proteins is energy, which can be defined as the ability or capacity to do work. The breakdown of large molecules into smaller molecules—associated with release of energy—is catabolism. The building up process is termed anabolism. The breakdown of proteins into amino acids is an example of catabolism, while the formation of proteins from amino acids is an anabolic process.

Exergonic reactions are energy-releasing reactions and are generally catabolic. Endergonic reactions require energy and include anabolic reactions and the contraction of muscle. Metabolism is the total of all catabolic, exergonic, anabolic, endergonic reactions.

Adenosine Triphosphate (ATP) is the intermediate molecule that drives the exergonic transfer of energy to switch to endergonic anabolic reactions used in muscle contraction. This is what causes muscles to work which can require a breakdown, and also to build in the rest period, which occurs during the strengthening phase associated with muscular contraction. ATP is composed of adenine, a nitrogen containing base, ribose, a five carbon sugar (collectively called adenosine), and three phosphate groups. ATP is a high energy molecule because it stores large amounts of energy in the chemical bonds of the two terminal phosphate groups. The breaking of these chemical bonds in the Krebs Cycle provides the energy needed for muscular contraction.

Glucose

Because the ratio of hydrogen to oxygen atoms in all carbohydrates is always the same as that in water—that is, 2 to 1—all of the oxygen consumed by the cells is used to oxidize the carbon in the carbohydrate molecule to form carbon dioxide. Consequently, during the complete oxidation of a glucose molecule, six molecules of carbon dioxide and six molecules of water are produced and six molecules of oxygen are consumed.

The overall equation for this reaction is:

C6H12O6 + 6 O2 → 6 CO2 + 6 H2O

(38 ATP molecules)

Because the gas exchange in this reaction is equal, the respiratory quotient (R.Q.) for carbohydrate is unity or 1.0:

R.Q. = 6 CO2 / 6 O2 = 1.0

Fats

The chemical composition for fats differs from that of carbohydrates in that fats contain considerably fewer oxygen atoms in proportion to atoms of carbon and hydrogen. When listed on nutritional information tables, fats are generally divided into six categories: total fats, saturated fatty acid, polyunsaturated fatty acid, monounsaturated fatty acid, dietary cholesterol, and trans fatty acid. From a basal metabolic or resting metabolic perspective, more energy is needed to burn a saturated fatty acid than an unsaturated fatty acid. The fatty acid molecule is broken down and categorized based on the number of carbon atoms in its molecular structure. The chemical equation for metabolism of the twelve to sixteen carbon atoms in a saturated fatty acid molecule shows the difference between metabolism of carbohydrates and fatty acids. Palmitic acid is a commonly studied example of the saturated fatty acid molecule.

The overall equation for the substrate utilization of palmitic acid is:

C16H32O2 + 23 O2 → 16 CO2 + 16 H2O

Thus the R.Q. for palmitic acid is 0.696:

R.Q. = 16 CO2 / 23 O2 = 0.696

Proteins

Proteins are composed of carbon, hydrogen, oxygen, and nitrogen arranged in a variety of ways to form a large combination of amino acids. Unlike fat the body has no storage deposits of protein. All of it is contained in the body as important parts of tissues, blood hormones, and enzymes. The structural components of the body that contain these amino acids are continually undergoing a process of breakdown and replacement. The respiratory quotient for protein metabolism can be demonstrated by the chemical equation for oxidation of albumin:

C72H112N18O22S + 77 O2 → 63 CO2 + 38 H2O + SO3 + 9 CO(NH2)2

The R.Q. for albumin is 63 CO2/ 77 O2 = 0.818

The reason this is important in the process of understanding protein metabolism is that the body can blend the three macronutrients and based on the mitochondrial density, a preferred ratio can be established which determines how much fuel is utilized in which packets for work accomplished by the muscles. Protein catabolism (breakdown) has been estimated to supply 10% to 15% of the total energy requirement during a two-hour aerobic training session. This process could severely degrade the protein structures needed to maintain survival such as contractile properties of proteins in the heart, cellular mitochondria, myoglobin storage, and metabolic enzymes within muscles.

The oxidative system (aerobic) is the primary source of ATP supplied to the body at rest and during low intensity activities and uses primarily carbohydrates and fats as substrates. Protein is not normally metabolized significantly, except during long term starvation and long bouts of exercise (greater than 90 minutes.) At rest approximately 70% of the ATP produced is derived from fats and 30% from carbohydrates. Following the onset of activity, as the intensity of the exercise increases, there is a shift in substrate preference from fats to carbohydrates. During high intensity aerobic exercise, almost 100% of the energy is derived from carbohydrates, if an adequate supply is available.

Aerobic vs. anaerobic exercise

Studies published in 1992[23] and 1997[24] indicate that the level of aerobic fitness of an individual does not have any correlation with the level of resting metabolism. Both studies find that aerobic fitness levels do not improve the predictive power of fat free mass for resting metabolic rate. However recent research from the Journal of Applied Physiology, published in 2012 Sep. 27, PMCID:PMC3544497, compared Resistance Training and Aerobic training on body mass and fat mass in overweight adults: "STRRIDE AT/RT. When you consider time commitments against health benefits, AT is the optimal mode of exercise for reducing fat mass and body mass as a primary consideration, RT is good as a secondary factor when aging and lean mass are a concern. RT causes injuries at a much higher rate than AT. [1] Compared to RT, it was found that AET resulted in a significantly more pronounced reduction of body weight by enhancing the cardiovascular system which is what is the principle factor in metabolic utilization of fat substrates. RT if time is available is also helpful in post exercise metabolism, but it is an adjunctive factor because the body needs to heal sufficiently between RT episodes, whereas with AET, the body can accept this every day. RMR, and BMR are measurements of daily consumption of calories. [2] [3] The majority of studies that are published on this topic look at aerobic exercise because of its efficacy for health and weight management.

