#but love to see it and if i dont then DL; DR
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Introductions are in order, I suppose.
Lore, (Dr.) Adrastea, and Percy are our names. Lore is preferred, but we will tell you which to use if needed.
21, genderweird, plural, kinky bi/ace domme, @spiraleyedlore is my main.
Minors dni, cis man doms you aint wanted here.
Everything you see here is fantasy. I will be posting some very intense stuff here, but let it be known it doesn't reflect my real political or philosophical beliefs. If it still pisses you off, you might be the problem, not me. Every post is also from the perspective of Me as the domme, unless i actively say otherwise. Make sure you read everything here before dming me.
Don't fucking add extra "oh this is totally me" shit to my original posts (and id prefer if you didnt do it in general tbh). Its about Me, not you. And don't fuckin call Me titles out of the blue, you may call Me a title once you've earned it, with the only exception being Goddess. If you read this, tell me your regular drink order when you go to a cafe.
Now that pet peeves and general stuff is out of the way, kink likes and dislikes are under the cut. Keep in mind, this list is always updating and being elaborated on.
Obsessed:
Hypnosis, mind control, possession (as in ghost stuff), memory play, worship, personality play
Love em:
Drone stuff, tech control, genderplay, orientation play (esp just altering peoples sexuality to be just Me), forcefem/forcemasc, ego death and rewriting, hypnotized service (making people draw or write or do other things for me), cnc, intox (weed or alcohol, though i am open to other things!), dollification
Like em:
detrans (never permanent), rapeplay, fauxcest (esp sister stuff), cuck, findom, bimboification, boot stuff, emotional sadism, dombreaking
Occasionally in the mood (ask before engaging in it)
physical sadism, possessiveness (needs to be close, genuine, and im allowed to act on it partly, not just a scene thing), petplay, ageplay, mommy kink, vore, musk/scent kink, class play
Not into it:
feet, breeding, pregnancy, feeder/feedee, extreme inflation/extremely large parts, actual incest kink
Dont bring it up around me (i might block you if your posting this, nothing personal. this isnt a dni)
hdg aka human domestication guide (for personal association reasons), sissy anything, eating disorder kinks, watersports, scat, ab/dl, raceplay, real sexism and transphobia, b*mb* sl**p
Ask me to tag stuff!! If you want me to tag a certain kink I regularly post, ask or dm me and I will try my best to tag it. Also, if I have you blocked on my main but you wish to be unblocked, send an anon with your blog you want unblocked, and I might unblock it if I'm feeling merciful~
I use a modified stoplight system for check ins during scenes. I will either ask directly, or use a stoplight emoji to ask how you are feeling! If you aren't familiar with it, green means continue on, yellow means to take a minute and check in/slow down, and red means to stop completely. I will always respect these, no matter how intense the scene is. I also use blue, which you can use if you like the specific thing I am doing and want more. If you read this far, tell me a fun fact when you first dm me. Never be afraid to use these in scene, I would rather know you are comfortable during the scene.
Remember that kink isn't reality. I am still a person behind this screen, and you are too. I will play an exaggerated version of ourself here, and let my most controversial kinks be known. I try to be safe with my kink play, but I practice RACK and know that some kinks may come with inherent risks.
Final rules! Be respectful, don't lie to me (if you break my trust im not fuckin with you anymore), and don't be an actual bigot. Now go have some fun, n get a little bit Worse for Me~
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why r u so mad about ppl preferring ten x madame de pompadour to ten x martha like ten/martha will never be a thing. ten don’t want anything to do with martha. he literally said to her face she wouldn’t replace rose… and she never did… isnt canon enough for you
hm.
im glad im only a scorpio on this alone. if martha deserved better than ten then so do all of em but anyway:
this ask is giving 2006/07 i dont want to see tenth doctor in a romantic relationship with a person of color because i can't project myself or relate to them if they arent the very thing being catered to me ever since the silent pictures vibes. u know the same vibe when rtd was told to not regenerate 14 in 13's clothes. just. Ick.
but im not mad. its just interesting for a ship so big as tenrose, it is usually correlated with hating madame de pompadour and/or joan and/or river [though in joan's case they hate her not because shes racist but because shes not rose]
though comics tend to release to combat that in multi doctor stories where they jump through various alternate universes of themselves where the doctor sees themselves settled down with dr. grace holloway (for 8th dr multi doctor stories) and professor melody williams/river song (for 11th dr multi doctor stories) where in those cases, they are frightful of the concept settling down at all. [take note that both times, he settles down in the same house that he owns bc of that unit paycheck on the dl] so i am curious that with this new drs, the equivalent of this would be 13 14 15 being terrified of settling down with rose because they had grown past her as this point.
i prefer the doctor in a polyromantic ace relationship than their umpteenth 🌟tragic heteronormative romance with yt human woman number 23445788764443356743🌟 i want 14 to sweep martha off her feet in pure joy and kiss her passionately while badmouthing tf out of 10 like 9 11 12 13 do with no filter before cradling her like a baby because hes about to crumble under his brand new identity complex and then take her kid to an amusement park and then 14 trips over a brick and dies. hell i rather have nina sosanya play a whole different lady in nod to doctor who recycles their actors trope as a way to introduce a love interest to 14
that amusment park one weirdly sounds like a 8th doctor audio. pls 🙏🏾 dont make it into one i couldnt handle schezro let alone the rest of his content. Empire of the Wolf made me so fucking worried for rose marion tyler like im just she back home 🫣. as for rose tyler from the sea devil universe still out about. whoop his ass. if billie come back as HER? MISS COVER MODEL MISS DICTATOR MISS EMPRESS ROSE?
