Our 3rd annual meet-up will piggyback on the LowCarb USA conference in San Diego, CA, August 3-6.

Questions for Dr. Ronald Krauss

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Juliegee
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Questions for Dr. Ronald Krauss

Postby Juliegee » Wed Apr 29, 2015 2:39 pm

To make the best use of our limited time with the various experts we will be visiting during our Meet-up in May, let's compile our questions for them here. For those who plan to attend (and for those who can’t join us), please share your questions for Dr. Ronald Krauss here. Obviously, those who are in attendance, will have the opportunity to have their questions addressed first; but we will do our best to get ALL questions answered and report back.

Ronald M. Krauss, MD is a world-renowned physician and researcher as well as a much publicized author in both the lay press and medical journals. He is a UCSF Adjuvant Professor, Endocrinologist, and the Director of Atherosclerosis Research at Children’s Hospital Oakland Research Institute. Dr. Krauss' research program focuses on plasma lipoprotein metabolism and related traits that influence risk for coronary artery disease. His laboratory developed and applied methodology that led to the discovery of a common genetically-influenced atherogenic lipoprotein phenotype that underlies cardiovascular disease risk in patients with obesity, type 2 diabetes, and metabolic syndrome. To learn more about Dr. Krauss, see below:

http://www.chori.org/Principal_Investig ... rview.html
http://profiles.ucsf.edu/ronald.krauss

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Re: Questions for Dr. Ronald Krauss

Postby GenePoole0304 » Wed Apr 29, 2015 6:53 pm

How did he finally treat Jonathan of Triple your HDL and what was his genotype?

http://livinlavidalowcarb.com/blog/the- ... more/15544

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Re: Questions for Dr. Ronald Krauss

Postby Stavia » Wed Apr 29, 2015 9:00 pm

We know we have higher LDL (total and particle number) than e3s and e2s. How critical does he feel our higher LDL is in us developing AD? (Not CVD). Is it a just a marker of the apoe4 (and obviously predisposes to CVD through the usual processes) or is it involved directly in the pathogenesis of AD in us?

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Re: Questions for Dr. Ronald Krauss

Postby KatieS » Thu Apr 30, 2015 6:17 am

Along the same lines, how critical is HCY, and with lowering HCY with B12/folate/TMG/NAC to an optimal level, can we lower AD risks? Some studies suggest that supplement lowered HCY does not alter CV outcomes.

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Re: Questions for Dr. Ronald Krauss

Postby rep » Fri May 01, 2015 1:18 pm

What diet does he recommend for apoe4s?

What diet does he recommend for apoe4s with high LDL-P?

Would he make any changes in those diet recommendations if the apoe4 person were a hyper synthesizer AND hyperabsorber of cholesterol?

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Re: Questions for Dr. Ronald Krauss

Postby Ski » Sat May 02, 2015 10:50 am

Kitano wrote:Along the same lines, how critical is HCY, and with lowering HCY with B12/folate/TMG/NAC to an optimal level, can we lower AD risks? Some studies suggest that supplement lowered HCY does not alter CV outcomes.


Then that means whatever you are lowering is a symptom not a cause! In that same manner, then no drug should work as its artificially altering something and we know thats not true. So if that study is true then Id say HCY is merely a symptom of something else going on that is causing issues, then youre right, lowering HCY means nothing but then it also means its not contributing to heart disease. I dont see how it can work both ways.

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Re: Questions for Dr. Ronald Krauss

Postby KatieS » Sat May 02, 2015 12:32 pm

I'm on HCY supplements which have lowered HCY as expected by almost a quarter, but does it actually lower disease (CV &AD) risks?

"But despite the beneficial results from the aforementioned studies, recent reports have indicated that the homocysteine-lowering effects may not lead to changes in CVD risk or mortality. In May 2008, Albert et al published results from their randomized trial in The Journal of the American Medical Association. The team sought to test whether a combination of folic acid, vitamin B6, and vitamin B12 reduced the risk of cardiovascular events among women with and without CVD. Participants in the treatment group were given a combination pill of the three vitamins for 7.3 years. At the end of the trial, folic acid, vitamin B6, and vitamin B12 supplementation did not affect cardiovascular events in high-risk women despite the significant homocysteine reductions.

