Interventions had OPPOSITE impact on lab results!

[Julie G]

Is there a way to post a grid? I had copied and pasted the values from a spreadsheet... I pasted them again and entered spaces to space them out, but when I looked at the preview, it looked exactly the same.

Sorry, meant to address this. You can't "post" a grid, but you can attach a spreadsheet. Just click on "attachments" below and follow instructions.

[apod]

Have you looked into thyroid hormones or micronutrients (like copper) ? These come to mind when thinking about LDL clearance rates. 1238kcal/d sounds pretty extreme to me while eating 50g of protein and exercising -- I barely hold my weight at 2200-2600/d while eating 100g/d of protein.

[jcosmo]

All great info. Your homocysteine is a little high, but not bad. Are you addressing with the trifecta (b12,folate, B6) of Bs?

I'm taking a daily B complex vitamin with 100 mcg B12 as methylcobalamin (and 1-2 mg sublingual in a separate supplement), 400 mcg folate as methylfolate, and 35 mg of B6 (as 25 mg pyridoxine and 10 mg P5P).

Your hbA1c is terrific, which really makes me wonder about two things: 1.) could your glucometer be off? 2.) hard to synchronize that with your higher insulin.

I have a diabetic cat, and I tested my own BG several times with the Relion Confirm meter, comparing it to the Nova Max, before I started using it with him. Each time, the results were within 5 mg/dL of each other... though that was over a year ago.

Do you know how much of an impact sleep deprivation has on insulin resistance? I wonder if repeated loss of sleep leading up to the last blood test could account for the higher than expected fasting insulin.

Regarding the elevated triglycerides, I wonder how much of that could be a result of higher fructose intake. Blackberries and bell peppers had not been part of my diet until recently.

We're wondering if the CR isn't serving you well. Perhaps your body is misperceiving a chronic energy shortage and your liver is ramping up cholesterol "energy" to compensate. I wonder how your numbers would change if you kept the same healthy diet and lifestyle habits, BUT only practiced CR every other day? Just a thought.

I can try that, though I wonder how it might compare to alternate day fasting, which I've been considering for the next round of interventions. I searched the forum for information about it and didn't find much here, but from the (albeit limited) scientific literature that I've been able to find, it appears to have a beneficial impact on lipid profile without the metabolic adaptation that happens with daily CR.

Sent from my XT1710-02 using Tapatalk

[Tincup]

While I did not attempt perfection you can use

Code: Select all

[/code ] (I've added an extra space before the closing bracket so you can see) for a table. You can iterate with preview & spaces to get it more lined up.

Hence:
[code ]
NMR LP      Date Range     Calories     Protein     CHO      Fiber      Net CHO    Fat    SFA   PUFA   MUFA
12/2/2016    10/29 - 12/1      1487      61          53       35        17          127     48     10     24
10/27/2017   9/24 - 10/26      1407      53           35       18        17          116     40     8      33
11/24/2017 	 10/27 - 11/23      1457      48          51       33        18          127     31     11     59
1/3/2018 	 11/30 - 1/02      1238      50          70        38        23           95      27     10     34
[/code ]

Becomes:

[code]
NMR LP      Date Range     Calories     Protein     CHO      Fiber      Net CHO    Fat    SFA   PUFA   MUFA
12/2/2016    10/29 - 12/1      1487      61          53       35        17          127     48     10     24
10/27/2017   9/24 - 10/26     1407      53           35       18        17          116     40     8      33
11/24/2017 	 10/27 - 11/23  1457      48          51       33        18          127     31     11     59
1/3/2018 	 11/30 - 1/02      1238      50          70        38        23           95      27     10     34

(sorry preview did not have a wrap - but you get the idea - I'm not going to correct it)

For what it is worth, here is some of my lipid experience with fasting & keto diets:

My standard lipids get worse with a long fast. For example on day 7, TG's might go from 55 up to 80, LDL will increase from 105 to 175 & etc. In my world, this is not "getting worse," but that is a matter of perspective. Talked to Dr. Gundry about the TG's and he suggested it was because they were being used for fuel. In fact, he's always bragging about his TG's in the 30's and his wife's in the 20's and would like us <50. I told him I can only get my TG's < 50 by eating a carby meal the night before the test. He commented that it was lower as my body was keeping the TG's in storage, as they weren't needed due to my carb intake.