NOT
i would love for ten to be strictly friends with the new miss empress rose. get that martha karma real quick ehehehehe after all rtd did say they need freema for somethin and im sure seeing 10 get treated the same way he treated martha by no other than empress rose herself -AND THEN EMPRESS ROSE FLIRTS WITH MARTHA??? FINGERS CROSSED??? im just saying that i personally will ride on that for 8 black history months and christmases straight like woo
also real glad it is collectively decided by every one that tentoo is just john smith not corin so yay thanks big finish and titan comics
#{lets see if i can scare this anon away listen i even made a graphic for this damn it. u better appreciate it i went all out for you}#{porn blogs and micro antiblack anons: this is why i dont share my shipping opinions much bc they stick to tv and i stick to everything}#{usually all this i gave to my aunt and we would have phone discussions and she would watch and call be like hey yeah! i see it}#{and she would say: but really it wasnt that for martha. it was the writing choices that was disapproved because not wanting another 💞}#{it went from classism for rose to racism for martha and she points that it wasnt catered to black fans in the rtd era}#{so yeah ten x martha wouldn't be a thing but only because test audiences and fans refused it due to the studios racial bias}#{10 wanted everything to do w martha. he just used rose as excuse and because of that 12 and 13 vocally to his face hates him for it}#{and we all fell for it: everybody did because like 12 said: its the bambi eyes. hook line and sucker}#{he wanted martha the whole time but he kept playing that hot n cold game to the wrong girl just bc it worked on 2 later 3 yt blonde women}#{4 yt women because of miss kylie minogue! all of a sudden he dont know how to counterflirt when a blk woman flirts back?}#{yes thats right im throwing miss claire pope AND IN THE GABBY GONZALES COMIC OF THE PPL OUTSIDE HER FAMILY LAUNDROMAT??}#{but yeah after losing donna suddenly supiciously hes not racist but extremely genocidal to death and death alone like hm.}#{his actions speak extremely louder than his words and in turn so does the fandom and its writers}#{4 yt blondes and hes willing to believe in them despite him having to permanently lose them but completely have lil faith in the blk one?}#{ ten never actually go back to martha. be fair if i forgave the person that enslave her family for a missing year? yeah i wouldnt either}#{we could never be together because of a yt woman i chose to leave behind three times with her mum for 'safety' boy bye}#{and i go around and almost in one whole episode almost left her behind AGAIN for madame de pompadour another blonde yt woman?}#{like i ship them i ship all of em but if they were all hanging off a cliff side? 🤧 😔 we gather here today in the loss of 🌹 and depomp}#{dont worry at least 9 would leap after rose.}#bw: out of ethos#answered#anonymous#bw: long post#{i made a long post just so i surprise you with a cute billie graphic thats all. that the main topic}
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Small Nov Wins
1 - cant bring myself to study, got out of bed 10:30-ish am. While lazing around i read royal servant and do random internet stuff and watched romee's vlogs. Ate breakfast and i somehow has no appetite?? This is rare. e, cicil kompre began at 15:30 pm (i know, i waste my time a lot). Pengumuman wahana mpi wow yay kalideres makara and budi asih
2 - the weather was pleasantly cloudy. poli anestesi anak, simul. went to what used to be calais, its called flavola now. at this point i quite need some calories because i only ate bubur ayam and its like 2-3 pm ish. Eventually the hunger is gone, arrived home at about 4-ish, drank protein to curb my hunger (nanggung dinner). dad said sumn that annoyed me so after maghrib i just lazed in bed, not feeling like doing anything (even though there’s lots of exams and hw lmao), fell asleep
3 - woke up at 2 am, prated, randomly searched for angel - chancellor and taeyeon’s lyrics and i basically wept at 4 am. i assumed the song was just like,,, a guy talking to a girl, his angel, you know. EXCEPT,,,,,,,,. the 2 MVs was also rly222 beautiful 🥺. Poli geriatri today, didnt even see patient because there was no more at that time (status salin nadia). ate ichiban salad (surprisingly quite good) at dm bcs i rly do be functioning better outdoors, made matcha latte with full cream milk ((powder)), cicil PT
4 - can finally wake up late. finished 1 sitasi pt, made ikk ppt, bujing lina called about diarrhea and nausea meds, laddered the leader for tomorrow’s exam and it,, was,,, me,, group call with shiko. frantically studied for EA
5 - PT (finished in 45 mins), simul as a leader, with STEMI, VF and hypoglycemia case. somehow made it through. i suck at dosages omggg. PP by car with mom (not rly that tired) but i SLEPT after i got home and had no mood to study helpppp
6 - did my first swab test today. i pushed the doctors hand when she’s doing oropharyngeal swab im sorryyyy 😂. slept. matcha. cicil kompre
7 - still havent finished ikk (deadline: today), and still havent studied for geri and ikk AND i still managed to take a nap. why. Read a bit of kompre. Not sleepy after matcha, but insted i reread bj alex and tsubaki chou lonely planet until 2 am the next day #rippriorities
8 - im having matcha latte seven days in a row as of today :))))) woke up at 10:30 am, went to flavola with atikah and got strawberry yakult (tasted like es mony), arrived home at abt 7-ish am and there no dinner, so i drank protein and ate japota honey butter. My breakfast was chicken porridge, so my diet is sooo liquid today. Rip proper nutrition (ate buryam, lumpia, japota for the whole day and drank 3 beverage). Cicil kompre and studied geri
9 - suma geri, slept, cicil kompre, ny head kind of hurts
10 - my head still hurts, suma ikk with dr herqu and dr retno, didnt take swab result by car because the TRAFFIC in soetta so my brother took it. Thankfully negative.
