Comments by SWSL
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    “assume that topsoil was more nutrient dense than it often is now, making fruit less nutrient potent.”
    No doubt, and this is a prime argument for mineral supplementation. Might be true for C content also? I wonder if there’s any indication for what ancestral vitamin C levels were. Or healthy tribes we have studied in modern times.

    In any case, if we are supplementing to the limits of what our bodies will actually accept in food, then the question is why do we have to work so hard to overcome our natural limits? Did we evolve to need liposomal C for optimal health? Are we forcing the issue with a “more is better” mentality without an adequate understanding of the larger dynamics?

    The idea of going with food-sourced (super-foods included) nutrition versus isolated elements in supplements has been a key point with Rhonda. Not rigid, but an orientation that makes good sense.

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      Great, thanks! Two counter-point thoughts to consider-

      1) We are starting to understand the ROS are not just terrible bad enemies of life, but like everything else, integral to our system. The ROS seem to play a role as signalers. A balance between ROS and anti-oxidant levels may promote better health than simply hammering our bodies with anti-oxidants with no regard for the value of ROS in the dynamic? Rhonda did address this to a degree here with the discussion on exercise and blunting of beneficial effects and the linked research.

      2) How do we reconcile historical dietary levels of C in the course of evolution with the idea of forcing huge over-supplies of it on our systems? Again, are we so sure that pushing for higher than an ancestral diet would provide is better for us on a daily basis?

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        “are we so sure that pushing for higher than an ancestral diet would provide is better for us on a daily basis?” Great question. Would the maximum natural blood plasma level from oral intake be the optimal self-leveling amount?

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        I’m also concerned after listening to Sinclair that sourcing non-degraded NMN is not practical yet. He basically comes out and says people are likely getting degraded products, no matter how expensive.

        Looking into things I found that there is another NAD+ precurser as indicated here:

        I wonder why this has not entered the discussion. Something we are missing?

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          Too bad the link doesn’t work when Foundmyfitness tacks on it’s own parts to the actual webaddress. I don’t understand why FMF does that. Original link:

          Link when added to news adds this? …../

          So, check the above link if interested since the original won’t work as “news” Good stuff!

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            This seems to support the hypothesis that “AD actually a vascular and metabolic disease” per Francisco Gonzalez-Lima

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              Seems that they are patenting a combo of NMN with other goodies that can help keep the NAD+ production from dropping as homeostasis pushes back.

              direct link to Patent application:

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                Here is a good article: Although only tangentially related to your question, it can give you some useful background.

                My advice is that you probably should get some more information. I think there is reasonable consensus that it is the LDL particles themselves – that is, the number of them – that confers risk. Not the amount of cholesterol they carry. So getting an actual LDL-P number assay done (NMR) would be helpful.

                Past this, if your LDL-C is very high, then your LDL-P will almost certainly be high also. Whether you choose to use statins or not should be a discussion between you and your doctor. Otherwise what is the point of having a doctor?

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                  Thank you, I’ll take a look. My doctor was unfamiliar with FH, and I had to request the lipoprotein(a) test which showed my low density lipoprotein(a) was around the 300 range. Triglycerides 41, HDL 87. TC 249. I did request the Lp(a) test on the advice of my mother, who does see a cardiologist, and diagnosed her with FH by specifically requesting lipoprotien (a) testing. The problem with FH is that diet has no positive effect on Lp(a), although I’m sure I could make my LDL worse. It’s a genetic defect. Now, my lifestyle makes it much more likely I would survive the heart attack… bonus I guess. The issue is that statins seem to lower numbers overall, to include HDL, and might have negligible improvements. So much of this research I have been able to find deals with people with high triglycerides and poor HDL, when really, the only marker I have that would indicate I’m not incredibly healthy is the 400+ lipoprotien. I’m military insurance, so my doctor is whoever I happen to have at the time at the military treatment facility, and I don’t exactly have a valid reason to request a referral to a cardiologist. I mean, I’m a marathoner and my resting heart rate is 55 BPM (female).

