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Lipidaholics Anonymous Case 291: Can losing weight worsen lipids?

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Lipidaholics Anonymous Case 291:   Can losing weight worsen lipids?

As a result of the epidemic of insulin resistance (IR) plaguing the world, and for sure the United States, the evils of carbohydrates are becoming realized. Large numbers of patients are now following any one of the many low carbohydrate, and even

 

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0 # pauleis 2013-06-23 04:09
Hi Dr. Dayspring,
Thank you for what seems to be the first in-depth analysis of the "Paleo-Lipid" condition. You state
"Many of the low carbers and Paleo folks not only
ingest increased saturated fat but also
cholesterol (love their eggs and shellfish) – would
one expect that to also contribute to
the increased cholesterol levels seen in some? The
answer is no:"

Do you consider that to be true for everyone, including "hyper-responde rs" and "hyper-absorbers"?
Thank you
Paul
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0 # tdayspring 2013-06-23 11:43
Quoting pauleis:
Hi Dr. Dayspring,
Thank you for what seems to be the first in-depth analysis of the "Paleo-Lipid" condition. You state
"Many of the low carbers and Paleo folks not only
ingest increased saturated fat but also
cholesterol (love their eggs and shellfish) – would
one expect that to also contribute to
the increased cholesterol levels seen in some? The
answer is no:"

Do you consider that to be true for everyone, including "hyper-responders" and "hyper-absorbers"?
Thank you
Paul

Quoting pauleis:
Hi Dr. Dayspring,
Thank you for what seems to be the first in-depth analysis of the "Paleo-Lipid" condition. You state
"Many of the low carbers and Paleo folks not only
ingest increased saturated fat but also
cholesterol (love their eggs and shellfish) – would
one expect that to also contribute to
the increased cholesterol levels seen in some? The
answer is no:"

Do you consider that to be true for everyone, including "hyper-responders" and "hyper-absorbers"?
Thank you
Paul



Paul: That is true in almost anyone because the vast majority of cholesterol that will be absorbed in the gut is of biliary. not exogenous (eaten) origin. Typically the pool of cholesterol that will be absorbed is 85% exogenous origin and 15% eaten. In a normal person ~50% of that pool will actually make it in. So unless one is eating tremendous amounts of cholesterol, dietary cholesterol is not a player. Even in a hyperabsorber, most of the cholesterol absorbed will have been produced within their cells, returned to the liver within lipoproteins, excreted into the bile by hepatocytes and then enter the gut where it will be subject to to absorption or excretion in stool.
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0 # tdayspring 2013-06-23 11:44
Quoting tdayspring:
Quoting pauleis:
Hi Dr. Dayspring,
Thank you for what seems to be the first in-depth analysis of the "Paleo-Lipid" condition. You state
"Many of the low carbers and Paleo folks not only
ingest increased saturated fat but also
cholesterol (love their eggs and shellfish) – would
one expect that to also contribute to
the increased cholesterol levels seen in some? The
answer is no:"

Do you consider that to be true for everyone, including "hyper-responders" and "hyper-absorbers"?
Thank you
Paul

Quoting pauleis:
Hi Dr. Dayspring,
Thank you for what seems to be the first in-depth analysis of the "Paleo-Lipid" condition. You state
"Many of the low carbers and Paleo folks not only
ingest increased saturated fat but also
cholesterol (love their eggs and shellfish) – would
one expect that to also contribute to
the increased cholesterol levels seen in some? The
answer is no:"

Do you consider that to be true for everyone, including "hyper-responders" and "hyper-absorbers"?
Thank you
Paul



Paul: That is true in almost anyone because the vast majority of cholesterol that will be absorbed in the gut is of biliary. not exogenous (eaten) origin. Typically the pool of cholesterol that will be absorbed is 85% exogenous origin and 15% eaten. In a normal person ~50% of that pool will actually make it in. So unless one is eating tremendous amounts of cholesterol, dietary cholesterol is not a player. Even in a hyperabsorber, most of the cholesterol absorbed will have been produced within their cells, returned to the liver within lipoproteins, excreted into the bile by hepatocytes and then enter the gut where it will be subject to to absorption or excretion in stool.


Note typo above: 85% of absorbed cholesterol is of ENDOGENOUS not exogenous origin. Sorry TD
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0 # pauleis 2013-06-23 22:27
Dr Dayspring:

Thank you for your prompt response. So does this mean, more or less, that 7.5% of serum cholesterol is of dietary origin - so that, say, cutting cholesterol by half would reduce LDL-C by +/- 3.75%? Or is this too simplistic? And is this pretty much the same for everyone?

Thank you, Paul
.
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0 # tdayspring 2013-06-24 02:55
Quoting pauleis:
Dr Dayspring:

Thank you for your prompt response. So does this mean, more or less, that 7.5% of serum cholesterol is of dietary origin - so that, say, cutting cholesterol by half would reduce LDL-C by +/- 3.75%? Or is this too simplistic? And is this pretty much the same for everyone?

Thank you, Paul
.


We are speaking generalities: Every single person is different. Of the gut pool of cholesterol that is available for absorption, on average 15% will be of exogenous and 85% of endogenous (cellular) origin.Of that pool, 20-80% will be absorbed depending on the multiple physiologic steps involved. Without doing labeled cholesterol studies there is no way to derive the figure that you tried to guess in your question. Of course our mission is to lower LDL-P -it is not really meaningful what we do to LDL-C
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0 # pauleis 2013-06-24 04:32
Dr Dayspring,

Thank you again - only (hopefully) one more question - you gave a range - 20-80% to further refine the "...~50 of that pool..."; Is there also an expected range for the "...15% wil be of exogenous..."?

Thank you, Paul
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0 # tdayspring 2014-07-15 23:22
Quoting pauleis:
Hi Dr. Dayspring,
Thank you for what seems to be the first in-depth analysis of the "Paleo-Lipid" condition. You state
"Many of the low carbers and Paleo folks not only
ingest increased saturated fat but also
cholesterol (love their eggs and shellfish) – would
one expect that to also contribute to
the increased cholesterol levels seen in some? The
answer is no:"

Do you consider that to be true for everyone, including "hyper-responders" and "hyper-absorbers"?
Thank you
Paul


Unless one is eating gigantic amounts of cholesterol it would be most unlikely that ingested cholesterol quantities would equal biliary amounts. Thus in the vast majority of cases the gut pool of cholesterol available for absorption would be mostly of biliary origin. Also folks hypersynthesizi ng cholesterol (due to fat intake) tend to be hypoabsorbers.