11 - lulus kompre alhamdulillah, the examiner were Prof Saptawati and dr. Dani from THT. Dr dani still remembered me :"") they were very kind. Went to tamel for first wahana: klinik makara UI. Picked up masker first at mahmudas place, and then went to depok. On the way i was interviewed by maba 2020 wtf im so old. Cleaned up my room with the fam, printed sumn in barel (its quite empty there)
12 - first day at klinik makara ui. i WALKED. such wow. fixed my shoes in kutek. had breakfast in barel and bahari for lunch-dinner. somehow i felt very drained. bought Dapur Alya (nutella and regal) and 2 salads from Salad Point since there was 11.11 promo. Put all of them in the fridge. Read Fools and its sooo good omg
13 - had salad and left over bahari rice for brekkie. went to clinic by grabbike :)))), had my first teleconsultation experience today, a chemical trauma case. suma ea with the help of shiko
14 - woke up at 5:20 ish and i jogged a bit at ui lmaoo. fisip - ft - fisip. By 6:30 im already back at my room. 1 hour can be spent a lot of different ways, it turns out. Washed my clothes. Ate monstercheese pizza. Slept a bit. Went to blok m with ara (she was late as always, surprised her with koi milk tea), ate futago ya (greasy cheesy milky goodness, enak tapi eneg afterwards), bought red bean bread at la mouette, bought discounted onigiri bento box at papaya. We went to m bloc space, looked around, ate gelato at kebunide (blueberry: yum, fresh, kiiinda feels artificial, salted caramel: delicious but makes me thirsty) and did photobox at connectoon. Walked to mrt asean but turns out!! for weekends mrt is closed at 8pm. Took grabbike to sudirman, seeing the pretty city and people just hanging out, playing skateboards on the wide sidewalks.
15 - planned to go jogging with salemba frens but i woke up late (06:45), so i just lazed around. Ate onigiri bento (super worth it for 25k for the proteins), fell asleep again 10ish to 14:30 lmaoo. The doms from yesterday was present even on the right side of my lower back 🙂 the red bean bread made me feel full, and the red bean was not too sweet, which i love. Reviewed some meshwork materials i missed. Fianti called and we talked abt her and hari
16 - had mujigae for sahur and fish bite for iftar. The fish was not as soft as fish streat, but the flour was definitely better and crunchy. But it doesnt have the seasoning micin like fish streat do. The pasta was quite a lot im in food coma afterwards. Fell asleep, and my stomach was so gassy that i woke up in the middle with a headache that does not play around. Fortunately it dissapeared in the morning
17 - breakfast is rice kimchi and abon lmaoo just pretend it makes sense. The scrubs i ordered finally arrived. I fell asleep AGAIN, WHYYYY. Lost my streak in DL, i guess i can stop using it for now.
18 - finished reading blood link, girlll i thought the human died at the end. Did not buy food today wow. Took a nap and cicil kompre.
19 - brekkie at barel. Helped measuring antropometry today at clinic, and also measured my own. The fucked up thing was that i THOUGHT my body fat is still at 28% compared to the past (dr rina's research). So i looked at the old paper AND. I USED TO HAVE. 35% FAT 🙂 even my memories are in denial and are fooling me. All this time i thought i was at 28 🙂 did swab at rsui. The one swabbing was from fkui 2012 and we had small talk. It hurted more than lmk :( now this does feel like drowning in water (cause before i said "nah its not like water in nose"). Took angkot back to tamel, bought piscok lumer pocin and its soooo gooood ugh
20 - i feel like if i have breakfast with leftover rice and abon and sozzis i get hungry faster lmaoo. Ordered ken karaage from kukusan, yaa okela for 25k with ongkir. Did online posbindu education through wa. BTS BE COMEBACK 🥺 i maximized my wifi time (no wifi at tamel) so i listened to the whole album. My mobile data is at 200MB lol. Read a good longreads from the atlantic, about down synd and genetic screening. The writing is so so good im just blown away. And teary eyed.
