Difference between revisions of "Ketone Levels"
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− | There are three important [[Ketones]] involved in [[Ketogenic Diet]]s, Acetoacetic acid (AcAc), Acetone, and Beta-hydroxybutyrate (BOHB). Their levels can vary somewhat independently, and the target levels for different results are not well defined. Blood levels of BOHB from 0.5 to around 3-5.0 mmol/L have been labeled 'nutritional ketosis' and levels over 4.0 mmol/L are probably best for treatment of Epilepsy. | + | There are three important [[Ketones]] involved in [[Ketogenic Diet]]s, Acetoacetic acid (AcAc), Acetone, and Beta-hydroxybutyrate (BOHB). Their levels can vary somewhat independently, and the target levels for different results are not well defined. Blood levels of BOHB from 0.5 to around 3-5.0 mmol/L have been labeled 'nutritional ketosis' and levels over 4.0 mmol/L are probably best for treatment of Epilepsy. My suspicion is that there is a "Goldilocks range" of ketone levels, with higher values indicating insufficient protein intake. It's possible that 1.0-1.5 mmol/L of blood BOHB might be ideal for athletes in order to prevent impaired performance. |
=Relative Levels= | =Relative Levels= | ||
[[File:KetonesProgressiveStarvation.jpg|none|thumb|300px|Changes in blood ketone levels during progressive starvation<ref name="Cahill2006"/>.]] | [[File:KetonesProgressiveStarvation.jpg|none|thumb|300px|Changes in blood ketone levels during progressive starvation<ref name="Cahill2006"/>.]] | ||
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=Target Levels= | =Target Levels= | ||
There are no well-defined targets for Ketone levels at which particular changes occur. The list below is a sampling of the levels I've found used. | There are no well-defined targets for Ketone levels at which particular changes occur. The list below is a sampling of the levels I've found used. | ||
+ | * The classic 1983 study by Dr Phinney measured the athletes blood BOHB as 1.28 mmol/L at rest<ref name="Phinney-1983"/>. This makes me wonder if there is a "Goldilocks effect" to ketone levels. Too high may indicate too little protein, and poor glycogen stores, that may impair endurance performance. | ||
* The level required to be ketogenic (hyperketonemia) has been suggested as 0.2 mmol/L measured as the combination of AcAc and BOHB in whole blood as this is slightly above the levels seen in "normal" individuals<ref name="Robinson-1980"/>. Personally, I'd argue this is too low to be considered ketogenic, as this level is seen in people on a high carbohydrate diet after a night's sleep. | * The level required to be ketogenic (hyperketonemia) has been suggested as 0.2 mmol/L measured as the combination of AcAc and BOHB in whole blood as this is slightly above the levels seen in "normal" individuals<ref name="Robinson-1980"/>. Personally, I'd argue this is too low to be considered ketogenic, as this level is seen in people on a high carbohydrate diet after a night's sleep. | ||
* The book "The Art and Science of Low Carbohydrate Living" calls the range 0.5 to 5.0 mmol/L of blood ketones "nutritional ketosis"<ref name="Phinney-2011-p31"/> | * The book "The Art and Science of Low Carbohydrate Living" calls the range 0.5 to 5.0 mmol/L of blood ketones "nutritional ketosis"<ref name="Phinney-2011-p31"/> | ||
Line 55: | Line 56: | ||
=References= | =References= | ||
<references> | <references> | ||
+ | <ref name="Phinney-1983">SD. Phinney, BR. Bistrian, WJ. Evans, E. Gervino, GL. Blackburn, The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation., Metabolism, volume 32, issue 8, pages 769-76, Aug 1983, PMID [http://www.ncbi.nlm.nih.gov/pubmed/6865776 6865776]</ref> | ||
<ref name="Balasse-1989">EO. Balasse, F. Féry, Ketone body production and disposal: effects of fasting, diabetes, and exercise., Diabetes Metab Rev, volume 5, issue 3, pages 247-70, May 1989, PMID [http://www.ncbi.nlm.nih.gov/pubmed/2656155 2656155]</ref> | <ref name="Balasse-1989">EO. Balasse, F. Féry, Ketone body production and disposal: effects of fasting, diabetes, and exercise., Diabetes Metab Rev, volume 5, issue 3, pages 247-70, May 1989, PMID [http://www.ncbi.nlm.nih.gov/pubmed/2656155 2656155]</ref> | ||
