My Lipids under Dr. Gundry's Protocol

[LA18]

Juliegee, thanks for posting your numbers. I’m working hard on my diet and it’s helpful to see what can potentially happen on the Gundry protocol. My particle count is still high, despite many dietary modifications in accordance with Dr. Gundry’s recommendations, so I’m still in the process of figuring out what works best for me.

Regarding this, I was wondering about how many calories per day you consume and whether you have difficulty maintaining a reasonable weight/BMI. This has definitely been a struggle for me – I keep losing and am getting too thin. There are some things I can’t tolerate (e.g., avocados and coconut oil), so I rely pretty heavily on olive oil and nuts (probably too much so) for calories. I don’t eat gluten, dairy, or any processed food. I’ve moved away from eating red meat, but have been eating some turkey and fish. I’ve also added omega 3 eggs to my diet, which has had virtually no effect on my lipid panel (results posted below – I added eggs 10/14). This is my third panel and not much has changed, perhaps because I’m still eating too much saturated fat. I’m just not sure what to replace it with, given my food sensitivities and diabetes. I’m also frustrated by my too high insulin resistance score and triglycerides, as I eat low carb (about 50 grams/day). I’m also e4/4.

7/14, 9/14, 11/14
TC – 160, 154, 164
LDL – 160, 154, 164
HDL – 48, 51, 52
TG* - 50, 64, 64

LDL-P 1495, 1395, 1344 (same despite decrease in meat, especially red, consumption)
HDL-P – 30.2, 35.1, 32.9
Small LDL – 678, 706, 707 (sigh)
LDL size 20.8, 20.6, 20.6
LPIR* 34, 42, 42

*In July I was eating about 30 grams of carb a day. In Sept. and Nov. I was eating about 50 grams per day.

[Gilgamesh]

Hey Julie,

Agree with STavia that your markers are in fact excellent. Congrats!

Stavia, per these results, I agree with your stance on using the LEAST amount of dietary fat necessary to obtain ketosis. That philosophy has worked well for me in the past. I strongly believe there is much evidence to support ketosis for the neuroprotection element, but applying exercise and CR (which I've consistently done) reduces the need for dietary fat and may be the safest path for us.

Agree strongly.

I wonder, though, whether ketosis is really helping ε4s -- esp. homozygotes -- at all. CR and exercise very likely are, but the Axona studies show no sig. effect on ε4-carriers. And, alas, these effects are often "dose-dependent". There generally are too few homozygotes to make claims about them, but even when a marginal effect on "ε4-carriers" is reported, that often means that the effect on homozygotes is nil, or maybe even negative.

Anyway, just read this on my break:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3213220/

Conclusions
In conclusion, despite the relatively small size of this study, genetic influences on cognitive scores in response to induced ketosis were noted. The main modulator of induced ketosis appears to be the carriage status of APOE4. It may not be a coincidence that APOE4 is also the major genetic risk factor for late onset AD. The failure of APOE4 carriers to respond to ketosis may indicate a more insidious metabolic problem. APOE4 carriers may be overly reliant on glucose and hence, over a lifetime, cerebral neurons are deprived of the metabolic advantages conferred by ketone body metabolism and this may be crucial to etiology of AD [36]. Importantly, this type of pharmacogenomic profiling not only offers insights into the disease process, it also allows targeting of patients who are most likely to respond to therapy. In this way, better and more effective therapeutics can be developed.

Depressing.

But the good news about the "dose-dependency" phenomenon in general is that the studies showing exercise is better for ε4-carriers probably mean that homozygotes benefit even more than what's reported in the studies.

All the mono fats he suggests can shift ones omega3 index unfavorably to more inflammatory status

GenePoole - Any reference for that? I've never seen anything suggesting mono. fats would have that effect.

GB

[Julie G]

GenePoole0304, good questions. I didn't track my dietary intake with software (as I have before) so I can't answer your questions precisely. My only added dietary fat was from high polyphenol EVOO. Depending on the source, we know that it contains anywhere from 8-20% SFA. I ate MORE fat in the second trail, testing Gundry's assertion that there is no upper limit for EVOO. (There is for me ) I also ate MORE non-starchy veg than in the second trial. Re. lectin containing foods, I avoided legumes with the exception of occasional chick peas/garbanzo beans as they are naturally lower in phytic acid. I also continued to enjoy tomatoes, cucumbers, and peppers identically in both trails. I am dusting off my cron-o-meter & once again measuring and recording everything in an effort to improve my numbers.

Interesting & helpful to see how dramatically TGs shift with re. to time/fasting, George. Thanks for sharing. I guess I agree that a shift from TGs of 50 to 62 may not be awful but an LDL-P shift from 1089 to 1370 is definitely moving in the wrong direction

Hep, you are too kind. I wondered about thyroid. THAT would be a variable that would confound everything. I think I'm good there and will soon have confirmation per the testing required for Dr. Bredesen's protocol. Trust me, THAT was on my radar as a possibility. My inflammation markers are decent: CRP- .05, Homocysteine- 7.7.