21 - ran a bit, solid class (gastro, rheum, infection), embryo, webinar about sleep by dr Gita Anindyajati, SpKJ, bought ayam geprek gold chick (lotsss of oil since i ordered tempe, jamur, egg, bought pop cookies. matcha cheese was actually better than i expected (the combination somehow fits), dark chocolate and marshmallow is very chocolatey like mom’s brownies, and vegan strawberry cookie with a hint of mint. i wonder how they replace the egg. I wonder why after i run i dont feel hungry for a moment. bloating just gooes away
22 - joined kris' healthy weekly event (lmao) in tamsur. They went to epiwalk first. Its difficult for me to run w mask, ngl. Went back to tamel, embryo, ate leftover meal from gold and chick, felt somehow drained to the bone so i just laid in bed and lazed and lazed. Theres no soreness, but the weakness was generalized lmao. Ordered bbq chicken almond salad from salad point, it was actually quite fulfilling and delishhh (added chili sauce to the dressing). Literally laid in bed from 7 until i fell asleep and woke up at 6 the next day. Finished readin shame application lmao
23 - i still feel tired ckckck. No doms, but i feel like i just want to lay down. got DV patient today at clinic, its most likely derm numularis??? Ate salad and dark choco marshmallow cookies in the evening and that cookie. Is so damn sweet im just thinking about the increase in my blood sugar. And i like sweets so!!! Never thought id find sumn too sweet. Washed my clothes and cicil ukmppd (i put things about studying ukmppd in habitica now)
24 - ate tanoshi sushi and ufo ramen for bfast, ate the sushi again for lunch and after waking up from my sleep i tried kokku ramen (so so, but the egg yolk's good)
25 - bfast: superbubur, protein shake and cookies. (did not make me feel full long enough). Ordered burger from EATG (so so, burger bener is better) for lunch. Last day at makara ui. Ara arrived coz shes staying here in tamel. Waiting for mom to arrive from cibubur, she arrived at about 20:30. I passed out at home
26 - first day in pkm kalideres, i volunteered to be pj to avoid RSUD. my room is a mess, i feel tired after i go back. maybe its the physical withdrawal (?) because i dont walk like when im on klinik makara. came to pkm thinking i wont do anything (orientation only) but the 6 of us ended up going. i was at igd. i saw nail extraction and injected ats for another patient
27 - talked for almost an hour with the doctor at poli lansia. went home, felt sooo tired, i slept and actually showered after maghrib. originally planned to go to sbux but i was just tired af. my mood was horrible at home.
28 - turns out i started my period today. i havent studied at all during pkm kalideres era. embryo. slept again. read some manga by nishin something with the psychological and BL genre.
29 - embryo. cut my hair, showered, and felt better. fell asleep on dr gita's lecture. Drank cimory banana milk with a bit of matcha powder. I dont know if its the sleep, or a bit of caffeine, but my mood feels better and im more awake. Cicil ukmppd with a slow pace. Read itasaku ff. Slept at about 2 am
30 - surprisingly, i dont feel sleepy when i wake up. poli anak today, surprisingly i got perinatology case (jaundice). presented it on pleno. for bfast i ate 3 slice of bread (2 with meat and cheese, 1 choco and cheese) and protein shake, lunch: a slice of choco cheese bread and a banana, fell asleep, dinner: 1 bakwan, a banana and nextar. i can feel that the calories i got today is even less than what i usually got (and usually i already try to limit calories that i am counting the intake amout and made sure im not too far from my bmr lmaoo (~1100)
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(fic anon) its hard to find good fics for dl tbh.... just any of your favs? :) (i really like ‘another way out’ tho)
http://diabolikpersonals.tumblr.com/tagged/fic-recs I have a tag for fics! :D beware that I posted links to a few piss fics so if u see a post tagged as “unsanitary” then thats...thats one of em
I would love to link you to a bunch of my favorite fics but unfortunately a lot of them got taken down or the author moved them to a private page and I dont know if im allowed to share them. ._.;; but uh im gonna promo tl;dr again because it’s still so cute and I love it a whole lot
I’m glad you like another way out!!! ahahaha, I havent updated any of my fics in a while..........I should get started on that soon x_x
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Is Keto Bad For Cholesterol?
We’ve all heard the story. Maybe we’ve even been the protagonist.
Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.
Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.
“Could I be killing myself?”
“Are my health improvements just a mirage?”
In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?
The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.
In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.
In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.
Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.
But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.
I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….
I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.
What Could Be Causing LDL Elevations On Keto? Weight Loss
I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:
But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.
When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.
If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”
Low Thyroid Function
The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.
Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.
Eating Too Damn Much
Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.
Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.
Genetic Variance
Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.
Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.
Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.
Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.
This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).
Too Much Butter
Huh? Too much butter, Sisson? Is such a thing even possible?
Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve. That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.
Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.
I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.
For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.
So, What Can You Do If You See An Increase in LDL? Start Chugging Soybean Oil
Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.
You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.
Stop Being a Keto Caricature.
Half a package of cream cheese for a snack.
Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.
I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.
Eat Less
Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.
You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy. Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.
Balance Your Fats
The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.
For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.
Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.