Anaerobic exercise, such as weight lifting, builds additional muscle mass. Muscle contributes to the fat-free mass of an individual and therefore effective results from anaerobic exercise will increase BMR.[25] However, the actual effect on BMR is controversial and difficult to enumerate. Various studies[26][27] suggest that the resting metabolic rate of trained muscle is around 55kJ per kilogram, per day. Even a substantial increase in muscle mass, say 5 kg, would make only a minor impact on BMR.

Longevity

In 1926, Raymond Pearl proposed that longevity varies inversely with basal metabolic rate (the "rate of living hypothesis"). Support for this hypothesis comes from the fact that mammals with larger body size have longer maximum life spans (large animals do have higher total metabolic rates, but the metabolic rate at the cellular level is much lower, and the breathing rate and heartbeat are slower in larger animals) and the fact that the longevity of fruit flies varies inversely with ambient temperature.[28] Additionally, the life span of houseflies can be extended by preventing physical activity.[29] This theory has been bolstered by several new studies linking lower basal metabolic rate to increased life expectancy, across the animal kingdom—including humans. Calorie restriction and reduced thyroid hormone levels, both of which decrease the metabolic rate, have been associated with higher longevity in animals.[30][31][32][33]

However, the ratio of total daily energy expenditure to resting metabolic rate can vary between 1.6 and 8.0 between species of mammals. Animals also vary in the degree of coupling between oxidative phosphorylation and ATP production, the amount of saturated fat in mitochondrial membranes, the amount of DNA repair, and many other factors that affect maximum life span.[34]

Organism longevity and basal metabolic rate

In allometric scaling, maximum potential life span (MPLS) is directly related to metabolic rate (MR), where MR is the recharge rate of a biomass made up of covalent bonds. That biomass (W) is subjected to deterioration over time from thermodynamic, entropic pressure. Metabolism is essentially understood as redox coupling, and has nothing to do with thermogenesis. Metabolic efficiency (ME) is then expressed as the efficiency of this coupling, a ratio of amperes captured and used by biomass, to the amperes available for that purpose. MR is measured in watts, W is measured in grams. These factors are combined in a power law, an elaboration on Kleiber's law relating MR to W and MPLS, that appears as MR = W^ (4ME-1)/4ME. When ME is 100%, MR = W^3/4; this is popularly known as quarter power scaling, a version of allometric scaling that is premised upon unrealistic estimates of biological efficiency.

The equation reveals that as ME drops below 20%, for W < one gram, MR/MPLS increases so dramatically as to endow W with virtual immortality by 16%. The smaller W is to begin with, the more dramatic is the increase in MR as ME diminishes. All of the cells of an organism fit into this range, i.e., less than one gram, and so this MR will be referred to as BMR.

But the equation reveals that as ME increases over 25%, BMR approaches zero. The equation also shows that for all W > one gram, where W is the organization of all of the BMRs of the organism's structure, but also includes the activity of the structure, as ME increases over 25%, MR/MPLS increases rather than decreases, as it does for BMR. An MR made up of an organization of BMRs will be referred to as an FMR. As ME decreases below 25%, FMR diminishes rather than increases as it does for BMR.

The antagonism between FMR and BMR is what marks the process of aging of biomass W in energetic terms. The ME for the organism is the same as that for the cells, such that the success of the organism's ability to find food (and lower its ME), is key to maintaining the BMR of the cells driven, otherwise, by starvation, to approaching zero; while at the same time a lower ME diminishes the FMR/MPLS of the organism.

Medical considerations

A person's metabolism varies with their physical condition and activity. Weight training can have a longer impact on metabolism than aerobic training, but there are no known mathematical formulas that can exactly predict the length and duration of a raised metabolism from trophic changes with anabolic neuromuscular training.

A decrease in food intake will typically lower the metabolic rate as the body tries to conserve energy.[35] Researcher Gary Foster estimates that a very low calorie diet of fewer than 800 calories a day would reduce the metabolic rate by more than 10 percent.[36]

The metabolic rate can be affected by some drugs, such as antithyroid agents, drugs used to treat hyperthyroidism, such as propylthiouracil and methimazole, bring the metabolic rate down to normal and restore euthyroidism. Some research has focused on developing antiobesity drugs to raise the metabolic rate, such as drugs to stimulate thermogenesis in skeletal muscle.

The metabolic rate may be elevated in stress, illness, and diabetes. Menopause may also affect metabolism.

Cardiovascular implications

Heart rate is determined by the medulla oblongata and part of the pons, two organs located inferior to the hypothalamus on the brain stem. Heart rate is important for basal metabolic rate and resting metabolic rate because it drives the blood supply, stimulating the Krebs cycle. During exercise that achieves the anaerobic threshold, it is possible to deliver substrates that are desired for optimal energy utilization. The anaerobic threshold is defined as the energy utilization level of heart rate exertion that occurs without oxygen during a standardized test with a specific protocol for accuracy of measurement, such as the Bruce Treadmill protocol (see metabolic equivalent). With four to six weeks of targeted training the body systems can adapt to a higher perfusion of mitochondrial density for increased oxygen availability for the Krebs cycle, or tricarboxylic cycle, or the glycolitic cycle. This in turn leads to a lower resting heart rate, lower blood pressure, and increased resting or basal metabolic rate.