TDD
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0 # ebyman 2013-06-25 18:38
Tom,
Interesting case on the paleo diet.
Given that
A) it appears that a ketotic state can lead to fatty acids being converted to cholesterol, and
B) a low-carb diet improves insulin resistance,
can we reasonably conclude that for IR patients at risk for CAD, the best diet is an ALMOST-ketotic diet? (i.e. consume just enough carbs, probably in small but frequent ingestions, to keep the body from entering a ketotic state). I'm wondering if the additions of oatmeal and apples to the case-patient's diet were just enough to tip her away from ketosis and its associated cholesterol production.
For patients who are that serious about getting the "perfect" balance in their diet, should we order a box of UA test strips so they can figure out when they're spilling ketones, and what level carb intake is needed to prevent it?
EB
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0 # tdayspring 2013-06-25 19:24
Eric - regarding your question above: We will never truly know the answers you seek without properly designed trials: The true Paleo folks want to be ketotic as they perceive multiple benefits on many chronic disease states including cancer and dementia. Right now we estimate a third of low carb/high fat eaters develop seriously high LDL-P (and high LDL-C - no discordance). If we believe using conventional tools that they are at risk and they elect not to stop full ketosis (with some degree of saturated fat restriction, than (because they are hypersynthesize rs of cholesterol, a statin would seem to be a logical option, although many in the Paleo community are very anti-drug.

For those not so ketosis driven, lessening saturated fat is needed (the amount to restrict is likely very variable per given individual and would be determined by trial and error) to reduce LDL-C and LDL-P.

The nutritional alterations in the woman in case 191 that worked for her - might not work for the next and both Oatmeal and apples do bring more carbs back into play - so serious markers of IR should be followed.

The serious Paleo guys monitor ketones by a blood stick (not urine) 3-4 times a day. These are very serious dudes!

Regards, TD
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0 # Paula 2013-06-27 01:28
6/26/13 Hi Dr. Dayspring. I consulted the Bible (Gary Taubes' GC, BC) and p. 25-26 mentions the Masai nomads in Kenya (a facially very beautiful people by the way) in 1962 who had blood cholesterol levels among the lowest ever measured in spite of living exclusivly on milk, blood and occasionally meat of the cattle they herded. Nearly 3000 cal a day of mostly saturated fat.
George Mann, early director of the Framingham Heart Study, examined the Masai & concluded they refuted Keys' hypothesis. Mann reported that the Masai indeed had extensive atherosclerosis despite their low cholesterol without suffering heart attacks or any other symptoms of CVD.
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0 # tdayspring 2013-06-27 01:37
Quoting Paula:
6/26/13 Hi Dr. Dayspring. I consulted the Bible (Gary Taubes' GC, BC) and p. 25-26 mentions the Masai nomads in Kenya (a facially very beautiful people by the way) in 1962 who had blood cholesterol levels among the lowest ever measured in spite of living exclusivly on milk, blood and occasionally meat of the cattle they herded. Nearly 3000 cal a day of mostly saturated fat.
George Mann, early director of the Framingham Heart Study, examined the Masai & concluded they refuted Keys' hypothesis. Mann reported that the Masai indeed had extensive atherosclerosis despite their low cholesterol without suffering heart attacks or any other symptoms of CVD.




This scenerio where people get atherosclerosis in the face of low LDL-C isusually where there is discordance with LDL-P. Had LDL-P been measured, you likely would have found the cause of their atherosclerosis (very high LDL particle nukber). Of course back then LDL-P testing was not available. Never forget it is lipoproteins that traffic sterols into the artery TD
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0 # Paula 2013-06-27 03:02
Quoting tdayspring:
Quoting Paula:
6/26/13 Hi Dr. Dayspring. I consulted the Bible (Gary Taubes' GC, BC) and p. 25-26 mentions the Masai nomads in Kenya (a facially very beautiful people by the way) in 1962 who had blood cholesterol levels among the lowest ever measured in spite of living exclusivly on milk, blood and occasionally meat of the cattle they herded. Nearly 3000 cal a day of mostly saturated fat.
George Mann, early director of the Framingham Heart Study, examined the Masai & concluded they refuted Keys' hypothesis. Mann reported that the Masai indeed had extensive atherosclerosis despite their low cholesterol without suffering heart attacks or any other symptoms of CVD.




This scenerio where people get atherosclerosis in the face of low LDL-C is usually where there is discordance with LDL-P. Had LDL-P been measured, you likely would have found the cause of their atherosclerosis (very high LDL particle number). Of course back then LDL-P testing was not available. Never forget it is lipoproteins that traffic sterols into the artery TD


But how do you explain their apparent lack of CVD? Perhaps they are protected from it, as you hypothesize might be the case with "Paleos" (tho the Masai of course drink milk which makes them non-Paleo). I wonder if their "lack of CVD" WAS only apparent. Perhaps drinking milk which has a lot of sugar in it was a problem as far as particle #. Other subject: Your saying my ApoB of 98 was way too high and should be < 80 but this link re ApoB targets says quite a bit else...
emedicine.medscape.com/article/2087335-overview
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-1 # RE: Lipidaholics Anonymous Case 291: Can losing weight worsen lipids?bbradfor 2013-06-30 01:01
Hi Dr. Dayspring; I found this article both a relief and alarming as I am very similar to this woman. I started a low carb diet over a year ago and my TC and LDL-C just keep climbing, although i've lost almost 20 pounds. I do exercise 3-5 days per week. My Dr. insists I go on statins, but will -not measure my apo-B. I am also menopausal. I thought from reading Gary Taubes and Peter Attia most statins only increase HDL-C (mine is already high) and do not work to reduce Apo -B. Your final comment appears to state otherwise. thank you
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0 # tdayspring 2013-06-30 02:32
Quoting bbradfor:
Hi Dr. Dayspring; I found this article both a relief and alarming as I am very similar to this woman. I started a low carb diet over a year ago and my TC and LDL-C just keep climbing, although i've lost almost 20 pounds. I do exercise 3-5 days per week. My Dr. insists I go on statins, but will -not measure my apo-B. I am also menopausal. I thought from reading Gary Taubes and Peter Attia most statins only increase HDL-C (mine is already high) and do not work to reduce Apo -B. Your final comment appears to state otherwise. thank you