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                    You could listen to the Dayspring lipid podcasts that Peter Attia posted last week on his site:

                    It touches on many of the topics you mention here. Recent evidence is that high HDL isn’t actually protective–all drugs that increase it appear to have failed to produce lower levels of CVD. So at best, it is a marker for some other process that may be protective.

                    Also, don’t confuse Lp(a) with LDL-P. LDL-P comes from an assay (usually NMR) that counts/calculates the LDL particles per liter of blood. Lots of small LDL particles are thought to be much more atherogenic than lower numbers of large LDL particles – even if the amount of cholesterol they carry (LDL-C) is the same. If your LDL-C is what is 300, it is still within the realm of possibility that your LDL-P is okay. But you would need to get the NMR test to tell you that.

                    Lp(A) is an LDL particle with an additional lipoprotein – apolipoprotein A – added to it. Peter Attia had an earlier podcast that went into some detail on Lp(a):

                    If you did have your Lp(a) tested and it is high, then you should listen to this. It is currently much more difficult to treat than high LDL and many doctors know nothing about it. Just treating it with a statin is unlikely to be sufficient.

                    Also, keep in mind that FH is not a single genetic condition, but rather a host of genetic predispositions to high blood cholesterol levels. Some probably do respond to changes in diet.

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                      Best summary of Attia/Dayspring current lipidology knowledge I’ve seen! A keeper. Thanks!

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                        Yes, I definitely had my Lp(a) tested, and last one was 333 (I pulled my last labs just to double check my numbers.) Looking for info on this topic that few know very much about was one of the things that led me here. I have been listening to some of Peter Attia’s stuff over the past couple of days to include the Lp(a) podcast you referenced, and it’s been interesting. I’ll take a look at the ones you posted, as well. Thanks!

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                          I’m glad you’re investigating your options. Ask your doctor for a referral to a FH / lipoprotein specialist. Also check out the Valter Longo interviews with Rhonda. Beg Peter Attia to review your case.

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                    Not as straight forward as one would think. check out the week of Tom Dayspring podcast to learn more than you ever wanted about the world of lipids.

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                      Thank you! Looks like a ton of information here. It’s been a difficult topic to research because so much of the things you find are from “all fat is bad, cholesterol is bad” sources, and statin topics range from they are either life-saving or incredibly damaging.

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                        Yes check out the Dayspring interviews. You could skip to the last one on statins and also get his take on niaciin that segment. . Attia puts Dayspring on top as his lipidolgy guru and they both also respect Dr Ron Kraus. All of these folks and Rhonda appear to endorse each other and together they carry more weight as peers. Attia is not supportive of Ivor Cummins' approach, though not apparently totally against, he has disputed the focus on calcium and the cac test’s utilify. Poke around to find details. Attia could be wrong, but hes a very experienced and scientific doc as well as a serious athlete and works with the top lipidologists. So as much as Ivor Cummins (the engineer ) appeals to common sense, I have to go with Attia/Dayspring/Kraus conclusions first and foremost.

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                      Hi. I also have chronic Lyme and do the Buhner protocol and have been better on it by far. I have not taken supplements during my 3 day fasts nor during my time restricted fast hours. I plan to start doing 5 day fasts regularly when life allows and have wondered the same as you.

                      BUT I am very low symptom now. I only do a few of the many recommended herbs at this point.

                      To answer your question, I understand that yes staying in ketosis (very low carb load) is crucial and the other clear directive for effecting autophagy in a prolonged fast is cutting protein out. Check out the Fasting Mimicking Diet developed by Dr Valter Longo. I will guess that if that diet yields significant results similar to prolonged fasting, then taking herbs or herbal teas should be ok. As for tinctures, those could introduce alcohol (carbs) or glycerin and those are more questionable.

                      My thoughts are to stick with teas or capsules and make sure your supplements fit within the guidelines of the fasting mimicking diet macros and calorie profile (google FMD for details people have gleaned from Longo and patents filed) and you can be assured that your fast with supplements will be at least as helpful as the FMD while also maintaining the helpful effects of the Buhner protocol as well. Good luck and healing to you!