By measuring heart rate we can then derive estimations of what level of substrate utilization is actually causing biochemical metabolism in our bodies at rest or in activity. This in turn can help a person to maintain an appropriate level of consumption and utilization by studying a graphical representation of the anaerobic threshold. This can be confirmed by blood tests and gas analysis using either direct or indirect calorimetry to show the effect of substrate utilization. The measures of basal metabolic rate and resting metabolic rate are becoming essential tools for maintaining a healthy body weight.

See also

References

  1. ^ a b c McNab BK (1997). "On the Utility of Uniformity in the Definition of Basal Rate of Metabolism". Physiological Zoology. 70 (6): 718–720. doi:10.1086/515881.
  2. ^ Ballesteros FJ, Martinez VJ, Luque B, Lacasa L, Valor E, Moya A (2018). "On the thermodynamic origin of metabolic scaling". Scientific Reports. 8: 1448:1–1448:10. Bibcode:2018NatSR...8.1448B. doi:10.1038/s41598-018-19853-6.
  3. ^ Manini TM (2010). "Energy expenditure and aging". Ageing Research Reviews. 9 (1): 1–11. doi:10.1016/j.arr.2009.08.002. PMC 2818133. PMID 19698803.
  4. ^ McMurray RG, Soares J, Caspersen CJ, McCurdy T (2014). "Examining variations of resting metabolic rate of adults: a public health perspective". Medicine & Science in Sports & Exercise. 46 (7): 1352–1358. doi:10.1249/MSS.0000000000000232. PMC 4535334. PMID 24300125.
  5. ^ Stiegler P, Cunliffe A (2006). "The role of diet and exercise for the maintenance of fat-free mass and resting metabolic rate during weight loss" (PDF). Sports Medicine. 36 (3): 239–262. doi:10.2165/00007256-200636030-00005. PMID 16526835.
  6. ^ "Calculating BMR and RMR: Diet and Weight Loss Tutorial". CaloriesPerHour.com. Archived from the original on 2008-01-05. Retrieved 2008-01-26.
  7. ^ a b c McKechnie, Andrew E. (2008). "Phenotypic flexibility in basal metabolic rate and the changing view of avian physiological diversity: a review". Journal of Comparative Physiology B. 178 (3): 235–247. doi:10.1007/s00360-007-0218-8. ISSN 0174-1578. PMID 17957373.
  8. ^ Rezende, Enrico L.; Bozinovic, Francisco; Garland, Jr., Theodore (2004). "Climatic adaptation and the evolution of basal and maximum rates of metabolism in rodents". Evolution. 58 (6): 1361–1374. doi:10.1111/j.0014-3820.2004.tb01714.x. ISSN 0014-3820.
  9. ^ Liknes, Eric T.; Scott, Sarah M.; Swanson, David L. (2002). "Seasonal acclimatization in the American goldfinch revisited: To what extent do metabolic rates vary seasonally?". The Condor. 104 (3): 548. doi:10.1650/0010-5422(2002)104[0548:SAITAG]2.0.CO;2. ISSN 0010-5422.
  10. ^ Weber, Thomas P.; Piersma, Theunis (1996). "Basal metabolic rate and the mass of tissues differing in metabolic scope: Migration-related covariation between individual knots Calidris canutus". Journal of Avian Biology. 27 (3): 215. doi:10.2307/3677225. ISSN 0908-8857. JSTOR 3677225.
  11. ^ a b Harris J, Benedict F (1918). "A Biometric Study of Human Basal Metabolism". PNAS. 4 (12): 370–373. Bibcode:1918PNAS....4..370H. doi:10.1073/pnas.4.12.370. PMC 1091498. PMID 16576330.
  12. ^ Roza AM, Shizgal HM (1984). "The Harris Benedict equation reevaluated: resting energy requirements and the body cell mass" (PDF). The American Journal of Clinical Nutrition. 40 (1): 168–182. doi:10.1093/ajcn/40.1.168. PMID 6741850.
  13. ^ Müller B, Merk S, Bürgi U, Diem P (2001). "Calculating the basal metabolic rate and severe and morbid obesity". Praxis. 90 (45): 1955–63. PMID 11817239.
  14. ^ Mifflin MD, St Jeor ST, Hill LA, Scott BJ, Daugherty SA, Koh YO (1990). "A new predictive equation for resting energy expenditure in healthy individuals". The American Journal of Clinical Nutrition. 51 (2): 241–247. doi:10.1093/ajcn/51.2.241. PMID 2305711.
  15. ^ Frankenfield D, Roth-Yousey L, Compher C (2005). "Comparison of predictive equations for resting metabolic rate in healthy, nonobese and obese adults: A systematic review". Journal of the American Dietetic Association. 105 (5): 775–789. doi:10.1016/j.jada.2005.02.005. PMID 15883556.
  16. ^ McArdle W (2006). Essentials of exercise physiology. Lippincott Williams & Wilkins. p. 266. ISBN 9780495014836.
  17. ^ Dunford M (2007). Nutrition for Sport and Exercise. Brooks/Cole. p. 57. ISBN 9780781749916.