Tough to truly understand CV risk without apoB or LDL-P measurements. One could have high LDL-C, but if LDL particles are large LDL-P might be normal and not associated with CV risk. Main action of statins is to lower apoB but they often need help if the level is very high. Statins can with variation raise HDL-P which is likely beneficial. What they do to HDL-C is is not related to benefit
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-1 # RE: Lipidaholics Anonymous Case 291: Can losing weight worsen lipids?herbertg 2013-07-01 05:31
Tom,
Thanks for this enthralling and fascinating case. Does anyone know what it is in those outliers with a high LDL-P that make them resistant to LDL becoming trapped in the sub-endothelial space?
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+1 # RE: Lipidaholics Anonymous Case 291: Can losing weight worsen lipids?NYG 2013-08-12 23:27
Some of what needs to be be considered by those going Paleo and hi sat fat I would think might be prior CAD status, family history, and their age. Those above 50 might already have CAD, and I wonder Dr. Dayspring if with advancing age going hi sat fat and seeing LDL-P soar might mean the same risk profile as those who have been on the SAD diet and have hi LDL-P count.
Your recommendation for reduced sat fat, and staying out of ketosis. albeit on a reduced carb diet seems to be the most sensible way to go in my view. I am not IR, but generate tons of LDL-P on low carb hi sat fat; or hi carb oriented diet. Strong history of CAD. I reduce the sat fat- add mono and poly, keep carbs low, and take meds. Lowest 5% LDL-P with that regimen.
The internet has a lot of nonsense on it regarding this topic; thanks for bringing clarity to very important issues.
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0 # rfshaffner 2013-08-25 13:17
Dr. Dayspring -- Thank you for this and all that you do to help educate everyone (laymen and doctors) on these vitally important topics.
I wonder how this patients' LDL-P numbers might have changed after being weight-stable for a period of time. You and others have mentioned that theory -- that the TC and LDL-P numbers were high from the dramatic weight loss. Do we have many (or any) cases of high numbers dropping back down, after the new norm is established and the body is no longer burning so much of its own fat?

Thanks again!
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-1 # tdayspring 2013-08-25 20:51
Quoting rfshaffner:
Dr. Dayspring -- Thank you for this and all that you do to help educate everyone (laymen and doctors) on these vitally important topics.
I wonder how this patients' LDL-P numbers might have changed after being weight-stable for a period of time. You and others have mentioned that theory -- that the TC and LDL-P numbers were high from the dramatic weight loss. Do we have many (or any) cases of high numbers dropping back down, after the new norm is established and the body is no longer burning so much of its own fat?

Thanks again!



Weight loss can be associated wiith a transient raise in TC and LDL-C but not LDL-P
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0 # tdayspring 2013-09-03 12:18
Quoting tdayspring:
Quoting rfshaffner:
Dr. Dayspring -- Thank you for this and all that you do to help educate everyone (laymen and doctors) on these vitally important topics.
I wonder how this patients' LDL-P numbers might have changed after being weight-stable for a period of time. You and others have mentioned that theory -- that the TC and LDL-P numbers were high from the dramatic weight loss. Do we have many (or any) cases of high numbers dropping back down, after the new norm is established and the body is no longer burning so much of its own fat?

Thanks again!



Weight loss can be associated wiith a transient raise in TC and LDL-C but not LDL-P



Extreme weight loss, as in anorexia can significantly raise TC and LDL-C but not LDL-P: the rise in the former is due to increase in LDL size, not LDL particle number. Fat cells are a major repository of cholesterol.

Dr Dayspring
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0 # makinghealthy 2013-09-01 07:37
It appears that one can stay in keto and reduce lipids.
By just adjusting the Sat: Mono: Poly ratios.
Some Individual experimenting required.
Fatty acids have different effects on LDL receptor take-up in the liver. One should use a variety of fatty acids.
lauric , Myristic and Palmitic are that fats that raise Apo B in serum ... Other saturated fats like stearic do not, nor do shorter chain fatty acids. Some fatty acids ( MUFA and PUFA ) will lower ApoB. So an individual needs to find the right balance for their particular gene expression

EG
Keto diets for epilepsy
"One of the major concern while giving a high fat diet is, maintaining lipid levels.We use a combination of oils & ghee ( different types of fatty acids ) to maintain lipid levels at or near normal values. We use a combination of Groundnut oil ( MUFA ), Corn oil or Safflower oil ( PUFA) and Ghee ( Clarified butter – Saturated fat ) in a proportion of 2:1:1."
http://www.ketogenicdietindia.org/inket_scr.asp.htm

Also here
Where olive and flax oils were used

Long term effects of ketogenic diet in obese subjects with high cholesterol level.

"The level of total cholesterol, LDL cholesterol, triglycerides and blood glucose level decreased significantly (P < 0.0001), whereas HDL cholesterol increased significantly (P < 0.0001) after the treatment in both groups."

http://www.ncbi.nlm.nih.gov/pubmed/16652223
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0 # makinghealthy 2013-09-01 08:14
Tables in this study show good reduction in APo B and good increase in Apo A-1. Not keto , but demonstrates how different fatty acids alter gene expression.
Have a look at table 3
Again need a balance all PUFA would not be good either.
http://ajcn.nutrition.org/content/53/3/660.long

Also thank you for this info I did not know this.
"Weight loss can be associated with a transient raise in TC and LDL-C but not LDL-P"
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0 # tdayspring 2013-09-03 12:20
Quoting makinghealthy:
Tables in this study show good reduction in APo B and good increase in Apo A-1. Not keto , but demonstrates how different fatty acids alter gene expression.
Have a look at table 3
Again need a balance all PUFA would not be good either.
http://ajcn.nutrition.org/content/53/3/660.long

Also thank you for this info I did not know this.
"Weight loss can be associated with a transient raise in TC and LDL-C but not LDL-P"


ApoA-I is not a validated target of therapy - in fact in several trials its rise had no correlation with outcomes. Tells us nothing about HDL functionality.