LAC1965, yes, I wanted to let others SEE that my numbers worsened following the Gundry protocol. It doesn't negate everything he promotes...just didn't work in this n=1 trial. Good for you for consistently tracking your numbers in response to dietary changes; frustrating, but ultimately the only way we can figure out what works. I didn't track my daily caloric intake during this trial, but my weight remained very stable. I've been eating LCHF for almost 3 years. At first, I had trouble with losing too much weight; not now. I'm small (like you) and have no desire to lose weight. I strength train and am more concerned with optimal health/maintaining muscle. Keep tracking, my friend. I'll be doing the same. I'm using my cron-o-meter again so that I can better see the effect my macronutrient ratios have on my lipids.

G, nice to see you posting. The Axona study you cite was an attempt to improve cognition in mild to moderate Alzheimer's. That's a pretty high standard. Also, don't forget the inherent flaw in the Axona strategy; that of adding ketone bodies, but failing to deal with underlying IR by reducing carbohydrates, especially simple sugars, etc. One writer described Henderson's approach as being akin to a sailor frantically trying to bail water out of a sinking boat without first patching the holes in the hull. Doing BOTH may yield different results.

[LillyBritches]

Just now seeing this. SWEETHEART. I KNOW you're disappointed, but I swear on everything I know, those aren't bad. And your HDL? :-O :-O :-O Julie. Jumpin' Jiminy Christmas. Has anyone, in the history of the world, EVER had HDL like that? I'm laughing out loud because that number is cray unbelievable. I'm fairly certain that trumps any other lipid marker, like, ever.

I mean...who has HDL at 86, let ALONE 97??? And your trigs are amazing, too! So. Your LDL is 142...still only BORDERLINE high. And your total is that high, partially, because your HDL is so freakin', crazily high (aka GREAT).

So with all due respect, I don't think "bad" is the correct descriptive term here. I parrot Andrea: your markers as a whole are fantabulous. Again - 18 BMI? Who the frick over 50 has that? LOLOLOL

C'mon, sweet friend. Stop Julie-bashing. Okay? OH. And this entire thing is a simple fix: eat differently. This was an experiment and, whereas it raised your HDL ever more (still SMH at that number - 97 - I'm simply aghast and not merely paying lip service), it raised your LDL and trigs (SLIGHTLY and they're STILL awesome), as well.

So, no fretting past your initial distress over this, okay? Love you. (((Julie)))

P.S. I've never gotten totally on board with the Gundry protocol for 4s...because I could never discern why he wants us to eat lots and lots of shellfish but NO salmon, tuna, etc. I mean, I get the whole no animal fats thing, and, granted - I've not researched his beliefs in-depth, but, still.

[Julie G]

You make me feel better, Sweet Lilly- Thank You. You're right, time to tweak. I'm not completely tossing Dr. Gundry's ideas out. As George keeps reminding us, he has amazing clinical results. I'm staying HFLC to stay in ketosis, just tempering my exuberance for EVOO a bit and adding a little more variability into my diet.

FWIW, we have lots of folks here with crazy high HDL. I think Kit is one. She has the best lipids of anyone I've ever seen; her HDL is over 100 and considerably HIGHER than her LDL . After seeing our Russ and my poor husband practically drink bottles of EVOO and still yield HDL in the 40s, I've decided genetics play a huge role there.

[Welcomeaboard]

I may have said this as I know I have thought about it. That is that Gundry's idea of eating 1 meal a day in winter seems to be his idea of trying to live like ancient man before he knew how not to try and starve himself to death. Sometime ideas of living like ancient man is absurd as I am sure if you asked ancient man if he enjoyed and welcomed the days of stress that starvation brought on he would probably just kill you and throw you on the grill and say nope thank god that meal came so easily. It may sound bad but they had Pacific Islanders practicing canabalism into the 1900's and they pretty much lived that ancient man life style as well.
As well as one of the pharaoh's of Egypt about 4500 years ago give or take a few hundred lived to 92 and you can bet your damn ass he was not on the ancient man starvation diet plan to reach 92. Or eating one meal a day because it was good for him.
There have been people documented living to their 70's to 100 years of age for 400 hundred years or more and I have not read where any of them said they chose to starve themselves so they could live long and prosper.
Now, in his defense the diet plan for certain people with bad genetics leading to cvd issues probably need some type of restricted diet to help them live past 50, including heart operations as required.

[Stavia]

Lily - exactly. Thanks for saying it in true Lily style. Julie darling, you are in excellent shape. 95% is good enough honey. PLEASE stop worring about the tiny imperfections.