  18. ^ Johnstone AM, Murison SD, Duncan JS, Rance KA, Speakman JR, Koh YO (2005). "Factors influencing variation in basal metabolic rate include fat-free mass, fat mass, age, and circulating thyroxine but not sex, circulating leptin, or triiodothyronine". American Journal of Clinical Nutrition. 82 (5): 941–948. doi:10.1093/ajcn/82.5.941. PMID 16280423.
  19. ^ a b Speakman JR, Król E, Johnson MS (2004). "The Functional Significance of Individual Variation in Basal Metabolic Rate". Physiological and Biochemical Zoology. 77 (6): 900–915. doi:10.1086/427059. PMID 15674765.
  20. ^ Durnin, JVGA (1981). "Basal metabolic rate in man". Report to FAO/ WHO/UNU. Rome: FAO.
  21. ^ McArdle, William D. (1986). Exercise Physiology (2nd ed.). Philadelphia: Lea & Febigier.
  22. ^ Lisa Gordon-Davis (2004). Hospitality Industry Handbook on Nutrition and Menu Planning. Juta and Company Ltd. p. 112. ISBN 978-0-7021-5578-9.
  23. ^ Broeder, CE; Burrhus, KA; Svanevik, LS; Wilmore, JH (1992). "The effects of aerobic fitness on resting metabolic rate". The American Journal of Clinical Nutrition. 55 (4): 795–801. doi:10.1093/ajcn/55.4.795. PMID 1550061.
  24. ^ Smith, DA; Dollman, J; Withers, RT; Brinkman, M; Keeves, JP; Clark, DG (1997). "Relationship between maximum aerobic power and resting metabolic rate in young adult women". Journal of Applied Physiology. 82 (1): 156–63. doi:10.1152/jappl.1997.82.1.156. PMID 9029211.
  25. ^ Ravussin, E; Lillioja, S; Christin, L; Bogardus, C; Bogardus, C (1986). "Determinants of 24-hour energy expenditure in man. Methods and results using a respiratory chamber". The Journal of Clinical Investigation. 78 (6): 1568–1578. doi:10.1172/JCI112749. PMC 423919. PMID 3782471.
  26. ^ Campbell, W; Crim, M; Young, V; Evans, W (1994). "Increased energy requirements and changes in body composition with resistance training in older adults". American Journal of Clinical Nutrition. 60 (2): 167–175. doi:10.1093/ajcn/60.2.167. PMID 8030593.
  27. ^ Pratley, R; Nicklas, B; Rubin, M; Miller, J; Smith, A; Smith, M; Hurley, B; Goldberg, A (1994). "Strength training increases resting metabolic rate and norepinephrine levels in healthy 50- to 65-year-old men". Journal of Applied Physiology. 76 (1): 133–137. doi:10.1152/jappl.1994.76.1.133. PMID 8175496.
  28. ^ Miquel, Jaime; Lundgren, Paul R.; Bensch, Klaus G.; Atlan, Henri (1976). "Effects of temperature on the life span, vitality and fine structure of Drosophila melanogaster". Mechanisms of Ageing and Development. 5 (5): 347–70. doi:10.1016/0047-6374(76)90034-8. PMID 823384.
  29. ^ Ragland, S.S.; Sohal, R.S. (1975). "Ambient temperature, physical activity and aging in the housefly, Musca domestica". Experimental Gerontology. 10 (5): 279–89. doi:10.1016/0531-5565(75)90005-4. PMID 1204688.
  30. ^ Hulbert AJ, Pamplona R, Buffenstein R, Buttemer WA (October 2007). "Life and death: metabolic rate, membrane composition, and life span of animals". Physiol. Rev. 87 (4): 1175–213. doi:10.1152/physrev.00047.2006. PMID 17928583.
  31. ^ Olshansky, SJ; Rattan, SI (2005). "What determines longevity: Metabolic rate or stability?". Discovery Medicine. 5 (28): 359–62. PMID 20704872.
  32. ^ Aguilaniu, H. (2005). "Metabolism, ubiquinone synthesis, and longevity". Genes & Development. 19 (20): 2399–406. doi:10.1101/gad.1366505. PMID 16230529.
  33. ^ Atzmon, G.; Barzilai, N.; Surks, M. I.; Gabriely, I. (2009). "Genetic Predisposition to Elevated Serum Thyrotropin is Associated with Exceptional Longevity". Journal of Clinical Endocrinology & Metabolism. 94 (12): 4768–75. doi:10.1210/jc.2009-0808. PMC 2795660. PMID 19837933. Lay summaryReuters (June 13, 2009).
  34. ^ Speakman, JR; Selman, C; McLaren, JS; Harper, EJ (2002). "Living fast, dying when? The link between aging and energetics". The Journal of Nutrition. 132 (6 Suppl 2): 1583S–97S. doi:10.1093/jn/132.6.1583S. PMID 12042467.
  35. ^ Grattan BJ Jr; Connolly-Schoonen J (2012). "Addressing weight loss recidivism: a clinical focus on metabolic rate and the psychological aspects of obesity". ISRN Obesity. 2012: 567530. doi:10.5402/2012/567530. PMC 3914266. PMID 24527265.
  36. ^ Whitman, Stacy "The Truth about Metabolism." Shape. September 2003. Archived 2011-04-23 at the Wayback Machine