Dr Dayspring
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+2 # RE: Lipidaholics Anonymous Case 291: Can losing weight worsen lipids?rfshaffner 2013-09-03 12:37
I just read Cholesterol Clarity. I believe Dr. Westman said that lipid panels can be misleading for those who are actively losing weight (probably for the same reason). He suggests waiting until the patient's weight is stable before giving much weight to lipid numbers.
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0 # tdayspring 2013-09-03 18:08
Quoting rfshaffner:
I just read Cholesterol Clarity. I believe Dr. Westman said that lipid panels can be misleading for those who are actively losing weight (probably for the same reason). He suggests waiting until the patient's weight is stable before giving much weight to lipid numbers.


Lipid panels yes, but not lipoprotein analyses. Do not confuse lipid testing with lipoprotein testing. Normally we wait 8-12-16 weeks before doing lipid/lipoprote in follow-up analyses after dietary or drug therapies. By that time the usually both lipid and almost always lipoprotein values are stabilized: however risk more accurately depends on LDL-P (apoB), so I also would not get upset if LDL-C increases as long as LDL-P or apoB do not.

Dr Dayspring
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0 # rfshaffner 2013-09-03 12:55
As Dr. Attia explains in a video on his website, Ancel Keys and others blamed saturated fats inappropriately . The focus on LDL has helped support that mistaken belief and make it last for decades.

I've found a number of nutrition studies that concluded saturated fats were bad only because they raised LDL (the outcome measured), and LDL was considered the #1 CV risk factor.

So this all makes perfect sense now. Saturated fats have not been shown to cause problems (except perhaps in the presence of plenty of carbs, where insulin levels are high). But they can cause LDL to go up, and until recently, that was assumed to be bad.
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0 # tdayspring 2013-09-03 18:03
Quoting rfshaffner:
As Dr. Attia explains in a video on his website, Ancel Keys and others blamed saturated fats inappropriately. The focus on LDL has helped support that mistaken belief and make it last for decades.

I've found a number of nutrition studies that concluded saturated fats were bad only because they raised LDL (the outcome measured), and LDL was considered the #1 CV risk factor.

So this all makes perfect sense now. Saturated fats have not been shown to cause problems (except perhaps in the presence of plenty of carbs, where insulin levels are high). But they can cause LDL to go up, and until recently, that was assumed to be bad.



Please note that there is no lab test called LDL - you are referring to LDL-cholesterol or LDL-C. Never confuse LDL-C with LDL-P. You are correct in stating that because saturated fat can raise LDL-C it is uniformly condemned - when in fact outcome trials in fact are needed. Often the high fat diet increases LDL size and hence LDL-C without raising LDL-P. That is not likely to be a concern.However there are some cases where a high saturated fat diet can raise both LDL-C and LDL-P, even to horrific levels, and until proven otherwise that has to be assumed to be risky.
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0 # rfshaffner 2013-09-03 19:01
I understand, and thank you!

When will LDL-C or ApoB become part of the std lipid panel? Will ATP IV (or whatever they come out with) spur that along?
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0 # rfshaffner 2013-09-03 19:03
I meant when will LDL-P or ApoB become part of the std test. (Until they do, too many will continue to focus on the wrong things.)
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0 # bbradfor 2013-09-04 00:23
Dr. Dayspring, in one of your many lectures I have listened to you mention that, or at least I understood that a poor man's apoB/a1 ratio is TC/HDL-C. Would you have a poor man's estimate for calculating apoB? They do not measure this in Canada; wondering if there might be a correlation to HDL-C that one could use? thanks very much
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0 # tdayspring 2013-09-04 13:41
Quoting bbradfor:
Dr. Dayspring, in one of your many lectures I have listened to you mention that, or at least I understood that a poor man's apoB/a1 ratio is TC/HDL-C. Would you have a poor man's estimate for calculating apoB? They do not measure this in Canada; wondering if there might be a correlation to HDL-C that one could use? thanks very much


Of course the term "poor man's" also means not as good. With respect to a free marker of apoB, it would be non-HDL-C which is calculated as TC minus HDL-C. Currently the accepted values is 30 mg/dL greater than the desired LDL-C although new data has shown we have to lower the non-HDL-C goals to ~ 10-15 mg/dL above LDL-C goals. Please note that apoB is widely available in Canada. Canada was the first country to incllude apoB into their treatment goals
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0 # Norm 2014-01-23 11:39
Hi Dr Dayspring,

What is your take on the theory that on a low carb diet it could be the lower thyroid function but not the saturated fat that might be affecting the clearance of LDL-P or LDL-C?

Thanks
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+1 # tdayspring 2014-01-23 15:27
Quoting Norm:
Hi Dr Dayspring,

What is your take on the theory that on a low carb diet it could be the lower thyroid function but not the saturated fat that might be affecting the clearance of LDL-P or LDL-C?

Thanks


Who knows? Like any hypothesis it would have to be proved or disproved in a properly designed clinical trial. Regardless, one can easily test to see if hypothyroidism is at play. Thyroid hormone is involved with the expression of LDL receptors (LDLr). There is less expression of LDLr in hypothyroid states leading to decreased apoB-particle clearance and thus higher levels of LDL-C, TC, and TG. Recently there has been a move to recognize subclinical hypothyroidism and in persons with significant CV risk, to treat.
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0 # busterblooth 2014-01-27 16:34
Dr. Dayspring,

Thanks for your interesting and informative comments on this topic. By way of background, I am a 33 year old physician. Approximately 12 weeks ago, I adopted a VLCKD. In the interim, I have lost 25 pounds (16% BF to about 10%), stopped snoring (says my wife), and stopped an ACEi. I would say that I a easily feel and look the best I have ever felt. I lift heavily 3-4/week and run 5-7 miles once or twice per week. In trying to put the following in proper perspective, I should also note no strong family history of early vascular disease, although an uncle and GF had CABGs in their 70s.

Regarding advanced lipid tests, my LDL-P is approximately 1400 (correlating to an LDL-C of 179, which represents a doubling from last value approximately 2.5 years ago), so it probably represents a rise in value. The remainder of my lab tests (including fasting insulin, which was below normal, actually) were stellar and in keeping with expected, in particular my HDL-P was 36.5, which I'm guessing based on the quartiles provided by Liposcience puts me 2.5 SD from their mean.