<ref name="HayBond1967">RW Hay, MA Bond, Kinetics of the Decarboxylation of Acetoacetic acid, Australian Journal of Chemistry, volume 20, issue 9, 1967, pages 1823, ISSN [http://www.worldcat.org/issn/0004-9425 0004-9425], doi [http://dx.doi.org/10.1071/CH9671823 10.1071/CH9671823]</ref> | <ref name="HayBond1967">RW Hay, MA Bond, Kinetics of the Decarboxylation of Acetoacetic acid, Australian Journal of Chemistry, volume 20, issue 9, 1967, pages 1823, ISSN [http://www.worldcat.org/issn/0004-9425 0004-9425], doi [http://dx.doi.org/10.1071/CH9671823 10.1071/CH9671823]</ref> |
Latest revision as of 07:07, 18 June 2017
There are three important Ketones involved in Ketogenic Diets, Acetoacetic acid (AcAc), Acetone, and Beta-hydroxybutyrate (BOHB). Their levels can vary somewhat independently, and the target levels for different results are not well defined. Blood levels of BOHB from 0.5 to around 3-5.0 mmol/L have been labeled 'nutritional ketosis' and levels over 4.0 mmol/L are probably best for treatment of Epilepsy. My suspicion is that there is a "Goldilocks range" of ketone levels, with higher values indicating insufficient protein intake. It's possible that 1.0-1.5 mmol/L of blood BOHB might be ideal for athletes in order to prevent impaired performance.
1 Relative Levels
- As shown above, the ratio of AcAc to BOHB can change dramatically during progressive starvation, with BOHB rising far higher than AcAc[1]. Also, during diabetic ketoacidosis (DKA), the ratio of BOHB:AcAc rises from normal (1:1) to as high as 10:1[2].
- Urine ketone levels vary with the time of day, often being lower in the morning[3]
- The ratio between AcAc and Acetone appears reasonably constant, and is based on the spontaneous, one way decomposition of AcAc into Acetone[4].
- Ketone levels in the general population tend to rise from a low level during exercise, but those on a ketogenic diet will typically see their ketones fall from their normal elevated level during exercise[5].
2 Target Levels
There are no well-defined targets for Ketone levels at which particular changes occur. The list below is a sampling of the levels I've found used.
- The classic 1983 study by Dr Phinney measured the athletes blood BOHB as 1.28 mmol/L at rest[6]. This makes me wonder if there is a "Goldilocks effect" to ketone levels. Too high may indicate too little protein, and poor glycogen stores, that may impair endurance performance.
- The level required to be ketogenic (hyperketonemia) has been suggested as 0.2 mmol/L measured as the combination of AcAc and BOHB in whole blood as this is slightly above the levels seen in "normal" individuals[7]. Personally, I'd argue this is too low to be considered ketogenic, as this level is seen in people on a high carbohydrate diet after a night's sleep.
- The book "The Art and Science of Low Carbohydrate Living" calls the range 0.5 to 5.0 mmol/L of blood ketones "nutritional ketosis"[8]
- The follow on book "The Art and Science of Low Carbohydrate Performance" suggests that BOHB levels of 0.5 mmol/L to 3.0 mmol/L is "optimal"[9], with benefits starting at 0.5 mmol/L and improving to 3.0 mmol/L, but levels above 3.0 mmol/L not producing additional benefits[10]. (It is unclear what research these levels are based on.)
- For epilepsy, the recommendation is for AcAc to be 80-160 mmol/L as measured by urine dipstick[11], though this level is not necessarily sufficient[12].
- The range of 2 to 7 mmol/L[13] or 2 to 5 mmol/L[14] has been suggested in some literature as a "therapeutic" range.
- A study of 74 children on the ketogenic diet for epilepsy found that blood BOHB levels of greater than 4 mmol/L were correlated with better seizure control than those with lower levels[12].
- A 28 day study of five Parkinson's patients on the Ketogenic Diet had blood BOHB levels averaging 6.6 mmol/L (range 4.8 to 8.9) and showed some signs of improvements, though the study was too small for any conclusions to be drawn [13].
3 Example levels
From "Physiological roles of ketone bodies as substrates and signals in mammalian tissues"[7]:
Situation | Ketone Levels (Blood levels of AcAc + BOHB) |
---|---|
Fed | ~0.1 |
Fasted 12-24 Hours | Up to 0.3 |
Fasted 48-72 Hours | 2-3 |
Fasted 5-6 weeks (plateau) | ~8 |
Post exercise | Up to 2 |
Late Pregnancy | Up to 1 |
Late Pregnancy, fasted 48 hours | 4-6 |
Neonatal | 0.5-1.0 |
Hypoglycemia | 1-5 |
Uncontrolled diabetes | Up to 25 (dangerous ketoacidosis) |
4 See Also
- The classifications and types of Low Carbohydrate Diet.