Further reading

  • Tsai, AG; Wadden, TA (2005). "Systematic review: An evaluation of major commercial weight loss programs in the United States". Annals of Internal Medicine. 142 (1): 56–66. doi:10.7326/0003-4819-142-1-200501040-00012. PMID 15630109.
  • Gustafson, D.; Rothenberg, E; Blennow, K; Steen, B; Skoog, I (2003). "An 18-Year Follow-up of Overweight and Risk of Alzheimer Disease". Archives of Internal Medicine. 163 (13): 1524–8. doi:10.1001/archinte.163.13.1524. PMID 12860573.
  • "Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: Executive summary. Expert Panel on the Identification, Evaluation, and Treatment of Overweight in Adults". The American Journal of Clinical Nutrition. 68 (4): 899–917. 1998. doi:10.1093/ajcn/68.4.899. PMID 9771869.
  • Segal, Arthur C. (1987). "Linear Diet Model". College Mathematics Journal. 18 (1): 44–5. doi:10.2307/2686315. JSTOR 2686315.
  • Pike, Ruth L; Brown, Myrtle Laurestine (1975). Nutrition: An Integrated Approach (2nd ed.). New York: Wiley. OCLC 474842663.
  • Sahlin, K.; Tonkonogi, M.; Soderlund, K. (1998). "Energy supply and muscle fatigue in humans". Acta Physiologica Scandinavica. 162 (3): 261–6. doi:10.1046/j.1365-201X.1998.0298f.x. PMID 9578371.
  • Saltin, Bengt; Gollnick, Philip D. (1983). "Skeletal muscle adaptability: Significance for metabolism and performance". In Peachey, Lee D; Adrian, Richard H; Geiger, Stephen R (eds.). Handbook of Physiology. Baltimore: Williams & Wilkins. pp. 540–55. OCLC 314567389. Republished as: Saltin, Bengt; Gollnick, Philip D. (2011). "Skeletal Muscle Adaptability: Significance for Metabolism and Performance". Comprehensive Physiology. doi:10.1002/cphy.cp100119. ISBN 978-0-470-65071-4.
  • Thorstensson (1976). "Muscle strength, fibre types and enzyme activities in man". Acta Physiologica Scandinavica. Supplementum. 443: 1–45. PMID 189574.
  • Thorstensson, Alf; Sjödin, Bertil; Tesch, Per; Karlsson, Jan (1977). "Actomyosin ATPase, Myokinase, CPK and LDH in Human Fast and Slow Twitch Muscle Fibres". Acta Physiologica Scandinavica. 99 (2): 225–9. doi:10.1111/j.1748-1716.1977.tb10373.x. PMID 190869.
  • Vanhelder, W. P.; Radomski, M. W.; Goode, R. C.; Casey, K. (1985). "Hormonal and metabolic response to three types of exercise of equal duration and external work output". European Journal of Applied Physiology and Occupational Physiology. 54 (4): 337–42. doi:10.1007/BF02337175. PMID 3905393.
  • Wells, JG; Balke, B; Van Fossan, DD (1957). "Lactic acid accumulation during work; a suggested standardization of work classification". Journal of Applied Physiology. 10 (1): 51–5. doi:10.1152/jappl.1957.10.1.51. PMID 13405829.
  • McArdle, William D; Katch, Frank I; Katch, Victor L (1986). Exercise Physiology: Energy, Nutrition, and Human Performance. Philadelphia: Lea & Febiger. OCLC 646595478.
  • Harris, JA; Benedict, FG (1918). "A Biometric Study of Human Basal Metabolism". Proceedings of the National Academy of Sciences of the United States of America. 4 (12): 370–3. Bibcode:1918PNAS....4..370H. doi:10.1073/pnas.4.12.370. PMC 1091498. PMID 16576330.

External links

Abnormal basal metabolic rate

Abnormal basal metabolic rate refers to a high or low basal metabolic rate (BMR). It has numerous causes, both physiological (part of the body's normal function) and pathological (associated with disease).

Energy consumption

Energy consumption is the amount of energy or power used.

Expensive tissue hypothesis

The expensive tissue hypothesis (ETH) relates brain and gut size in evolution (specifically in human evolution). It suggests that in order for an organism to evolve a large brain without a significant increase in basal metabolic rate (as seen in humans), the organism must use less energy on other expensive tissues; the paper introducing the ETH suggests that in humans, this was achieved by eating an easy-to-digest diet and evolving a smaller, less energy intensive gut. The ETH has inspired many research projects to test its validity in primates and other organisms.

The human brain stands out among the mammals because its relative size compared to the rest of the body is unusually large compared to other animals. The human brain is about three times larger than that of our closest living relative, the chimpanzee. For a primate of our body size, the relative size of the brain and that of the digestive tract is rather unexpected; the digestive tract is smaller than expected for a primate of our body size. In 1995, two scientists proposed an attempt to solve this phenomenon of human evolution using the Expensive Tissue Hypothesis.

Glycogen

Glycogen is a multibranched polysaccharide of glucose that serves as a form of energy storage in animals, fungi, and bacteria. The polysaccharide structure represents the main storage form of glucose in the body.