In trying to understand the implications of these changes, I found the 2012 paper by Mackey, et al (http://www.ncbi.nlm.nih.gov/pubmed/22796256), which I can't seem to find commented on anywhere else, despite what seem to be some important implications.

I would love to hear your thoughts and comments on the paper. My understanding of it is the following:

(1) LDL-P remained a strong independent predictor of IMT and incident CAD, with a RR of 1.29 per 1 SD above mean.

(2) Inverse correlations between HDL-C and CAD may be reflective of secondary effects on HDL-C of other factors, since inverse correlations between HDL-C and IMT were attenuated after adjusting for HDL-P.

(3) After adjusting for covariates, LDL-C, LDL-P, and HDL-C, HDL-P maintained a strong inverse relationship to both IMT and incident CAD. The numbers were impressive: -22.2 μm IMT per 1 SD above mean, and 0.75 RR for CAD per 1 SD above mean. Importantly, after adjusting for HDL-C, very high-levels of HDL-P still correlated strongly and inversely with incident CAD, suggesting the protective effect of "high HDL" likely is mediated by the high particle number, rather than high HDL-C (which had a strong direct relationship with IMT/CAD after adjusting for HDL-P).

Reflective of my situation, I conclude that I am probably a hyper-responder who needs to cut back a bit on saturated fat and perhaps add back 50-100 grams of starches and ensure no micronutrient deficiencies are affected LDLr processing. Despite this, my understanding of this paper suggests that my current 1 SD increase in LDL-P (and 30% increased risk) is largely offset by my >2 SD increase in HDL-P (suggesting that 30% increased relative risk may be more like 15%).

Thanks in advance...
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0 # kells 2014-02-02 01:29
Interesting. I wonder if my husband would benefit from similar dietary changes as this patient. He's 51, type 1 diabetic (diagnosed at age 4), very well-managed, physically active, quite healthy overall, stocky build but not overweight (per BMI and waist circum), great BP and lipid profile…except for LDL-P, which he just had tested for the first time: 1,730 nmol/L. Eats moderate carb.
TC 189; LDL-C 120; HDL-C 55; TG 68; small LDL-P 651 (is that a concern?); LDL size 21.2; most recent A1-C 6.5; LP-IR
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0 # tdayspring 2014-02-02 21:21
Quoting kells:
Interesting. I wonder if my husband would benefit from similar dietary changes as this patient. He's 51, type 1 diabetic (diagnosed at age 4), very well-managed, physically active, quite healthy overall, stocky build but not overweight (per BMI and waist circum), great BP and lipid profile…except for LDL-P, which he just had tested for the first time: 1,730 nmol/L. Eats moderate carb.
TC 189; LDL-C 120; HDL-C 55; TG 68; small LDL-P 651 (is that a concern?); LDL size 21.2; most recent A1-C 6.5; LP-IR


We cannot comment on individual therapies. Understand that a total LDL-P of > 1600 nmol/L is above the 80th percentile population cut point and is considered high risk. Should be discussed with a professional cognizant of such biomarkers
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0 # kells 2014-02-03 15:55
Thank you, understood, of course. Though I am a physician, my Hubby is working with a new doctor who ordered the advanced lipid profile and whose advice is to try VLC for a while (
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0 # tdayspring 2014-02-04 21:52
I have commented on the MESA paper many times: watch my lectures on HDL complexities or go to www.biomarker bliki and read the HDL treatise by Remaley and myself Under topics choose HDL

Your are correct: LDL-P is an independent predictor of CIMT risk

Low HDL-C is for the most part meaningless in an indiividual patient as it is at best an epiphenomenon reflective of other CV pathologies -- one of them being elevated LDL-P. When we see low HDL-C we need to search for other (treatable) risk factors. If none are found (after a serious work up) then the low HDL-C may have little clinical meaning

You are also correct that HDL-P is a much better biomarker than HDL-C - but the problem is that it is still possible to not be protected by high numbers of HDL particles of the HDL [particles themselves are dysfunctional. Unfortunately we have no readily available marker of HDL fucntionality. Who knows if your HDL particles have or do not have antiatherogenic capabilities.

I agree with your suggested therapeutic ideas.

Finally, relative risk has little meaning in individual patients. Without an assessment of HDL functionality your statement or reasoning about the elevated HDL-P mitigating your risk may be true or it may not be true -- We need to know is everyone with high LDL-P doomed or for whatever reason are there folks (like you) with high LDL-P who really are not at risk.

TD
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+1 # Ketosis or saturated fat?stathie@gmail.com 2014-04-29 03:59
Dear Dr. Dayspring,

Your explanation seems to imply that the danger is solely from the following situation: when "ketone bodies are in excess, β-hydroxybutyri c acid utilizes a dehydrogenase enzyme and converts to acetoacetate which can then enter the cholesterol synthesis pathway by joining with acetyl-CoA in reforming HMG-CoA which in turn then enters the cholesterol synthesis pathway". But what does this have to do with saturated fat? Presumably nutritional ketosis (i.e. excess ketone bodies) is possible without excess saturated fat, which, by your explanation above, could lead to excess cholesterol synthesis.

So what is the danger: saturated fat, or being in nutritional ketosis?

Many thanks,
ST
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0 # RE: Ketosis or saturated fat?tdayspring 2014-05-28 11:28
Quoting :
Dear Dr. Dayspring,

Your explanation seems to imply that the danger is solely from the following situation: when "ketone bodies are in excess, β-hydroxybutyric acid utilizes a dehydrogenase enzyme and converts to acetoacetate which can then enter the cholesterol synthesis pathway by joining with acetyl-CoA in reforming HMG-CoA which in turn then enters the cholesterol synthesis pathway". But what does this have to do with saturated fat? Presumably nutritional ketosis (i.e. excess ketone bodies) is possible without excess saturated fat, which, by your explanation above, could lead to excess cholesterol synthesis.

So what is the danger: saturated fat, or being in nutritional ketosis?

