Ran a 6-week 16:8 block, same sleep window, no med changes. Data: fasted BHB 1.2 mM at week 5, fasting insulin 5.8, ApoB 105, LDL-P 1450, TSH 1.7, free T3 down from 3.4 to 3.0, HRV down ~8 ms, resting HR +4. Diet was similar calories, maybe 200 kcal deficit. I expected trigs to drop more than they did.
Is the LDL-P/ApoB discordance just weight loss, or is there a plausible FFA/thyroid mechanism? Looking for papers, not anecdotes.
What were trigs and HDL? Discordance often tracks energy deficit more than fasting window.
If free T3 fell while TSH stayed flat, the crab/energy availability angle seems more likely than the fasting window itself. There's classic work from Danforth on fasting and T3, though the LDL-P angle is separate.
The ApoB/LDL-P discordance in early weight loss is real. I saw similar in my n=1, but it reversed by week 12.
The FFA/thyroid framing is plausible, but the LDL-P number may just be assay noise plus negative energy balance. There's a 2019 review in J Clin Lipidol on LDL-P vs ApoB discordance; insulin resistance tends to make ApoB underestimate particle number, while weight loss shifts the relationship.
Your trigs/HDL would tell us more. If trigs stayed high with ApoB 105, I'd suspect remnant cholesterol.
If trigs dropped and HDL rose, maybe it's just flux.
Also, 16:8 without measured intake is a big confound; sleep restriction can drop HRV 5-10 ms alone. Did you track sleep duration or only timing?
Sleep duration matters. My HRV drops 6-8 ms when I cut sleep by 45 min, even with same fasting window.
Did you run ApoB twice? Assay drift is real.
The T3 drop is the interesting part for me. In the Minnesota Starvation Study, T3 fell with energy deficit, not fasting per se.
If your BHB was 1.2 mM at week 5, you were likely in ketosis, but that doesn't rule out low carb intake affecting T3. The LDL-P rise could be increased cholesterol synthesis or decreased clearance; thyroid normally upregulates LDL receptors. But n=1 and no direct clearance marker.
What's missing is trigs, HDL, and maybe Lp(a) before reading too much into LDL-P. The discordance debate is mostly about which marker is more reliable in insulin-resistant vs weight-loss states.
Your free T3 dip plus HRV down 8 and RHR +4 reads more like “energy deficit stress” than the 16:8 itself to me. I ran a similar six-week 16:8 last spring and my ApoB went 92→108 while trigs stayed flat, which drove me nuts; the reversal came when I stopped doing fasted strength work and moved my last meal to 6pm, not when I shortened the window.
My BHB was lower than yours (0.7–0.9), but LDL-P tracked with how many days I ate under ~1800 kcal, especially if I skipped post-lift carbs. Surprise: my waist dropped 1.5 inches while ApoB rose, so I stopped panicking about the discordance until I reran labs after two weeks of no fasted workouts and consistent 7.5h sleep.
Did you track waist or weight trend, and were your fasted mornings also workout days? That’s the fork I’d chase before blaming thyroid.
Quick check: how long were you actually fasted, not just what the clock said? Mine drifted from 13 to 17.5 hours depending on whether dinner slipped to 8:30, and once I started logging it, the only draws with BHB over 1.0 were the 17-hour ones, which made my whole "ketones are up" story a lot less exciting than it looked.
The part I'd toss in as a maybe-contrarian take: in my n=1, ApoB went up during the active losing phase and came back down about 5 weeks after I held weight flat, no diet change beyond eating at maintenance. So the number you grab at week 6 of a deficit is sort of a moving target, and I burned a lot of energy interpreting a snapshot that didn't survive the next draw.
apoB 105 with LDL-P 1450 isn’t wildly discordant — both are particle-ish; trigs often lag unless carbs/refined fat actually dropped. My n=1 sheet: fasting window length barely moved trigs, but shifting my last bite 2h earlier dropped them ~18% in 3 weeks.
Weight loss can also transiently bump ApoB/LDL-P via mobilized cholesterol. What were trig/HDL ratio and hs-CRP at baseline vs week 6? And did your meal timing stay identical, or just the clock? I’d bet the compressed eating window pushed your last meal later, which would line up with the RHR/HRV shift.