Glycogen functions as one of two forms of long-term energy reserves, with the other form being triglyceride stores in adipose tissue (i.e., body fat). In humans, glycogen is made and stored primarily in the cells of the liver and skeletal muscle. In the liver, glycogen can make up 5–6% of the organ's fresh weight, and the liver of an adult weighing 70 kg can store roughly 100–120 grams of glycogen. In skeletal muscle, glycogen is found in a low concentration (1–2% of the muscle mass) and the skeletal muscle of an adult weighing 70 kg stores roughly 400 grams of glycogen. The amount of glycogen stored in the body—particularly within the muscles and liver—mostly depends on physical training, basal metabolic rate, and eating habits. Small amounts of glycogen are also found in other tissues and cells, including the kidneys, red blood cells, white blood cells, and glial cells in the brain. The uterus also stores glycogen during pregnancy to nourish the embryo.Approximately 4 grams of glucose are present in the blood of humans at all times; in fasted individuals, blood glucose is maintained constant at this level at the expense of glycogen stores in the liver and skeletal muscle. Glycogen stores in skeletal muscle serve as a form of energy storage for the muscle itself; however, the breakdown of muscle glycogen impedes muscle glucose uptake, thereby increasing the amount of blood glucose available for use in other tissues. Liver glycogen stores serve as a store of glucose for use throughout the body, particularly the central nervous system. The human brain consumes approximately 60% of blood glucose in fasted, sedentary individuals.Glycogen is the analogue of starch, a glucose polymer that functions as energy storage in plants. It has a structure similar to amylopectin (a component of starch), but is more extensively branched and compact than starch. Both are white powders in their dry state. Glycogen is found in the form of granules in the cytosol/cytoplasm in many cell types, and plays an important role in the glucose cycle. Glycogen forms an energy reserve that can be quickly mobilized to meet a sudden need for glucose, but one that is less compact than the energy reserves of triglycerides (lipids). As such it is also found as storage reserve in many parasitic protozoa.

Harris–Benedict equation

The Harris–Benedict equation (also called the Harris-Benedict principle) is a method used to estimate an individual's basal metabolic rate (BMR).

The estimated BMR value may be multiplied by a number that corresponds to the individual's activity level; the resulting number is the approximate daily kilocalorie intake to maintain current body weight.

The Harris–Benedict equation may be used to assist weight loss — by reducing kilocalorie intake number below the estimated maintenance intake of the equation.

Hypermetabolism

Hypermetabolism is the physiological state of increased rate of metabolic activity and is characterized by an abnormal increase in the body’s basal metabolic rate. Hypermetabolism is accompanied by a variety of internal and external symptoms, most notably extreme weight loss, and can also be a symptom in itself. This state of increased metabolic activity can signal underlying issues, especially hyperthyroidism. Patients with Fatal familial insomnia, an extremely rare and strictly hereditary disorder, also presents with hypermetabolism; however, this universally fatal disorder is exceedingly rare, with only a few known cases worldwide. The drastic impact of the hypermetabolic state on patient nutritional requirements is often understated or overlooked as well.

Hypermetabolism typically occurs after significant injury to the body. In hospitals and institutions, the most common causes are infections, sepsis, burns, multiple traumas, fever, long-bone fractures, hyperthyroidism, prolonged steroid therapy, surgery and bone marrow transplants. Hypermetabolism may occur in particular in the brain after traumatic brain injury. The cause and location of hypermetabolic symptoms within the body can be accurately detected by PET scan. Symptoms will usually subside once the underlying illness or injury is treated.

Institute of Medicine Equation

The Institute of Medicine Equation was published in September 2002. It is the equation which is behind the 2005 Dietary Guidelines for Americans and the new food pyramid, MyPyramid.

The Institute of Medicine equation uses a different approach to most others. The equation doesn't measure basal metabolic rate, but uses experiments based on doubly labelled water. The scientists at the Institute of Medicine said in their report that the factorial method tended to underestimate calorie expenditure.

Kleiber's law

Kleiber's law, named after Max Kleiber for his biology work in the early 1930s, is the observation that, for the vast majority of animals, an animal's metabolic rate scales to the ¾ power of the animal's mass. Symbolically: if q0 is the animal's metabolic rate, and M the animal's mass, then Kleiber's law states that q0 ~ M¾. Thus, over the same timespan, a cat having a mass 100 times that of a mouse will consume only about 32 times the energy the mouse uses.

The exact value of the exponent in Kleiber's law is unclear, in part because there is current no completely satisfactory theoretical explanation for the law.

Max Kleiber

Max Kleiber (4 January 1893 – 5 January 1976) was a Swiss agricultural biologist, born and educated in Zurich, Switzerland.

Kleiber graduated from the Federal Institute of Technology as an Agricultural Chemist in 1920, earned the ScD degree in 1924, and became a private dozent after publishing his thesis The Energy Concept in the Science of Nutrition.

Kleiber joined the Animal Husbandry Department of UC Davis in 1929 to construct respiration chambers and conduct research on energy metabolism in animals. Among his many important achievements, two are especially noteworthy. In 1932 he came to the conclusion that the ¾ power of body weight was the most reliable basis for predicting the basal metabolic rate (BMR) of animals and for comparing nutrient requirements among animals of different size. He also provided the basis for the conclusion that total efficiency of energy utilization is independent of body size. These concepts and several others fundamental for understanding energy metabolism are discussed in Kleiber's book, The Fire of Life published in 1961 and subsequently translated into German, Polish, Spanish, and Japanese.

He is credited with the description of the ratio of metabolism to body mass, which became Kleiber's law.

Metabolic age

Metabolic age is calculated by comparing one's basal metabolic rate to the average of one's chronological age group. Basal metabolic rate is the amount of energy consumed per unit of time when all environmental factors are considered neutral, the digestive system is in a post-absorptive state (meaning that the digestive system is inactive, which requires about twelve hours of fasting in humans), and the energy expenditure is only sufficient to support normal functioning of the vital organs, the heart, lungs, nervous system, kidneys, liver, intestine, sex organs, muscles, and skin. Formulas for estimating basal metabolic rate take into account age, weight, height, activity level, body fat mass, and lean body mass.