Many thanks,
ST


Saturated fat is what best activates cholesterolgeni c genes
TD
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0 # Unclear root causembertler 2014-05-27 17:41
First- tremendous article. I see this lecture frequently cited on this interesting and very real phenomenon- most helpful! One question- at the end, there appears to be conflicting recommendations , as noted in the comment above. Is the root issue of cholesterol over-synthesis primarily driven from "saturated fat" in an over abundance, or is the root issue being in a ketogenic state? It is unclear to me if saturated fat is reduced, and that saturated fat is replaced with MUFA/PUFA (still remaining in a ketotic state), if this cholesterol over synthesis remains possible? Are the metabolic pathways you note for saturated fat (where ketone/choleste rol production cross paths) possible with MUFA/PUFA? In this case, the patient appears to have "softened" both sat fat intake and ketosis, somewhat confusing the true driver in this instance.
Thx again, your insight into these real problems is appreciated by the entire community!
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0 # RE: Unclear root causetdayspring 2014-05-28 11:25
Quoting mbertler:
First- tremendous article. I see this lecture frequently cited on this interesting and very real phenomenon- most helpful! One question- at the end, there appears to be conflicting recommendations, as noted in the comment above. Is the root issue of cholesterol over-synthesis primarily driven from "saturated fat" in an over abundance, or is the root issue being in a ketogenic state? It is unclear to me if saturated fat is reduced, and that saturated fat is replaced with MUFA/PUFA (still remaining in a ketotic state), if this cholesterol over synthesis remains possible? Are the metabolic pathways you note for saturated fat (where ketone/cholesterol production cross paths) possible with MUFA/PUFA? In this case, the patient appears to have "softened" both sat fat intake and ketosis, somewhat confusing the true driver in this instance.
Thx again, your insight into these real problems is appreciated by the entire community!


Seems like saturated fat is a more powerful ligand for increasing the activity of sterol regulatory binding element proteins which is the nuclear transcription factor that activated cholesterolgeni c genes. Anecdotaly the switch to unsaturated fat in such patients can dramatically lower cholesterol synthesis. However it is often harder to maintain ketosis.
TDD
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0 # RE: Unclear root causejosemr 2014-07-15 20:34
Quoting tdayspring:
Quoting mbertler:
First- tremendous article. I see this lecture frequently cited on this interesting and very real phenomenon- most helpful! One question- at the end, there appears to be conflicting recommendations, as noted in the comment above. Is the root issue of cholesterol over-synthesis primarily driven from "saturated fat" in an over abundance, or is the root issue being in a ketogenic state? It is unclear to me if saturated fat is reduced, and that saturated fat is replaced with MUFA/PUFA (still remaining in a ketotic state), if this cholesterol over synthesis remains possible? Are the metabolic pathways you note for saturated fat (where ketone/cholesterol production cross paths) possible with MUFA/PUFA? In this case, the patient appears to have "softened" both sat fat intake and ketosis, somewhat confusing the true driver in this instance.
Thx again, your insight into these real problems is appreciated by the entire community!


Seems like saturated fat is a more powerful ligand for increasing the activity of sterol regulatory binding element proteins which is the nuclear transcription factor that activated cholesterolgenic genes. Anecdotaly the switch to unsaturated fat in such patients can dramatically lower cholesterol synthesis. However it is often harder to maintain ketosis.
TDD

Dr Dayspring,
Wouldn't this then confirm what many have been saying for decades that saturated fats can indeed cause elevated lipid profiles? It's a bit confusing. What role, if any, does being ketogenic have on this process?
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0 # RE: Unclear root causetdayspring 2014-07-15 23:32
Quoting josemr:
Quoting tdayspring:
Quoting mbertler:
First- tremendous article. I see this lecture frequently cited on this interesting and very real phenomenon- most helpful! One question- at the end, there appears to be conflicting recommendations, as noted in the comment above. Is the root issue of cholesterol over-synthesis primarily driven from "saturated fat" in an over abundance, or is the root issue being in a ketogenic state? It is unclear to me if saturated fat is reduced, and that saturated fat is replaced with MUFA/PUFA (still remaining in a ketotic state), if this cholesterol over synthesis remains possible? Are the metabolic pathways you note for saturated fat (where ketone/cholesterol production cross paths) possible with MUFA/PUFA? In this case, the patient appears to have "softened" both sat fat intake and ketosis, somewhat confusing the true driver in this instance.
Thx again, your insight into these real problems is appreciated by the entire community!


Seems like saturated fat is a more powerful ligand for increasing the activity of sterol regulatory binding element proteins which is the nuclear transcription factor that activated cholesterolgenic genes. Anecdotaly the switch to unsaturated fat in such patients can dramatically lower cholesterol synthesis. However it is often harder to maintain ketosis.
TDD

Dr Dayspring,
Wouldn't this then confirm what many have been saying for decades that saturated fats can indeed cause elevated lipid profiles? It's a bit confusing. What role, if any, does being ketogenic have on this process?


Depending upon their genetic makeup, either excess saturated fat and/or ketosis can increase cholesterol synthesis in some but not all persons. The bigger question is what would be the long term consequences of that
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0 # Lipidholics AnnonymousShannon Monahan 2014-10-13 15:42
In ketosis my all the markers in my lipid panel got worse. I would like some insights into the causes and factors.
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0 # RE: Lipidholics Annonymoustdayspring 2014-10-13 17:28
Quoting Shannon Monahan:
In ketosis my all the markers in my lipid panel got worse. I would like some insights into the causes and factors.