African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA
African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA
Elk: roughly 40% SFA, 30% MUFA, 30% PUFA
Moose: roughly 33% SFA, 33% MUFA, 33% PUFA
I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.
Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):
Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.
Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.
Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.
Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.
They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.
Are Traditional Lipid Markers Even Relevant for Keto Dieters?
Maybe, maybe not.
But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.
You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.
I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.
We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them.
True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.
What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.
Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.
References:
Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.
Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.
Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.
Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.
Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.
Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.
De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.
Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.
The post Is Keto Bad For Cholesterol? appeared first on Mark's Daily Apple.
0 notes
Text
Is Keto Bad For Cholesterol?
We’ve all heard the story. Maybe we’ve even been the protagonist.
Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.
Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.
“Could I be killing myself?”
“Are my health improvements just a mirage?”
In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?
The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.
In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.
In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.
Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.
But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.
I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….
I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.
What Could Be Causing LDL Elevations On Keto? Weight Loss
I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:
But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.
When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.
If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”
Low Thyroid Function
The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.
Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.
Eating Too Damn Much
Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.
Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.
Genetic Variance
Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.
Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.
Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.
Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.
This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).
Too Much Butter
Huh? Too much butter, Sisson? Is such a thing even possible?
Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve. That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.
Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.
I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.
For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.
So, What Can You Do If You See An Increase in LDL? Start Chugging Soybean Oil
Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.
You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.
Stop Being a Keto Caricature.
Half a package of cream cheese for a snack.
Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.
I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.
Eat Less
Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.
You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy. Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.
Balance Your Fats
The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.
For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.
Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.
African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA
African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA
Elk: roughly 40% SFA, 30% MUFA, 30% PUFA
Moose: roughly 33% SFA, 33% MUFA, 33% PUFA
I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.
Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):
Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.
Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.
Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.
Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.
They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.
Are Traditional Lipid Markers Even Relevant for Keto Dieters?
Maybe, maybe not.
But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.
You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.
I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.
We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them.
True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.
What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.
Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.
References:
Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.
Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.
Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.
Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.
Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.
Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.
De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.
Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.
The post Is Keto Bad For Cholesterol? appeared first on Mark's Daily Apple.
0 notes
Text
Is Keto Bad For Cholesterol?
We’ve all heard the story. Maybe we’ve even been the protagonist.
Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.
Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.
“Could I be killing myself?”
“Are my health improvements just a mirage?”
In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?
The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.
In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.
In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.
Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.
But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.
I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….
I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.
What Could Be Causing LDL Elevations On Keto? Weight Loss
I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:
But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.
When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.
If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”
Low Thyroid Function
The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.
Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.
Eating Too Damn Much
Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.
Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.
Genetic Variance
Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.
Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.
Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.
Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.
This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).
Too Much Butter
Huh? Too much butter, Sisson? Is such a thing even possible?
Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve. That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.
Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.
I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.
For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.
So, What Can You Do If You See An Increase in LDL? Start Chugging Soybean Oil
Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.
You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.
Stop Being a Keto Caricature.
Half a package of cream cheese for a snack.
Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.
I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.
Eat Less
Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.
You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy. Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.
Balance Your Fats
The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.
For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.
Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.
African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA
African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA
Elk: roughly 40% SFA, 30% MUFA, 30% PUFA
Moose: roughly 33% SFA, 33% MUFA, 33% PUFA
I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.
Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):
Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.
Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.
Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.
Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.
They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.
Are Traditional Lipid Markers Even Relevant for Keto Dieters?
Maybe, maybe not.
But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.
You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.
I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.
We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them.
True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.
What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.
Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.
References:
Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.
Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.
Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.
Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.
Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.
Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.
De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.
Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.
The post Is Keto Bad For Cholesterol? appeared first on Mark's Daily Apple.
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Is Keto Bad For Cholesterol?
We’ve all heard the story. Maybe we’ve even been the protagonist.
Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.
Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.
“Could I be killing myself?”
“Are my health improvements just a mirage?”
In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?
The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.
In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.
In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.
Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.
But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.
I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….
I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.
What Could Be Causing LDL Elevations On Keto?
Weight Loss
I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:
But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.
When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.
If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”
Low Thyroid Function
The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.
Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.
Eating Too Damn Much
Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.
Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.
Genetic Variance
Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.
Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.
Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.
Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.
This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).
Too Much Butter
Huh? Too much butter, Sisson? Is such a thing even possible?
Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve. That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.
Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.
I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.
For what it’s worth, whole food dairy like full-fat yogurt, kefir, and cheese do not have the same effect on lipids as butter. They also happen to be keto-friendly and more nutrient-dense.
So, What Can You Do If You See An Increase in LDL?
Start Chugging Soybean Oil
Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.
You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.
Stop Being a Keto Caricature.
Half a package of cream cheese for a snack.
Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.
I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.
Eat Less
Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.
You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy. Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.
Balance Your Fats
The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.
For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.
Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.
African kudu (antelope family): 35% SFA, 24% MUFA, 39% PUFA
African impala (antelope family): 51% SFA, 15% MUFA, 33% PUFA
Elk: roughly 40% SFA, 30% MUFA, 30% PUFA
Moose: roughly 33% SFA, 33% MUFA, 33% PUFA
I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.
Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):
Focus on monounsaturated fats and fat from meat, rather than isolated sources of saturated fat like butter and coconut oil. You probably don’t have to eliminate those fats. Just don’t make them the centerpiece of your diet.