All the components in the body require various levels of energy to be maintained. Body fat requires much less energy than lean muscle, as lean muscle is much more metabolically active and therefore requires more energy expenditure to remain in homeostasis. If comparing two individuals, with all variables being equal, the person with more lean muscle mass will have a higher basal metabolic rate, and therefore, a lower metabolic age in comparison to those with the identical chronological age.

Physical activity level

The physical activity level (PAL) is a way to express a person's daily physical activity as a number, and is used to estimate a person's total energy expenditure. In combination with the basal metabolic rate, it can be used to compute the amount of food energy a person needs to consume in order to maintain a particular lifestyle.

Rate-of-living theory

The rate of living theory postulates that the faster an organism’s metabolism, the shorter its lifespan. The theory was originally created by Max Rubner in 1908 after his observation that larger animals outlived smaller ones, and that the larger animals had slower metabolisms. After its inception by Rubner, it was further expanded upon through the work of Raymond Pearl. Outlined in his book, The Rate of Living published in 1928, Pearl conducted a series of experiments in drosophilia and cantaloupe seeds that corroborated Rubner’s initial observation that a slowing of metabolism increased lifespan.

Further strength was given to these observations by the discovery of Max Kleiber’s law in 1932. Colloquially called the “mouse-to-elephant” curve, Kleiber’s conclusion was that basal metabolic rate could accurately be predicted by taking 3/4 the power of body weight. This conclusion was especially noteworthy because the inversion of its scaling exponent, between 0.2 and 0.33, was the scaling for lifespan and metabolic rate.

Respiratory quotient

The respiratory quotient (or RQ or respiratory coefficient), is a dimensionless number used in calculations of basal metabolic rate (BMR) when estimated from carbon dioxide production. It is calculated from the ratio of carbon dioxide produced by the body to oxygen consumed by the body. Such measurements, like measurements of oxygen uptake, are forms of indirect calorimetry. It is measured using a respirometer. The Respiratory Quotient value indicates which macronutrients are being metabolized, as different energy pathways are used for fats, carbohydrates, and proteins. If metabolism consists solely of lipids, the Respiratory Quotient is 0.7, for proteins it is 0.8, and for carbohydrates it is 1.0. Most of the time, however, energy consumption is composed of both fats and carbohydrates. The approximate respiratory quotient of a mixed diet is 0.8. Some of the other factors that may affect the respiratory quotient are energy balance, circulating insulin, and insulin sensitivity.It can be used in the alveolar gas equation.

Resting metabolic rate

Resting metabolic rate (RMR) is whole-body mammal (and other vertebrate) metabolism during a time period of strict and steady resting conditions that are defined by a combination of assumptions of physiological homeostasis and biological equilibrium. RMR differs from basal metabolic rate (BMR) because BMR measurements must meet total physiological equilibrium whereas RMR conditions of measurement can be altered and defined by the contextual limitations. Therefore, BMR is measured in the elusive "perfect" steady state, whereas RMR measurement is more accessible and thus, represents most, if not all measurements or estimates of daily energy expenditure.Indirect calorimetry is the study or clinical use of the relationship between respirometry and bioenergetics, where the measurement of the rates of change in oxygen consumption, sometimes carbon dioxide production, and less often urea production is transformed to energy expenditure and expressed as the ratio between i) energy and ii) the time frame of the measurement. For example, following analysis of oxygen consumption of a human subject, if 5.5 kilocalories of energy were estimated during a 5-minute measurement from a rested individual, then the resting metabolic rate equals = 1.1 kcal/min rate.

A comprehensive treatment of confounding factors on BMR measurements is demonstrated as early as 1922 in Massachusetts by Engineering Professor Frank B Sanborn, wherein descriptions of the effects of food, posture, sleep, muscular activity, and emotion provide criteria for separating BMR from RMR.

Schofield equation

The Schofield Equation is a method of estimating the basal metabolic rate (BMR) of adult men and women published in 1985.This is the equation used by the WHO in their technical report series. The equation that is recommended to estimate BMR by the US Academy of Nutrition and Dietetics is the Mifflin-St. Jeor equation.The equations for estimating BMR in kJ/day (kilojoules per day) from body mass (kg) are:Men:

Women:

The equations for estimating BMR in kcal/day (kilocalories per day) from body mass (kg) are:

Men:

Women:

Key:

W = Body weight in kilograms

SEE = Standard error of estimation

The raw figure obtained by the equation should be adjusted up or downwards, within the confidence limit suggested by the quoted estimation errors, and according to the following principles:

Subjects leaner and more muscular than usual require more energy than the average.

Obese subjects require less.

Patients at the young end of the age range for a given equation require more energy.

Patients at the high end of the age range for a given equation require less energy.

Effects of age and body mass may cancel out: an obese 30-year-old or an athletic 60-year-old may need no adjustment from the raw figure.

To find actual energy needed per day (Estimated Energy Requirement), the base metabolism must then be multiplied by an activity factor.

These are as follows:

Sedentary people of both genders should multiply by 1.3. Sedentary is very physically inactive, inactive in both work and leisure.

Lightly active men should multiply by 1.6 and women by 1.5. Lightly active means the daily routine includes some walking, or intense exercise once or twice per week. Most students are in this category.