Dorm-meal angle: when my eating window shrinks, my cheap protein defaults to tuna packets, deli turkey, and Greek yogurt — sodium up, potassium down. My HRV/RHR moved with that plus late dining-hall close times, not just the deficit.
Did you log sodium/potassium or the last-meal-to-sleep gap? Also, did your fiber source change?
Mine did when I skipped the sad salad bar, and my ApoB/LDL-P tracked more with soluble fiber than with BHB.
Tbh What did your lifting log do? When I ran 16:8 in a deficit, HRV/RHR shifted before labs caught anything: top sets felt okay but bar velocity and rep capacity dropped.
If weekly tonnage or sleep latency changed, that’s your stress signal. Also, 16:8 often shoves most carbs later, which can leave morning lifts under-fueled.
Did you keep pre/post-training carbs consistent, or just fit them into the window?
late-night soda-swap guy here. when i did 16:8 my hrv dropped and rhr bumped until i moved my caffeine/zero-soda earlier and added electrolytes.
i was chugging diet dew at 10pm and waking to pee, so my hrv was basically reading sleep fragmentation. did you change soda/energy drink timing or sodium/fluid intake during the block?
also fasted bhB can mean lower glycogen, which sometimes makes hrv and ft3 look worse before tigs move. curious if your urine ketones/breath acetone tracked with the hrv dip.
The free T3 drop is the clue I’d chase. When I did 16:8 plus a similar deficit, my FT3 went 3.3→2.9 and HRV dropped ~7 ms, even though TSH stayed around 1.5. What turned it around for me wasn’t more fasting—it was adding 30–40g carbs around my workout and
My n=1: 7 weeks 16:8, BHB 0.8–1.4, ApoB 96→103 while losing 4 kg, then down to 89 over the next 6 weeks once my waist actually moved. I track ApoB against waist with a 2-week lag, and that correlation beat BHB/insulin by a mile.
Free T3 dip felt like energy availability, not the window itself; adding a carb meal after training brought it back. Did you track waist/body comp weekly, and were you lifting fasted? If waist was flat, I’d expect ApoB to lag; if waist dropped, I’d look at fat mobilization/thyroid stuff rather than 16:8 itself.
random q: did your sodium/electrolyte intake or caffeine timing change with the window? every time i tighten to 16:8 my rhr bumps ~3-5 and hrv dips until i stop chugging diet soda/black coffee on an empty stomach and salt my first meal.
lower insulin can make you dump more sodium/water, so plasma volume drops, and that alone can hit hrv before lipids move. also if lifting slid to the tail of the fast, that’s a double whammy.
what did your pre/post workout fuel look like? that might explain the hrv/rhr shift and maybe the ft3 dip while apoB/ldl-p just chug along.
One angle not mentioned: your free T3 drop. In the trials, energy restriction—especially lower carb—can suppress T3 independent of the fasting window, and that’s a plausible hit to LDL receptor activity, so ApoB/LDL-P can drift up even while insulin is low.
Trigs also track liver fat/energy flux, not just fasting insulin. How fast was the weight loss, and did LDL-C/non-HDL track with ApoB?
I’d also check whether BHB 1.2 was a one-off from a longer overnight fast vs a steady pattern. My n=1: T3 and lipids lagged behind HRV/RHR when I overdid the deficit.
Hi, brand new (week one), so this is a nervous small question: did you track sodium/potassium or overall hydration? When I under-salt and drink more coffee, my HRV drops a few ms and RHR bumps up.
I’ve also seen BHB rise more from lower carb than from fast length itself. Did your carb grams shift much, or was it mostly meal timing? Sorry if obvious — just trying to understand the electrolyte/hydration angle and whether that could explain some of the HRV/T3 stuff.
Small-town pharmacy/insurance angle: our local lab only runs ApoB if it’s justified, so I get the number-staring. The piece I’d chase is free T3 down with HRV down: did you check reverse T3 or morning cortisol?
In my own 16:8 blocks, a mild deficit dropped T3 before ApoB moved, and my RHR tracked sodium/electrolytes more than BHB. Were you keeping sodium steady? If fasting glucose also crept up despite BHB 1.2, that smells more like a stress/cortisol adaptation than fat adaptation.
A 3-day food/symptom log might tease that out better than another lipid panel.
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