Eat more avocados, avocado oil, olives, olive oil, and mac nuts for monounsaturated fat. Salads are a great nutrient-dense way to incorporate high-MUFA foods.
Eat more fish. A couple portions of farmed Atlantic salmon were enough to improve LDL-P in overweight men and women. And compared to plain keto, keto + omega-3s from fish has a superior effect on inflammation and metabolic health.
Eat more kudu and impala (if you can get it). Sort of kidding. But really, eat them if you can.
They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.
Are Traditional Lipid Markers Even Relevant for Keto Dieters?
Maybe, maybe not.
But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.
You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.
I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.
We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them.
True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.
What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.
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Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.
References:
Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.
Phinney SD, Tang AB, Waggoner CR, Tezanos-pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991;53(6):1404-10.
Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metab Clin Exp. 1983;32(8):757-68.
Kleinveld HA, Naber AH, Stalenhoef AF, Demacker PN. Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free Radic Biol Med. 1993;15(3):273-80.
Rosqvist F, Smedman A, Lindmark-månsson H, et al. Potential role of milk fat globule membrane in modulating plasma lipoproteins, gene expression, and cholesterol metabolism in humans: a randomized study. Am J Clin Nutr. 2015;102(1):20-30.
Raatz SK, Johnson LK, Rosenberger TA, Picklo MJ. Twice weekly intake of farmed Atlantic salmon (Salmo salar) positively influences lipoprotein concentration and particle size in overweight men and women. Nutr Res. 2016;36(9):899-906.
De luis D, Domingo JC, Izaola O, Casanueva FF, Bellido D, Sajoux I. Effect of DHA supplementation in a very low-calorie ketogenic diet in the treatment of obesity: a randomized clinical trial. Endocrine. 2016;54(1):111-122.
Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.
The post Is Keto Bad For Cholesterol? appeared first on Mark's Daily Apple.
Is Keto Bad For Cholesterol? published first on https://drugaddictionsrehab.tumblr.com/
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The Basics on Getting a Bigger, Stronger Back https://ift.tt/2UqrlNn
Hey everyone! I wrote this up in a deleted post on /advancedfitness and didnt want it to completely go to waste, so thought that Id post it here.
The question asked was specific to using Barbell Rows to get a bigger back, but I went on a little bit of a rant about back training in general, so here it is!
Ok, so, idk what your specific goals are, but if youre looking to develop a big back, then heavy bent over rows and heavy deadlifts should be incorporated into your program.
Some questions that you probably have: What type of bent over row should you be doing? What is the ideal torso-floor angle? Where should the bar be touching my torso?
The answer: yes. Whatever works best for you, but remember that variety/variations in a movement (as in purposely varying the movement, not just performing it with shitty form) is going to help target all intended muscles and lead to a fuller, more mechanical efficient back.
Some places to start/tips: first off, you should be able to row the same, or greater than your bench, period. If you cant, that means that your chest is way too developed/your back is under developed and this can lead to a whole host of mechanical issues and potential injuries.
Types of rows: i do three "types" of rows in my powerlifting routine (normally done in super sets, but they arent necessary) .
Bench Press/Supinated grip, relatively upright row supersets: right after I do a bench, I do a row with an underhand grip in a relatively upright position (maybe at a 70 degree angle from the floor) with the same weight and for the same reps as my bench. The bar ends up hitting just below my belly button and activates my biceps, upper back, and traps (they hit lats aswell, but I dont feel them as much there due to the relative upright position of the row). Quick note: these are the only rows that I do with a supinated grip (underhand grip, facing away from your body), all others are pronated (overhand) grip
Military press (or OHP) and Pendlay Row supersets: I put these two together because when Im MPing or OHPing Im cleaning the bar off the floor (the more explosive work in your routine, the better), so its nbd to just throw some more weight on and hammer out some rows. With these, Im close to parallel with the floor (hip is hinged, hams and glutes are loaded, back is in a neutral position, etc, kind of like a starting deadlift position). Your ripping the bar straight off the ground, hitting your torso (higher than your belly button, for me its maybe 2-3 inches below my sternum), and lowering the bar back to the ground. The key with these guys is explosiveness. You want to really be engaging your lats when you rip the bar off the ground, and if that means a little body english, then so be it. You dont need to maintain a 100% rigid torse through this movement, you should be doing each rep with intent. Just remember to maintain proper posture throughout the movement and dont round your back.
The "deadlift" row: I follow Cailer Woolam alot because Deadlifts are the best lifts and he is Dr. Deadlift (seriously, the guys a fucking freak at DLs) he does a modified bent over row where he incorporates a lot of body english into the movement , and honestly, these are fucking amazing for back development. Ill typically do these with barbell shrug super set (cailer style where you generate force with your legs. Theres a vid of him explaining somewhere on youtube), and I go heavy with both (like 3+ plates for reps). I cant recommend these enough, as they not only develop a great, strong back, but by using your legs to help drive the bar up, youre engaging your whole body, and developing explosive power (which translates into all other rows and deadlifts).
So those are your rows, but what else could you be doing?