This is a different context than someone on a high carb diet who's high TG's are due to a full fuel storage system and no place to put anything....

On a high carb, low fat diet I had "stellar" lipid results, but my glucose control got worse. I was pretty optimized on low carb high fat & fasting here:, a link to all our Gundry history is here..

The high trigs might be due to the fructose.

You might test after a five day fast - that would give you a baseline with no food. Then see what makes it better. With the execption of a TG/HDL ratio <=1 and getting sdLDL low, I'm not concerned about the rest of it, but that is me. A CAC makes a lot of sense.

[jcosmo]

Have you looked into thyroid hormones or micronutrients (like copper) ? These come to mind when thinking about LDL clearance rates. 1238kcal/d sounds pretty extreme to me while eating 50g of protein and exercising -- I barely hold my weight at 2200-2600/d while eating 100g/d of protein.

I haven't checked copper, but I did check T4, T3 uptake, and Free T4 Index on 11/24. All were within normal range:

T4: 6.2 ug/dL (4.5 - 12)
T3 Uptake: 30% (24 - 39)
Free T4 Index: 1.9 (1.2 - 4.9)

I also started taking kelp supplements every other day (200% DV iodine) a few weeks before that test since I've been using sea salt instead of iodized salt for several years now.

I'm adding coconut oil to my diet again. When I started limiting saturated fat in November, I found myself drinking a glass or two of wine on several occasions if my caloric intake was at or below 1200 at the end of the day. (Before that, I was using equal parts coconut oil and macadamia nuts blended and frozen in ice cube trays for that purpose.)

Sent from my XT1710-02 using Tapatalk

[apod]

I haven't checked copper, but I did check T4, T3 uptake, and Free T4 Index

This is what comes to mind with copper (granted, I've never really heard of anyone outside of this blog having a sub-optimal copper intake and seeing high lipids):

http://perfecthealthdiet.com/2011/03/an ... arb-paleo/

Jaminet writes: "Copper deficiency is, I believe, the single most likely cause of elevated LDL on low-carb Paleo diets. The solution is to eat beef liver or supplement."

[Orangeblossom]

I'm not an expert here, but just noted on the exercise about the HIIT but what about general exercise for example walking or swimming? Maybe tweaking that might help? I mean in general, not sure of benefits on cholesterol (although think it can help HDL, I read). I noticed you said you were adding eggs and dairy, I find my LDL is Ok with those and other fats as well. Maybe as others have mentioned to be it is individual and might be worth tweaking and testing to see what works for you? Kind thoughts, sounds frustrating.

PS I read this on that blog mentioned, cholesterol code? Which would tie in with you as you are lean. However unsure if is a response to LCHF as such if you were doing that previously.

"I believe the largest influence of one being a hyper-responder is how lean and/or fit they are"...interesting. http://cholesterolcode.com/hyper-responder-faq/

[jcosmo]

I Googled "lower sdldl" and found a review of research showing that statins don't lower it, but alternate day fasting does! (I know what confirmation bias is, but I DIDN'T go looking for ADF specifically.)
https://www.marksdailyapple.com/statins ... olesterol/

I don't take a multivitamin with copper, but Cron-o-meter shows that I meet the requirement at least every other day. Still, I might add it to the next test.

Sent from my XT1710-02 using Tapatalk

[jcosmo]

Still searching. This post says that niacin lowers sdLDL: http://drbganimalpharm.blogspot.com/200 ... a-out.html

How does Slo-Niacin (vitamin B3) work?

It hits the ketone receptors which is anti-inflammatory and subsequently leads to lower sdLDL, annihilation of the 'death band' LDL-IVb (the most dense and lethal), and raises the HDLs OUT OF THE ROOF.