Two recent meta-analyses questioned the efficacy and benefit of B vitamin supplementation to reduce CVD risk. The August 15, 2010, issue of The American Journal of Cardiology published the results of a meta-analysis led by Miller. The group compiled results from randomized controlled trials of folic acid supplementation to prevent CVD events and reported that supplementation did not affect the risk of CVD or stroke. The second meta-analysis performed considered eight large, randomized, placebo-controlled trials involving 37,485 participants. Clarke et al concluded that folic acid supplementation for the purposes of lowering homocysteine levels had no significant effect within five years on cardiovascular events, overall cancer occurrence, or mortality.5"
http://www.todaysdietitian.com/newarchi ... 11p8.shtml

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Re: Questions for Dr. Ronald Krauss

Postby rep » Thu May 07, 2015 11:53 am

Please ask Dr. Krauss to consider Julie's statement regarding ketosis:
We are THE known population with decreased cerebral glucose metabolism decades before cognition declines. What gets tricky for us is HOW to best create those ketones without driving up our risk for CAD/CVD as we also tend to hyper-absorb dietary cholesterol. Many of our members practice CR, IF, exercise, reduce starchy carbs, and use MUFAs to more safely create ketone bodies. Ketone supplements, like MCT, can also drive up LDL-P. As you've wisely ascertained, ketone esters MAY end up being our ticket... but even less research has been done there :roll:

We're kind of between a rock and a hard place. It's pretty clear that we could greatly benefit from ketones; but we're struggling with how to balance brain health with heart health.


Then, given that, what does Dr. Krauss think about the use of a product such as KetoCaNa (Prototype Nutrition) for E4s? Would that supplement be okay for those with high LDL-P? How about high blood pressure, given the salts? Lastly, would that product be okay for those with high LDL-P who are hyper-producers and hyper-absorbers of cholesterol?

BTW, it is my understanding that the KetoCaNa should not drive up LDL-P the way MCT oil can, correct? Also, Dr. Krauss will receive these questions ahead of time, right? I'd like him to have time to take a look at the KetoCaNa product and do some research if need be.

Please, let's get more questions lined up for Dr. Krauss!!!

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Re: Questions for Dr. Ronald Krauss

Postby pgf54 » Sat May 09, 2015 5:36 am

Does Dr Krauss consider Adma levels a cardio risk factor? and what are his views on L-Arginine supplementation measures to address/improve nitric oxide synthesis, taking into account those of us that have an Apoe4 allele which is supposedly unable to activate endothelial cells to produce No.? and thus worsening cardio vascular function.
Don't wait for your ship to come in, row out to meet it.

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Re: Questions for Dr. Ronald Krauss

Postby Juliegee » Sat May 16, 2015 9:56 pm

I stumbled upon an interesting editorial written by Dr. Krauss a year ago that seems to corroborate Dr. Gundry's focus on using sdLDL (LDL-III and LDL-IV) as opposed to small LDL-P to better refine CVD risk.

All Low-Density Lipoprotein Particles Are Not Created Equal
http://atvb.ahajournals.org/content/34/5/959.long

I especially found this section intriguing given our prior discussions about ApoC-III. He seems to be echoing Dr. Frank Sacks position, that it is the presence of ApoC-III that renders LDL atherogenic:
Another consideration with regard to heterogeneity of LDL particles is their content of specific proteins and perhaps lipids that could refine assessment of pathophysiologic properties of lipoproteins, as proposed originally by Alaupovic.20 Of particular interest is apoCIII, a small molecular weight protein that has been found consistently to be strongly associated with risk of CVD when present on apoB-containing lipoproteins,21 likely because of the combined effects of increased very low density lipoprotein (VLDL) secretion,22 impaired VLDL remnant catabolism,23 and proinflammatory activity.24Recently, it has been reported that whereas LDL particles containing apoCIII are significantly associated with CHD risk, this relationship is substantially weaker for the majority of LDLs lacking apoCIII.25 Notably, apoCIII is particularly abundant in very small LDL particles.26 Other subspecies of sdLDL that may have particularly high atherogenic potential are those with increased content of glycated apoB27 and increased electronegative charge.


I'd love an update on his thoughts regarding ApoC-III when we meet with him.


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