Fucking. Dead. Lifts. Deads, all the deads: conventional deads, sumo deads, stiff leg deads (great for lowback, hams and glutes), Romanian deads (similar to stiff leg but a little more low back), box deads, w.e. just do them. All of them, and do them heavy, amd do them often. Even if youre just a body building broseph, heavy compound lifts (specifially deads and squats) trigger the release way more growth horomones than any isolation excersise possibly could. You get the most bang for your buck with these, and theyre worth it. Personally, I deadlift two days a week, one is purely conventional deadlifts and the other is purely sumo deads. They are similar, but they emphasis different areas of the body during the lift: Sumos hit the legs and hips a bit more, Conventional hits the back a bit more (especially low back).
Proper form chin ups/pull ups: you want wings? Do some fucking pull ups. Most people dont do them for a single reason: theyre hard (ego hits to the bros). Typically, Ill do chins/pulls between each of my sets for a couple of excersises. These dont need to be till failure, but if youre doing 3 pull ups per set of squats (or w.e) and you do 6 sets of squats, well, youve now done 18 pull ups in that work out. Progressively overload this as you see fit. If you cant do a pullup/chin up right now, learn with assistance bands (dont use the machine), there are plenty of tutorials on youtube.... Just be sure not to bag yourself lol. One more thing to note, Pull ups vs Lat Pulldown machines: Pull ups are a true multi-joint compound excersises that you cant cheat on (with proper form), while the Lat Pulldown machine is a much more isolated movement that you can easily "cheat" on. Generally, Pulls ups > Pull downs and the Pull have high muscle activation (through EMG readings) than Pull downs.
Hanging highpulls and/or hanging cleans: these may be a little difficult if youre not use to doing more explosive movements, but they're both amazing back exercises. A key to them is not letting the weight touch the ground between reps, which means more time under tension, which translates to more gains and greater strength. Honestly, these do more for my upper back than any other excersises (while hitting mid and lower back too), as youre really ripping the bar up to your shoulders.
Squats and front squats. How the hell do you expect to squat heavy if you dont have a strong enough back/core to stabalize the weight? (You cant). These will indirectly work your entire back (front squats engage your core and upper back, I find, more due to you fighting with gravity from flopping forward).
Fuck, I went on a rant. Call this one Road Rage Rob Random Rant.
Remember: chest and arms make you look strong, but legs and back actually make you strong.
Ill see myself out lol
Edit: accessory exercises to consider.
Face Pulls: learn to love them as they are one of the best isolation movements for the upper back (I super set them with Arnold Shoulder Presses for added masochism).
Inverted body weight rows: set a bar up in the rack, and maybe a bench outside of it to put your legs on (creating a parallel row or even a decline row). Super set these with push ups to get a nive even push-pull work out.
Back flies: same idea as a chest fly, but for your back, I find they really hit the center of my mid- upper back.
SO, what are some of your favourite back exercises?!
submitted by /u/RoadRageRob666 [link] [comments] December 10, 2018 at 04:57PM
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Small August Wins
1 - DL, did my part for PKP, read a bit about leprosy reaction (PKP related), watched a cute movie tune in for love, ara stayed over at my home, edited 1 pld article
2 - exercised a bit, edited 3 pld articles, DL, finished ppt tinpus PKP, walked to the nearby lake with ara, ate nasgor smoked chicken (been a while!) and jco donuts and my tummy is happy, felt afraid with DV exam huft. I hope I can prepare myself properly
3 - DL, edited 1 article, went to school together w ara, deep fried by dr adhi for my minicex (but i am grateful for the opportunity), emir took a while to pick me up (he left home 1530 and arrived 1715) so i did some status work, arrived at home super hungry but moms food is delicious and wow glucose is finally in (after previously supported by nasi uduk and 1 jco donut) and the pain from today sort of fades away.
4 - DL, tried to study as much as i could (the panic is real), went to kencana to get dr adhis signature at 12 but he replied my chat at about 1330 🙃 , finished self reflection, group called with my group for exam prep
5 - did not DL bcs i fell asleep!! Thank god for streak freeze, met up with dr adhi in poli regarding minicex bcs turns out he brought my status etc, hes very kind 🥺 dr yudo kindly took his time to answer questions via wa voicenote even though he had a tiring day 🥺 bless all the kind people in this world
6 - DL, alhamdulillah passed the exam with dr sondang and dr larissa even though i was being a dumb ass student (thankfully theyre patient enough). Honestly panicked during the morning, i was super afraid. Searched some drug dosage for renata. I hope she passes the remed!!
7 - slept and lazed all day :( edited 1 article, dv closing. Managed to say thanks to dr yudo even though i was lowkey near tears bcs i cant for the life of me say something even mildy emotional, DL at like 15 mins before midnight
8 - finally at lvl 3 DL by cheating with my notes lmaoo, ate burgers and half pizza by dcheese pizza but had mencret2 the next day lmaooo, watched bosscha virtual sky sightseeing
9 - DL, watched Summer Vacation, edited 2 articles, put some sheet mask on (the numbers surely diminished since my cousin took some 🙂 ), pretty much watched youtube all day. At night i dreamed going to a villa that kinda looks like matamori, and the villa near it was also booked by other groups of friend, and i was recording snow falling from the sky and snow on the cliffs, but there was also a snake under the bed, and writing patients resume -_-(?)