[LanceS]

I may have said this as I know I have thought about it. That is that Gundry's idea of eating 1 meal a day in winter seems to be his idea of trying to live like ancient man before he knew how not to try and starve himself to death. Sometime ideas of living like ancient man is absurd as I am sure if you asked ancient man if he enjoyed and welcomed the days of stress that starvation brought on he would probably just kill you and throw you on the grill and say nope thank god that meal came so easily. It may sound bad but they had Pacific Islanders practicing canabalism into the 1900's and they pretty much lived that ancient man life style as well.
As well as one of the pharaoh's of Egypt about 4500 years ago give or take a few hundred lived to 92 and you can bet your damn ass he was not on the ancient man starvation diet plan to reach 92. Or eating one meal a day because it was good for him.
There have been people documented living to their 70's to 100 years of age for 400 hundred years or more and I have not read where any of them said they chose to starve themselves so they could live long and prosper.
Now, in his defense the diet plan for certain people with bad genetics leading to cvd issues probably need some type of restricted diet to help them live past 50, including heart operations as required.

Remember that Gundry did an undergrad in evolutionary biology or something similar at Yale. 4 years of deep thinking about genetics and diet prior to med school. It is my understanding that he believes that successful animals don't physically overstress themselves. That means that they maintain their ability to feed themselves, while minimizing the energy output needed to do so. This fits with much of what exercise junkies are doing these days. 10 mile runner? Most today are doing more strength training fewer miles, but the ones they run are faster. Many marathoners and ultra athletes are having very severe responses to their energy load which many attribute to ROS. When I read his book, I had the distinct impression that minimal calories were a design goal built into our specie. Energy conversion seems to him to be a necessary means to a happy life and not an end to be a badge of honor like we Americans celebrate it. So Michael Phelps and his 9000 calorie breakfasts might seem to catch more fish but compared to a regular guy with nice spear pole (who lives his life reasonably and is reasonably equal in other lifestyle/genetic elements) would likely live longer. Swimming is probably the worst example I could have used as at a high level like Phelps' it seems to be almost completely HIIT.

Regards the seasonal cycling, you should take some time to read caloriesproper.com (Lagakos), and yes perhaps some Kruse. We now live in an age where turning the lights off is a conscious and oft deferred decision. Their point regarding seasonal cycles has to do with sleeping seasonally, eating seasonally, etc. These docs often understand this stuff down to how the seasonal cycles affect the thermodyamics of energy generation etc.

Lastly, read up on hormesis which I think is the specific rationale for Gundry's fasting recommendation. By fasting the genes are activated that make the animal feel threatened... so for example some docs advocate annual five day fasts in order to activate longevity genes -- i.e. drive sugar low and activate apoptosis where cells are killed off if they have abnormal energy requirements (cancer). Mind you that Gundry may not advocate 5 days of fasting, but I believe hormesis is the underlying reason why he advocates fasting. I think Gundry would say that we live in eternal summer... where sweets and and short nights tell our body to store fat for winter... and we miss the winters which is where we used to get our annual dose of hormesis.

Not saying they have the answers, but there is a lot of wisdom and knowledge behind their words. And frankly, I think delving into the substance of what they have said may still reveal contradictions, but you may be surprised that there are nuggets you find useful.

The world is in the midst of an obesity epidemic. Go to an american airport during vacation times to see just how sick the average american is. The notion that a few individuals with bad genetics might need a Gundrian approach is completely out of touch with today's reality.

[SusanJ]

Hugs girlfriend. I know that oh shit moment when you see the results and they are NOT what you expected or wanted. At least your small LDL didn't shoot up by orders of magnitude like mine did on top of everything else.

Just another thought. I know that you were eating more fish, and you also have MCAS. Fish, unless truly processed immediately can be high histamine (as is spinach, tomato, etc). That's why I absolutely do not eat shrimp (I don't relish the idea of reaching for the epipen after dinner.) Some research is connecting histamine to both glucose and lipid metabolism. I've been down the rabbit hole for some time (following histamine's role in inflammation, which is the root of all evils), and still haven't emerged with any specific insights other than I am watching my histamine load and take Histame with fish or other high histamine foods. Physically I can feel the difference of watching histamine load, but whether it translates into lipid changes, will have to wait until my next labs.

Ref:

In summary, H1R and H2R signaling may play important roles in glucose and lipid metabolism, which seems to be mediated through both central and peripheral pathways. H1R signaling would be involved in central nervous system and pancreatic tissue to regulate glucose metabolism, while H2R signaling would be mainly related to peripheral action in the liver and skeletal muscle via adiponectin system to regulation both lipid and glucose metabolisms.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913336/

These results indicate that histamine could have a certain effect on lipid metabolism in liver cells... Furthermore, HDC expression in the pancreatic islet cells (73) also suggests a close relationship between histamine and energy metabolism, along with insulin and glucagon. The system effects of histamine on energy or lipid metabolism, which would modify atherogenesis, are still controversial.

https://www.jstage.jst.go.jp/article/ja ... 3_122/_pdf

[Julie G]

A total Oh Shit Moment (Love that!) VERY interesting, Susan. The plot thickens. I totally agree that irritated mast cells are big players in AD and CAD, especially for me. Very intriguing that fish may be a trigger

Thanks to you and everyone for your support- means a lot. I'm sorting it out. My T-Shirt says: ApoE4- Work-in-Process.