- An introduction to the Ketogenic Diet.
- My experiences with ultrarunning on the Ketogenic Diet
- How the Ketogenic Diet can be used for the treatment and management of disease.
- Health Risks of the Ketogenic Diet
- The time frame and changes that occur with Ketoadaptation
- What are Ketones
- How to measure Ketones
- What ketone levels to aim for
- The pros and cons of the Ketogenic Diet for athletes
- The Types of Ketogenic Diet
- My Ketogenic Recipes
- Non-Ketogenic Low Carbohydrate Diets
5 References
- ↑ 1.0 1.1 George F. Cahill, Fuel Metabolism in Starvation, Annual Review of Nutrition, volume 26, issue 1, 2006, pages 1–22, ISSN 0199-9885, doi 10.1146/annurev.nutr.26.061505.111258
- ↑ L. Laffel, Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes., Diabetes Metab Res Rev, volume 15, issue 6, pages 412-26, PMID 10634967
- ↑ Eric. Kossoff, Ketogenic diets : treatments for epilepsy and other disorders, date 2011, publisher Demos Health, location New York, isbn 1-936303-10-8, Kindle Offset 2274
- ↑ RW Hay, MA Bond, Kinetics of the Decarboxylation of Acetoacetic acid, Australian Journal of Chemistry, volume 20, issue 9, 1967, pages 1823, ISSN 0004-9425, doi 10.1071/CH9671823
- ↑ EO. Balasse, F. Féry, Ketone body production and disposal: effects of fasting, diabetes, and exercise., Diabetes Metab Rev, volume 5, issue 3, pages 247-70, May 1989, PMID 2656155
- ↑ SD. Phinney, BR. Bistrian, WJ. Evans, E. Gervino, GL. Blackburn, The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation., Metabolism, volume 32, issue 8, pages 769-76, Aug 1983, PMID 6865776
- ↑ 7.0 7.1 AM. Robinson, DH. Williamson, Physiological roles of ketone bodies as substrates and signals in mammalian tissues., Physiol Rev, volume 60, issue 1, pages 143-87, Jan 1980, PMID 6986618
- ↑ Phd Stephen D. Phinney MD, Rd Jeff S. Volek Phd, The Art and Science of Low Carbohydrate Living: An Expert Guide to Making the Life-saving Benefits of Carbohydrate Restriction Sustainable and Enjoyable, 2011, publisher Beyond Obesity LLC, isbn 978-0-9834907-0-8, Page 31
- ↑ Jeff Volek, Stephen D. Phinney, The Art and Science of Low Carbohydrate Performance: A Revolutionary Program to Extend Your Physical and Mental Performance Envelope, 2012, publisher Beyond Obesity, isbn 978-0-9834907-1-5, Page 155
- ↑ Jeff Volek, Stephen D. Phinney, The Art and Science of Low Carbohydrate Performance: A Revolutionary Program to Extend Your Physical and Mental Performance Envelope, 2012, publisher Beyond Obesity, isbn 978-0-9834907-1-5, Page 157
- ↑ Eric. Kossoff, Ketogenic diets : treatments for epilepsy and other disorders, date 2011, publisher Demos Health, location New York, isbn 1-936303-10-8, Page 201
- ↑ 12.0 12.1 DL. Gilbert, PL. Pyzik, JM. Freeman, The ketogenic diet: seizure control correlates better with serum beta-hydroxybutyrate than with urine ketones., J Child Neurol, volume 15, issue 12, pages 787-90, Dec 2000, PMID 11198492
- ↑ 13.0 13.1 TB. Vanitallie, C. Nonas, A. Di Rocco, K. Boyar, K. Hyams, SB. Heymsfield, Treatment of Parkinson disease with diet-induced hyperketonemia: a feasibility study., Neurology, volume 64, issue 4, pages 728-30, Feb 2005, doi 10.1212/01.WNL.0000152046.11390.45, PMID 15728303
- ↑ RL. Veech, B. Chance, Y. Kashiwaya, HA. Lardy, GF. Cahill, Ketone bodies, potential therapeutic uses., IUBMB Life, volume 51, issue 4, pages 241-7, Apr 2001, doi 10.1080/152165401753311780, PMID 11569918