10 - DL, read pem psikiatri cbt batch 1 optima, 25 CBT PADI, a fruitful 2,5 hr discussion with dr Heriani, SpKJ
11 - DL, poli with mendel hari and dr Khamelia, SpKJ, mustered some courage to do the ppt, phoned the patient to ask a little bit more, fell asleep and thank god i’ve prayed isya
12 - DL, lazied and played get rich, felt sick and was sick, nose congested, head starting to hurt, i dont know what is it that triggered my emotions but when my dad asked "tiff kok bersin2?" i felt like i have no privacy and they were too intruding and i wept silently in my room (bcs ppl outside can hear) and yall my nose just goes 100% blocked. aint accepting air today. Massaged my face around the sinus area until i can somehow breathe nicely and fall asleep. (took about half and hour of snot cleaning, drinking and mulling around)
13 - since i felt bad abt lazying i started my day early. Woke up at 5. Put on tretinoin, 15 CBT PADI, DL, naskah psikiatri WIP (Work in progress). It rained today. The sky was grey half of the day, which I LOVE. I felt better and more cheery, especially at abt 4-5 pm when it was raining hard and im snuggled in bed. The laptop stand arrived and bitch it was fucking amazing. My back and neck muscles felt less awkward and/or sore working at my ergonomically-awful table and chair combo turned ok thanks to laptop stand!!
14 - DL, poli with dr cika, crashed aras place (drank thai tea, ate flip burger and sausages), it felt refreshing to be in a different place rather than seeing my room all day everyday. Afterwards ara indah and i ate po noodle bar, the taste was kind of herbal (not brothy) in a good way. Tried some sort of gyoza, it was good too. Juan got accepted at USU civic engineering. Went to atikahs place, passed a red light and i got ppl a bit annoyed lmao sorry :(((, talked with atikah until 1-2ish pm
15 - richeese and fried rice for brunch time, went back home (felt socially refreshed!) to see 2 bottles of sbux coffee i ordered, claras nastar and vit d supplement from tokped. Did RPS and ikhtisar for naskah. DL. Sbux' coffee still upsets my stomach lmao but it did keep me awake and focused enough til 11 pm
16 - DL, after staying over at friends place i feel.suer content to be just at home. Ate while watching erna limdaughs vids, sleeeept
17 - DL, naskah WIP, whipped myself to go do naskah by drinking caramel macchiato and playing coffee - bts. It tasted better when i hear jks soothing voice
18 - DL, finally panicked a bit and did ppt, read a bit abt bipolar, chugged hazelnut dolce latte and somehow its not bitter anymore it actually tasted good. Talked w mendel and hari a bit abt the patient
19 - the dr actually showed up to zoom while i was opening other screen and i didnt realize (ultra embarrassing!!!) basically my diagnosis for axis I and II were wrong. She was kindly explaining and i was more dissapointed with myself but at least its all over? Talked w hansel a bit. Revised a bit of naskah. Submitted hardcopy of naskah and refleksi to mbak Asma. Went to ara. DL, ate gwen's dimsum (quite good and fulfilling). Planned to go to kashiwa but we ended up getting bakmi akiaw. Went back "home" to DM, took only 35 mins.
20 - DL, slept half of the day since im on my period (what even is daily structure), woke up in the evening, decided to start “the folk of the air” series. Binged the first book in one go, from 8 pm to 1 am lmaoo
21 - DL, finished the series at night. it’s nice but not as good as six of crows duology. bts comeback with dynamite!! :) i love them. its scary to think they are still progressing and going up and getting better stats. When will it all stop?
22 - discussion with dr natalia spKJ at 7.30 am, DL, drank matcha latte at starbucks airport hub (been a while! It doesnt taste quite good as i remembered) while backing up HD data at drive and some padi CBT (finished TO 3. After all this time, only to 3?!), felt a bit better after i went out, read a falling cohabitation again
23 - DL, danced to baepsae, slept in the afternoon (my body is too weak nowadays)
24 - DL, psychiatry closing, 1 pamela reif vid, 2P (CBT PADI)
25 - DL, made latar belakang for propeks nemo
26 - DL, 4P, rapat nemo
27 - DL, met up with atikah pupuy @ toska, tried yogurt and fruit, mac and cheese, vegan mentai rice and had dinner @ bakmi gm. mom somehow told (and allowed) me to go back home (it was 9 am and i was abt to stay over at atikah’s)
28 - DL, i dont feel like doing anything helppp, i know there’s stuff that im supposed to do but i cant bring myself to do it. a week will pass by, a month, and before you know it exam will arrive
29 - DL, ordered burgushi, i literally have no strength to go at static bike (can only do for a couple of mins), didnt rly do anything else bcs im in a slump nowadays
30 - its scary that the month is almost over again. my life just goes away like that but i still dont feel like doing anything, DL, tried to follow some dances on youtube to move my body
31 - DL, 2A, 4P
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