How that can happen is discussed withing the above case. You should also checkout another case discussion: http://www.lecturepad.org/index.php/commentaries-and-opinions/1283-lipid-changes-on-a-very-low-carb-ketogenic-diet-my-own-experience
Dr Dayspring
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0 # APO E4 allelerameau9 2014-11-03 13:37
I have read that possession of the APO E4 allele, which is apparently found in ~25% of the population, may be the reason that some low-carbers (your clinicians estimate perhaps a third) seem to have this problem of rocketing LDL-C and LDL-P numbers. It happened to me, and I had this marker checked, and indeed I have one APO E4 allele. So I started being better about ignoring Sat. fat and my LDL-C is down 40 in a few months (only did NMR on the second test). LDL-P is a tad over 1600, but I'm hoping that retesting in a few months will see that down as well.
Does your experience indicate that perhaps the APO E4 allele is the reason some people have this issue?(Apparent ly APO E4 is an Alzheimer's marker in addition to being a CVD marker - for the reasons above? - and indeed my mom died of Alzheimer's.)
Thanks,
James
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0 # RE: APO E4 alleletdayspring 2014-11-03 13:41
Quoting rameau9:
I have read that possession of the APO E4 allele, which is apparently found in ~25% of the population, may be the reason that some low-carbers (your clinicians estimate perhaps a third) seem to have this problem of rocketing LDL-C and LDL-P numbers. It happened to me, and I had this marker checked, and indeed I have one APO E4 allele. So I started being better about ignoring Sat. fat and my LDL-C is down 40 in a few months (only did NMR on the second test). LDL-P is a tad over 1600, but I'm hoping that retesting in a few months will see that down as well.
Does your experience indicate that perhaps the APO E4 allele is the reason some people have this issue?(Apparently APO E4 is an Alzheimer's marker in addition to being a CVD marker - for the reasons above? - and indeed my mom died of Alzheimer's.)
Thanks,
James


ApoE genotype not involved with this lipid response
TD
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0 # Follow up...rameau9 2014-11-03 15:21
Any thoughts as to why only a third of low-carbers have this response? It would seem that some physical phenomenon is driving this, and some apparently reasonable/scie ntific MD's think that this allele is the key.

Thanks,
James
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0 # RE: Follow up...tdayspring 2014-11-03 15:33
Quoting rameau9:
Any thoughts as to why only a third of low-carbers have this response? It would seem that some physical phenomenon is driving this, and some apparently reasonable/scientific MD's think that this allele is the key.

Thanks,
James


Seems like the genes regulating cholesterol synthesis are activated in some but not others. So transcription factors and their agonists and antagonists are at play. Unknown at this time. TD
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0 # Follow up 2...rameau9 2014-11-03 15:44
Also, any thoughts as to why APO E4 is apparently a marker for CVD, if this is not the reason? What other physical phenomenon would be in play here?

Thanks,
James
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0 # RE: Follow up 2...tdayspring 2014-11-03 16:24
Quoting rameau9:
Also, any thoughts as to why APO E4 is apparently a marker for CVD, if this is not the reason? What other physical phenomenon would be in play here?

Thanks,
James

Multiple factors including hyeprabsorption of cholesterol and xenosterols and decreased clearance of apoB particles leading to elevated apoB and LDL-P
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0 # Sorry if I'm being dense here...rameau9 2014-11-04 05:58
I get it that the lipid response to reducing saturated fat is not connected with APO E4 status.

What I'm really curious about is whether this allele explains the extreme rise in LDL-P to begin with. Dr. Davis of Wheat Belly fame says that E4 puts one "between a rock and a hard place" nutritionally, since regular Paleo is contraindicated , but the need for care with regard to sugars still obtains.

All my numbers (that I know about) are fine, except LDL-P, which seems to be the only one that counts. I'm very happy indeed on Paleo for the last 9 months, feeling better than ever, weight down another 12 pounds even though I've been low-carb since 2002, A1C heading south, and brain fog totally gone, which is the best of all. Sometimes when walking I feel like I'm dancing on air.

Hard to know what to do, as I'm not eager to add back 50-100 carbs worth of oats, an apple and such that seems to have served this patient so well. I'm not as young or athletic as she is.

Hence my quandary! What is to be done?!

Thanks,

James
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0 # Calcium scan?rfshaffner 2014-11-04 11:33
James,
Jimmy Moore (the low carb blogger and author) had similar results -- everything improved except LDL-P. No one knows whether or not high LDL-P is s problem or not in such a case. (We're still learning.)
Jimmy Moore had a calcium scan performed and found that his arteries are clean (no plaque build-up), so I gather he feels good about his results, in spite of the high LDL-P numbers.
Perhaps you should have a scan done ,too.
Richard
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0 # Calcium scanrameau9 2014-11-06 14:47
Dear Richard,

I was trying to observe the rule about not making comments on the subject of one's own stuff, in deference to Dr. Dayspring's rules and this amazingly informative site.

Actually, I had one two years ago, and have some plaque. My doctor put me on 10mg liipitor, and in a matter of months my LDL-C was at 81. After being snowed in at Mr ChickenParm last winter for several days and gaining weight, I decided to follow the advice of my kung fu son and try Paleo. Instant wonderful results! But blood work a few months later had the LDL-C score doubled! So I cut back on satfat with good results (NMR test losing 40 on LDL-C but revealing this LDL-P issue), found out I'm E4, and repeated calcium scan, which showed a slight worsening, which I took to be good news in that apparently it's rare to actually reverse plaque. Hopefully it's stable.

As I flirted with metabolic syndrome and Type 2 before going low-carb 12 years ago, I suppose it could be that the damage was/is already done. However, my direct ancestors live a long time (dad is 94 and going strong, despite being told he had a silent heart attack somewhere along the line) and I would love to live out this genetic tendency.

I think if my calcium scan score were 0 that I would not be here at all!

Trying to figure out what's past, what's present, especially with incomplete data (other VAP test was ~10 years ago) and otherwise good health, is apparently tricky.

n=1. I will try to find a sweet spot where I can follow Paleo without driving up LDL-P, with testing often to track the numbers.

Thanks to both you and Dr. Dayspring.

James
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0 # Increase in triglycerides on LCHF dietSamttee 2014-12-24 16:36
Very informative discussion. Is there a way to account for increased triglycerides on a LCHF (lots of saturated) diet? Non fasting TC was 250, tris over 500, subject was in ketosis.
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0 # RE: Increase in triglycerides on LCHF diettdayspring 2014-12-26 19:47
Quoting Samttee:
Very informative discussion. Is there a way to account for increased triglycerides on a LCHF (lots of saturated) diet? Non fasting TC was 250, tris over 500, subject was in ketosis.