Again, how do we produce ketones?
--low low low carb diet
--low low carb diet
--low carb diet
--physical low-moderate intensity activity > 1-2 hours (max HR 50-60%)
--fasting > 5-6 hours
--intermittent fasting 12-36 hour fasts (we all do this in the Paleo blogosphere, Crossfit, evolutionary lifestyles)
--starvation
--drink human breastmilk (just kidding)
--eat a lot of medium chain SATURATED fatty acids (coconut oil, coconut butter, MCT oil, coconut milk/meat, grassfed goat cheese/milk, grassfed butter oil (greenpasture.org), grassfed butter/ghee/cream, etc)

There's also a lot of review of evidence that saturated fat lowers sdLDL and increases HDL on the same site: http://drbganimalpharm.blogspot.com/sea ... es%20sdLDL

Though I don't know if E4s get the same results. But I do intend to cut fructose and alcohol out of my diet again.

Editing to add: He is NOT advocating niacin, but the other mechanisms of inducing ketosis. Found on the second link posted above:

Does overdosing on niacin aid the above? Unfortunately 'no'. The mechanism of action is that niacin mimics all of the above (increases hGH, testosterone, steroids, ketosis, fasting and exercise). Adverse effects of niacin include: gout, diabetes and liver test elevations. Again I like niacin b/c it works but I don't love it. It doesn't appear to work on everyone in the year 2008-2009 and likely the future. Numerous nutritional and environmental toxicities apparently have shifted the cardiology and endocrinology playing field since the niacin trials were published, including the HATS 2001 NEJM publication by BG Brown et al.

[jcosmo]

Found by Google search for the phrase "small dense LDL" and APOE4: http://ajcn.nutrition.org/content/73/4/736.full

This research article suggests that alcohol is the only factor significantly correlated with the difference in LDL-C between subjects of each APOE genotype. (Though they didn't look at particle size or sdLDL count.) All the more incentive to drop it from my diet.

Alcohol drinking determines the effect of the APOE locus on LDL-cholesterol concentrations in men: the Framingham Offspring Study
Dolores Corella, Katherine Tucker, Carlos Lahoz, Oscar Coltell, L Adrienne Cupples, Peter WF Wilson, Ernst J Schaefer, and Jose M Ordovas
Am J Clin Nutr April 2001
vol. 73 no. 4 736-745

The results of regression models of the association between APOE alleles and alcohol intake, after control for possible confounding factors, are summarized for men and women separately in Table 4⇓. We observed a highly significant interaction (P = 0.001) between alcohol intake and the effect of APOE allele status on LDL-cholesterol concentrations in men. In women, this interaction term was not significant. The results obtained with these models confirm the interaction between APOE allele group and alcohol intake shown in Figure 1⇑. The interaction between alcohol intake and APOE allele status remained significant in men after age, BMI, saturated fat intake, energy intake, and tobacco smoking were controlled for. The regression coefficients for the interaction terms indicated that the LDL-cholesterol-lowering effect observed in carriers of the E2 allele (−0.532 mmol/L; P < 0.001; Table 4⇓) was absent in male nondrinkers (0.538 mmol/L; P < 0.01). Likewise, the usual elevating effect observed in carriers of the E4 allele on LDL cholesterol (0.157 mmol/L; P < 0.05) was also absent in male nondrinkers (−0.339 mmol/L; P < 0.05). The interaction described between alcohol and APOE allele type was present in all categories of saturated fat intake. The interaction term between APOE allele type and saturated fat intake was not significant when included in these models and it was removed in subsequent analyses.

This might explain why I'm seeing studies that say SFA alter lipid profiles beneficially for E4s, and others that say the opposite...

Previous studies reported significant interactions between APOE allele type and plasma lipid responses to both dietary and pharmacologic therapies (39). However, most of these studies did not investigate the effects of the interactions between alcohol intake and APOE allele type on lipid concentrations, and the diet studies focused on fat and cholesterol intakes rather than on alcohol intake.

The results of the present study support the importance of considering alcohol intake and sex when examining genotype-phenotype associations. In the present study, the inclusion of a sex interaction term in the multivariate model, stratification by alcohol intake and genotype, and the additional control for confounders such as dietary fat allowed the identification of an interaction between APOE allele type and alcohol intake. In studies in which these factors were not considered, the alcohol interaction effects may have been masked and therefore ignored.