Moderately active men should multiply by 1.7 and women by 1.6. Moderately active means intense exercise lasting 20–45 minutes at least three time per week, or a job with a lot of walking, or a moderate intensity job.

Very Active men should multiply by 2.1 and women by 1.9. Very active means intense exercise lasting at least an hour per day, or a heavy physical job, such as a mail carrier or an athlete in training.

Extremely active men should multiply by 2.4 and women by 2.2. Extremely active means an athlete on an unstoppable training schedule or a very demanding job, such as working in the armed forces or shoveling coal.These equations were published in 1989 in the dietary guidelines and formed the RDA's for a number of years. The activity factor used by the USDA was 1.6. In the UK, a lower activity factor of 1.4 is used. The equation has now been replaced by the Institute of Medicine Equation in September 2002 in the USA, however is still currently used by the FAO/WHO/UNU.

Specific dynamic action

Specific dynamic action (SDA), also known as thermic effect of food (TEF) or dietary induced thermogenesis (DIT), is the amount of energy expenditure above the basal metabolic rate due to the cost of processing food for use and storage. Heat production by brown adipose tissue which is activated after consumption of a meal is an additional component of dietary induced thermogenesis. The thermic effect of food is one of the components of metabolism along with resting metabolic rate and the exercise component. A commonly used estimate of the thermic effect of food is about 10% of one's caloric intake, though the effect varies substantially for different food components. For example, dietary fat is very easy to process and has very little thermic effect, while protein is hard to process and has a much larger thermic effect.

The Hacker's Diet

The Hacker's Diet (humorously subtitled "How to lose weight and hair through stress and poor nutrition") is a diet plan created by the founder of Autodesk, John Walker, outlined in an electronic book of the same name, that attempts to aid the process of weight loss by more accurately modeling how calories consumed and calories expended actually impact weight. Walker notes that much of our fat free mass introduces signal noise when trying to determine how much weight we're actually losing or gaining. With the help of a graphing tool (Excel is used in the book), he addresses these problems. Factoring in exercise, and through counting calories, one can calculate one's own total energy expenditure (basal metabolic rate, thermic effect of food, and day-to-day exercise) and cut back calorie intake or increase exercise to lose weight.

Thermogenics

Thermogenic means tending to produce heat, and the term is commonly applied to drugs which increase heat through metabolic stimulation, or to microorganisms which create heat within organic waste. Approximately all enzymatic reaction in the human body is thermogenic, which gives rise to the basal metabolic rate.In bodybuilding, athletes wishing to lose fat purportedly use thermogenics to increase their basal metabolic rate, thereby increasing their energy expenditure. Caffeine and ephedrine are commonly used for this purpose. 2,4-Dinitrophenol (DNP) is a very dangerous thermogenic drug used for fat loss; it will give a dose-dependant increase in body temperature, to the point where it can induce death by hyperthermia. It works as a mitochondrial oxidative phosphorylation uncoupler, disrupting the mitochondrial electron transport chain. This stops the mitochondria from producing adenosine triphosphate, releasing energy as heat.

Wolff–Chaikoff effect

The Wolff–Chaikoff effect, discovered by Drs. Jan Wolff and Israel Lyon Chaikoff at the University of California, is a presumed reduction in thyroid hormone levels caused by ingestion of a large amount of iodine. In 1948, Wolff and Chaikoff reported that injection of iodine in rats almost completely inhibited organification (thyroglobulin iodination) in the thyroid gland. However, recent research into the study shows that the thyroid hormone levels of the rats were not checked prior to injections.

Patients with Graves' disease are more sensitive than euthyroid patients, and iodine has been used to manage Graves' disease.

The Wolff–Chaikoff effect is known as an autoregulatory phenomenon that inhibits organification in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream. This becomes evident secondary to elevated levels of circulating iodide. The Wolff–Chaikoff effect is an effective means of rejecting a large quantity of imbibed iodide, and therefore preventing the thyroid from synthesizing large quantities of thyroid hormone. Excess iodide transiently inhibits thyroid iodide organification. In individuals with a normal thyroid, the gland eventually escapes from this inhibitory effect and iodide organification resumes; however, in patients with underlying autoimmune thyroid disease, the suppressive action of high iodide may persist.

The Wolff–Chaikoff effect lasts several days (around 10 days), after which it is followed by an "escape phenomenon," which is described by resumption of normal organification of iodine and normal thyroid peroxidase function. "Escape phenomenon" is believed to occur because of decreased inorganic iodine concentration inside the thyroid follicle below a critical threshold secondary to down-regulation of sodium-iodide symporter (NIS) on the basolateral membrane of the thyroid follicular cell.

The Wolff–Chaikoff effect has been used as a treatment principle against hyperthyroidism (especially thyroid storm) by infusion of a large amount of iodine to suppress the thyroid gland. Iodide was used to treat hyperthyroidism before antithyroid drugs such as propylthiouracil and methimazole were developed. Hyperthyroid subjects given iodide may experience a decrease in basal metabolic rate that is comparable to that seen after thyroidectomy. The Wolff–Chaikoff effect also explains the hypothyroidism produced in some patients by several iodine-containing drugs, including amiodarone. The Wolff–Chaikoff effect is also part of the mechanism for the use of potassium iodide in nuclear emergencies.

This page is based on a Wikipedia article written by authors (here).
Text is available under the CC BY-SA 3.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.