Remember TG are three fatty acids attached (esterified) to glycerol so an increased intake of SFA can increase TG in some folks
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0 # Hypocaloric ketosiserella@gmail.com 2015-03-28 16:13
As usual, when I reread your posts, there is always an extra pearl which I extract, a thing I missed on the first time through...
Do you have an opinion on hypocaloric (not nutritional) ketosis?
I don't mean the anorectic, I'm looking at the trend towards intermittent fasting - so no food between 7pm and noon. I recommended it to a diabetic patient of mine to aid in weight loss, her LDL skyrocketted, and her endo told to start eating breakfast again, her LDL went down. Her macronutrients were unchanged, total calories were likely the same because she really didn't lose any weight (ate the same total calories in a compressed eating window of time).What is the mechanism of the increase in LDL in this scenario? Thanks for your time and your insights.
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0 # RE: Hypocaloric ketosistdayspring 2015-03-28 16:18
Quoting :
As usual, when I reread your posts, there is always an extra pearl which I extract, a thing I missed on the first time through...
Do you have an opinion on hypocaloric (not nutritional) ketosis?
I don't mean the anorectic, I'm looking at the trend towards intermittent fasting - so no food between 7pm and noon. I recommended it to a diabetic patient of mine to aid in weight loss, her LDL skyrocketted, and her endo told to start eating breakfast again, her LDL went down. Her macronutrients were unchanged, total calories were likely the same because she really didn't lose any weight (ate the same total calories in a compressed eating window of time).What is the mechanism of the increase in LDL in this scenario? Thanks for your time and your insights.



Without measuring sterols or LDL-P it is hard to guess: My thought is the body (adrenals) needed to make corticosteroids due to starvation and there was a sudden marked increase in cholesterol synthesis nwhich would influence LDL-C

TD
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0 # Hypocaloric ketosiserella@gmail.com 2015-03-28 16:13
As usual, when I reread your posts, there is always an extra pearl which I extract, a thing I missed on the first time through...
Do you have an opinion on hypocaloric (not nutritional) ketosis?
I don't mean the anorectic, I'm looking at the trend towards intermittent fasting - so no food between 7pm and noon. I recommended it to a diabetic patient of mine to aid in weight loss, her LDL skyrocketted, and her endo told to start eating breakfast again, her LDL went down. Her macronutrients were unchanged, total calories were likely the same because she really didn't lose any weight (ate the same total calories in a compressed eating window of time).What is the mechanism of the increase in LDL in this scenario? Thanks for your time and your insights.
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+1 # intermittent fastingerella@gmail.com 2015-03-28 16:31
As a followup question, I don't know that this person was actually in ketosis. It is quite possible that her IF was not prolonged enough to achieve that state. Can you comment on LDL increases in non-ketotic fasting (ie there would not be an excess of acetoacetyl-CoA with which to make extra cholesterol).
Thanks again.
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0 # intermittent fastingerella@gmail.com 2015-03-28 16:31
As a followup question, I don't know that this person was actually in ketosis. It is quite possible that her IF was not prolonged enough to achieve that state. Can you comment on LDL increases in non-ketotic fasting (ie there would not be an excess of acetoacetyl-CoA with which to make extra cholesterol).
Thanks again.
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0 # RE: intermittent fastingtdayspring 2015-03-28 16:39
Quoting :
As a followup question, I don't know that this person was actually in ketosis. It is quite possible that her IF was not prolonged enough to achieve that state. Can you comment on LDL increases in non-ketotic fasting (ie there would not be an excess of acetoacetyl-CoA with which to make extra cholesterol).
Thanks again.



You do not have to have ketosis to increase cholesterol synthesis. We see many folks with LC diets who are not ketotic increase cholesterol synthesis - likely depends on their unique cholesterolgeni c genes response too a diet. Need to measure sterols in these folks routinely.

Causes of rising LDL: Hyperabsorption of sterols, hypersynthesis of cholesterol, decreased clearance of LDL particles (many issues might be at play) or hepatic overproduction of apoB particles which is usually do to increase hepatic lipid substrates)

TD
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0 # My doctor can't test for LDL subsmarcnz 2015-03-31 02:28
I live in Australia and in December 2014 I had a full blood check
18-Dec-2014:
Total Cholesterol:10.1
Triglyceride: 6.2
Measured Cholesterol Fractions:
HDL (protective): 1.19
LDL (atherogenic): 6.59
Total/HDL ratio: 8.5
HbA1c: 8.8
in SI units: 73
Blood pressure: 165/130
Weight: 125kg - Height 180cm
I decided to go on a Ketogenic Diet since then. The doctor gave me statin and other few drugs. I have been taking insulin before as well, which did not help much with the hyper and hypoglicemic states. So I decided to see what would happen.
Follow up test:
27-Mar-2015
Total Cholesterol:10.3
Triglyceride: 6.2
Measured Cholesterol Fractions:
HDL (protective): 1.03
LDL (atherogenic): 6.48
Total/HDL ratio: 10.0
HbA1c: 7.8
in SI units: 61
Blood pressure: 190/130
Weight: 113kg - Height 180cm -> 11kg lost
Doctor very happy with glucose results. She said she has never seen me with such a great value HbA1c. However the concerns are:
LDL way too high. I asked her if she could test for the particles but she said there is no such test available! Really?
Other issue is the blood pressure. It went dangerously high at 190/130!
She said I must take the medication for the cholesterol and blood pressure otherwise I will be in big trouble very quickly.
I have been very good on the Keto diet. I am keeping my Carbs at 25 ~30g /day max, the Proteins below 70g and the total calories within 1000~1500 range. Sometimes over the weekend, I went above, still keeping 65+% FAT average. My craving for chocolate has totally disappeared. I have stopped the insuline after a couple of weeks when I noticed that it had no or very little effect on the sugar level, which I can't explain. Before being on ketosis state, when I had Blood Sugar Level (BSL) on meter around 10, I took 20 units of insulin and it went down to 7 or 8 within the next couple hours. However back high the next morning. When I had 14 I took 40 units.
Since ketosis state (measured using a meter), when I took insulin when at 10 or 11 (start of the diet), it moved very little. I increased insulin the next day and the next up to 40 units and still no or very little effect. Before ketosis, I would have woken up all sweaty and weak in the middle of the night and had some carbs! I try insulin from another box in case the one I had was not working. Same thing. So I decided to drop insulin altogether. The BSL meter still reads high range (7.8 - 9.4), but never any spike or drop, which makes me happy.
I am not sure about the LDL as it can't be tested down its particles. The doc said that no matter the LDL, they are all bad and build in the arteries. However, I must have my blood pressure in order.
What do you suggest?
Thank you for such a great article.
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